THE BREATH HOLDING AND THE VENTILATORY CARBON DIOXIDE
257
THE REMTIONSHIP BETWEEN THE BREWNG POINT OF BREATH HOLDING AND THE VENTILATORY RESPONSE TO CARBON DIOXIDE Pan's Pmaskevas Vasaou A thesis submitted in conformity with the requirements for the degree of Master of Science Graduate Department of Physiology University of Toronto O Copyright by Paris P. Vasiliou (1998)
Transcript of THE BREATH HOLDING AND THE VENTILATORY CARBON DIOXIDE
THE REMTIONSHIP BETWEEN THE B R E W N G POINT OF BREATH HOLDING AND THE VENTILATORY
RESPONSE TO CARBON DIOXIDE
Pan's Pmaskevas Vasaou
A thesis submitted in conformity with the requirements for the degree of Master of Science Graduate Department of Physiology University of Toronto
O Copyright by Paris P. Vasiliou (1998)
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The Rektionship Betweea the Breikiag Point of Breath Holding and the Ventilatory Response to Carbon Dioxide
Paris P. Vasilioo, M.Sc, 1997 Department of Physiology, University of Toronen
The first part ofthe study examined the relationship between the breakhg point of
breath holding and the ventilatory response to carbon dioxide. Seventeen subjects
perfomed a modined rebreathing test with prior hyperventilation at three iso-oxic levels
(PO, = 40, 80, 150 mmHg) and the chemorefiex parameters (Vb, Tp, Sp, Tc, Sc, and
m), and the dnve to breathe (V) were quantifieci. Subjects also perfiormed maximal
breath hoids under four conditions (TLC, TLCsw, FRC, FRCsw). No reiationships were
found between any of the chemorefiex (Vb, Tp, Sp, Tc, Sc, and MR) parneters and the
breath holding conditions (TLC, TLCsw, FRC, FRCsw). Males were found to have a
higher perïpheral threshold, and higher peripheral and centrai sensitivities than females
(p < 0.05). A strong relationship was found between the drive to breathe (V) and FRC (r
= 0.9377) and FRCsw (r = 0.952 1 ) breath holding conditions in male subjects. A weaker
relationship was found between the drive to breathe (V) and TLCsw (r = 0.7499) breath
holding condition in male subjects.
The second part of the study examineci the effect of swdowing on breaîh holding
Mie. Seventeen subjects perfonned maximai breath holds under four conditions (nC,
TLCsw, FRC, FRCsw). Fourteen of the seventeen subjects were found to have a
significant (p < 0.05) increase in breath hold thne with swallowing in both TLCsw and
FRCsw. The mean b r d hold t h e (SE) for TLC hcr& fiom 74.8 i 7.4 to 81.8 1: 8.4
seconds. Themean breath holdtime (SE)forFRC increased fkom 31.3 + 3.7 to 36.2 k5.1
seconds. This represents an increase of 9 % and 13% respdvely. A signincant @<O.OS)
decrease was dso found in the final end-tidal partial pressure of oxygen for both TLCsw
and FRcsw.
1 would like to thank my supervisor Dr. Robert C. Goode, for agreeing to take me on as a
graduate mident. 1 would also Iike to thank him for his encouragement and enthusiasrn. In
a worfd where many supervisun dont care about their students personal iife. Dr. Goode
acted not only as a supervisor towards me, but also as a friend, who took the time to
inquire not only about my academic Me but also about my personal and social life as well.
Always encouraging me to relax and have some fiin. He made my first couple of months in
Toronto more pleasant.
I would like to express my sincerea gratitude to my CO-supervisor Dr. James Dufin. I am
grateful for his advice, help, and patience and for continuously being available to answer
rny thousands of questions. Dr. Duffin's insight as scientists has been an inspiration to me.
Dr. D u f i has provided me with technical and research skills that will prove invaluable for
years to corne. Thank You.
For making the laboratory such a great place to work and leam. and for making my
graduate school expenence so memorable, I would like to thank my fiends and
coiieagues: Ricardo Maliba, Timothy Mertens, Robert Mertens, Rachel Rotenberg and Dr.
G. F. Tian.
In appreciation of their generously donated the , CO-operation, and wiiiingness to subrnit
to the conditions of the experiment without personal gain, I sincerely thank the subjects
who volunteered to be in this study.
A special thank you goes out to Dr. L'mberto De Boni, for his cheerful attitude and open
door poticy (even though the sign on the door said "'office hours at 4:00 p.m.").
Dr. De Boni was a h instrumental in the procurement of much needed fündiog.
I would especiaiiy like to thanlc Ravi Mohan for all his encouragement and support. I am
very grateful to have met and made such a fiend and colleague. t look forward to our
many friture colIaborations.
I would like to thank my brother Taso Vasiliou, for his continual, albeit quiet, support and
encouragement. One could not ask for a berter brother than him.
Finally, to my best fnend Marina Vasilatos, who has not only put up with my lunacy al1
these years, but dso has provided me with unconditional support and encouragement. of
which magnitude I c m only begin to express with my gratitude. I shall be forever thankttl
for her belief in my abilities. Your light shines brighter than al1 others.
1 ciedicnte thîs thesis to those zuho h u e Jurd the gmatest itnpact on rity life:
TABLE OF CONTENTS
Table of Contents ........................................................................................ iv
.. List of Abbreviatioas and Symbols ........... ...................................................vu
List of Figures ....................................................~................~..~-.............-...-.. x
List of Tabl es... ........................................................................................... xv
. . List of Appendices .................................................................................. xvu
I .O introduction ..............~............................................................................ 1
1.1 Control of Breatbg ...................................................................... -2
1 . 1 . 1 Peripheral Chemoreceptors and The Peripherai Chemorehx Response ...................................... .6
1.1.2 Centrai Chemoreceptors and The Central Chernoreflex Response ....................................... 10
1.1.3 Mathematical Mode1 of The Chernoreflex Control of Breathuig .................................... 12
1 -2 Examining the Ventilatory Response to Carbon Dioxide.. ............-.--. 16
.......................................................... 1 -2.1 Rebreatfüng Technique -16
1 -2.2 Modifieci Rebreathulg Technique ............................................. 1 8
1 -3 Historical Background of Breath Holding.. ................................. 1 9
1.5 Lung Volumes ................................................................................ 28
1 -7 Sdowing and Respiration ........................................................... - 3 5
1 -8 Breath Holding and Its Relatioaship to ................................ nie Ventilatory Response to Carbon Dioxide -38
2.0 Objectives of The Study ........................................................................ 42
3 -2 Apparatus ....................................................................................... -43
3.5 Data Analysis .................................................................................. -52
............................................................................ 3.6 Statistical Analysis 54
4.1 Gene ral ........................................................................................... 57
4.2 Basal Ventilation ............................................................................. -57
4.3 Iso-oxic Rebreathhg ....................................................................... -58
4.3.1 Peripheral Chernoreflex .......................................................... -71
4.3.2 Central Chernoreflex .............................................................. -73
4.4 Mathematicai Mode1 of the Chernoreflex Drive to Breathe ............... -74
4.5 Breath Holding ............................................................................... -90
4.6 Breath Holding Relationships ........................................................... -93
5.0 Discussion .......................................................................................... 116
5.1 Critique of Methods ....................................................................... 1 16
.............................................................. 5.1.1 Selection of Subjects 1 16
.................................................................. 5.1 -2 Rebreathing Tests 117
............................................................. 5.1.3 Breath Holding Tests 118
.................................................................... 5.2 Critique of Results 120
........................................................... . 5.2.1 1 Basal Ventilation 120
................................................. 5 .2.1.2 Peripheral Chemoreflex 121
..................................................... 5.2.1 -3 Central C hemoreflex 122
...................................................................... 5.2.2 Breath Holding 123
5.2.3 Breath Holding and Its Relationship to ..................... The Ventilatory Response to Carbon Dioxide ... 127
.................................................................. .............. 6.0 Conclusion.. .. 131
................................................................................................ References 132
.............................................................................................. Appendix I.. 141
Appendix II .............................................................................................. 144
............................................................................................. Appendbc III 147
............................................................................................. Appendix IV 149
..................................................................... .................. Appendix V .... 167
............................................................................................. Appendix VI 185
............................................................................................ Appendix W 186
Appendix Vm .......................................................................................... 221
GLOSSARY OF ABREVIATIONS AND SYMBOLS
GENERAL DEFiMTIONS
ASCII American Standard Code for Information Exchange
ATPS Arnbient Temperature and Pressure, Saturateci with water vapor
BTPS Body Temperslture, ambient Pressure, Saturated with water vapor
CSF Cerebral Spinal Fluid
Ws~nea Shortness of Breath
lx7 Hydrogen ion concentration
Hypercapnia A greater than n o d arteriai carbon dioxide tension
Hyperoxia A greater than nonaai amount of arterial oxygen tension
Hyperventilation Increased puLnonary ventilation in excess of metabolic requirements
Hypocapnia A less than normal amount of arterial carbon dioxide tension
Hypoxia A less than normal amount of arterial oxygen tension
[K7 Potassium ion wnceatration
-g Pressure in units of millimeters of mercury
PAR-Q Physical Activity Readiness Questionaire
PSR Puhonary Stretch Receptors
RRN Respiratory Related Neurons
BREATH HOLDING PARAMETERS
BHT Breath Hoid Tirne
FRCsw Functional Residuai Capacity with swallowing
TLCsw Total Lung Capacity with Swaiiowing
STATISTICAL NOTATIONS
ANOVA A d y s i s of Variance
n Number of Subjeds
P Robabiiity
p 0.05 Probabiiity of Sipnincant Diffaence
r Correlation Coefficient
SD Standard Mation
SE Standard Error
REBREATHlCNG PARAMEXERS
As Hypoxic shape parameter
Cs Asymptotic value of PQ
Sc Centrai-chemorefkx sensitivity to carbon dioxide (~=rnmHg-min')
s P Peripheral-chemoreflex sensitivity to carbon dionde&-mdg-&')
Tc Central-chernoreflex threshold for carbon dioxide (mrnHg)
TP Peripheral-chemoreff ex threshold for carbon dioxide (mmHg)
V Ventilation min-')
Vb Basai Ventilaton &min-')
Vc Centrai-chemoreflex ventilation component
VP Peripheral-chemordex ventilation component
LXJNG VOLUMES and CAPACITIES
ERV Expiratory Rese~e Volume (L)
FRC Funaionai Residuai Capacity (L)
IRV Inspiratory Resewe Volume (L)
VT Tidal Volume (L)
VC Vital Capacity (L)
RESPIRATORY VARIABLES
CO2 Carbon Dioxide
Ot Oxygen
P*% Partial Pressure of Carbon Dioxide in arterial b1ood
Pa(% Partial Pressure of Oxygen in artenai blood
Ph Partial Pressure of Carbon Dioxide in dveolar blood
p% Partial Pressure of Oxygen in alveolar blood
Pc@ Partial Pressure of Carbon Dioxide
POr Partial Pressure of Oxygen
P d 0 2 End-tidal Partial Pressure of Carbon Diorcide
PETQ End-tidal Partid Pressure of Oxygen
prC02 Partial Pressure of Inspireci Carbon Dioxide
PrOz Partiai Pressure of ulspired Oxygen
LIST OF FIGURES
A diagraxn of the controt of breathing by the chernordexes.
A general schematic showing some of the feedback control involveci in the controt of breathing.
Diagnun of the location of the carotid bodies in the neck.
nie dveoiar ventilation response to arteriaf carbon dioxide at several coastants levels of arterial oxygen mediated by the peripheral chemoreceptors.
Diagram of the location of the centrai chemoreceptors
The alveolar ventilatory response to arterial carbon dioxide mediated by the central chemoreceptors.
The chernoreflex control of breathing. Straight limes: the dveolar ventilation response to arterial carbon dioxide mediated by the central and peripherd chernoreflex
Mode1 of the control of breath holding and origui of sensation.
The &kt of inspited oxygen concentration @OZ) on breath holding tirne at two levels of inspireci volume, VC (vîtal Capacity) and FRC (Functiond Residual Capacity).
The 'Breaking point' curve d e m g the coexisting values of alveolar Pm and P m , at the breaking point of breath holding, starting 60m various States.
Compiled data nom iiterature showing the relationship between initial Iung volume and breath holding time with normoxia.
Effect of 1ung volume (expresseci as pa cent vital capacity) at the breakhg point of breath holding with 02 on tolerance for C a , expressing PAC& at brealririg point as per cent of PACa when initial volume was at vital capacity (Inaximum).
A block diagram illustrating the experimental set-up of the modified rebreathing technique.
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Trace diagnim illutrathg eqdiiration of &a dioxide ( m e ) [bottom row] in alveolar, arteriai and tissue compartmeuts? evidenced by a plateau on the chart recorder C a trace for subject 4, (papa speed 100 mmsec-').
Trace diagram during breath holding iliustrating initial and final end-tidal carbon dioxide (mmHg) [top row] and oxygen ( m g ) [bonom row] lweis for subject 4, (paper speed 100 mm-sec-').
Figure illutraihg the presence or absence of a ventilatory response to the test conditions appiied.
Mean i (SE) basai ventilation response for ail subjects (n=17) at dinerent oxygen partial pre~sufes. No sigmficam difference was found in the mean basai ventilation of all subjects at the different isooxic lwels (p > 0.05).
Mean f (SE) basal ventilation respoose for male subjects (n=7) subjects and fernale subjects @=IO) at different partial pressure of oxygen levels. No signifiant difference was fond in the mean basai ventilation of all subjects at the diierent iso-orcic levels (p > 0.05).
The time course of end-tidal partial pressure of oxygen at all three iso-oxic levels (40,80, 150 mmHg), for subject 6.
The time course of end-tidal partial pressure of carbon dioxide at dl three iso-oxic levels (40, 80, 150 mmHg), for subject 6.
Mean rate of rise (MR) (SE) of end-tidal partial pressure of carbon dioxideat ali three iso-oxic levels (40, 80, 150 mmtIg), for al subjects (n=17). A signifiani diffcrence was found in the mean metabolic rate of dl subjects between iso-oxic levels of 40 and 80 mmHg and between iso-oxic levels of 40 and 150 mmHg (p < 0.05).
Mean rate of nse (MR) * (SE) of end-tidal partial pressure of carbon dioxideat d three iso-oxk leve1s (40, 80, 150 rnmHg), for femde (n=IO) and male (n=7) subjects. A sisnifiant diffkrence was found in the mean metabolic rate of fernale subjects between iso-oxic levels of 40 and 80 mmHg and between iso-oxic Ieveis of 40 and 150 mmHg (p < 0.05).
The ventilatory response of subject 2 who has a Iow response (i-e. low senstMty) to carbon dioxide at variuos isosxic levels (40, 80, 150
The ventüatory response of subject 11 that has a high response (Le. low sensitivity) to carbon dioxide at variuos iso-oxic levels (40, 80, 150 mmHg).
4.7 Mean * (SE) peripheral chemordex threshold for ail subjezts (s17) and 76 at aii iso-oxic levels. A significmt diffefence was found h the mean peripheral chernoreflex threshold between iso-oxic leve1s of Pa = 40 and 80 mg, and between 40 and 150 mmHg @ < 0.05).
4.7a Mean f (SE) peripheral chernoreflex heshold for male subjects (n=7) and 77 femaie subjects (~10) at different partial pressure of oxygen levels. A sipïficant dïfkeace was found in the mean periphd chernoreflex threshold of fernale subjects between isu-oxic leveis of PQ = 40 and 80 mmHg, and between 40 and 150 mmHg @ < 0.05). A significant difference was found in the mean peripheral chemore$iex threshold between male and female subjects at an iso-oxic levei of 40 mmHg (p < 0.05).
4.8 Mean (SE) peripherd chemordex sensitivity for ail subjects (n=17) and 79 at aii isooxic levels. A sipifiaint Merence was found in the mean peripheral threshold of all subjects between iscwxic levels of 40 aad 80 mmHg and between isooxic lwels of 40 and 150 m d g (p < 0.05).
4.k Mean k (SE) peripheral chemoreflex sensitivity response for male subjects 80 (n=7) and f d e subjects ( ~ 1 0 ) at different p h a l pressure of oxygen levels. A signifimt diffience was found in the mean peripheral chemorefiex sensitivity of male and f d e subjects between isooxic ievels of P&= 40 and 80 mrnHg, and 40 and 150 mmHg (p < 0.05). ). A signincant Merence was found in the mean peripheral chemoreflex threshold between male and fernale subjects at an iso-oxic level of 40 mmHg @ < 0.05)-
4.9 Mean * (SE) central chemoreflex threshoid for aU subjects (n=17) and at 82 ail isosxic levels. No significant difference was found in the mean peripheral threshold of ail subjects between iso-oxic levels of 40, 80 and 150 mmHg (p > 0.05).
4.9a Mean t (SE) central chemoreflex threshold for male subjects (n=7) and 83 fernale subjects @=IO) at different partial pressure of oxygen levels. No sigdi~anf ciifference was found in the mean central chemorefiex tbreshold of male and female subjects between al1 iso-oxic levels (p > 0.05).
4.10 Mean i( SE) ceneal chemoreflex senstMty for al1 subjects (FI 7) and at 85 all iso-oxic levels. No significant difference was found in the mean peripheral threshold of ail subjects between aii iso-oxic iwels (p > 0.05).
xii
Mean t (SE) central chernoreflex threshold response for male subjects ( ~ 7 ) and female subjects @=IO) at différent partiai pressure of oxygen leveis No sigoincant diffe~erice was formd in the mean central chernordex threshold of male and f d e subjects between aii iso-oxic lwels (p c 0.05)- A signifiant dinerence was found in the mean peripheral chernoreflex threshoId between male and female subjects at an isooxic l d of80 mmHg @ < 0.05).
Mean i (SE) of the chernordex drive to breathe fcr all subjects (n.17). No sigdicant difference was found in the mean chernoreflex drive to breathe between aii breath holding conditions @ > 0.05).
Mean f (SE) of the drive to breathe for male subjects (n=7) and female subjects @=IO) at diffaent partial pressure of oxygen levels. A sisnificant difference was found in the mean central chernordex threshold of male and f i e subjezts b e e n aii iso-oxic levels (p < 0.05).
The mean breath hold times SE for ail subjects (n=17), under ï L C and TLCsw breath holding conditions. Mean breath hold t h e during TLC incregsed tiom 74.8 * 7.4 seconds without swdowing to 81.8 * 8.4 seconds with swaiiowing. A siwcant difference was fond in the mean increase of breath hold time with swaiiowing (p < 0.05).
The mean breath hold times * SE for male (n=7) and female (n=10) nibjects under TLC and TLCsw breath holding conditions. A signincant difference was found in the mean increase of breath hold time with swaiiowing in both male and f d e subjects (p < 0.05).
The mean breath hold times * SD for each subjects and dl subjects under FRC and FRCsw breath holding conditions. Mean breath hold &ne during FRC increased from 3 1.3 * 3.7 seconds without wdowing to 36.2 5 -9 seconds with swaiiowing. A significant difference was found in the rnean increase of bregth hold time with swallowing @ < 0.05).
The mean br& hold times * SE for d e (n=7) and fernale (&-!O) subjects under TLC and TLCsw breath holding conditions. A signincant Merence was found in the mean increase of breath hold time with swaiiowing in d e subjects (p < 0.05).
The mean Borg scale score * SE for all subjects (IF 16) obtained under all breath hold conditions (FRC, FRCsw, TLC, and TLCsw). Analysis using a two-way repeated measures -sis of variance, showed that the increase in the mean score with 3wd0whg was statisticaiiy significant (P < 0.05).
4.15 The relationship between Vb vs breath hold time (TLC and FRC) for ail 109 subjects (n=17). The corre1ation d c i e n t (r) for TLC and FRC was r = 0.5131 and r = 0.4522 respectively.
4.16 The relatiomhip between Tp vs breath hold time (TLC and FRC) for all 1 10 subjects (11-17). The mrrebtion coefficient (r) for TLC and FRC was r = 0.0787 and r = 0.0768 respectively.
4.17 The relationship between Sp vs breath hold time (TLC and FRC) for aü 11 1 subjects (n=17). The correlation coefficient (r) for TLC and FRC was r = 0.0141 and r = 0.241 7 respectively.
4.18 The relatiomhip between Tc vs breath hold time (TLC and FRC) for al1 1 12 subjects (1~17). The correlation coefficient (r) for TLC and FRC was r = 0.1 105 and r = 0.041 2 respectively.
4.19 The relationship between Sc vs breath hold time (TLC and FRC) for aü 113 abjects (n=17). The correlation coefficient (r) for TLC and FRC was r = 0.2452 and r = 0.0678respectively.
4.20 The relationship between MR vs breath hold t h e (TLC and FRC) for all 114 abjects ( ~ 1 7 ) . The correlation coefficient (r) for TLC and FRC was r = 0.0889 and r = 0.0346 respectively.
4.21 The relationship between the chernoreflex drive to breathe (V) vs breath 115 hold tune (TLC and FRC) for all subjects (n=17). The correlation coefficient (r) for TU: and FRC was r = 0.0787 r = 0.4624 respectively.
LiST OF TABLES
Table
4.1
4.2
4.3
4.4
4.5
4.6
4.7
4.8
Table of antbropometric data recordeci fkom each subject that participateci in the investigation
Mean basal ventiiation (Vb) (SE), m min-' for all subjects (1147). Basal ventilation rangeci fiom a low of 8.33 * 0.99 m min" at an isooxic level of 150 nmiHg to a high of 9.52 1.01 min-' at an isooxic level of 40 -i3
The mean rate of rise (MR) (SE) of end-tidal pamal pressure of carbon dioxide at ai l three iso-oxic levels (40, 80, 150 mmHg), for di subjects (n=17). Mean vafues for metabolic rate increased fiom 4.2 * O. 1mnHgmin-' at an isu-oxic level of 150 mmHg to 4.6 * O. 1 mnHg=mK1 at an iso-oxic level of 40 m d g .
The mean peripheral chemorefiex threshold (Tp) * (SE), for al1 subjects (n=17) and at all iso-oxic levels. The mean values for the peripherd threshold declined fiom 42 * 0.7 mmHg at an iso-oxic level of 1 50 mmHg to 40 0.8 mmHg at an iso-oxic level of 40 mrnHg-
The mean peripheral chemoreflex sensitivity (Sp) * (SE), for al1 subjects (1~17) and at ail iso-olric levels. The overall mean values for the peripheral seositivities increased fiom 1.8 * 0.5 ~-min-'-rnrnH~-' at an isooxic Ievel of 150 d g to 4.6 0.8 ~ - m h - ' - r n m ~ ~ ~ ' at an iso-oxic level of 40 rnmHg.
The mean centrai chemoreflex threshold (Tc) (SE), for al1 subjects (n=17) and at ali iso-oxic levels. Overall mean values for the central threshold declined f?om 48 1 -0 M g at an iso-oxic level of 1 50 mmHg to 47 1.6 mmHg at an iso-oxic level of 40 m d g .
The mean centrai chemoreflex sensitivity (Sc) * (SE), for all subjects and at aii iso-oxic levels. There was no trend in the mean Sc when compareci to ail iso-oxic levels.
The overall mean values for the chemoreflex drive to breathe (V) * (SE) for ail subjeni ( ~ 1 7 ) increased fiom 16.3 1.6 L-IIIK' with TLC to 16.9 * 1.7 L-IIIK' with TLCsw. The overd mean values for the chernoreflex drive to breathe (V) * (SE) for ail subjects ( ~ 1 7 ) Uiîreased f?om 15.9 I 2.2 min-' with FRC to 16.8 2.3 min-' with FRCsw
Page
4.9 The mean breath hold tunes k (SE) for each subjects and d subjects, under TLC and TLCsw breath holding conditions. Mean breath hold time miring TU: increased nom 74.8 * 7.4 seconds without swallowing to 8 1.8
8.4 seconds wah d o w i n g .
4.10 The mean breath hold times (SE) for each subjects and 1 subjezts, under FRC and FRCsw breath holding conditions. Mean breath hold time during FRC increascxi nom 3 1.3 * 3.7 seconds without swallowing to 36.2
5.1 m n d s with swallowing
4.1 1 The mean initial PH (SE), for d subjects (n=17), under ali breath hold conditions (FRC, FRCsw, TLC, and TLCsw)
4.12 The mean final P d * (SE), ), for a l i subjects (n=17), under all breath hold conditions (FRC, FRCsw, TLC, and TLCsw)
4.13 The mean initial P d & * (SE), for ail subjects (n=17), under aii breath hold conditions (FRC, FRCsw, TLC, and TLCsw)
4.14 The mean final P d G * (SE), ), for dl subjects (n=17), under aii breath hold conditions (FRC, FRCsw, TLC, and TLCsw)
4.15 The mean Borg sale score k SE for ali subjects (n=16) obtained under aii breath hold conditions (FRC, FRCsw, TLC, and TLCsw). The mean score I SE increased fiom 7.4 * 0.3 during TLC to 8.3 a 0.2 duMg TLCsw, and from 7.7 * 0.3 during FRC to 8.5 k 0.2 during FRCsw. Andysis using a one-way repeated measures andysis of variance, showed that the increase in the mean score with swdowing was statisbidy significant (P < 0.05).
4.16 Correlation between chemoreflex parameten and ail breath hold conditions (FRC, FRCsw, TLC, TLCsw) for d subjects (n=L 7) and in both males and fernales.
LIST OF APPENDICES
Apperacii'ce Page
Copy ofthe consent form 141
Copv of the physicai activity readiness questionnaire form (PAR-Q) 144
Copy of the Borg scale which measures physiological mess 147
Breath-by-breath plots of the ventilatory response to carbon dioxide 149 during the modifieci rebreathing tests a - Q iso-oxic (40, 80, 150 MnHg) rebreathing tevels (n = 1 7)
Breath-by-breath plots of end-tidal partiai pressure of oxygen during the 167 modified rebreathing tests at al1 is0i)xic (40, 80, 1 50 m d g ) rebreathing levels (n = 1 7)
Breath-by-breath plots of end-tidal partial pressure of carbon dioxide 185 during the modified rebreathing tests at al1 i m x i c (40, 80, 150 mmHg) rebreathing levels (n = 1 7)
Raw data obtained during the modified rebreathing tests at d l iso-oxic 203 (40,8û, 150 mmHg) rebreathing levels (n =17)
Raw data obtained d u ~ g the breath holding test at al1 breath holding 221 conditions (FRC, FRCsw, TLC, TLCsw) rebreathing levels (n = 1 7)
1.0 r n 0 D U r n O N
LMng organisms require the coutinuous co~lsumption of oxygen and expulsion of
carbon diorcide from th& system Deviation nom this path will inevitably lead to the
progressive disniption of biochemid, cellular and physiological processes thw together
are necessary for homeostatic Me.
Due to the importance of the respiratory system in living organisms, respiratory
control and reguiation has been imrestigated for many years by physioiogists. Aithough
respiratory control and regulation has been studied for neariy LOO years, there is mil
disagreement withh the respiratory physiology research cornmwity as to the ventilatory
responses during hypoxia and hypercapnia The fust objective of this investigation is to
use a modifieci rebreathhg technique (Read, 1967; Dufnn and McAvoy, 1988; Rapanos
and Dunin, 1997; Mohan and Dufnn, 1997) to characterire the ventilatory response to
carbon dioxide at various iso-oxic levels.
There are moments (Le., threat of entry of a noxious media into the respiratory
system), when it becornes necessary to deviate from the normal homeostatic respiratory
process (i.e., in an open 'nonnmic' and 'nomocapnic' environment) and operate in a
closed 'trypoxic' and 'hypercapnic' environment. By breath holding for short periods of
tirne, one can d e i y enter this mfàvorable environment. One can therefore consider breath
holding as a very important and vitai subsidiary h c t i o n of ventilation, a type of
respiratory regulation essential for sutvival avdable at a moment's notice.
Whiie breath holding in air becornes uncornfortable at fïrst, and will evenhially
h m e intolerable, it does not pose any r d threat to Me, as the resumption of respiration
q u i c e retums the homeostatic conditions. Unfortunately, the same can not be said of
breath holding undemater, where the consequences of severe hypoxia becorne
catastrophic and can lead to death via drowning (Craig, 1961, 1976). Several snidies have
shown that breath holding Mie can be increased by performiag Valsahta and Mailler
manoeuvres (Riggs et al., 1974; and Bartlett, 1977), while Aipher et al., 1977 showed that
perfiorming a mental task wuid also prolong breath hold the. However, these methods of
prolonging breath holding thne seem diflicuït and unnatual to perfonn during an
emergency. Therefore, a more simple and more natural method of prolonging breath
holding time during an emergency must be considered. The second objective of this
investigation is to examine the effectiveness of a swaiiowing motion wifl have on breath
holding tirne.
I.1 Contd of B r d i h g
The initiation and regdation of ventilation is controlled by special chernosensitive
organs that sense changes in body fluid composition (ie., carbon dioxide, oxygen, and pH).
Foremoa among these specialized chernosensory organs are the peripheral and central
chemoreceptors. These chemoreceptors increase ventilation when they are stimulated, and
this is ofien r e f e d to as the peripheral and centrai chernoreflex responses, respeaively
(Cunningham et al., 1986; Casey et al., 1987; hifnn and McAvoy, 1988; hifnr5 1990).
The chemoreflexes can be thought of as a control mechanisrn and cm be seen in Figure
1.1. A change in hydrogen ion concentratons expressed as the partial pressure of carbon
dioxide at both the peripheral and c d chemoreceptors, as weU as, a change in the
partial pressure of oxygen at the peripheral chemoreceptors are the stimuli for the
activation of the chemoreflexes. In addition to the per iphd and central chemoreflex
response, ventilation is also driven by a wakefûi stimulus (neural drive) as d e s c r i i by
Fink (1961). Fink showed tbat the wakefùi stimulus produces a base line vemilation d e d
the basai ventilation (Vb) when the chemoreflexes are not stimulateci.
The chemoreflex controi of breaîhing can be d e s c n i in tenns of a negative
feedback regulator txying to maintai. homeostasis. Should hydrogen ions CK] (the
regdateci variable) increase above either the peripheral or centrai chemoreflex threshold,
ventilation wouid aiso increase. This incregse in ventilation results in the excess [H7 being
washed away. The chemordexes includes the chemoreceptors (peripheral and/or central),
th& afiFerent comections to the respiratory neurons in the medulia, output to the
respiratory motor neurons, efferent wmections to the respiratory muscles and the
produced change in ventilation Figure 1.2). The feedback portion of the loop is formed by
the chemordexes, which moaitor levels of Pc@, M, and Pa (Figure 1.1). The fonvard
portion of the negative f d b a c k loop consists of the pulmonary and cardiovascular
systems and refers to the effects of chging pulmonary ventilation upon the stimuli sensed
by the chemoreceptors (Figure 1.1). Both the fonvard and feedback portions of the
negative feedback loop, as well as other modulatory factors, such as, core temperature,
and plasma By, combine to influence the ventilatory response. Although both
mechanisms are of importance to the respiratory respoose, it is usually the peripheral
chemorrceptors of the feedback loop that respond most rapidly to changes in blood gases.
The main parameters which characterize the chemorefiex response to a Stimulus
are tbreshold and SeLlSifMty. The threshold parameter can be defineci as the chemoreseptor
PC@ below which no change in ventilation is generated and above which ventilation
increases linearly with M e r increases in P a (Read, 1967; Casey et al., 1987).
r , Pulmonary and Cardiovascuiar
systems ,l
Peripheral and Central Chemoreflexes
FIGURE 1.1: A diagram of the control of breathing by the chemoreflexes. [Reproduced
with permission, fiom Dufnn (1990). Canadian Journal of Anaesthesia 37(8): 933-9421.
FIGURE 1.2: A general scheme showhg some of the feedback control involved in the
cmtrol of breathing.[ Repmduced with permission fkom, Dufnn et al., (1992).
Unpubiished work].
The sensitivity parameter can be defineci as the increase in ventilation due to an
increase in P C a at the chemorecepton and is measured by the dope of the response curve
above threshold. This parameter increases with decreasing Pa levek.
2.I.I P e h e m l C n e m ~ ~ e c e p t ~ ~ ~ and me Pmphemi Cnemorejù= Response
The peripheral chemoreceptors are located more peripherally in relation to the
respiratory centers than the central chemoreceptors. The peripheral chemorecepton are
composed of two distinct groups; the aortic bodies and the carotid bodies (Heymans and
Heymans, 1927; Kao, 1972; Lahiri 1991). However, t is the carotid bodies that play a
more signincant role in chemoreception in humans (Nye 1994). The carotid bodies are
spherical in shape and reside at the bifùrcation between the extemal and intemal branches
of the carotid artenes (Figure 1.3). The d d bodies are regarded as chemorecepton for
artenal blood, and are specifidy sensitive to aiterations in blood PB, PC@ and pH.
It has been shom that there are two types of ceiis Iocated in the carotid bodies.
Type 1 celis are regarded as chernoreceptive ceilq and Type 2 cells categorized as
sustentaailar or supporthg ceiis ( G o d e z et ai., 1995). It is the Type 1 ceiis that are
responsible for the sensitivity to low oxygen, high carbon dioxide, and pH changes. The
carotid body is innervated by the carotid sinus newe, the glossopharyngeal nerve, and by
the gangiiogiomedar nerve. Type 1 ceiis are innervateci by çensory neurons which may
innenatte more than one cell (Fidone and G o d e q 1986; Lahiri, 1991; Nye, 1994;
& d e z et al., 1995; Nattie, 1995).
Historically, the penphed chemorecepton have been wnsidered senson of
hypoxia with a secondary response to carbon dioxkie. This means that, if the partial
pressure of oxygen decnased to hypoxic levds and the partial pressure of carbon dioxide
decreased beIow the level of the peripherai and central thresholds for carbon dioxide, one
wouid see an increase in ventilation
Reœnt eyidence @ufnn and McAvoy, 1988; Dufnn 1990; Rapanos and Dufnn,
1997; Mohan and hrfnn. 1997) has suggested a different view. It may be preferable to
consider the peripherai chemoreceptors primariEy as hydrogen ion sensors, with hypoxh
playing a secondary role, to inmase the SeaSitivity of the chemoreceptor. @utnn, 1990;
Rapanos and hrffiiS 1997; Mohan and DU£@ 1997). In other words, one would not see
an iacrease in ventiiation if the partiai pressure of oxygen decreased to hypoxic leveis and
the partial pressure of carbon dioxide was decreased down below the level of the
peripheral and cenaal threshofds for carbon dioxide.
In contrast to oxygen, there appears to be a clear threshold for chemoreceptive
activity due to inmeashg Pcq or m, below which there is no stimulation of ventilation
(Figure 1.4). The increase in ventilation has k e n shown to be a hear response with a
PC@ threshold of approxhate1y 39 mmHg (Du& and McAvoy, 1988). The dope of this
response increases with a lowering of the Pa Neken and Smith, 1952; Cunningham et
al., 1986; Cunningham, 1987; Ddlh, 1990; Weil and Swaason, 1991). The effects of
hypoxia and inmeased PCa redt in a peripheral chemoreceptor response that is greater
than the sum of its two parts, which therefore has been called a multiplicative effect
(Ndson and SmÎth, 1952; Strange Pe$ersen and Vq'by-Christensen, 1975; Robbins, 1988;
Dufnn.
FIGURE 1.3: Frontal view of the right carotid artery bifùrcation in the rabbit. The
cornmon carotid artery (1) gives rise to the i n t e d (2) and extemal (3) airotid artenes.
The carotid body (4) is locateà on the &anal carotid artery close to the bifurcation.
Sensory fibers fiom the petrosal ganglion (5) mach the carotid body via the carotid sinus
neme (6). The superior ceivical ganglion (7) also innemates the b i d o n area,
including the motid body via the gangiiogiomenilar nerves (8). [Reproduced with
permission, nom G o d e z et al., 19%. Regdation of Breathing, pp. 3931.
FIGURE 1.4: The alveolar ventilation response to arterial carbon dioxide at several
constants levels of arterial oxygen mediated by the peripheral chanoreceptors.
[Reproduced with permission fkom, Ihfk (1990). Canadian Journal of Anaesthesia 37(8):
933-9421.
Lî.2 Cenarrl Cn-aos a d me Cenaal ~~ Responu The location of the central chemoreceptor area is based mainly on the work done
by Loeschcke (1965) and Mitchell (1%5). Initia&, the emphasis of the location of the
cmtral chemoreceptors was on the surnice of the dorsal medulla, but more recently
investigation has foaised on the Ventdateral MeduUary Shell (Loeschcke et al., 1973; .
Loeschcke et al., 1976; Bruce et al., 1987; Nattie, 1995). Many widespread locations of
chemoreceptive cells have been proposed, but not all areas and hypotheses agree.
However, it is generally agreed that there is a centrai chemoreceptive area in the bminstem
and that it drives ventilation when stllnulated by M or changes in PCG (Figure 1.5).
The central chemoreceptors are sunoundeci by extracellular BWd. The composition
of which is govemed by the cerebral spioal fluid (CSF), local blood flow, and local
metabolism The central chemorecepton cm be stimulated by hydrogen ion changes in the
CSF in a very short penod of the, but apparently not by changes of M in the blood.
This is due to the existence of a blood-brain bamer between the cerebral blood and the
bmb, which prevents the passage of hydrogen ions fkom blood to brah. When blood PCQ
rises, carbon dioxide diffiises tieely across the membrane into the CSF from cerebral blood
vessels, thereby £king hydrogen ions which stimulate the central chemorecepton to
increase ventilation proportionately. This pathway cm be seen in Equation 1.
Equation 1:
The hear Form of the Henderson-Hasselbalch equation (Equation 2) illustrates
the relationship between M and PCG and explains how an increase in carbon dioxide
would result in an increase in CSF m.
Eqnation 2: CK] = 24 Pca I @ C a l
Therefore, t is via the of the CSF by which the C a level of the blood
reguiates the ventilation. The increased arterial Pc@ also acts as a cerebral vasodilator
which in tum causes an increase in caebral blood Qow. The ensuing increase in ventilation
causes a redudon in blood Pc@ and therefore in the CSF as weU The M of the CSF
inmeases in pater proportions than thet of blood for a &en change in PCG, due to the
CSF's low buffering capacity (West. IWO).
The centrai chemorecepton act as hydrogen ion sensors, and Figure 1.6 @utnn
1990) shows the central chernoreflex response to an increase in PCG. There are numerous
complexities associated with the central chemoreflq which are due mainly to the
chemoreceptor location in the medulla and the existence of the previously mentioned
blood-brain barrier. Tirne course changes in PCQ at the central chemoreceptors in
relationship to changes in the arterial circulation also add to the complexity of the central
chemoreflexes. The reason that changes in PC& at the central chemoreceptors lag behind
those in arterial blood is, in part, due to the blood flow rate of 0.01 m l d in the brain
tissue. They are therefore slow to respond to changes in arterial carbon dioxide. It takes
approximately 5 minutes for the system to respond M y . The thne constant in this case can
be estimateci as the reciprocai of the blood perfusion per volume of chemoreceptor tissue
(Le., 1ûû seconds) @ufiin. 1990).
The ventilatory drive due to the chemoreflexes (paipheral andor centrai) and the
neural drive is illustrated in Figure 1.7 (Dufnn. 1990).
îhe chernoreflex drive to breathe has b e n guantined by Lloyd and Cunningham
(1963). These algebraic relations between the chemoreceptor stimuli and pulmonary
ventilation have been expanded to fit the current model of the chemoreflexes, as foUows:
Equation 3: V = Vc +Vp +Vb
where: v =totalvetlfilabm Vc = îhe central-chemorefiex verrtilaticm c~flzpo~len!: Vp = the peripherai-ctiemoreflex wntUo11 cornpotlent
Vb = the m o n compment independart of tbe chernordexes
The ventilatory response to carbon dioxide mediated by the central chernoreflex may be algebraicaliy modelled as foiiows:
Equation 4: Vc = Sc (PC@ - Tc)
where: Vc = ceutraidemorefiex canpcment of vertilatim ([PCa 2 Tc] and WC = O, if PC& < TC]) PC@ = end-tidal partial pressure of carbon dioxide Sc = centrai-ctiernoreflex sensitivity to carbon dioxide Tc = centrai-chemorefiex dmshold for carban dioxide
The ventilatory response to carbon dioxide mediated by the peripheral-chernoreflex and uicluding the hypoxic interaction may be algebraically modelled as foilows:
Equation 5: Vp = Sp (PCQ - Tp) where:
Vp = peripheral-cùemoreflex coqxment of v d k i o u ([PC&h Tp] and p p = O, if P C 4 < Tp]) PCOz = partial pressure of carbon dioxide Tp = peripheral-cùemoreflex threstiold for carbon dioxide. Sp = periphed-chemoreflex sadivity to carha dioxide
where: Sp = As
(Pa - Cd where:
P~=partialpressureofaxygeo As = an hypoxic shape parameter Cs =an asymptatic VaIueofpOZ
AU the parameters described in these equafions can be detennined by the program
of experiments desaibed in section 3.4 (Protocol) of the Methods section
FIGURE 1.5: Schematic representations of the topographical anatomy of the traditional
central chemorecptor locations on the ventrolateral meduila. The rostrd chernosensitive
area (M) is also d e d Mitchell's area. The caudal chernosensitive area (L) is also called
Loeschcke's area, and the intermediate area (S) is also cailed Schlaefke's area.
[Reproduced with permission, from Name (1995). Regdation of Breathing, pp. 4741.
FIGURE 1.6: The alveolar ventilation response to arterial carbon dioltide mediated by the
central chemoreceptors. meproduced with permission from, Duffn (19%). Canadian
J o d of ARaesthesia 37(8): 933-9421.
- pot=40
P4=m a
4
9
a
a
Basal Ventilation (Vb)
FIGURE 1.7: The chernoreflex control of breathing. Straight lines: the aiveolar
ventilation response to arterial carbon dioxîde mediated by the central and peripheral
chemorefiex. [Redrawm f k o ~ hifnn (1 9%), Personal notes].
2.2 Eramriring the Yen- RspacPe h Cmbon DùmcEc
Traditionaily, there have been several approaches to meanire the venthtory
response to carbon dioxide mediaiecl by the chemoreflexes. These include the steady-state
technique, the transient techni~ue, the ciynamïc end-tidal forcing technique, and the
rehathulg technique. The experhental technique used in these experirnents to measure
the ventilatory response to carôon dioxide mediateci by the chemoreflexes was the
rebreathg technique whïch was introduced by Read in 1967 and modified by Dutnn and
McAvoy (1988).
1-21 Rebreathing Technique
As opposed to other methods, the rebreathing technique induces hypercapnia in a
progressive maaner over several minutes. This elicits a graduai ventilatory response in
individuals due to the wntinuously changing PCG. The underlying p ~ c i p l e behind the
rebreathing technique is that a subject breathes in and out of a bag so that the P C Q in the
bag steadiiy rises due to the rnetaboIic C a production of the individual.
It was obmed that if a subject rebreathes nom a small bag cuntaining 7 % carbon
dioxide in oxygen, equiliirium between mixeci venous blood PC&, arterial blood PCa,
dveolar PCG, and the P C a in the rebreatbing bag is estabLished quickly. This meant that
any one of these compartments couid be monitored and be representative of the P C a in afi
the other regiom. Thus, which can easily measured during an m e n t allowed
the investigator to monitor the level of carbon dioxide in the brain tissue non-invasively.
Due to the large ansistomosis of arferial venous blood vesseh in the region of the central
chemoreceptors and the high metabolic rate, the blood in this region is commonly refmed
to as maed venous blood Measurment of this has been enabled by rebreathùig methods
designed by Collier (1956), Hackney et al (i958) and Campbell and Howeil(l962).
It has been shown that an eqdi'brium between the rebreathing bag, the lungs and
mixed venous blood develops w i t h 15 seconds of rebreathing. More importady, it was
noticed that if rebreatbing is continued, the end-tidai PC@ increases at a constant rate
which is dependent on the C a stores of the body and the metabolic production of CO2
(Fowie and Campbell, 1964). Since the storage of C a in the lung and the bag is negiigible
and independent of the ventilation, the C a provided a stimulus which acted as an
independent variable.
Read (1967) modifieci earlier methods of the rebreathing technique. A smaller bag
was used, dong with an initial carbon dioxide level close to that of mixed venous blood.
The subject breathed a hyperoxic and hypexcapnic gas mixture which allowed for quick
equilibration to mixed venous levels, while the high oxygen silenced the peripheral
chemorecepton in the process. When rebreathing is initiated with 7 % CO2 in a s m d bag,
negligiiale amounts of C a exchange between blood and gas during 4 minutes of
rebreathing. The rate of artenal P C ~ change is therefore vimially independent of the
ventilatory response. This is an important Eictor leading to a stable relation between
arterial P C a and brain tissue P C ~ .
The negiigible C a exchange during rebrathing can be explaineci by the P C ~
@'brium established between mixed venous blood, the lungs, and the rebreathing bag
ceases. The oxygen uptake coatinues and the volume of the gas in the lung is reduced
progressively. When a small bag is used, this progressive shrinkage concentrates the C a
already present in the lung and bag and C a =change fkom blood to gas remains
negligiïle despite a progressive rise of PC@ (Read and Leigh, 1967). The distinct
advantage tbis method has over other rebreatbing techniques is that it creates an open-
loop w h d y a linear relationship is established between end-tidal PC@ and brab tissue
Pca d e c t e d by the level of ventilation mead and Leigh, 1967).
t 2.2 Mortiyed Rebreallting Technique
The Read reôreatbing techaique (1967) was modined by biffin and McAvoy
(1988) in two ways. It has been modified to permit the breath-by-breath measurement of
the ventilatory responses to hypoxia and hypercapnia and to d o w for the detection of
carbon dioxide threshoids for both the peripheral and centrai chemoreflexes (Figure I .7).
Firstly, the modified rebreathing test is commenced only after a short period of
hyperventüation, in order to lower the body stores of carbon dioxide. This is done so that
the equiiibration and subsequent rebreathing commences at a carbon dioxide tension below
that of the peripheral chernoreflex threshold. As a result, both the peripheral and central
chemordex t hresholds are measured.
Secondly, an oxygen feedback system maintains isooxic conditions for a desired
level of 02 throughout the testing period. Therefore, this method has the ability to
determine the effects of hypoxia on the sensitivity and threshold of the peripheral
chemordex fesponse to &on dioxide as wel as, the ventilatory response to hypolea
independent of carbon dioxide.
Not only is tbis method fast which aliows for repeated observations, it aiso
overcomes the issue ofdymmic changes in cerebrai biood flow. Mer equiiibration at the
mixed venous Ievei, carbon dioxide increases without an increase in ventilation untii the
peripheral chernoreflex theshold (Tp) is reached. Above this threshold, ventilation
ïncreases lineariy with carbon dioxide mtii the centrai chemoreflex threshold (Tc) is
reached Above the central threshold, veotüation increases Iinearty with carbon dioxide but
at an increased rate.
The dope of ventilation versus carbon diorcide between the two thresholds
(penpheral and centrai) is taken as the sensitivity of the peripherd chemoreflex (Sp)
ventilatory response to carbon dioxide- The dope of ventilation versus carbon dioxïde
above the second threshold (central) is taken as the sensitivity of the combined (Sp + Sc)
peripheral and central chemoreflex v d a t o r y response to &on dioxide.
1.3 H i i Baekgmund of Breath Holding
Respiratory control and regulation has been investigated by many of the early
respiratory physiologists, and a substantîal amount of this work involveci the study of
breath holding It is due mainly to this early work that many of the principles that govern
the control of breath holding have been established.
It is known that the maximum duration of breath holding varies fiom subject to
subject, wen among members of the same famiy (Grassi et al., 1994). These variations of
maximum breath hold times are due in part to weil deked factors These include;
psychological factors (Schneider, 1930; Eügg et al., 1974; Bartiett, 1977; Blanton et al.,
1983; Aipher et al., 1986), and at least four interdependent physiological variables: initial
iung volume, pH, P a , and IQ (Fowleq 1954; Chapin, 1955; MitEioefer, 1959; Godney
and Campbell., 1968).
These interdependeut physiological variables combine to f o m the chernoreflex
drive to breathe, which as mentioned, was guantined by Lloyd and Cunningham (1963),
and were expauded (Equation 3) to fit the m e n t mode1 of the chemoreflexes
Equation 3: V = Vc +Vp +Vb
Early work by Hiif and Flack (1908) and Douglas and Haldane (1 909) showed that
the prevenfion of hypoxia ïncreased the duration of breath holding. Klocke and Rahn
(1959) aiso showed that one can ïncreme breath hold duration by hyperventilation prior to
breath holding, to lower the initial partial pressure of carbon dionde. Likewise, Godfiey
and Campbeii (1 968) showed that elevation of the initiai partial pressure of carbon dioxide
shortened breath holding duration.
An inverse relationship between oxygen and carbon dioxide was s h o w to exist by
Douglas and Haldane (1909) and by Otis Rahn and Fenn (1948). Muxworthy ( 195 1)
showed that there was a hear relationship between breath holding duration and initiai
lung volumes, concluding that static lung volumes and their storage capacity played a role
in deteminhg the duration of breath holding.
In 1959, Mithoefer mggesteci a mode1 for the control of breath holding from the
early evidence that, the partial pressure of carbon dioxide and oxygen, dong with static
lung volumes interact in some rnanner to determine breath holding duration. It seems
logical that chernical stimuli and storage capacity should interact in a marner that would
detennine the breath holding duration. However, if we go back to the work done by W
and Flack (1908). we can clearly see that there is no simple explanation for the dwation of
breath holding in terms of PCG, Pa, and h g volumes- W and Flack (1908)
demonstrateci this by having their subjects rebreathe h m a bag ofexpired air for a period
of time fk greater than they wuld hold their break This was accomplished despite the
fact that at the breaking point of rebreathiog, the P a was fkr higher and the Pa fu
lower than at the breaking point of breath holding. Fowier (1954) also demonstrateci that,
ifsubjects breathed a few breaths of a gas which did not alter their blood gas levels, breath
holding was able to resume and that this process wuid be repeated several times
coI1SeCUtnrely despite increasing leveh of P C ~ and decreasing levels of Pa. This led
Fowler to suggest that the vagus nerve played a role in this phenornenon. More recently,
Hume et ai. (1995) reported that relieffrom the distress of breath holding can be obtained
by halfa breath cycle, either by expiration or inspiration They showed that although relief
was greatest during inspiration, there was stiU a signifiant relief from expiration. Rume et
al., (1995) suggest thaî this relief from the distress of breath holding is due to vagal input
via pulmonary saetch recepton (PSR).
Work by Fowler (1954) lead to the conclusion that mechanical factors in addition
to the chemicai and lung volume (storage) mors are involved in deterrnining the duration
of breath holding. Further evidence by Go- and Campbel (1968) and Godney,
Edwards and WarreU (1969) showed that it was possible to breath hold at a higher partial
pressure of carbon dioxîde and srniiller lung volumes than existai at the breaking points of
previous breath holds. This suggested that there must be more than the inter-relationship
between the partial pressures of carbon dioxïde and oxygen and lung volumes in
detemirhg br& holding duration.
A cormon characteristic fature desaied by respiratory physiologists during
breath holding was the imroluntary contractions of respiratoory muscles that occur as one
approaches the breakhg point of breath holding. Fowler (1954) beiiwed that the
unpleasant sensations which occurred during breath holding were due to the involuntary
musailsr contractions, and were mediated by chemicai h o r s . This concept was
supported by evidence h m Agostoni (1963) and by Campbell et al. (1967).
Agostoni (1963) showed that as breath holding proceedeû, involuntary
contractions of respiratory muscles took place. These spontaneous rhyihmic contractions
begm shortly &er the beginning of breath holding and increase in amplitude and frequency
until the breaking point. (Agostoni, 1963; Whitelaw et al., 1987). Diaphragmatic
electrographic recordings by Agostoni (1 963) showed that the onset of this involuntary
muscuiar activity was related to the parthi pressure of carbon dioxide and not to lung
volume.
Further evidence supporthg Fowler's concept that the inter-relationship of
chemicai, storage, and mechanid factors were irmolved in determinhg breath hold
durabon came from Guz et al. (1966) and Campbell et ai. (1967). Guz et al. (1966)
demonstrateci that the discomfon of breath holding could be attenuated thereby increasing
the breath holding duration despite worsenllig blwd gas levels. Guz et al. (1966)
accomplished this by blocking puimonary afferents via the (Vagus) and
(Olossopharyagd) cranial oerves. Campbell et al. (1967) showed that total padysis of
respiratory musculature by curare ( i coMaous human subjects) increased breatii holding
duration even at highly elevated partial pressures of carbon dioxide.
Godfiey and Campbell (1968) stated that any mode4 on the control of breath
holding must be compatible with the following SEperimental observations made over the
years:
i) Breath holding time is inversely proportional to the partial pressure of carbon dioxide.
5) The pamal pressun of carbon dioxïde rises linearty throughout the breath hold.
Üi) Breath holding time is shortened by hypoxk
iv) For any *en level of P a and Pa, breath holding time is direaly proportional to
lmg volume.
V) At the breaking point of breath holding, a single breath of gas wdi enable the breath
hold to be resumed, despite a higher PCQ, and a smaller lung volume.
vi) Total paralysis by curarisation removes the unpleasmt sensation occurred during
breath holding and prolongs the breath holding Mie.
This led to the development of a mode1 (Figure 1.8) by Go- and Campbell
(1968) to explain the control of breath holding. Each square in the diagram (Figure 1.8)
represents a hc t ion generator, each block acting in two ways. It receives one or more
input signals, modifies them (Le., addition, multiplication) and then provides an output
signal. If one follows Figure 1.8 nom left to right, we see that the increased chernical drive
(in this case PCQ) during breath holding acts in conjunction with the non-chernical drive
and sumrnates to produce a central, driving-stimulus build-up. This in tum, creates a drive
for ventilation which is passed on to the motor pathways of the brain and spinal cord and
thus drives the lower motor neurons goveming the respiratory muscles. N o d y , these
muscles would contract; however, due to the breath holding, the decrease in lung volume
is prevented, which r d t s in a disproportion developing b ~ e e n the tension in the
respiratory muscles and the motor &kt produced. In tum, muscle, tendon and joint
receptors are stimulated, which produces a . output signal into the sensory pathway. nie
effect of lung volume in this modd is shown to be acting at the level of the muscle and
joint receptors, CL^ peripherally). M g r and Campbell (1968) believed that the
responses to changes in lung volume acts at the Ievel of muscle-joint receptors in the chest
WaIl*
There are two main types of respiratory sensations; respiratory proprioception and
respiratory discornfort (Shea et al., 1995). These sensations arise ffom several afferent
sources wbich include: puimonary stretch receptors (PSR), lower and upper airway
reoeptors, and thoracic wall receptors. Respiratory proprioception is the sense of the
mechanical motion, displacements, position, and forces, whether these sensations arise
Eom somatic receptors or receptors in the lungs and other visera. Respiratory discornfort
is often lumped under the single terrn "dyspnea" (Shea et al., 1995).
hiring the course of n o d respiration, there are many structures that corne into
play and move together. These structures inchde: the rib cage, spine, skin, airways, lungs,
abdominal contents, and muscles of the head, ne& and chest (Shea et ai., 1995). Studies
have shown wddicombe, 198 1 ; Sant7Ambrogio, 1982) that there are a variety of viscerai
mechanoreceptor fiom the airway and lungs that discharge in response to movement and
pressures in the nomial range of breathing. Other studies m o n 1981) have shown that
muscle, tendon and joint receptors are abundant in somatic respiratory structures. Studies
have also shown (Bolser et al., 1989; Coffey et al., 1971; Davenport et ai., 1985;
Gandevia et al., 1989) that the afferents from the muscle, tendon and joint recepton
termiaate on motor centers throughout the nervous system: spine, brainstem, cerebeiium
and cortex These afférents play an important role in limb motion proprioception
(McCloskey, 1978), and therefore, these afférents are also important in respiratory
proprioception
Go- and Campbell (1968) showed that when al1 the known chernical, lung
volume, a d o r mechZrnical f'actors are considered, there still remaineci a large non-
cheinicai -or which could be abolished by hmg or chest movement. They beiïeved that
this f ~ o r is most iikely due to an inherent build-up of cenaal excitation witlnn the central
newous system. This build-up is removed with each respiratory cycle through information
carried by the vagus nerve but not by the Heting-Breuer reflexes. Similar suggestions
have been made by Fowler (1954) and Domhorst (1963), who suggested that there is a
pool of respiratory netuons which is dischargeci by each breaîhing cyde.
Godfiey's and Campt?eli7s (1968) mode1 of the control of breath holding
incorporates the various breath holding factors into one of three groups:
1) peripheral and centrai chemosensory response to change in P C 9 (Le., chernical stimuli).
2) length-tension (volume-pressure) inappropriateness (Le., lung volume stimuli).
3) a hypothetical "central excitatory aate" that builds up duMg breath holding and is
discharged when respiratory drive inmeases to a tolerance thres hold (i. e., mechanical
stimuli).
Mithoefer (1965) defined the breaking point of breath holding as the voluntary
termination in response to the development of a net stimulus too strong to be tiirther
resisted by a voluntary effort. Nthough the definition is accurate in a qualitative sense, it
FdïlS to define its supra-threshold strength in a quantitative manner. The term 'Breaking
Point' embodies no partïcdar dimension; it can be expressed in tenns of any appropriate
parameter under obmation, with the most common being time and alveolar gas tension.
As stated previously, the breakîng point is brought on by the interaction of variables,
which may be classineci as 'chernical', 'storage', 'mechaaical', and 'psychologicai' factors.
2.4 mernical SrUnrrlr
The chernid stimuli which interact to b ~ g about the end of breath holding are
due to changes in the partiai pressure of earbon dioxÏde (PCG), the partial pressure of
oxygen (iQ) and to an increase in the concentraton of m. These variables which also
interact with lung volumes (static and dynamîc) are determined mainly by: i) the gas
composition of the Uispired breath (Le., P a and Pa), ü) the metabolic rate (i-e., the rate
of C 9 rise) and üi) the level of carbon dioxide stores in the body and the b d h g
capacity for carbon dioxide at the onset of breath holding. The effects of inspired oxygen
concentration on breath holding t h e nom two studies are shown in Figures 1.9
(Mïthoefer, 1965) and 1-10 (NuM, 1993).
Engel et al. (1946) had their subjects perform breath holds at vital capacity, while
Otis et al (1948) had their subjects perform breath holds at bctional residual capacity at
various initial Ievels of oxygen, The effect of oxygen in detennining the breaking point of
breath holding is clearly seen in Figure 1.9. At vital capacity, the breath holding t h e is
increased by 75 per cent when breath holding is begun with LOO % oxygen as compared to
breath holding in room air. This effect is consistent with that of other studies (Friedman,
1945; Hill and FIack, 1908; Robard, 1947), which showed that breath holding Mie can be
increased by 50 to 80 %, by breath holding at higher levels of inspird oxygen. The effect
was greatest in d e r lung volumes and breath holding time increased threefold.
Although there have not been any systematic studies on the interaction of carbon
dioxide stores or metabolic rate in determinhg the breakhg point of breath holding, sorne
conclusions can be drawn upon anaiysis of published data.
pca 7 Motor Respirato~ Muscle/Joint Sensory 1 Pathways Muscles Receptors Pathways
40 f(t)
A
9
Ill- *
Sensation
Chernical Factors
Centrd L n g Excitatory Volume
State
FIGURE 1.8: Mode1 of the control of breath holding and origin of sensation.
~eproduced wiîh pemiission fiom G o c k y and Campbell, 19681.
Klocke and Raho (1959) showed that breath holding time increased when the
body's initial stores of carbon dioxide were l o w d with prior hypewenfilation and Hiu
and FIack (1908) showed that hyperventilation with oxygen for two minutes increases
breath holding time &y about threef01d. From these studies the broken line seen in Figure
1.9 is constructed. It shows the theoreticai breath hold tirne with two minutes of prior
hypemedation at various lewels of inspired oxygen concentrations. Figure I - 1 O (NUM
1993) also shows the results of breath holding with normal levels of oxygen as well as
with increasecî and decreased leveis of inspireci oxygen.
I.5 lwng volrunes
B reath ho I ding time is directly proportional to the initial lung volume for a given
mixture of inspirecl gas, other factors being constant (Mithoefer et al., 1953; Vacca, 1946).
This relationship between initial lung volume and breath hold tirne is a direct result of the
fact that a restriction in lung volume is an independent ventilatory stimulus which interacts
with the chernical stimuli Osrpoxia and hypercapnia) and detemines the breaking point.
This relationslip is cleariy demonstrated in Figure 1. i 1 (Mithoefer, 1965), which is a
composition of data tiom severai studies on the relationship between breath holding tune
and initial lung volume. 11 is evident fiom Figure 1.1 1 that the longest breath holding tirnes
are achieved at vital qaci ty and the shortest breath holding times when the initial Iung
volume is at residiiril volume. In fact, at b c t i o d residuai capacity, the breath hold t h e
is ody 40 per cent as long as it is at vitai capacîty and only 24 per cent of vital capacity at
residual volume. The broken line in Figure 1.1 1 indicates hypotheticaily what the breath
FIGURE 1.9: Wect of inspirai oxygen concentration (Pa) on breath holding time at
two levels of inspired vohune, VC Capacity) and FRC (Funaionai Residuai
Capacity). Broken line indicates predicted elevation of VC auve that would be produceci
by two minutes of iiypervdation. [ Reproduced with permission from Mithder, l965].
Alveolar PCO, (rnmHg) O 50 100 150 200
\ \ Normal \ alveolar
point After
30 % oxygen AAer breathing
breathing 15 % oxygen
I A fter hyperventilation
I I
O 5 10 15 20 25 30 Alveolar PO, (kPa)
FIGURE 1.10: The 'Breakhg point' w e defines the coexisting values of alveolar Pa
and P C 9 , at the breakhg point of breath holding, starting fiom various States. The normal
dveolar point is shown (P9 100 mmHg: P C 9 40 m e ) and the w e d a m w shows the
changes in alveolar gas tensions which occur during breath holding. [Redrawn %om Nuna,
19931.
INITIAL LUNG VOLUME - L,
FIGURE 1.11: Compiled data nom Merature showing the relationship between initial
lung volume and breath holding tirne when iaspired gas is air. Number of obsemdons
indicated at each point. [Reproduced with permission fiom Mithoefe, 19651.
hold time would be at a lung volume of zero (8 seconds). This corresponds to the time for
circulation h m the lungs to the brain
A relationship exists between nnal Iung volume and the p d pressure of dveolar
carbon dioxide (P-) at the breakhg point of breath holding (Mithoder, 1959). This
relationship is i11ustrated in Figue 1.12 (Mithoefer, 1965). The graph shows that the
to!erance for hypercapnia diminishes with decreasing lung volume. There are several
reasons for the decrease in lung volume. The main one being that there is a continuous
uptake of oxygen by the body and a decrease in carbon dioxide exchange in the alveoli.
Another eEect of lung volume and its change, is mediated by afEerents arising fiom
the chest waIi and the lungs itself(Godf?ey and CampbeU, 1968). This is explained by the
fact that the 'distress' leading to the termination of breath holding is due to the frustration
of the r e k motor response from the pulrnonary afférents. The motor response consists of
an involuntary contraction of the respiratory muscles, which bas been found to increase
progressively during breath holding (Agostoni, 1963). These involuntary contractions
should produce movement which are detected by tendon and joint recepton in the chest
wall itself (Godfiey and Campbell, 1968). However, because movement is prevented
during breath holding, an 'happropriateness' results between the respiratory muscle
activity and the lack of movement. This leads to an inherent build-up of centrai excitation
within the central newous system and to the uncornfortable sensations felt during breath
holding.
FIGURE 1.12: Effect of lung volume (expressed as per cent vital capacity) at the
breaking point of breath holding with 02 on tolerance for C a , expressing Pko2 at
breakhg point as per cent of PA^+ when initial volume was at vital capacity (maximum)
[Reproduced with permission fiom Mithoefer, 19651.
z 3 100- s œ
X
2 90- 8 I
f 8 0 LU
- FINAL VOLUME-%K.
O 20 40 60 80
Agostoni (1963) d e s c n i the phases of br& holdmg based on his work on
respiratory muscle iictiviry, as reflected by electromyognun and iritrapleural pressure
changes. He d e s c n i two phases: an initial quiescent phase of voluntary inspiratory
muscle inactMty, followed by a second phase of involuntary efforts against a ctosed giottis
(Le., involuntary muscle actbity).
Psychological factors have an influence on breath holding duration Udortunately,
the study of psychologicai factors affecting breath holding time has d e r e d from a lack of
observations and an experimentai model. W and mack (1908) observeci that "one of the
important factors in detennuiing breath holding duration seems to be that of pluck and
resolution to withstand discodort. This varies in the same individual according to the
state of their nervous system".
Later studies (Riggs et al., 1974; Alpher et al., 1977; Bartlett, 1977) have
demonstrated the important influence of psychological factors on breath holding duration. -4
These studies examined the effects of perfomiing some type of relieving manoeuvre in
order to elicit a prolonged breath hold duration. Riggs et al. (1974) had their subjects
perfonn Muelier manomes (inspiratory efforts against glottis). They found an inaease
in breath hold t h e and attributed this to Serents input âom the inspiratory muscles.
However, Bartlett (1977) found that perfomiing a Valsaiva manoeuvre was e@y as
efféctive as the M d e r manoeuvre in prolonghg breath holding time. Bartlett proposed
that these resuits are consistent with the theory that stimulation of pulmooary stretch
receptors in the extrathoracic trachea must account for the increase in breath hold the.
Bardett (1977) also had a control manoeuvre in his study, in which subjects
squeezeci a rubber bulb. Bartlett found that Worming the bulb squeezing manoeuvre was
equally as &&e as the Valsalva and M d e r manoeuvres in prolonging breath holding.
These findings showed that a manoeuvre that does not imroive the respiratory system c m
proiong breath hold tirne-
Aipher et al. (1977) also demonstrated that a manoeuvre that does not involve the
respiratory system can prolong breath holding tirne. They demonstrated that subjects could
prolong their breath holding performance using a physical task (e.g., rubber bulb squeeze),
a mental task (e.g., mental arithmetic) or a combination of both.
These studies clearly indicate the importance of psychological factors during
breath holding. It also establishes the fact that there is more than one type of psychological
factor involveci. There is a cognitive factor and a psychomotor factor.
One drawback that is seen with the studies mentioned above is that al1 breath holds
were performed at hctional residual capacity (FRC) ody. It is strongiy felt that these
manoeuvres should have been done over the tiill range of iung volumes to mly determine
the efféctiveness of these manoeuvres in prolonging breath holding, and to what extent the
psychological factor plays a role in breath holding.
I.7Swallowing and Respiration
The human oropharypx has muitiple hctions hcluding voice production,
dowing, and respiration. These activities mua be coordinated so uiat mutual
compromise does not occuf.
Swdowing is a complm intermittent behavior involving not ody the inhiion of
respiration and closure of the larynx, but a cornplex movement of the pharym< and
epigiottis as well, and therefore invohes all the accessory muscles of breathuig in this
region SwaUowhg therefore nquires modiEiC8fion of the normal respiratory rhythm, in
which the nomai fbnction depends not oniy on pattemesi a* within the swallowing
system, but with the respiratory system as well.
Inhi ion of respiration tends to ocaa predominady during the expiratory phase
of the respiratory cycle in hunaos. It occurs 89 % of the time during the expiratory phase
of the respiratory cycle when the bolus swallowed is a solid and 71 % of the t h e when the
bolus is a Liquid. It has also been shown that an apneic pause of 0.5-3 -5 seconds (average
1.5 seconds) accorqanies swallowuig in adult humans (Dowty, 1968). As a consequence,
swdowing results in a specitic modincation of the associated respiratory pattern.
(Preiksaitis et al., 1992). Studies have also indicated that the respiratory pattem associated
with swallowing is also modulated by the volume of the swallowed bolus (Preiksaitis et
al., 1992).
Clinid and experimental evidence also supports the existence of
neurophysiological, structurai, and hnctional interdependenœ between the upper
respiratory and digestive systerns. The intermingiing of respiratory-related, swaiiowing-
related, and vocalization related ceUs both in the dorsal and ventrai medulla wodd suggest
that some neurons may be involved in combinations of these diierent aaMties (Larson et
al., 1994). Although the exact rnechanisms are not understood, respiration is probably
inhiiited by a command fiom the swallowing central pattem grnerator (McFariand et al.,
1994).
Of 63 fiilly e e d respiratory related neurons @RN's), 40 (63 %) modulated
their actMty wit& vocalizaton, and 3 (5 %) modulateci their activity with swallowing.
Thirteen (21 %) of the RRETs modulated their actMty with vocalization, respiration, and
swallowing. Seven (13 %) of the RRETs were moduked oniy with respiration (Larson et
ai., 1994). However, the basic phyaologicai relationship between breathg and
swallowing still remains p0ori.y understood (M&n et al., 1994).
SwaUowhg beghs with signais carried in the vagus and gfossophaxyngeal n e m s
to the micleus of the solitary tract and to the neighbo~g retiCuIar formation, a region that
coordhates swallowing @est and Taylor, 199 1).
Io general, swdowing invoives the cumbined action of 50 paired muscles,
supporthg bones and cartilage7 and virtudly all levels of the central nervous system
(Cunningham et al., 1991). Swallowuig can be divideci into three stages: 1) the voluntary
stage, which initiates the swaiiowhg process, 2) the pharyngeal stage, which is involuntary
and constitutes the passage of a bolus through the pharynx into the esophagus, and 3) the
esophageal stage, which is another involuntary phase that promotes the passage of a bolus
h m the pharymc to the stomach (Ganong, 1995).
In particular, swallowing involves the movement of the larynx, pharynx and
trachea in response to sigaals from theû associateci afferent nerve fibers. Specifically,
afferents nom the trigemird nerve, fâcial newe, glossopharyngeal, and hypoglossal nerve.
Swallowing a h causes traasient pressure fluctuations within the thoracic cavity, and
depending on the size of the bolus swallowed, t cm also cause abdominal, thoracic,
shoulder, and head movement.
The pharyngeai stage of swdowing is a reflex act requiring the Uaegrated action
of the respiratory and Swallowing centers. In man, the mon semitive areas for initiating
the d o w i n g r d e x are the anterior and posterior pillers and the posterior pharynx
These areas are inervated by the glossopharyngeal and vagus nenes (Wang et al., 1964).
There have been several investigations (Heath et al., 1968; Godfky and Campbeü,
1969) which report that voluntary swdowing movements increase breath holding times.
However, these authors did not give any references for this statement and a search of the
literature yielded ody one reference (Dowty, 1968) concemhg the effects of swallowing
an and increased breath hold time. Dowty (1968) quoted another author (Meltzer, 1883),
who claimed that "swdiowing generdy had an inhibitory effeçt on other activities, so that
it codd prolong breath holding by 10-15 seconds." Meltzer (1883) also suggested that
swailowing can inhibit labor pains, hiccups and pede erections. Mortunately, the study
was not scientincaiiy valid as the author served as both the investigator and the ody
subject. Fdy, Huang et al. (1981) examined the effects of wallowing or the Muiier
maneuver on heart rate during breath holding for 30 seconds out of water and during face
immersion Although Huang et al. 198 1, found that the heart rate was not decreased with
swallowing or the Muller maneuver, no mention was made about its effects upon breath
holding Mie.
The relationsbip between the limits of breath holding and the ventilatory response
to hypoxia and hypercapnia has been reviewed by Feiner et al. (1995). In this review, they
report that both the hypoxic ventilatory response and the hypercapaic ventilatory response
infiuence breath holding the, and suggest that, the reWe importance of the hypoxic
ventdatory response and hypercapnic ventilatory response has not yet beea established.
Mani& et ai. (1981) found that Iapauese peari divers (Am) have a blunted hypoxic
ventdatory response and Bjurstrom and Schane (1987) reporteci a similar blunted hypoxic
ventilatory responsê in synchronized Swimmers. Recemly Feiner et al. (1995) reporteci that
the hypoxïc ventiiatory response was a predctor of breath holding performance in a
n o r d population
Blunted hypercapnic ventilatory responses have also been observed. Both Masuda
et ai. (1982) and Song et ai. (1963) observed a Lowered hypercapnic ventilatory responses
in other groups of Ama Schaefer (1965) found that submarine escape tower trainers also
arh'bited a blunted hypercapnic ventilatory responses. Lower hypercapnic ventilatory
respoRSeS have also been found in underwater hockey playen (Davis et al., 1987)- Royal
Navy divers (Florio et al., 1979) and in elite breath hold divers (Grassi et ai., 1994).
However, rnost of these midies have measured ventilatory responses and not
breath holding abÏÏ (Flono et al., 1979; Masuda et al., 198 1; Maaida et ai., 1982;
Schaefer, 1965; Song et al., 1963). In other studies, bot& the hypoxic ventilatory response
and hypercapnic ventilatory response were investigated in relation to breath holding ability
(Bjurstrom and Schoene, 1987; Davis et al., 1987; Feiner et ai., 1995; Grassi et al., 1994).
AU of these studies, with the exception of Feiner et al. (1995), compared mean values in
the group of interest to the vvahies in a control population In so doing, their conclusion
could be stroasty influenceci by selection bias or by corifoundmg variables that were not
measured. In addition these s~idies cannot conchide how strongly ventilatory responses
determine breath holding ability in normal individuais.
One must also question the methods used to measure the ventilatory responses to
carbon âioxide in these studies. The majority of these studies used the steady-state
technique to characterize the subjest's veatilatory response to carbon dioxide (Schaefer,
1%5; Florio et ai., 1979; Masuda et ai., 1981; Masuda et al., 1982; Bjurstrom and
Schoene, 1987; Davis et al., 1987; Grassi et al., 1994; Feiner e$ al., 1995). There are
inherent -es in using the steady-state technique to characterize the subject's
ventilatory response to carbon dioxide, the min one being that the increase in hypoxia
during the experïment wiil ause an increase in cerebral blood flow, which in turn, wiil
cause a washout of the stimulus itself. mers studies have used earlier versions of the
rebreathing method (1967) to characteriz the subject's ventilatory response to carbon
dioxide (Song et ai., 1963; Davis et al., 1987). The problem with the rebreathing method
in these studies is that the investigators used a large rebreathing bag. By ushg a large
rebreathing bag, the ability to ensure proper mixing and quilibration between the bag and
the subjects is decreased considerably.
Feiner et al. (1995) examined both the hypoxic and hypercapnic ventilatory
responses in a normal population. They concludeci that "the hypoxic ventilatory response,
but not the hypercapnic ventilatory respoase, is a signincant predictor of breath holding
perfomuuce." They used an isocapnic steady-state method in detennining the hypoxic
ventilatory response, and a hyperoxic steady-state method in determinuig the hypercapnic
ventilatory response. It is my beiief that the modified rebreathing technique @uffin and
McAvoy, 1988; Mohan and hifnn, 1997) d e s c n i eariier is a more e f f d v e and reliable
methoci for determinhg the venfilatory respoases to carbon dioxide than the steady-state
technique.
The m d e d rebreathing technique @utnn and McAvoy, 1988) is an e f f i v e and
reliabie method for determinhg the vernilatory responses to carbon dioxide (Mohan and
Dutnn, 1997). One modification, the use of iso-oxic rebreathing, aiiows for the
chernordexes to be rnea~u~eû at any constant P a A second modification, having the
subjects hyperventilate prior to the rebreathing test, allows kvestigaton to study the
effects of hypoxîa on the chanoreflexes independent of carbon dioxide. This method also
dows for both the peripheral threshold (Tp) and central threshold (Tc) to be determineci.
It also p d s memurement of basal ventilation (Vb), peripheral-chemorefiex sensitivity
(Sp) and central-chemoreflex sensitivity (Sc). F ' i y , it dows for the meaSuTement of the
interaction of both the peripheral and central chemoreflexes.
1. To quantify the parameters (Tp, Tc, Sp, Sc, Vb) of the ventilatov response
(chernordexes) to carbon dioxide and hypoxk, and the parameters (BHT, initial
P&ad and P&-, and nnal P & a and P&w of breath hoidhg.
2. To determine if the chemoreflex parameters are predictors of maximal breath
holding duration.
3. To predict the ventilatory drive (V) at the breakjng point of breath holding using
the measured chemoreflex parameters.
4. To determine if breath holding duration can be increased by the actions of a
swdowing rnovement.
3. I Selediort ofsubjects
A sample s k estimation based on previow data @ufnn and McAvoy, 1988;
Feiner et ai., 1995) suggested that the study required a minimum of ten subjects.
Seventeen subjects were recniited fiom the general population to complete the
investigation, This was done to dow for withdrawals nom the study or for failure to
complete the tests.
The investigation was compieted after the protocoi had been approved by the
University of Toronto Cornmittee for Human Experimentation and after the volunteen
gave their Ulformed consent (Appendk 1). Although the subjects did not undergo a
physical examination, al1 subjects were asked if they had any previous history of
respiratory andor cardiovascular disease. Subjects were also required to read and
complete a Physical Activity Readuiess Questionnaire (PARQ) (Shephard, 1988; Chislorn
et al., 1975) (Appendk 2). Ali subjects were healthy, non-smoking individuals with no
history of respiratory or cardiovascular disease. The nibjects were asked to refrain from
any exercise and stimulant or depressant substances (Le., caffeine, dcohol) for at least two
hours prior to the commencement of testing.
3-2 Appwabcs
During the rebreathing part of the study, the subjects wore nose clips and breathed
through a mouthpiece. Durhg the breath holding part of the investigation, the subjects
wore nose clips and breathed through a mask (Vital Signs hc., Medium Size). Both the
mouthpiece and ma& were connected to one side of a wide-bore Y valve (Collins P-3 19,
80 ml dead space). The Y-valve dowed the abject to switch themselves b m breathing
rwm air to breathhg h m the rebreathing bag.
The experimental set-up of the apparatus for the reûreathing tests can be seen in
Figure 3.1 (DufEn, 1990). The rebr-g bag of approxhately 5 iitres, was enclosed in a
ngid container which was comected to a spirometa (Morgan Spirdow, Model 130)
using a 50 mm diameter wide-bore tube in order to monitor ventilatiom The amount of gas
volume that was displaced in the rebreathing bag was also displaced in the ngid container.
This displacement was translated into an analogue signal by the spirometer.
A s d diameter tube (Briiel& Kjaer Gas Sample Tube UD 5037) connecteci to
the Y-valve close to the mouthpiece dowed for the continuous sampbg of the respired
gases (partial pressure of carbon dioxide and oxygen) with an oxygen/carbon dioxide gas
monitor (Brciel & Kjaer Anestfietic Gas Monitor Type 1304). Once analyzed, the gases
were retunied to the rebreathing bag via another small diameter tube connected Ma a
different port. The sample flow rate of the respired gases was 90 ml-min".
Carbon dioxide was analyzed by the Brüel& Kjaer gas monitor by photoacoustic
infhred spectroscopy (0.1 % or 0.5 mmHg resolution), while oxygen was d y z e d by
magnetoacoustics (1 % or 5 mmHp resolution).
The analogue signais of ventilation, and the partial pressures of carboa dioxide and
oxygen were displayed on a chart recorder (Graphtec Linear Recorder Mark W, Model
WR 3 101), at a paper speed of 100 mmin" . The chart recording was examineci for the
presence of a plateau, shortly after switchhg to the rebreathing bag. This was done to
determine that a proper equili'bration had been achieved between the mixed venous,
14
art& and aiveolar partial pressure of &n dioxide in the subjects (Figure 3.2). The
chart recorder was aiso used to determine the initial and M levels of end-tidal Pa and
P a during breath holding, as weli as, the total duration of the breath hold (Figure 3.3).
Breath hoid duration was compareci for accuracy using a digital stop watch (Thex
Triathlon Mo& B5)-
The analogue signals were converted to digital si@ ushg a 16-bit analogue-to-
digital converter (Digital PCM Recordhg Adapter, Vetter Model 3000 A) and were then
recorded for storage on video tape using a video cassette recorder (JVC S t e m Hi-fi
VCK HR-D840 Model 500c). The signals were also digitized by a 12-bit analogue-to-
digital converter (SP Innovations) so as to be displayed and analyzed by computer (Atari
1040 ST). This on-he computer anaiysis caicdated ventilation, tidal volume, inspiratory
and expiratory times as weU as end-tidal partial pressures of carbon dioxide and oxygen on
a breath-by-breath basis.
Upon termination of each test, the data input was saved in the fom of an ASCII
(American Standard Code for Information Interchange) file. This file was then importeci
into a spreadsheet program (Micros& Excel version 7.0, Windows 95). Conversions &om
ATPS to BTPS were performed using equations prograrnmed into the spreadsheet.
Hart rate (1 beat-min-' resolution) and oxygen saturation (1 % resolution) was
continuously monitored Ma a finger puise-oximeter probe (Briiel& Kjaer Type 8552).
In addition, the h g volume W C , iRC, VC, and VI) readings for each subject
were obtained using a C o k Respirometer (Mode1 P-900). AU lung volumes were
converted fiom ATPS to BTPS using programmeci quations in the spreadsheet.
Spirom eter
L
1 b - Oxygen I
Gas Analyser IQ w
Corn puter
FIGURE 3.1: A block diagram iilustratiag the experimental set-up of the modined
rebreathing technique. ~eproduced with permisson nom, Du86n (1990) Canadian
Journal of Anaesth* 3 7(8): 933-9421.
- FIGURE 3.2: Trace diagram illustrating quilibration of carbon dioxide (mmHg) [bottom
row] during rebreathing test in alveolar, arterial and tissue comparîments, evidenced by a
plateau on the chart recorder C a trace for subject 4, (paper speed 100 mm-sec-').
FIGURE 3.3: Trace diagram during breath holding illuseating initiai and final end-tidai
catbOn dioxide (mmHg) [top row] and oxygen (mmHg) [bottom row] levels for subject 4,
(paper speed 100 mm.soc").
3.3 Calrbrafroui
The entire apparahis was caliirateû prior tu the begüming of each experiment- The
gas monitor was adjusted to the atmospheric barometric pressure, and &n dioxide and
oxygen were caii'brated with known concentrations of gases @OC Gases Inc.), which
spanwd the e>cperimental range. A one litre syringe (Hans Rudolph Inc. 1 Iitre calibration
syringe, Series 5540, 1000 ml * O. 1 %) was useci to calibrate the spirometer by drawing
and pumping volumes of air in and out of the rebreathhg b a g The heart rate and oxygen
saturation were also calibrateci More each experiment, by matchhg the values displayed
on the gas monitor to that of the on-line microcornputer and correcting for any
discrepancies.
3.4 hotucd
The protocol for the investigation was such that each subject was required to be
tested on three separate occasions, with a minimum of 24 hours between each test day.
Upon each visit to the laboratory, the subject first perfonned three rebreathing tests, one
at each of three levels of oxygen (40, 80, 150 mmHg). The end-tidal partial pressure of
oxygen was maintained at one of three conditions by a controUed feedback wbich added
oxygen to the rebreathing bag at a controlled me. Each rebreathing test was separated by
a 30-minute interval. The subject then perfonned four breath holding tests under one of
four conditions (TLC, TLCsw, FRC, FRCsw). Each breath holding test was separated by
a 10-mimde interval. There was also a 30-minute interval between the last rebreaîhing test
and the fint breath holding test.
Both the rebreathmg and the breath holding conditions were raadomly chosen by
the subject immediateiy pnor to the begimhg of each testhg &y. The iso-oxic
rebreathiug leveis were never made known to the subject, and the breath holding
conditions were only revealed to the subject jua prior to the actual breath hoid.
The rebreatbhg tests conshed of a five minute period of voluntary
hypewenfilation (the respiratory rate of the iryperventîlation range- around 12 4
breaths-e') in order to d u c e the body's stores of carbon dioxide to a partial pressure
that was below both the peripherai and central chemoreceptor thresholds. The
hypewentilation itseifwas one of a slow and deep breathing pattern so as to avoid post-
hypaventilation ventilatory decline or short term potentiation (Folgering and Durhger,
1983). The hypewentilation lowered the subjects' end-tidal partial pressure carbon dioxide
Ievels dom to between 18-22 mmHg, which is above the Ievel that produces dininess in
subjects (Dempsey, 1975).
Mer five minutes of hypenentilation, the subject was asked to expire rnanmally,
switch to the rebreathùig bag @y tuming the Y-valve) and take three deep breaths. The
subjects were then instnrcted to relax and to foiiow their normal breathing pattem. The
subjects were asked to take three deep breaths immediately after switching ont0 the
rebreathing bag. This was done so as to ensure proper mWng and eqdi'bration between
the p d pressures of carbon dioxide and oxygen in the rebreathing bag and the partial
pressures of carbon dioxide and oxygen in the alveoh, arterial blood, and mixed venous
blood.
Rebreathing fiom the bag continueci until either the ventilation reached 100
~.mixi', the partial pressure of carbon dioxide reached 60 &g, or the oxygen saturation
reached 60 percent, at which time the subject was instnicted to switch back to breathing
rwm air. Once the test had been tenainated and the subject was breathing room air, they
remaineci seated for approxhately 3 min, in order to recover-
The breath holding tests wmmenced approxhtely 30 minutes after the
termination of the reûreathhg tests. Subjects were instnicted to hold their breath for as
long as possible under one of four conditions and to exhale at their breaking point.
The breath hold effort given by the nibjects was vetified for coosistency using
Borg's 10 point categorical Rating of Perceiveci Exertion (RPE) sale (Borg 1982)
(Appendix 3). The sale is related to physiologie stress and can be used to estabhsh
exercise iatensity for the purpose of training (Borg, 1982). Scaiing instructions were
provideci prior to each experimental session The follouhg is the text of the scaling
instnrctions (adapted fkom Robertson et al., 1992) that were given tu the subject prior to
each experimental breath hold condition The swie you see before yyou contains mrmbers
fiom O fo 1 O. nie m b e r s represent a range of feelingsfrom "no urge to brearh of ail"
( d e r O) to ''mm?m?mum urge to breath" (mrmber 10). When your feelings of urgency
me at maximal intem-ty, r e p d wzih a munber 10; when your feelings of urgency are al
a minimal intelt~~~ty, r e p n d with a number O. " Immediately foliowing the end of each
breath hold, subjects were asked "How strong was your urge to breath at the breaking
point.
Once the abject was seated comfortably wearing the nose clips and the puise
oxheter7 they were hitructecl as to which one of the four breath holds they were going to
do for that particular test. AAer king @en verbal confirmation by the investigator to
begh, the subjects proceeded to hold their breaths.
The four breath hold conditions were as follows:
9
ii)
iii)
iv)
Total lmg capacity (TLC). The nibjects heid th& breath &er a maximal
inspiration and d e d when they reached their breakhg point.
Total hmg capacity with swallowing (TLCsw). The subjects held their breaîh &er
a manmal inspiration, swaiiowed and continueci to hold their breath when they
reached their nrst breaking point, and tinally exhaleci when they reached their
second breakurg point.
Functional residuai capacity (FRC). The subjects held theû breath after a normai
expiration and exhaled when they reached their breaking point.
Futlctional residual capacity with swatlowing (FRCw). The subjects held their
breath after a normal expiration, swallowed and continued to hold their breath
when thqr reached their fht breakhg point, and W y exhaled when they reached
their second breaking point.
3.5 Data Anafysis
Analysis of the variables measuted d u h g the rebreathing tests used data coiiected
eorn the time each subject switched to the rebreathing bag until they switched back to
breathing rom air. Data for the £irst 30 seconds were omitted to exclude the quilibration
period and any post-hyperventi.lation potentiation of breathing (Wagner and Elàridge,
1991).
Data for each subject were plotted as ventilation versus partiai pressure of carbon
dioxide for each of the three isooxic partial pressure of oxygen rebrenthing conditions
(40, 80, 150 mmHg). These graphs uidicated the presence or abseace of the peripheral
52
andor central chemoreflex tbresholds 3.4). The f h t point above which ventilation
i n d with carbon diorcide, was interpreted as the tbreshold for either the peripheral
chemorefiex (Tp) or the threshold for the central chemorefiex (Tc), depending on the
subject and the iso-oxic level of the test.
Straight line segments were fitted to the appropriate segments of the graph @gure
3.4). To detennine the basai ventilation (Vb), a h e segment which was equal to the mean
ventilation was fïtted to the graph. A reduced major axis was nned to the segment of the
graph that was between the thresholds, and its dope was taken to be the penpheral
chemorefiex sensitivity (Sp). A second reduced major axis was fitted to the segment of the
graph that was above the second threshold (ipresentf, and its dope was taken to be the
nim of the peripheral chemorefiex and central chemoreflex sensitivities (Sp + Sc).
The r d u d major axk (Kemuick and Kaidane, 1950) is a line with a slope of
SyISx through the mean (%y). The reduced major axis is used because a linear regression
line is not appropriate for this type of data in that it assumes that variability is present only
in the y-axis and ignores the variability of the carbon dioxide partial pressure
measurement. Using estimates of the tbresholds, the thresholds were varied until the
lowest sum of squares was obtained by the line segments.
Data for each subject from the rebreathing tests were also plotted as the end-tidal
partial pressure of carbon dioxide versus the. This was doue in order to caicuiate the rate
of rise of carbon dioxide in each subject, and would later be used, dong with the breath
hold data, to predict a breaking point for each subject. Data for each subject fiom the
rebreathing tests were also plotted as the end-tidal partial pressure of oxygen versus tirne.
This was done in order to ver@ that the oxygen had indeed remaineci at the predetermined
iso-oxic level.
Adysis of the vanabtes m m e d duMg the breath holding tests used data
d e c t e d fkom the t h e the subject began to hold thek breath until the subject's f h t
exhalation &er breath holding began.
Data for each subject were plotted as breath hold time without swallowîng versus
breath hold time with swallowing for each of the two breath hold conditions (TLC and
FRC). Data for each subjezt were also plotted as breath hold t h e (with and without
swallowhg) verais ail the chemoreflex parameters mesureci as well as with the
chemoreflex drive to breath 0.
3.6 S-d Anal*
Anthropometric data collecteci Eom the subjects are expressed as mean * SD.
Statistical analysis of the parameters measured during the rebreathing tests was done using
a one way repeated m m e s (RM) analysis of variance (ANOVA). When a significant
ciifference was obtained, a Student Newman-Keds post-hoc d y s i s was performed to
isolate differences among treatment means. AU resuits are expressed as mean * SE, and
the level of significance chosen for the statistical procedure was p < 0.05. Statistical
analysis of the data was perfonned using the Jandel Scientific Statistical Package Sigma
Stat (windows version 7.0).
Statistid analysis of the parameters measured during the during the breath holding
tests was doue using a two way (condition x the) repeated measufes (RM) analysis of
variance (ANOVA). Main dectS of condition (di breath hold conditions), and time (all
test days) and condition x time interactions were analyseâysed When a significant F-ratio
(corrected for the repeaîed meamres Factor) was o b e d . , a Student Newman-Keuis pst-
hoc anaiysis was perfbrmed to isolate differeaces among treatment meam. AU r d t s are
expressed as mean * SE, and the level of sigdicance chosen for the statistical procedure
was p < 0.05. Statisticai analysis of the data was perfomed ushg the Statisticai Package
for the Soaal Sciences (SPSS/PC+, windows version 7.0).
Statistid analysis of the Rate of Perceived Exertion (RPE) values obtaùied durhg
the breath holding tests was done using a Wdcoxon Signed Rank Test. AU results are
expressed as mean * SE, and the level of significance chosen for the statistical procedure
was p c 0.05. Statisticai anaiysis of the data was perfionned using the Statisticai Package
for the Social Sciences (SPSS/PC+, windows version 7.0).
30 35 40 45 50 55 60
End-tidal Pco, (mmHg)
FIGURE 3.4: This graph indiates the presence or absence of a ventilatory response to
the test conditions applied and indicaies the presence or absence of the peripheral andor
central chernoreflex thresholds. The fïrst point above which ventilation increased with
carbon dioxide was interpreted as the threshold for either the peripherai chemoreflex (Tp)
or the threshold for the centrai chemoreflex (Tc), dependhg on the subject and the iso-
oxic level of the test. To detennine the basal ventilation (Vb), a line segment which was
equal to the mean constant of ventilation was fitted to the graph.
4.1 General
Seventeai healthy subjects (10 female and 7 male) from the University of Toronto
population participateci in the study. The amhropometric data for al1 the participants is as
foiiows and can also be seen in Table 4.1.
The ages of the nibjects ranged nom 18-27, with a mean age of 73.2 years I 2.6
(SD). Subject height ranged from 1.5-1.9 m, with a mean height of 1.7 meters k 0.1 (SD).
Subject weight ranged from 43.2-93 -2 kg, with a mean weight of 65.8 kg + 14.4 (SD).
Vital capacity ranged from 2.4 - 6.6 L(BTPS), with a mean of 4.3 L (BTPS) k 1.1 (SD).
Female subjects (n=10) ranged in age from 20-27, with a mean age of 33 .O years 5
2.2 (SD), a mean mas, of 59.6 kg f 13.2, and a mean height of 1.6 m + 0.1. Vital capacity
was calculated to be 5.6 L (BTPS) k 0.6. Male nibjects (n=7) ranged in age from 18-37
and had a mean age of 23.4 years + 3.3, a mean mass of 74.7 kg + 1 1.4, and a mean height
of 1.8 m f 0.1. Vital capacity was calculated to be 5.3 L (BTPS) 2 0.9.
4.2 B a d Ventilation
Basal ventilation (Vb) was measued below the peripherai and centrai
chemoreceptor thresholds immediately d e r the hyperventilation period (excluding the
initial 60 seconds, see next section) at the beginning of each rebreathing test. Mean basal
ventilation was found to Vary considerably between subjects. Mean basal ventilation
ranged tiom a iow of 2.44 I 0.23 (SE) min-' for wbject 17 at Pa of 150 mmHg to a
kgh of 20.75 * 3.87 ~-mia" at a Pa of 40 mmHg for subject 15. Resdts for ail subjects
are @en in Table 4.2. As can be seen fiom Table 4.2 and Figure 4.1, mean basal
ventilation for aU subjects increased with decreasing Pa. No significant difference was
found in the mean basai ventilation of ail subjects at all iso-oxic levels (p > 0.05) using a
one way repeated meanires ANOVA Figure 4. L a illustrates the ciifferences in basal
ventilation between male and female subjects. No significant dzerence was found in the
mean basal ventilation of male subjects between all iso-oxic levels (p :, 0.05) using a one
way repeated measures ANOVA No signincmt dinerence was found in the mean basal
ventilation of female subjects between al1 iso-oxic levels (p > 0.05) using a one way
repeated measures ANOVA No sigdcant difference was found in the mean basal
ventilation between male and female subjects between al1 iso-oxic levels (p > 0.05) using a
one way repeated rneasures ANOVA
4- 3 Is* Oxic Rebreathing
rUI subjects completed three rebreathing teas at each iso-oxic level. M y s i s of
the iso-oxic ventilatory response to hypoxia and hypercapnia revealed that several subjects
had an exponential decline of ventilation before reachhg their chernoreflex threshold. This
exponentiai decline in ventilation was due to a dedine in ventilation following a short-term
potentiation ( STP) of ventilation induced by voiuntary hyperventilation (Wagner and
Eldrige, 1991). In order to mesure Our results without the influence of this decline, data
analysis began only after a period of three tirne constants (60 seconds) had passed. The
time constant varied from subject to nibject, but was found to be between 10-20 seconds.
The time course of end-tidal partial pressure of oxygen at ail t h e iso-orcic levels
(40, 80, 150 mmHg), which were used during the rebreathing tests can be seen in Figure
58
The thne course of end-tidal pamal pressure of oxygen at d three iso-oxic leveis
(40.80, 150 mmHg), which were used during the rebreathiag tests can be seen in Figure
4.2 for subject 6. The the course of end-tidal partial pressure of carbon dioxïde a - aU
three iso-oxic levels (40, 80, 150 mnHgl7 which were used during the rebreathing tests
can be seen in Figure 4.3 for abject 6.
The rate of rise of end-tidal carbon dioxide partiai pressure at the various iso-oxic
Ievels was measured by ntting regression luies to the response. This rate of C a
accumulation in the rebregthing bag is indicative of the rate of C a production in the body
and is thus an estimate of metabolic rate. The response for each individual subject can be
seen in Table 4.3. Inter-subject and intra-subject variability was seen in the metabolie rate,
between iso-oxk levels. Mean rn~aboiïc rate for ail subjects (n=17) increased with
decreasing Pa. figure 4.4a illustrates the merences in mean metabolic rate of nse of all
subjects. A signXcant Merence was found in the mean rnetaboiïc rate of al l subjects
between ail iso-oxic Ievels @ < 0.05) using a one way repeated measures ANOVA. Figure
4.4a illustrates the merences in rnea. metaboiic rate of rise between male and female
subjects. No signifiant difference was found in the rnean metaboiic rate of male subjects
baween dl iso-oxic levels (p > 0.05) using a one way repeated measures ANOVA A
significant difference was found in the mean metabolic rate of f d e subjects betweem iso-
oxic l e ~ & of p4 = 40 and 80 d g , and between iso-oxic leveis of Pa = 40 and 150
rnmHg @ < 0.05) using a one way repeated measures ANOVA. No signincant différence
was found in the mean metabolic rate of between male and female subjects b e e n ail iso-
oxic l d s @ > 0.05) using a one way rrpe~ed rneasur;es ANOVA
Femde @=IO) Range Mean SD
Table 4.1: Anthropornetric data recordeci fkom each subject that participated in the investigation.
BASAL VENTILATION (Vb)
p.
Subject Gender 1 M
Table 4.2: Mean basal ventilation (Vb), in (~-rnin") * (SE) for al1 abjects (n=17). Basal
ventilation mged nom a low of 8.33 * 0.99 min-' at an imxic level of 1 50 mmHg to
a high of 9-52 * 1.01 min" at an isooxic level of 40 nmitIg.
Basai Venthtion (Vb) vs Partial Pressure of Oxygen
Partial Pressure of Oxygen (mmHg)
Figure 4.1: Mean basal ventilation (Vb) t (SE) for ail subjects (n= 17) at different partial
pressure of oxygen leveis. No sigdicant difference was fond in the mean basal
ventilation of ail subjects at al1 iso-oxic levels (p > 0.05) using a one way repeated
measures ANOVk
Basai Veatifatioii (Vb) vs Partid Pressure of Ocygen (Males)
Figure 4.la: Mean basal ventilation (Vb) + (SE) for male subjects (n=7) and f e d e
subjects @=IO) at different partiai pressure of oxygen levels. No sigdicant âiierence was
found in the mean basal ventiiaiion of males, femaies and betweea male and femde
subjects between di isosxic levels @ > 0.05) using a one way repeated m w e s
ANOVA.
PO2 vs Time
Figure 43: The time course of end-tidal partial pressure of oxygen at all three iso-oxic
levels (40,80, 150 rnmHg), for subject 6.
PC02 vs Time
Time (s)
Figure 43: The t h e course of end-tidal partial pressure of carbon dioxide at aU three
iso-oxic levels (40, 80, 150 mmHg), for subject 6.
Mttabolic Rate of Rise (MR)
Partial Prcssnre of Orygen (Pa)
Subject Gender 40 mmEg 80 mmHg 150 mmHg
5.0 4.8 4.6 4.2 3.8 3 -8
5.0 4.6 4.9
4.1 4.0 3 -7
4.8 4.6 4.4
4.0 4-7 4.1
5 .O 4.4 3 -8
3 -2 3.1 3.1
4.8 4.7 4.6
3.7 3 -7 3.8
5.2 4.7 4.9
4.6 4.1 4.0
4.7 4.7 4.3
5.2 4.9 5.0
5.3 4.5 4.4
4.4 4.3 3 -6
4.7 5.1 4.3
Table 4.3: The mean rate of rise (MR), in (mm~gmin") * (SE), of end-tidd partial
pressure of carbon dioxïde at all three iso-oxic lm& (40,80, 150 mmHg), for al subjects
( ~ 1 7 ) . Mean values for metabolic rate increased nom 4.2 * O. 1 mm~g-min'~ at an iso-
oxic level of 150 mmHg to 1.6 0.1 mm~g-mh-' at an iso-oxic level of 40 mmHg.
Metaboüc Rate of RM (MR) vs Partial Pressure of Oxygea
Partial Pressure of Oxygea (mmHg)
Figure 4.4 The mean rate of (MR) * (SE) of end-tidal partial pressure of carbon
dioxide at ail three iso-oxic IeveIs (40, 80, 150 d g ) , for a i l subjects (n=17). A
signifiant dinerence was found in the mean metabolic rate of a l l subjects between ail iso-
oxic leveis @ < 0.05) using a one way repeated measures ANOVA
Figure 4.4.: Mean rate of rise (MR) I (SE) of endotidal p h a l pressure of carbon dioxide
for female subjects @=IO) and male subjects (n=7) at dinerent partial pressure of oqgen
lwels. No signincant difference was found in the mean rate of rise of males and between
males and f d e s at all iso-oxic levels (p > 0.05). A si@cant ciiffierence was found in
fernales h e e n imxic levels of = 40 and 80 d g , and between 40 and 150
mmHg @ < 0.05) using a one way repeated meesures ANOVA..
v vs PCO*
Figure 45: The ventilatory response of subject 2 who has a low response (Le., low
sensitivity) to carbon dioxide at various iso-oxic levels (40,80, 150 rnmHg).
* O
** a
a", 5 49s.
30 35 40 45 50 55 60 65
end-tidai PC02 ( m d g )
Figure 4.6: The ventilatory response of subject 11 who has a high response (Le., high
sensitivity) to carbon dioxide at various iso-oxîc leveis (40,80, 150 mmHg).
The iso-oxic ventilatory respom to carbon dioxide varieci considerably f?om
subject to subject. The responses varied fkom a low response (i-e. low semitivity), a
moderate response (i.e. moderate seositivity), to a hïgh response (Le. high sensitivity).
Tbis varied response between subjects cm be seen in Figures 4.5 and 4.6, which shows the
iso-oxic vernilatory response to carbon dioxide in two subjects.
Figure 4.5 shows the vemilatoq response of subject 2 that has a low response (i. e.
low sensitivity) to carbon dioxide at various iso-oxic levels. Figure 4.6 shows the
ventilatory response of subject 11 that has a high response (i-e. high sensitivity) to carbon
dioxide at various i m x i c levels.
4.3.1 P m p h d CTtemorejlex
The peripheral chemoreflex threshold (Tp), varied between subjects and between
i m x i c levels. The resuits of ai l isooxic levels for aii subjects can be seen in Table 4.4
and Figure 4.7. The o v e d mean values for the peripheral threshold declined i?om 42 * 0.7 (SE) mmHg at an isooxic level of 1 50 mmHg to 40 * 0.8 mmHg at an isosxic levei
of 40 mmHg. A signiijcant diffaence was found in the mean peripheral threshold of ail
subjects between iso-oxic levels of 40 and 80 m . and between 40 and 150 mmHg
(p < 0.05) ushg a one way repeated measures ANOVA Figure 4.7a illustrates the
differences in pexipheral chemorefiex threshold in male and female subjects. No signincant
difference was formd in the mean peripheral chemorefiex threshold of male subjects
between al1 iso-oxic ievels (p > 0.05) using a one way rqeated measures ANOVA A
signifiant Merence was found in the mean @phexai chemoreflex threshold of témale
subjects between k x i c leveis of 40 and 80 mmHg, and 40 and 150 mmHg (p < 0.05)
71
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UMI
sensÏtivity of fernale subjects between ail iso-oxic levels (p > 0.05) using a one way
repeated measures ANOVA A siwficant difference was f o d in the mean centrai
Senativity between male subjects at aii isooxic levels and fernale subjects at an iso-oxic
level of 40 mmHg (p < 0.05) using a one way repeated measures ANOVA.
4.4 Mdematicaf Modd of the Gkeltu~eflex Drive tu Breathe
Intra-subject and inter-subject variation in the chemoreflex drive to breathe was
seen as caiculated by Equation 3 (page 12). The mean chemoreflex dnve to breathe (V) * (SE) ~*mui', as determineci under the four expenmental breath holding conditions (TLC,
TLCsw, FRC, FRCsw) for al1 subjects, cm be seen in Table 4.8 and Figure 4.1 1. The
overd mean values for the chemoretlex drive to breathe increased fiom 16.3 * 1 -6 ~ m i d
with TLC to 16.9 1.7 ~ * m i d with TLCsw, and fiom 15.9 * 2.2 ~ - m i d with FRC to
16.8 * 2.3 min-' with FRCsw. No significant difference was found in the mean
chemoreflex drive to breathe of al1 abjects between al1 breath holding conditions (p >
0.05) using a one way repeated measures ANOVA Figure 1 la illustrates the difference in
the mean dnve to breathe in fernale and male subjects. No si-gificant difference was found
in the mean drive to breathe of male subjects between ali breath holding conditions (p >
0.05) using a one way repeated measures ANOVA. A significant difference was found in
the mean dnve to breathe of f e d e subjects between FRCsw and n C s w breath holding
conditions (p < 0.05) using a one way repeated measures ANOVA. A significant
difference was found in the mean drive to breathe between f e d e and male subjects at ail
breath holding conditions (p < 0.05) using a one way repeated meanves ANOVA
Pa- Pressure of Oxygen (PO=)
Peripherai Threshold (Tp)
Subject Gender 1
Table 4.4: The mean peripheral chemoreflex threshold (Tp), in (rnmHg) * (SE), for ail
subjects ( ~ 1 6 ) and at ali iso-oxic levels. The mean values for the peripheral threshold
declined from 42 * 0.7 M g at an isu-oxic level of 150 mmHg to 40 0.8 mmHg at an
is0i)rQc level of 40 mmHg.
Penphernl Threshold (Tp) vs Partiai Pressare of Oxygen
Partial Pressure of Oxygen (mmHg)
Figure 4.7: The mean peripherai chernoreflex threshold (Tp) * (SE), for aii subjects
(n=16) and at ail iswxic levels. A sisnificant difrence was found in the mean penpheral
chernoreflex threshold of di subjects between iso-oxic levels of P@ = 40 and 80 mmHg,
and 40 and 150 mmHg (p < 0.05) using a one way repeated measures ANOVA.
Figure 4.7a: Mean penpheral threshold (Tp) 5 (SE) response for male subjects (n=7) and
female subjects (n=9) at aü iso-oxic levels. No signifiant dflerence was found in the mean
peripherai chemoreflex threshold of male subjects at al1 iso-oxic levels (p > 0.05) using a
one way repeated measures ANOVA. A significant diierence was found in the mean
penpherd chemoreflex threshold of female subjects between iso-oxic levels of Pa = 40
and 80 mtnHg, and 40 and 150 mmHg (p < 0.05) using a one way repeated measures
ANOVA. A signifiant ciifference was found in the mean peripheral chemoreflex threshold
of between ail iso-oxic Ievels for males and at an iso-oxic level of 40 mmHg for femaie
subjects (p > 0.05) using a one way repeated measures ANOVA.
Peripherai Sensitkity (Sp)
Partial Pressure o f Oxygen (PO3
Mem SD SE
Table 4.5: The mean peripheral chernoreflex sensitiviîy (Sp), in (~-min-'-mmH~~') (SE),
for ali subjects ( ~ 1 6 ) and at a l l iso-oxic levels. The overall mean values for the penpheral
sensitivities increased fiom 1.8 k 0.5 ~-min-~-rrnnH~~~ at an iso-oxic level of 1 50 mmHg to
4.6 * 0.8 ~*min"-nmH~-' at an iso-oxic level of 40 mmHg.
Peripheral Sensitivity (WminlmmHg)
PecipIted Sensitivity (Sp) vs Partial Preuuro of m e n (Males)
Peripherai Sensitivity (Sp) vs Partial Pressure o f Orygen (Females)
JO 80 150 Mean
Partial Pressure of Oxygen ( m e )
Figure 4.8.: Mean peripheral sensitivity (Sp) k (SE) response for male subjects (n=7) and
female subjects (n=9). A significant difference was found in the mean penpheral
chemorefiex sensitivity of male and female subjects between iso-oxic levels of 40 and 80
mmH& and 40 and 150 mmHQ (p c 0.05) using a one way repeated measures ANOVA. A
sipificant difference was found in the mean Sp between male subjects at an iswxic level
of 40 mmHg and females at al1 iso-oxic Ievels (p < 0.05) using a one way repeated
measures ANOVA.
Central Thresbold (Tc)
Partial Pressure of Oxygen (PO.)
Table 4.6: The mean central chernoreflex threshold (Tc), in (mrnHg) * (SE), for al1
subjects (n=17) and at ail isooxic levels. No trend can be seen in the centrai threshold
with the diierent iso-oxic levels.
Centraî Threshold (Tc) vs Partiai Pressure of Oxygen
Partial Pressure of Oxygen (mmHg)
Figare 49: The mean central chernoreflex threshold (Tc) (SE), for all subjects ( ~ 1 7 )
and at di isooxic leveis. No signifïcatlt difference was found in the mean peripheral
threshold of ai i subjects between all iso-oxïc be l s (p > 0.05) using a one way repeated
measures ANOVA.
Figure 4.9a: Mean central threshold (Tc) c (SE) response for male subjects (n=7) and
female subjects @=IO) at different partial pressure of oxygen levels. No siBnificant
diffaence was found in the mean central chernoreflex threshold of male and female
subjects between all iso-oxic levels @ > 0.05) using a one way repeated me8suTes
ANOVA. No si@cant Merence was found in the meen central chernoreflex threshold
between d e and f d e subjects between al1 isooxic levels (p > 0.05) using a one way
repéated measures ANOVA
Centrai SensiMe (Se)
Table 4.7: The mean central chernordex sensitivity (Sc), in (~-mlli '-rnrn~~-') * (SE), for
all abjects (1~17) and at ail isosxic levels. It can be seen that there is no particdm trend
in the mean Sc when wmpared to al1 isosxïc levels.
Centrai SensitMty (Sr) vs Partial Pressure of Orygen
P a r u Pressure of Oxygen (mmHg)
Figure 4.10: The mean centrai chemorefiex sensitivîty (Sc) I (SE), for al subjects (n=17)
and at ail isooxic levels. No signifiant differaice was found in the mean peripherai
threshold of dl subjects between all i m i c Ievels @ > 0.05) using a one way repeated
measures ANOVA
Centml k i t i v i t y (Sc) vs Partid Pressure of m e n
w 40 80 150 M e m
Partial Pressure of -en ( m m
Figure 4.10.: Mean central threshold (Sc) * (SE) response for male subjects (n=7) and
femaie subjects (n=10). No significant difference was found in the mean centrai threshold
of d e and f d e subjezts between aii iso-oxic levels (p > 0.05) using a one way
repeated memures ANOVA A significant difrence was found in the mean Sc between
male subjects at an isooxïc level of 80 mmHg and females at iso-oxic levels of 80 and 150
mmHg @ < 0.05) using a one way repated measures ANOVA. A significant difference
was fouml in the mean Sc between male subjects at an iso-oxic level of 150 mmHg and
females at iso-oxic levels of 80 and 150 mmHg @ < 0.05) using a one way repeated
measures ANOVA.
Drive To Breathe (V)
Breath Eold Condition
Subject Gender
Table 4.8: The overd mean values for the chemoreflex drive to breathe 0, in (~-mh-' )
i (SE) inaeased kom 15.9 * 2.2 (SE) ~-xnïn*' with FRC to 16.8 2.3 L-min-' with
FRCsw. The overail mean values for the chemoreflex drive to breathe increased fkom 16.3
1.6 min“ with TLC to 16.9 1.7 min-' with TLCsw.
Drive To Breathe (V) TLC vs FRC
1 TLC
Breath Hold Condition
Figure 4.1 1: No sigdicant difference was found in the mean chernoreflex drive to breathe
(V) + (SE) of all subjects (1147) between di breath holding conditions (p > 0.05) ushg a
one way repeated masures ANOVA
NOTE TO USERS
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4.5 Breatk Hddng
The mean breath hold times (seconds) SE for ail subjects, under d l breath
holding conditions (ïLC, TLCsw, and FRC, FRCsw), is shown in Table 4.9 and Table
4.10. There was intra-subject and inter-subject variation in breath holding times. Subject
10 had the longest breath hold time at 16 1.4 * 2.1 seconds and 90.7 * 6.3 seconds under
the TLCw and FRCnv conditions, respectively. Subject 3 had the shonest breath hold
tirne at 36.5 1.3 seconds under the TLC condition, while subject 6 had the shonest
breath hold time at 14.1 k 0.5 seconds under the FRCsw condition. However, in tenns of
the percent increase in breath hold tirne, the largest increases were seen by subject 13.
which had an increase of 25.4 % with swdlowing under the TLC condition and by subject
8, which had an increase of 38.9 % with swallowing under the FRC condition. The mean
breath holding times for ali subjects increased with swallowing * SE for both TLC and
FRC breath holding conditions. The rnean breath hold time during TLC increased fiom
74.8 * 7.4 seconds without swallowing to 81.8 * 8-4 seconds with swallowing. This
represents a 9.4 % increase in breath hold time for swallowing as compared to breath
holding without swailowing. The mean breath hold time dunng FRC increased from 3 1.3
* 3.7 seconds without swallowing to 36.2 * 5.1 seconds with swallowing. This represents
a 13.4 % increase in breath hold time for swallowing as compared to breath holding
without swallowing.
Figure 4.12 iUustrates the increase in mean breath hold time with swallowing under
the TLC breath hold condition. Analysis using a two-way repeated measures ANOVA,
showed that the increase in breath hold time with swallowing was significantly different
between swallowing and non-swailowing (p < 0.05).
Figure 4.12a illustrates the increase in mean breath hold time with nvdowing
under the TLC breath hold condition in male (n=7) and female (II= 10) subjects. .Wysis
ushg a two-way repeated measures ANOVq showed that the increase in breath hold t h e
with swdowing was significantiy different than non-swallowing (p < 0.05) in male and
fernale subjects. Analysis using a two-way repeated measures ANOVk showed that the
breath hold times between males and fernales was not significantly different for both
swdowing and non-swdowing under TLC breath holding condition (p > 0.05).
Figure 4.1 3 illuarates the increase in mean breath hold time with swailowing under
the TLC breath hold condition Analysis using a two-way repeated measures W O V A
showed that the increase in breath hold time with swallowing was significantly different
between swailowing and non-swatlowing (p < 0.05).
Figure 4.13a illustrates the increase in mean breath hold time with swallowing
under the FRC breath hold condition in male (n=7) and female (n=IO) subjects. Anaiysis
using a two-way repeated measures ANOVA, showed that the increase in breath hold tinte
with swallowing was significantly different than non-swallowing (p c 0.05) in male
subjects but not (p > 0.05) in female subjects. Analysis using a two-way repeated
measures N O V A , showed that the breath hold times between males and females was not
significantly different for both swallowing and non-swallowing under FRC breath holding
condition (p > 0.05).
The mean initial and final P& * (SE), for al1 subjects under al1 breath holding
conditions (TLC, TLCsw, and FRC, FRCsw) are shown in Table 4.11 and Table 4.12
respectively. The rnean initiai and final P d 0 2 * (SE), for all subjects under ali breath
holding conditions (TLC, TZCsw, and FRC, FRCsw) are shown in Table 4.13 and Table
4.14 respectively.
Analysis using a two-way repeated measures ANOVA showed that there was no
signifiaint difference (p > 0.05) in the mean initial P+ between (FRC, FRCsw, TLC
and TLCsw) breath hold cunditions. The mean 6nai P& decreased tiom 72.2 3.3
mmHg with FRC to 68.5 k 3.1 aimHg wÏth FRCsw. It ais0 decreased fiom 76.2 * 2.4
nmiHg with TLC to 73.0 * 2.7 mmHg with TLCsw. Analysis using a two-way repeated
measures ANOV4 showed that uie decrease in P m between EXC and FRCsw, and
between TLC and TLCsw is signincantiy Werent (p < 0.05).
Analysis using a two-way repeated measures ANOVA, showed that the mean
initiai P H 4 between (FRC and FRCsw) and (TLC and TLCsw) was not sipificantly
diierent (p > 0.05). The mean final P- increased from 44.0 1.3 mmHg with FRC to
44.7 1.2 mmHg with FRCsw). The mean final P & a increased from 45.7 0.9 mmHg
with TLC to 46.3 2: 0.9 mmHg with TLCsw. Analysis using a two-way repeated rneasures
ANOVk showed îhat the increase in P d G between FRC and FRCsw, and between
TLC and TLCsw is not signifïcantiy different (p > 0.05).
In order to assure that the subjects gave a maximal effort duruig each breath
holding test and to minimize intra-subject variabiiity, subjects were asked to rate their
perceived exertion fiom the test on a Borg sale (Borg, 1982). The mean Borg scale score
* SE for aii subjects under dl breath holding conditions is shown in Table 4.15 and Figure
4.14.
The mean Borg score * (SE) increased from 7.7 2 0.3 dunng FRC to 8.5 * 0.2
during FRCsw. nie mean Borg score * (SE) increased from 7.4 * 0.3 during TLC to 8.3
0.2 during TL,Csw. Analysis using a Wkoxon Signed Rank Test, showed that the
increase in the mean score with swallowing was aatisticdy dBerent (p < 0.05) for TLC-
Analysis using a Wdcoxon Signed Rank Test. showed that the increase in the mean score
with swallowing was not statisticaüy diierent (p > 0.05) for FRC.
4.6 Break Holding Relatùnsskips
Breath hold time (TLC, TLCsw, FRC, and FRCsw) was regressed against each of
the parameters measured during the rebreathing tests to determine if there was any
relationship between breath hold time and the measured chemoreflex parameters. These
relationships were looked at for dl subjects as wel as for al1 male subjects and al1 female
subjects. The results of the correlation's cm be seen in Table 4.16.
No relationship was found beîweea breath hold time (FRC, FRCsw, TLC. and
TLCsw) and basal ventilation. Figure 4.1 5 illustrates the relationship between Vb and
BHT for al1 subjects with TLC and FRC breath holding condition. The correlation
coefficient (r) for ail subjects was r = 0.5 13 1 and r = 0.4522, respectively for TLC and
FRC. The correlation coefficient (r) for males and fernales, is r = 0.2893 and r = 0.06 1 15
respectively with TLC breath holding condition. The correlation coefficient (r) for males
and fernales, is r = 0.2893 and r = 0.5906 respectively with FRC breath holding condition.
No relationship was found between breath hold time (FRC, FRCsw, TLC and
TLCsw) and the penpheral threshold. Figure 4.16 illustrates the relationship between Tp
and BHT for ail subjects with TLC and FRC breath holding condition. The correlation
coefficient (r) for all subjects was r = 0.0787 and r = 0.0768, respectively for TLC and
FRC. The correlation coefficient (r) for males and females, is r = 0.4101 and r = 0.030
respectively with ïLC breath holding condition The correlation coefficient (r) for males
and females, is r = 0.4065 and r = 0.030 respectively with FRC breath holding condition.
No relationship was found between breath hold time (FRC, FRCw, TLC and
TLCsw) and the peripherai sensitivity. Figure 4.17 illustrates the relationship between Sp
and BHT for di subjects with TLC and FRC breath holding condition. The correlation
coefficient (r) for ail subjects was r = 0.0 141 and r = 0.2417, respectively for TLC and
FRC The correlation coefficient (r) for males and femaies, is r = 0.4030 and r = 0.0265
respectively with TLC breath holding condition. The correlation coefficient (r) for males
and females, is r = 0.5 189 and r = 0.1 109 respectively with FRC breath holding condition.
No relationship was found between breath hold time (FRC, FRCsw, TLC and
TLCsw) and the central threshold. Figure 4.18 illustrates the relationship between Tc and
BHT for ali subjects with TLC and FRC breath holding condition. The correlation
coefficient (r) for dl subjects was r = 0.1 105 and r = 0.04 12, respectively for TLC and
FRC. The correiation coefficient (r) for males and femaies, is r = 0.1697 and r = 0.08 19
respectively with TLC breath holding condition. The correlation coefficient (r) for males
and fernales, is r = 0.0728 and r = 0.0245 respectively with FRC breath holding condition.
No relationship was found between breath hold time (FEK, FRCsw, TLC and
TLCsw) and the central sensitivity. F i p e 4.19 illustrates the relationship between Sc and
BHT for alI subjects with TLC and FRC breath holding condition. The correlation
coefficient (r) for ail subjects was r = 0.2452 and r = 0.0678, respectively for TL,C and
FRC. The correlation coefficient (r) for males and females, is r = 0.1916 and r = 0.2452
94
rrspectively with TLC breath holding condition The correlation coefficient (r) for males
and f d e s , is r = 0.1030 and r = 0.1822 respectively with ERC breath holding condition.
No relationship was found between breath hold t h e (FRC, FRCsw, TL,C and
TLCsw) and the metabolic rate of rise. Figure 4.20 illustrates the relationship between MR
and BHT for ail subjects with TLC and FRC breath holding condition The correlation
coefficient (r) for all subjects was r = 0.0889 and r = 0.0346, respectively for TLC and
FRC. The correlation coefficient (r) for males and females, is r = 0.5596 and r = 0.533 7
respectively with TLC breath holding condition. The correlation coefficient (r) for males
and females, is r = 0.5208 and r = 0.230 respectively with FRC breath holding condition.
A strong relationship was found between breath hold time (FRC and FRCsw) and
the chemoreflex drive to breathe for male subjects. The correlation coefficient (r) is r =
0.9377 and r = 0.952 1 respecticely. A weaker relationship was found between breath hold
time (TLCsw) and the chemoreflex drive to breathe for male subjects. The correlation
coefficient (r) is r = 0.7499. No relationship was found between breath hold tirne (FRC.
FRCsw, TLC and TLCsw) and the drive to breathe for al1 subjects and for females. Figure
4.21 illustrates the relationship between V and BE-iT for al1 subjects with TLC and FRC
breath holding condition. The correlation coefficient (r) for ail subjects was r = 0.0787 and
r = 0.4624, respectively for TLC and FRC. The correlation coefficient (r) for males and
females, is r = 0.4295 and r = 0.0975 respectively with TLC breath holding condition. The
correlation coefficient (r) for males and females, is r = 0.9377 and r = 0.4817 respectively
with FRC breath holding condition,
Mcan Breath Hold Tirne
Breath Hold Condition
TLC TLCsw Percent Change
73 -7 78.2 6.1%
43 -2 41.3 -4.3%
36.5 41 -7 14.3%
103.8 121.4 16.9%
101.5 108.6 7.1%
71.3 76.8 7.7%
76.2 69.5 -8.8%
68.9 72.0 4.6%
55.5 56.5 1.7%
137.1 161.4 17.8%
66.0 74.0 12.0%
63 -3 69.6 10.00h
38.0 47.7 25.4%
116.5 122.3 5.OYo
48.7 58.5 20.2%
53.3 61.6 15.5%
1 19.0 129.3 8.6%
Table 4.9: The mean breath hold times in (seconds) (SE) for each subjects and aii
subjects (n=17), under TLC and TLCsw breath holding conditions. Mean breath hold tirne
during TLC increased &om 74.8 * 7.4 seconds without swallowing to 81.8 * 8.4 seconds
with swallowing8
Breath Holding Time TLK vs TLCsw
ï
TLC TLCsw
Breath Holding Condition
Figure 4.12: The mean breath hold times (seconds) * (SE) for al1 wbjects, under TLC
and TLCsw breath holding conditions. Mean breath hold time during ïLC increased nom
74.8 7.4 seconds without swdowing to 81.8 & 8.4 seconds with swdowing. Andysis
ushg a two-way repeated measures ANOVq showed that the increase in breath hold the
with swdowing was significantly dierent (p < 0.05).
TLC n c ~ Bmth Holding Condition
Breath Holding Time TLC vs ïLCsw (Fernale)
TLC TLCsw
Breath Holding Condition
Figure 4.12.: Mean breath hold time with swallowing under the TLC breath hold
condition in male (n=7) and female (n=10) abjects. hdysis using a MO-way repeated
measures ANOV& showed that the increase in breath hold time with swallowing was
signîficantly different than non-swallowing (p < 0.05) in male and femaie subjects.
Analysis using a two-way repeated m u e s ANOVA, showed that the breath hold times
between d e s and fernales was not signincantiy different for both swallowing and non-
swailowing under TLC breath holding condition (p > 0.05).
Mean Breatb Hold
Breath Hold Condition
Tabk 4.10: The mean breath hold times * SE for each nibjects and dl wbjects (n=17),
under FRC and FRCsw breath holding condia011~~ Mean breath hold tirne during FRC
increased from 3 1.3 * 3.7 seconds without d o w i n g to 36.2 * 5.1 seconds with
Swauowing.
Bmth Holding Time FRC vs FRCsw
FRC
Birath Holding Condition
Figun 1.13: The mean breath hold times (seconds) * (SE) for subjects under FRC and
FRCsw breath holding conditions. Mean breath hold time during FRC increased from 3 1.3
*3 -7 seconds without swdowing to 36.2 * 5.9 seconds with swdowing. hdysis using a
two-way repeated measures ANOVA, showed that the increase in breath hold tirne with
swdowing was significantly different (p < 0.05).
Breath Holding Time FRC vs FRCsw (Maie)
FRC FRCm
Breath Holding Coadition
Breath Holding ïime FRC t-s FRCsw (Female)
FRC FRCsw
Breath Holding Condition
Figure 4.13~: Mean breath hold time with swallowing under the FRC breath hold
condition in male (n=7) and female (n=lO) subjects. Analysis using a two-way repeated
mezisnes ANOVA, showed that the increase in breath hold time with swallowing was
significantly difrent than non-swdowing (p < 0.05) in male subjects but not (p > 0.05)
in female subjects. Anaysis ushg a two-way repeated measures ANOVA, showed that the
breath hold tirnes between males aad females was not signifcantly different for both
swallowing and non-swallowing under FRC breath holding condition (p > 0.05).
Mern InitiaI End-Tidd Partial Pressure of Oxygen
Breath Eold Condition
FRC FRCsw TLC TLCsw
Table 4.11: The mean initiai PE+ * (SE) in mmHg, for al1 subjects (n=17), under al1
breath holding conditions (FRC, FRCsw, TLC, TLCsw). Analysis using a two-way
repeated measures ANOVA, showed that there was no signincm? difference (p > 0.05) in
the mean Uitid P d - between aii breath hold conditions.
Mean Final End-Tidai Partial Pressure o f Oxygen
Breath Hold Condition
FRC FRCsw TLC TLCsw
Table 4.12: The mean final P+- * (SE), in mmHg for al1 subjects (n=17), under al1
breath holding conditions. Analysis using a two-way repeated measures ANOVA, showed
that the decrease in the final PFpL with swallowing was statistically difEerent (p < 0.05).
Mean Initial End-Tidal Partial Pressure of Carbon Dioxide
-
Sabject Gender
Breath Hold Condition
FRC FRCsw TLC TLCm
Table 4.13: The mean initiai P d @ * (SE), in mmHg, for ali subjects (n=17), under ail
breath holding conditions. Analysis using a two-way repeated measures ANOV4 showed
that there was no significant difference (p > 0.05) in the initial PEfl& (p > 0.05).
Mean Final End-Tidal Partial Pressure of Carbon Dioaide
Breath Hold Condition
Subject Gender 1 FRC FRCsw TLC TLCsw
Table 4.14: The mean final P&Q * (SE), in rnmHg, for dl subjects (n=17), under di
breath holding conditions. Analysis using a two-way repeated measures ANOVA, showed
that the £inai P d Q with swdowing were not statistically dEerent (p > 0.05) than
without swallowing.
Rate of Perceived Exertion (RPE)
Breath Hold Condition
FRC FRCsw TLC TLCsw
Table 4.15: The mean Borg sale score I SE for al1 subjects (n= 16) obtained a11 breath
holding conditions. The mean score SE increased fiom 7.7 0.3 during FRC to 8.5 * 0.2 during FRCsw. The mean score SE increased fiom 7.4 * 0.3 during FRC to 8.3
0.2 during FRCsw.
Rate of Perceived Exertion TLC vs FRC
FRC TLCsw
Breath Hold Condition
Figure 4.14: The mean Borg scale score * SE for ail subjects (n=16) obtained under dl
breath holding conditions. Analysis using a Wicoxon Signed Rank test, showed that the
hcrease in the mean score with swallowing was statisticaliy significant (p > 0.05) between
TLC and TLCsw.
Chernoder Parameten vs Breath Hold Tme
Breath Hold Condition
Males
FRC FRCsw TLC TLCsw
Table 4.16: Table showing correlation's between chernoreflex parameters (Vb, Tp, Sp,
Tc, Sc), metabolic rate of rise (MR) and the drive to breathe (V) and breath hold time in
all conditions (FRC, FRCsw, TLC, T ' C m ) in ai l subjects and in both males and fernales.
Except for the drive to breathe (V) and breath hold t h e with TLC and TLCsw in males,
no other correlation's weie found between any of the parameters and breath hold the.
O 50 100 150 200
Breath Hold Erne (s)
Mean Vb vs Mean BHT (FRC)
O 20 H) 60 80 100
Breath Hold The (s)
Figure 4.15: ïhe relationship between the mean basal ventilation (Vb) vs breath hold time
(TLC and FRC) for aii subjects (n=17). The correlation coefficient (r) for TLC and FRC
was r = 0.5 1 3 1 and r = 0.4522, respectively.
Mean Tp vs Megn BHT (TL0
o f 1 4
O 50 100 150 ZOO
8- Hold T h e (s)
Mean Tp vs Mean BHT (FRC)
Brnth Hoid T h e (s)
Figure 4.16: The relationship between the mean peripheral threshold (Tp) vs breath hold
time (TLC and FRC) for al1 nibjects (n=17). The correlation coefficient (r) for TLC and
FRC was r = 0.0787 and r = 0.0768, respectively.
Breath Hold Time (s)
Mean Sp vs Mean BHT (FRC)
O 20 40 60 80 100
B m t h Hold Time ( 8 )
Figure 4.17: The relationship between the mean peripheral sensitivity (Sp) vs breath hold
time (TLC and FRC) for ail subjects (n=17). The correlation coefficient (r) for TL.C and
EXC was r = 0 .O 14 1 and r = 0.24 1 7, respectively .
mea an Tc vs Mean BHT (F'RC)
O 20 40 60 80 LOO
B r e d t Hdd Timt (s)
Figure 4.18: The relationship between the mean central threshold (Tc) vs breath hold tirne
(TLC and FRC) for aii subjects (n=17). The correlation coefficient (r) for I I C and FRC
was r = 0.1 1 05 and r = 0.04 12, respectively.
O 50 100 fSO 2 0
B m t h Hdd Tbnc (s)
Mean Sc vs BHT (FRC)
Figure 4.19: The relationship between the mean centrai sensitivity (Sc) vs breath hold
tirne (TLC and FRC) for al1 subjects (n=17). me correlation coefficient (r) for TLC and
FRC was r = 0.2452 and r = 0.0678, respectively.
Mean MR vs Mean BAT (TLC)
I 1 O 1 I
O 50 100 150 200
Sreath Hotd Time (s)
,Mean MR vs Mean BHT (FRC)
t L r 1 I
O 20 10 60 80 100
Bteath Hold Time (s)
Figure 4.20: The relationship between the mean rate of rise (MR) vs breath hold tirne
(TLC and FRC) for all subjects (n=17). The correlation coefficient (r) for TLC and FEK
was r = 0.0889 and r = 0.0346, respectively.
Mean V vs Mean BHT (TLC)
B m t h Hold Time (s)
Mean V vs Mean BHT (FRC)
Breath Hold Tiie (s)
Figure 4.21: The relationship between the chernoreflex drive to breathe (V) vs breath
hold tirne (TLC and FRC) for ail subjects (n=17). The correlation coefficient (r) for TLC
and EXC was r = 0.0787 r = 0.4624, respectively.
5.0 DISCUSSION
This investigation was uiitiaIly undextaken to m e r two questions: 1) is there a
relationship between b r d hold t h e and the ventilatory response to carbon dioxide in
Wects accustomed to holding their breath (Le., synchronized swimmers) and in the
general population (Le., persans who do not n o d y practice breath holding). 2) can
breath holding time be prolonged by way of swallowing. The experirnental design
incorporateci the selection of a relatively large number of subjects who performed each
rebreathing test three Mies (for a total of 9 rebreathing tests) and pediormed each breath
holding test three times (for a total of 12 breath hold tests). This rnethod required four
visits to the laboratory: one for orientation and three expenmental sessions. Since subjects
were donaîing their time and each visit required a minimum of 3 hours, it was extremely
diffidt to recru3 a large number of synchronized swimmers or other subjects that
practiced breath holding. Mer several of the synchroked swimmers dropped out of the
study, ody one synchronized swimmer was left in the study, and therefore, it was
impossible to test the original hypothesis.
Ideally, subjects of smilar gender, size and fitness should have been chosen.
However, since subjects were recruited strictly on a voluntary basis and the experùnents
were very time c o h g , such a simple population was extfemely diffidt to obtain.
Therdore, in order to allow the investigators to chose subjects f?om a large pool, both
f i e and d e subjects were used in the study, as weii as, both sedentary and athletic
subjects.
5.1.2 Rebreajkittg Tests
These experimenf~ used a revised version of Read's rebreatbing method @&in
and McAvoy, 1988; Rapanos and Du- 1997; Mohan and Du- 1997) which included
a pnor voluntary h~perventilation (5 minutes) to reduce the carbon dioxide stores in order
to study the ventilatory responses to carbon dîoxide below the centrai and penpheral
chemorefiex thresholds. In addition, a variable flow of oxygen adequate for metabolism
was administered to maintain the predetennuied isooxic levei. During the course of
rebreathing, the end-tidal partial pressure of oxygen was held constant while that of
carbon dioxide slowiy increased due to the effects of metabolism, from an initiai end-tidal
partial pressure of about 30 m g . Severai conditions were met to ensure that the
measmeci end-tidal partial pressure of carbon dioxide would reflect that of the central and
peripheral chemoreceptor environment duMg rebreatbing. First, the end-tidd partiai
pressure of carbon dioxide was the same as at the central and peripheral chemorecptors at
the start of rebreathing, and second, the rate of change of these partial pressures should be
the same during rebreathing.
To meet the fht condition, the inmai amount of carbon dioxide in the rebreathing
bag was adjusîed so that the end-tidal partial pressure of carbon dioxide rernained
unchangeci for severai breaths during the initial equiii'bration of the subject with the
rebreathllig bag. An observed plateau on the chart recordhg paper immediatety &er the
subject had switched to the rebreathing bag was indicative of proper equiltiration between
end-tidai carbon dioxide partiai pressure7 arterial and mixeci vmous blood (Figure 3.2). It
was assumeci that the partial pressure of carbon dioxïde in mixed venous blood
approximated that of the central chernoreceptors. Howwer7 this situation may not have
happened for scample, the hypocapnia achieved during hypemeatilation was unequai in
the centrai or other compartments due to changes in caebral blood flow.
The second requirement, for equal rates of rise of carbon dioxide partial pressures
at the central and peripheral chemoreceptors and end-tidal partial pressure as measured at
the mouth, was shown to be met at rest by the modeling experïments of Read and Leigh
(1 967), but may not be met under our experimeatai conditions for similar reasons.
The data was analyzed as detailed in the methods by f i h g either two or three
straight line segments rather than a generalized c w e fitthg technique (Figure 3.4). As
Figure 3.4 demonstrates, the thresholds were usuaiiy discernible by eye and the least
squares fit was used to veri@ their values without observer bias.
The choice of using the modified rebreatiiing method of hifi and McAvoy
(1988), dong with the additive chernoreflex rnodel, to chanicterize the ventilatory
response to carbon dioxide was confïrrned by our resultq as well as those obtained
previously @utnn and McAvoy, 1988; Rapanos and Dutnn, 1997; Mohan and Dufnn,
1997).
S. 1.3 B;reciak H&g T ~ L P
There were several potentïal areas of error that had to be overcome with the breath
holding part of this study. These included: subject motivation, proper fit of the breath
holding mask with the subject's fàce, and accidental or voluntary respiration through the
mouth or nose by the subject.
To more accurately assess the breath hoIding capability of a subject, it was
necessary for the subject to give a maimnal effort during each test. As an investigatcr, it
was extremely diffidt to detennine whether any given nibject a d y gave a maximû
effort. In order to try and minimize intra-subject var *il@, all subjects were asked to rate
th& perceived e d o n (urge tu breathe) to the breath hold test on a Borg scale
(Appendix 3). As can be seen nom Table 4.15 and Figure 4.14, intra-subject variability
varied slightiy and was statisticaiiy significant ody between TLC and TLCsw.
It was f o d during the pre-triai study, that it was more cornfortable, easier to use,
and reduced the chance of accidental or vohuitary respiration during breath hold to use a
face ma& as opposed to a mouth piece. However, the tàce mask was not without fault,
one king that there was a slight chance that some expired gases codd escape through the
sides of the mask if the fit was not secure enough. In order to overcome this problem, a
facemask (Vial Signs hc., Medium Size) that had an adjustable air bladder was use& The
air bladder allowed the mask to be contoured and adjusted to fit the face of the subject
more preciselyY
A gas sampling probe at the dista end b i d e the tace mask, enabled analysis of the
initial and final end-tidal partial pressures of carbon dioxide and oxygea The probe also
had a secondary purpose, wtiich was to make sure that none of the subjects were inhaling
or exhaling durhg the a d breath holding or d o w i n g part of the experiment. Shouid
a subject voluntarily or invoiuniady inhale or exhaie chhg bteath holding or swdowing,
the gas probe would immediately detect changes in end-tidal partial pressure of carbon
dioxide and oxygen, d t i n g in the temination of the test. Another way of verifying
subject adherenœ to the test pmtocol was by examinhg the chart recordhg for any signs
of deviation in the end-tidal pamal pressure of carbon dioxide and oxygen,
K t C w u e of R d
52. I Rebreding
S.2.l.l h a l Ven filafion
The measurements of sub-threshold or basal ventilation are in agreement with the
concept of a wakefbhess sthdus (Fink, 1961) governing ventilation below the
chernordex thresholds, for example, neural drive in the M o r d mode1 of the
chemoreflexes (Lloyd and C h - 1963). The nib-threshold ventdation (Table 4.2)
for each subject varied considerably, similx to previous fïndings in this laboratory (Duftin
and McAvoy, 1988; Baker et al., 1996; Rapanos and hifnn 1997; Mohan and Duffin
1997). Other investigaton have found a variety of ventilatoty responses to voluntary
hyperventilation ranging from penods of apnoea, eupnoea and increased ventilation, the
latter presumed due to short term potentiatioa (Folgering and Durlinger, 1983). As Meah
and Gardner (1994) point out, the responses are mixed and vary between individds, and
our observations support such a view. Basal ventilation ranged fiom 2.44 ~-d' to 20.75
mi ri', which is similar to previous measurements of 3.7 ~ m i d to 17.3 min*'
(Rapanos and hifnn, 1997) and 3 -9 ~ - m h i ' to 14.7 L ~ K ' (Mohaa and DufEn, 1997).
When examiaing basal vemilation between male and femaie subjects, no differences were
found.
B d ventilation did not hcrease! with hypoxh in this study, which is in agreement
with previous iwestigttions in this laboratory. Dufnn and McAvoy (1988), Rapanos and
Dufnn (1997) a d Mohan and Duffin (1997) used rebreathing after hypmentilation to
produce a progressive hypoxia at carbon dîoxide end-tidal partial pressures below the
chernoreflex thresholds, and found no ventilatory response umü the carbon dioxide level
exceeded a threshold.
r 2.1.2 ~milirer~~
The peripheral-chemordex thresholds for carbon dioxide were found to
vary Eom an overall mean of 42 mmHg at an isooxic end-tidal partial pressure of 150
mmHg to 39 nmiHg at an iw-oxic end-tidal partial pressure of 40 mmHg for the subjects
of these experiments. These estimates are similar to previous hdings &om this laboratory:
an overall mean threshold of 39 d g at im-oxic end-tidal partial pressure of 75 mmHg
@ufno and McAvoy, 1988). Penpheral-chemoreflex thresholds for carbon dioxide were
also found to Vary âom an overail mean of 41 mmHg at an imxic end-tidal partial
pressure of 100 mmHg to 39 mmHg at an isosxic end-tidal partial pressure of 40 mmHg
(Mohan and Dufnn. 1997). When examining periphed threshold levels between male and
f d e subjects males were found to have a statistically higher peripheral threshold level
than fernales.
The sensaMty of the peripheral chemorefkx to carbon dioxide varied markedly
with hypoxia and betweea subjects. The o v d mean value for 10 subjests of 1.7
~-m.in-*-rnrnH~~~ at an imxic end-tidal pamal pressure of 80 M g is close to that of
previous findings nom this laboratory of 3.5 ~ = m h - ' - r n m ~ ~ ~ ' for 8 subjects at an iso-oxic
end-tidal partial pressure of 75 nmiHg (ihflïn and McAvoy, 1988), and 2.7 L=min-
1 -rnmHg8' for 7 subjects at an iso-oxic end-tidai partiai pressure of 80 mmHg (Mohan and
DirfniS 1997). When examining p e r i p h d sensitivity Levels between male and f d e
subjects, males were found to have a statistically higher peripheral sensitivity level than
fernales.
5.29.3 Centrai CXemorejZa
The centrai-chemoreflex threshold for carbon dioxide during rebreathing
was found to decrease from an overall mean of 48 mmHg at an iso-oxic end-tidal partial
pressure of 150 mmHg to 47 mmHg at an iso-oxic end-tidal partial pressure of 40 mmHg.
However, the latter result was determined for only 9 subjects because in those nibjects
with highly sensitive peripheral chemoreflexes, the end-tidal carbon dioxide partial
pressure did not exceed the central chernoreflex threshold before reaching their ventilation
f i t . However, since this decline was not statistically significant one can not conclude that
hypoxia may influence the centrai chernoreflex threshold for carbon dioxide.
Previous results nom rebreathing experiments in this laboratory found overall
mean thresholds of 46 mmHg for 8 subjects @utnn and McAvoy, 1988), 48 mmHg for 6
subjects (Baker et al., 1996) and 48 m . g for 7 subjects (Mohan and Dufnn 1997).
When examining central threshold between male and fernale subjezts, no dinerences were
found.
The overall mean of the centrai-chernoreflex sensitivity to carbon dioxide in the 17
subjects in this study was 3.5 ~ - m i n " - m m ~ ~ ~ ' . This r d t is similar to previous
measurement o f 4.29 ~ - m i n " * m m ~ ~ ~ ' in 8 subjects (Ddh and McAvoy, 1988) and 5.0
~ * m i n " = m m ~ ~ ~ ~ in 7 subjects (Mobaa and Dufni5 1997), but greater than the 1.8 Lrnin-
'-mrnHg-' reported by Baker et al. (1996) in 6 subjects. When examining central sensitivity
levels between d e and femaie subjects, males were found to have a statistidy higher
central msithdy levei than f d e s .
Ui general, these difference between fernale and male aibjects with both the
pexipheral and central sensitivities reflect the cliffierences between individuais as found by
other experimenters (for review see McGurk et al., 1995). However, there has been no
previous herature reiated on the differe~lces between female and male subjects concerning
merences with the peripheral thresholds.
5.2.2 Br& Hdcling
In agreement with previous snidies (Engel et al., 1946; Otis et al., 1948;
Mithoefer, 1953; Vacca et al., 1 W6), ail nibjects had significantly longer breath hold times
when the tests were perfonned at the pater lung volume (TLC) than at the srnaiier one
(FRC). Also in agreement with previous hding (Engel et al., 1946; Otis et al., 1948;
Mithoefer, 1953; Vacca et al., 1946), abjects had an increase in end-tidal partial pressure
of carbon dioxide and a decrease in end-tidai parriai pressire of oxygen both with and
without swallowing. The overail mean decreas in the end-tidal partial pressure of oxygen
with swalIowing was statistically siifiaicant. However, only subject 10 had a really large
change (12 mmHg with TLCsw and 16 H g with FRCsw) in end-tidal partial pressure
of oxygen and dropped below 50 mmHg8 Subject 10 also had the longest breaîh holding
time both with and without swaüowing, and one of the larger increases (18% and 34%) in
breath holding time with swdowing, both at TU: and FRC, respectively. Although,
subject 10 did have a hypoxic final end-tidd partid pressure of oxygen, the subject did not
cornplain of or show any adverse signs of hypoxia (Le., non-responsiveness).
As previousty stated, there has been very iittie research done on breath holding and
d o w i n g (see section 1.6 and 1.7). Howevei, our findings are in agreement with the
three other refereices found in the literature that relate to breath holding time and
swallowing (Meltzer, 1883; Heath et al., 1968; Godfiey and Campbell, 1969) and show
that breath holding t h e can be increased by the simpIe act of swdowing- UnfortunateIy,
Heath et al. (1968) and W e y and Campbeil (1969) do not give any reason for this
phenornenon, and simply state that swdowing prolongs ones breath holding the. Meltzer
(1883) States that he wuld prolong his breath holding time by 10 to 15 seconds by
swallowing when reaching his breakhg point. Our study found that the mean breath
holding thne for ail subjects increased by 6.6 seconds while breath holding at TLC and
increased by 4.9 seconds whiie breath holding at FRC. Meltzer (1883) states that
swdowing causes an inhiiition of the breathing center. Despite the stimulation of the
respiratory center fiom an increase in the end-tidal partiai pressure of carbon dioxide and a
decrease in the end-tidal partial pressure of oxygen, MeIzter states that the inhibition
created by swallowing in the breathing center is much stronger than the stimuli to breathe,
and therefore, one receives a temporary relief from these sensations.
Although Meltzer's findings are in agreement with our OWII, Meltzer's study leaves
many unrinswered questions, and therefore, is diEcuit to compare with our study. Meltzer
was both the sole investiga~or and subject in his study-, he does not report on how many
trial nms were done, nor does he reveal at what lung capacity were the tests performed. In
addition, w data concerriing final end-tidal partial pressure for carbon diofide and oxygen
are &en. Aithou& swaüowing does i n b i respiration (Do-, 1968; Martin et ai.,
1994), it does so oniy momemarily, 0.5 to 3 -5 seconds @owty, 1968). It is therefore
unlikeiy that Melzer's reported increase in breath holding t h e of 10 to 15 seconds is due
simply to & i o n of the respiratory center caused by swallowing.
Therefore, if inhibition of the respiratory center by swallowing can accuunt for
only a 4 increase in breath holding time due to swallowing, how does swallowing
hcrease breath holding time despite an increase in the "urge to breathe". There must be
some affixent input inhibition fkom other areas of the body that temporarily alleviates the
discornfort of these respiratory sensations and so ailows breath holding to continue. These
aaérent areas include: recepton in the lungs (PSR), Iower and upper airway receptors,
and thoracic wd receptors.
It is possible that the action of swallowing is picked up by the above mentioned
receptors, specifically, the upper airway receptors and thoracic wall receptors, and that
these in tum send inhitory afferent sigds to the respiratory centers located in the brah
stem. Previous studies (Hü1 and Fiack, 1908) lend support to this theory. W and Flack
demoostrated that a person could prolong breath holding by rebreathing into a bag that
actually worsened their blood gas Ievels. More recently, Flume et al. (1995) also
dernollstrated the same concept by having their subjects perform an expiratov or
inspiratory movement at their breakhg point, but that did not change their blood gas
teveis. Hume et al. (1995) found that the subjects could prolong th& breath holdmg time
by this method. b e et al. (1995) suggested that the prolongation of breath holding Mie
and refief fkom the respiratory distress reSuIting fiom the inspiratory movement be due to
the inhriitory &écts of the pulmomy stretch receptors. In another study by Fiume et al.
(19%), breath holding time and relief f?om breath holding by rebreathing was studied in
n o r d subjects and in subjects with lung transplants or heart transplants. Flume et al.
(19%) found that heart transplanteci and hmg transplanted subjeçts had eaflier onset of,
and more rapidiy developing, distress during breath holding, which resufted in shorter
breath hold times than observed in normal subjects. Agah Fiume et al. (1996) attn'buted
this ciifference between the normal subjects and the subjects with either heart transplants
or lung transplants to puimonary stretch receptors.
These studies demonstrate and support the theory that the pulmonary stretch
receptors, thoracic waii receptors, and upper and lower ainvay receptors can increase
breath holding time despte unfavorable gas conditions, if these receptors are stimulateci.
However, this theory does not explain why an increase in breath holding t h e was
not seen in 1 subjects with swailowing nor wtry some subjects had a greater percent
increase in breath holding time with swallowing. One possible explanation as to why some
people had lower breath holding times with swallowing couid be due to the fact that the
bolus of saliva swallowed was extrernely small, and therefore, they didn't produce a great
deai of movernent in the head, abdomen, chest wall, and shoulders. The same argument
can also be used to defend the reasoa why some subjects had greater increases in breath
holding time with swdowing versus other subjects who had only minor increases in breath
holding the. It d d be argued that somehow, greater swallowing movements can cause
a greater inhibition of the respiratory center and a greater relief from the respiratory
discodort sensations that is caused by the worsming blood gas leveis during breath
holding. Perhaps, a greater swdowing movement activates or heightens the number of
a f k e n t s h d a t e d , which summate into a stronger inhiiition signai, thereby creatkg a
greater relief from the discornfort of breath holding, and thereby creating a greater
increase in breath holding time.
5-23 Bmd Holiting And ltr R è k h t d @ To 7ne Vindilatory Responsr to Cmbovr Diaride
The relationship between the duration of breath holding time and the ventilatory
response to carbon dioxide bas been studied for many years. As descn i in section 1.8,
there are varying views conceraing the ventilatory responses to hypoxia and hypercapnia
and th& relationship to breath holding tirne
Masuda et al. (1981) found that Japanese pearl divers (Ama) have a blunted
hypoxïc ventilatory response and Bjurstrom and Schoene (1987) also found a blunted
hypoxic ventilatory response in synchronized swhmers. Recently, Feiner et al. (1995)
reported that the hypoxic ventiiatory response was a predictor of breath holding
perfo~nance in a normal population. Blunted hypercap~c ventiiatory responses have dso
been observed. Masuda et al. (1982) and Song et al. (1963) observed lowered hypercapnic
ventilatory response in other groups of Ama. Schaefer ( 1 965) found that submarine escape
tower trainers also exbibiteci a blunted hypercapnic ventiiatory response. A lower
hypercapnic ventilatory response has also been found in undenvater hockey players @avis
et al., 1987), Royal Navy divers mono et al., 1979) and in elite breath hold divers (Grassi
et ai., 1994).
However, the r d t s fiom the present study did not find any relationships between
any of the chernordex pararneters (i.e., % Tp, Sp, Tc, Sc, Vb); measured during the
vemhtory cesponse to carbon dioxide rebreathlog tests and breath holding tVw in either
male or f d e subjects.
A strong correlation however was seen when comparing the drive to breathe (V) in
male subjects oniy and breath hold time with FRC (r = 0.9377) and FRCsw (r = 0.9521).
A weaker correlation was aiso seai when cornparhg the drive to breathe o . a n d breath
hold time with TLCsw (r = 0.7499). No correlation was seen when cornparhg the drive to
breathe (V) and aii breath hold conditions to f d e subjects and al1 subjects combineci.
Most studies have measured ventilatory responses and not breath holding ab-
(norio et ai., 1979; Masuda et al., 1981; Masuda et al., 1982; Schaefq 1965; Song et al.,
1963). Other studies have investigated both the hypoxic ventilatory response and the
hypercapnic ventilatory response dong with breath holding ability (Bjurstrom and
Schoene, 1987; Davis et al., 1987; Feiner et al., 1995; Grassi et al., 1994). AU of these
studies with the exception of Feiner et al. (1995) compared mean values in the group of
interest to the values in a wntrol population In so doing, their conclusion couid be
strongly influencecl by selection bias or by confounding variables that were not rneasured.
These shidies also cannot conciude how strongiy ventilatory responses determine breath
holding ability in normai indivïduaIs.
One must also question the methods used to measure the ventilatory responses to
carbon dioxide in these studies. The majority used the steady-aate technique to
characterize the subject's ventilatory response to carbon dioxide (Schaefer, 1965; nono et
al., 1979; Masuda et al., 198 1; Masuda et al., 1982; Bjurstrom and Schoene, 1987; Davis
et ai., 1987; Grassi et ai., 1994). While Feiner et al. (1995) used a partial rebreathuig
method to measure the vernilatory response to &n dioxide. As previously mentioned in
the Ultroductiob there are inherent disadvantages in using the steady-state technique to
characterize the subject's ventilatory response to carbon dioxide. The main one king that
the in- in Ca during the expriment wiil cause an incr- in cerebral blood flow,
which in turn, will cause a washout of the stimulus itself Othen studies used Read's
rebreathing method (1967) to ctiaracterize the subject's ventilatory respoose to carbon
dioxide (Song et al, 1963; Davis et al., 1987). The problem with the rebreathing method
in these studies is that the Urvestigaton used a large rebreathing bag. By ushg a large
rebreathing bag, the ability to ensure proper nn>ang and equilibration between the bag and
the subjects is decreased considerably.
Feiner et al. (1995), did examine both hypoxic and hypercapnic ventilatory
respoases in a normal population and concluded, %e hypoxic ventilatory response, but
not the hypercapnic ventiiatory response, is a si@cant predicîor of breath holding
performance." They used an isocapnic steady-state partial rebreathing method in
determinhg hypoxic ventilatory response and a hyperoxic steady-state method in
detemiining hypercapnic ventilatory respoose.
Because other shidies used other different methods to determine the ventilatory
response to carbon dioxide it is difEicuit to directiy compare the results of this study to the
others. However, recent studies @utso and McAvoy, 1988; Rapanos and Duffin, 1997;
Mohan and DufEn, 1997) have shown that the rebrrathing method used in this study to be
reliable in descrr'b'mg the ventdatory response to carbon dioxide. And so the results of this
study shouid be considered more closely
One very diflEicult question to m e r is why no relationslip was found between
breath holding time and the chemorefiex sensitivities. ûne would assume that a person
with a higher sensitnnty to hypercapnia wouid have a lower breath hold tirne than someone
with a lower sengtMty- Therefore!, even though a very reliable method of measuring the
chemorefiex sezdhdies was used compared to previous studies, no relationship was
found.
One possible e x p l d o n is that, aii the vafikles that determine br& holding
time (ie., lung volume, pH, PC&, P a and ventilatory drive to breathe) contribute in
vaxying amounts in each person. That is to say, in one subject (A), initial lung volume, pH,
drive to breathe conaibute more to the overd determinant of breath holding time than the
chernordex sensitivities, while in another subjecî (B), t is the chernoreflex sensitivities
that play the major determinant in breath holding duration. And so, in this way although
subject (A) has a higher setisitivity to carbon dioxide than subject (B), subject (A) could
have a longer breath holding t h e due to the fact that subject (B's) breath holding duration
is mody controiied by their sensitivity to carbon dioxide.
6.0 CONCLUSIONS
1. No relationships were found between any of the chemorefiex (Vb, Tp, Sp, Tc, Sc, and
MR) parameters and the breath holding conditions (TLC, TLCsw, FRC, FRCsw). No
reiatïonships were found between any of the chernoreflex parameters and the breath
holding conditions when w m p a ~ g mdes and fernales as well.
2. .We subjects were found to have signincantly (p < 0.05) greater levels of peripheral
threshold (Tp), peripheral sensitivity (Sp), and central sensitivity (Sc).
3. A strong wf~efatioa howwer was seen when cornparing the drive to breathe (V) in
male subjects ody and breath hold time with FRC (r = 0.9377) and FRCsw (r =
0.952 1). A weaker correlation was also seen when comparing the drive to breathe (V)
and breath hold t h e with TLCsw (r = 0.7499).
4. Fourteen of the seventeen subjects were found to have a significant (p<0.05) increase
in breath hold time with swallowing in both TLCsw and FRCsw. A significant
@<O.OS) decrease was found in the final end-tidal partial pressure of oxygen of both
TLCsw and FRcsw.
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A COPY OF TEE CONSENT FORM THAT WAS READ AND SIGNED BY ALL
SUBJECTS PRIOR TO THE COMMENCEMENT OF TESTING
DLPARTMENT OF PHWlOLOGY FACULTY OF MEDIQNE Medical Sciences Building Toronto, Ontario, Canada gL M5SlA8
Telephone: (41 6) 978-2674 Fax,- (416) 978-4940
Aw~-~-
UNlVERSrrV ûF TORONTO
VOLUNTEER CONSENT FORM
S u b j ~ s participatins in the inves@tioon must ùiitia(S coqlete the Phyncll Aetmcy Readiness Questjoiinaire (PAR-Q). This questiOrmaPt is b e i q administd in order to ensure tbat y w are not subject to arry stress refated cardiac aifmcntn It shauid be noteci thrrt this shidy is Linriteci to noksmokers.
Upon wmpletion of the qurriiomisirr y a i will be askeâ to retum to the Iaboratory on 6ve sepamte d o w There d be a rninirmmi of 24 houn between visits to the laboratory. You will bc: asked to abstain fiom &g and to avoid c a f f ' i e û mmtr for at lcaa 2 h a i n pnor to cuming to the laboratoiy. The length of eacb wiiIbeapprolrimatdy64b9ûrriirides.
fhe fint visi? d bc used to taaiaim. yai with the a p r i m d apparahcr acanrom you to breaibing ttimugh a mouthpiece and to the sendons of rebreathing, as weli as to becurne fimiinariad with the swallowing technique and the sensaiions f& wfien one apptOILChes the breaking point.
ïhe second and third visits to the laboraîory wiil be used to obtain data on the ventiiiory rwponse to Iow levels of oqgen and hi& levek ofcarbon &xi&.
The rdnathmg rmbod uscd in t b imrestigation Ïnciuda a prior hypcrvemilabon ro as to Iowa crrbai dioxide Iew&.
You will Wear a nose ciip aad breath through a mouthpiece which wiO aiiow one to switch fiom rocwn air to the rebreathing bag at the appopidt tirne. A hger probe puise oximeter will k wom tu measurt a r t d oxygen saturation and kart niue.
Mer sitting quietly fa 5 iriirriites bnathing room air. you wiii be asked to hypmmhte- Mer 5 minutes of hypaveentilation yau wil( thar swhh to the nbreathing bag. A samplnig tube wiii be used to coiltmuously monitor the room air as wed ss the carborr diode and oxygen levds,
The fourth and fifüi visits to the taboratory win be used to obtain data on the your breath holding abïrrty.
Carbon dioxide and oxygen k e b wiU be obtaniad b&n and afta brrath holding has bœn c o m p k d This wiU bedone b y h a v i n g y o u w c o r 8 ~ timt isspbcially & a î W i t h a ~ t u & a n d wiüùcpoationedin h n t of your mouth Hemt rate a d oxygen satudon wiff aIso be monitorcd aliring this phase of the mvtsÉigatios and W y the tirne tnken during tbe bteath hoM wiii also be obtamed
The sîress inaand Ehrring the breath haidhg phase of tk in-gain is rriiaimal. A feeLing of amiety and f c s t l ~ m a y a l s u befkitasoneapptoacbesthebreakingpoint.
l n d i v i a conseutmg to mcipate in this study may withdfaw at any tmie without any Mher obligation to the principle investigator and his cO.imresti&ator. F- participation in the investigation will be strict& con6idenriai. AIthooigh panicipation in the investigation w d l likely not provide any Unmediate b e n e the ezrpcrimmtal resuits obtained wiü contn'bute to the developmenî and advancemenî of the understarsding of the mechanisms t h c o m l respiration
Subjects haviag any questions regardmg the exper imd procedurt d o r participation are encouraged to ask any of the mvestigatow prior to si& the vohmtœr coastnt fbrm A copy of the form will be @en to di subjezu.
1 have read the above irrfofmation and derstand the test pr- and the nsks involveû. I consent participate in the investigation
Phone Numbtr, (Home):
Date
A COPY OF THE PHYSICAL ACTIVITY READINESS Q C T E S n O N m (PAR-Q) THAT WAS ADMINTSTERED TO EACH SUBJECT P W R TO
COMMENCEMENT OF TESTING
Ekprhted with permision h m the Canadian Society for E-YefciSe Physiology. The P A R 4 and You is a copyrighü!d pmexesk screen owned by the CSEP (1997).
-s.y-Boby- - ~ m i o y o u a m a m ~ y w bac - mmmbu. a tmwtny w q n t r a n g . c b a n r c h t t u ~ f o r y a u - ~ i r r U U - u p ~ b o o y ht stmdd n m e w m too hign nortoo Igw)
r r y a m w ~ * - -mmYow'-f ~ o c K W I ~ ~ N . ) Y O ~ I ~ O ~ T ~ O ~ M W
APPENDM III
A COPY OF THE BORG SCALE -CH MEASURES PHYSIOLOGIC STRESS REUTED TO THE SUBJECT'S RATE OF PERCEIWD EXERTION
RPE SCALE
O Nothing at al1
0.5 Very, very weak
1 Very weak
2 Weak
3 Moderate
4 Somewhat strong
5 Strong
6
7
8
9
10
Very strong
Very, very strong
BREATE-BY-BREATH PLOTS OF THE VENTILATORY RESPONSE TO
CARBON DIOXIDE DURING TEE MODIFIED REBREATEUNG TESTS AT
ALL ISO-OXIC (40,80,150 mmHg) REBREATHMG LEVELS (N=l7)
LEGEND OF FIGURES: POz= 40 mmEg
O PO2= 80 mmHg
PO2= 150 mmHg
NOTE TO USERS
Page(s) not included in the original manuscript are unavailable from the author or university. The manuscript
was microfilmed as received.
UMI
l I
30 35 40 45 SO 55 60 65
end-tidal PC02 (mmEIg)
v vs PCO*
30 35 40 45 50 55 60 65
end-tiâai P C 4 ( m g )
v vs PCO*
NOTE TO USERS
Page@) not included in the original manuscript are unavailable from the author or university. The manuscript
was microfilmed as received.
UMI
end-tidai PCOI ( m d g )
v vs PCO*
APPENDM V
BREATH-BY-BREATH PLOTS OF ENI)-TIDAL PARTIAL PRESSURES OF
OXYGEN DURING TEE MODLFlED REBREATEIING TESTS AT ALL
ISO-OXIC (40,80,150 m d g ) REBREATHING LEVELS (N=ll)
LEGEND OF FIGURES: 0 PO2 = 40 m d g
PO, vs Time
Time (s)
PO, vs Time
Time (s)
PO, vs Time
Time (s)
Time (s)
Time (s)
PO, vs Time
120 f E -- LOO
Time (s)
PO, vs Time
Time (s)
PO, vs Time
i . O---- J+-[
O 60 120 180 240 300 360 420 480 540 600
Time (s)
PO, vs Time
Time (s)
PO, vs Time
Time (s)
PO, vs Time
Time (s)
PO, vs Time
Ti me (s)
PO, vs Time
Time (s)
PO, vs Time
140 m m . 8
T i w (s)
PO, vs Time
Ti me (s)
PO, vs Time
Time (s)
PO, vs Time
Time (s)
APPENDM VI
BREATH-BY-BREATE? PLOTS OF END-TIDAL PARTIAL PRESSURES OF
CARBON DlOXIDE DURING THE MODIFED REBREATEING TESTS AT
ALL ISO-OXIC (40,80,150 mmHg) R E B R E A m G LEVELS (N=l7)
LEGEND OF FIGURES: + = 40 mmHg
PC02 vs Time
Time (s)
PCO, vs Time
Time (s)
PCO, vs Time
'ilme (s)
PCO, vs Tirne
Time (s)
Time (s)
SUBJECT 6
PCO, vs Time
Time (s)
PCO, vs Time
O 60 120 180 240 300 360 420 480 540
Time (s)
PCO, vs Time
Time (s)
PCO, vs Time
O 60 120 180 240 300 360 420 480 540 600
Tirne (s)
PCO, vs Time
Time (s)
PCO, vs Time
Ti me (s)
PCO, vs Time
Time (s)
PCO, vs Time
Time (s)
PCO, vs Time
Ti me (s)
PCO, vs Time
Time (s)
PCO, vs Time
Time (s)
PCO, vs Time
Time (s)
APPENDIX VII
RAW DATA OBTAINED DURING THE MODIFIED REBREATEfINÇ TESTS
AT ALL ISO-OXIC (40,80,150 mmHg) REBREATEING LEVELS (N=l7)
1 DAY ONE 1 DAY TWO 1 DAY THREE 1
S p (L.min-'-mdg) Tc SC (~-rnin-'-m.mH~) Rate of Rise (mmHg-min-')
1 DAY ONE 1 DAY TWO 1 DAY THREE 1
3 -4
47
0.85
5.9
, Tc @mg) Sc (L-rnin-'-rnmHg) Rate of Rise ( ~ g - m i n " )
5.0 - -
50
1.9
5 -9
Vb min-') 14-92 12.06 5.5 1
- 44
6.5
56 -
Sp (~-uih-'-mrnH~) Tc ( m g ) SC (~-min-'-rnrnH~) Rate of Rise (mmtigmin-')
50
I .3
4.7
4.6
51
2.4
3.9 a
- 55
1.6
6-9
4.4
- 42
2.9
3 -2
1.3
51
I . 1
3.6
REBREATHING DATA
Iso-Oxic Level(4û mmH@
1 DAY ONE
Sp (L=lnh-'-mrnHg)
Tc (mMg) Sc (L-min"-mrnHg) Rate of Rise (mm~gmin-')
1 DAY ONE 1 DAY TWO 1 DAY THREE 1 DAY FOUR 1
Iso-ûxic Level (1 50 mmH&
1 DAY ONE 1 DAY TWO 1 DAY THREE 1 DAY FOUR 1
1 DAY ONE 1 DAY TWO 1 DAY THREE 1
Sp (L-min%nm~g)
, Tc ( m g ) Sc (~=mln%nmH~) Rate of Rise (mm~g-min")
1.7 - -
4.8
Sp (~.mÜi'*rnmH~)
Tc ( m g ) Sc (Lmin~'*mrnHg) Rate of Rise (rndg-min-')
1.2
53
1.2
4.2
1.3 - -
4.7
- 45
2.1
4.7
1 .O
51
1.2
4.5
- 46
1.6
5.6
1 DAY ONE 1 DAY TWO 1 DAY THEEE 1
1 DAY ONE 1 DAY TWO 1 DAY THREE 1
Sc (L-min-'-mrnHg) Rate of Rise (mm~g-min-')
1.7 4.3
Sp (~-min-'-mrnHg)
Tc ( m m 3 ) Sc (L-minmin'-mdg) Rate ofRise ( m m H g = ~ ' )
1.2 3.8
1.2
53
1.8 3.8
3.1 3.9
1.4 - - 3.7
0.9
55
1.3 3.4
REBREATHING DATA
Isd3xic Level140 mmH@
1 DAY ONE ( DAY TWO 1 DAY THREE
1 DAY ONE 1 DAY TWO 1 DAY THREE 1
Sp (~-min-'-mm~~)
, Tc ( H g ) SC &,-minl-mm~~) Rate of Rise (mm~gmin")
DAY ONE DAY TWO DAY THREE
8.05 17.20 12.49
[ Rate of Rise (mm~gmin-') 1 4.7
-- 1 Rate ofRise (mrnHg--') r 1 4.6 1
2.2
49
1.2
5.1
1.5 l 0.5
47
0-9
4.9
4.5
45
2.1
4.4
4.8
REBREATHING DATA
Iso-ûxic Level (40 rnmH@
DAY ONE 1 DAY TWO 1 DAY THREE 1
1 DAY ONE 1 DAY TWO 1 DAY THREE 1
Sc ( ~ - d ' * m r n H ~ ) Rate of Rise ( ~ ~ i ~ ~ ~ ~ g r n i n " )
3.8 4.5
5.4 3 -6
5.3 5.9
REBREATHING DATA
1 DAY ONE 1 DAY TWO 1 DAY T I R E
Iso-ûxic Level ! 150 rnmH@
1 ~b &min-') DAY ONE
7.77
. Tc I - 47
2-9
3.8
Sc (L-&'-mmHg) Rate of Rise (mxnHg-min'')
DAY TWO
5.68
48
2-2
4.4
- 3.3
DAY THREE
9.43
DAY ONE DAY TWO DAY THREE
1 3 -43 13-12 15.28
1 DAY ONE 1 DAY TWO 1 DAY TKREE 1
Tc (mw3) SC (L-miri'-mm~g) Rate of Rise ( ~ g - m i n - ' )
- -
3.1
- -
2-9
52
0.8
3 -7
REBREATHING DATA
Iso-Chcic Level(4û mmH@
1 DAY ONE 1 DAY TWO 1 DAY THEEE 1
1 DAY ONE 1 DAY TWO 1 DAY THREE 1
REBREATHINC DATA
~ D A Y ONE ] DAY TWO 1 DAY THREE /
1 DAY ONE / DAY TWO ( DAY THREE 1
Sp (L-min-'*mrnHg)
Tc ( m e ) Sc (~-*'-mrntI~)
Rate of Rise (mm~g-min-')
- 43
1.1
4.1
- 40
1.3
3.7
- 42
1.7
3.8
1 DAY ONE 1 DAY TWO 1 DAY THREE 1
-- -
Sp (L-min~'-mrnHg)
Tc ( m g ) Sc (L-min-'*mmHg) Rate of Rise (mm~~min")
Sp (~-mi~i'-mrnHg)
Tc @mg) Sc (L-miri'-mmHg) Rate of Rise ( m m ~ g h - ' )
3.1 I
52 9.9
4.5
- -
4.2
51
8.6
5.3
- - . .
4.3
54
11.7
4.4
6.7
56
11.4
5.2
2.1
51
9.0
5.1
3.7
57
9-7
4-2
REBREATHING DATA
Iso-Oxic Levet (40 mmH4)
1 DAY ONE
Iso-ûxic Level @O mmH@
1 DAY ONE 1 DAY TWO 1 DAY THREE 1
s p ( ~ - m i e ~ - m n ~ ~ )
Tc ( w g ) Sc min-' =mmHg)
Rate of Rise (mrnHg-min")
- 38
1.1
4.2
Sp ( ~ m i n - ' - m m ~ ~ )
Tc (-8) Sc ( ~ m i r i ~ - m r n H ~ ) Rate of Rise (nim~~min-')
- 36
1.1
4.0
- 39 1.1
3.8
- 38
1.5
4.2
O
39
1-1
4.2
- 40
1.5
4.1
REBREATHING DATA
1 DAY ONE 1 DAY TWO 1 DAY THREE 1
DAY ONE DAY TWO DAY THREE
Vb &-min-') 8.26 8.81 -
R.E%REATHING DATA
DAY ONE 1 DAY TWO 1 DAY THREE 1
1 DAY ONE 1 DAY TWO 1 DAY THREE 1
S p (~*mixi ' -mm~g)
Tc (&g) Sc ( ~ . m . h % n m ~ ~ ) Rate of Rise (mrnHgmin-')
1.3
58
19.2
4.4
1.2
55
8.2
5.1
1.2
55
3 -4
5.2 -
REBREXTB[ING DATA
1 DAY ONE 1 DAY TWO 1 DAY THREE 1
DAY ONE 1 DAY TWO 1 DAY THREE
Sp (~-min"mmH~)
Tc ( m g ) Sc (~-min-'=tnmH~) Rate of Rise (rnmHg-min-')
0.5
48
3 -0
4.6
Sp ( L = ~ ~ l * m ~ g )
Tc ( H g ) SC (~-min"-mm~~) Rate of Rise (mm~gmin-')
- 46
3.8 4.8
0.4 - -
4-6
- 45
3 -2
4.1
- 50
3.9
4.9
- 47
2.3 3 -7
REBREXTEIING DATA
Isdhtic Level140 mmH@
1 DAY ONE 1 DAY TWO 1 DAY THREE 1
/ DAY ONE 1 DAY TWO 1 DAY THREE
Sp (~ -Gn ' -~nrn~~ )-
Tc ( m g ) Sc (~.xxlin-'*rnmH~) Rate of Rise ( m m ~ g m i d )
1 Rate of Rise ( m g - m K 1 ) 1 3.5 4.6 4.8
1 DAY ONE 1 DAY TWO 1 DAY THREE 1
--
5.9 - -
3.2
7.1 - -
5 -4
. - - - - -
Sp (L-min-'-me)
Tc (mm&?) Sc (~-min~'*rnmHg)
Rate of Rise (mm~gmlli')
5.8 - -
4.5
- 46
4.3
2.6
- 49
5.1
4.5
- 46
4.5
3 -9
REBREATHING DATA
1-c Level(4û mmH@
1 DAY ONE 1 DAY TWO 1 DAY ïEWZE 1
1 DAY ONE 1 DAY TWO DAY THREE
Sp (L-,-mln*'-mm~~)
Tc ( m g 1 Sc ( ~ - m i n - ' - m m ~ ~ )
--- - - - - - p- ---p -
Rate of Rise (mrn~~min- ' ) 1 4.4 5 -3 1 5 -6
Iso-Oxic Level / 150 IIlIILHg)
6.0 O
-
13.5 O
O
Rate of Rise (mrnHgmixf1)
Sp (L=mh-'-mmt~g)
Tc @dg) Sc (~-min%rmH~)
Rate of Rise (rnm~g.min-')
5.8 - -
4.1 3 -7 6.3 a
2.5
52
12.8
4.1
0.9
55
15.3
4.6
- - O
4.3
APPENDIX VIII
RAW DATA OBTAINED DURING 'IlE BREATB HOLDING TESTS AT ALL
BRlWï"ï HOLDING CONDITIONS (FRC, FRCsw, TLC, TLCsw) (N=17)
BREATH HOLDING DATA
Breath Holdina Condition (TLCsw)
r DAY ONE 1 DAY TWO 1 DAY THREE 1
DAY THREE . 77-12 148 80
O
48 7
DAYTWO 78.48 144 68 - 48 8
DAY ONE Breath Hold ïïme (s) t 65.48
1 Rate of Perceived Exertion 1 9 1 9 1 9 1
hitiai end-ticiai (mmHg) Final end-tidai Pa ( d g ) Initial ad-tidd PC@(mmHg) FÏnai enddai PC&(mmHg) Rate of Perceived Exertian
144 80
O
48
- 8
72-99 148 68 - 50
1 Rate of perceked Exertion 1 8 1 8 9 1
98.00 144 72 - 47
Breath Hold Tme (s) initial end-tidal Pa (mmHg) Finai end-tidal Pa (mmHg) initiai end-tidd PC& (mmHg)
Final aid-tidai P C a (mmHg)
Breath Hold Time (s) initial end-tidal Pa (mm&) Finai end-tidal POz(mftLHg) lnirial end-tidal PC@(mmHg) Final end-tidal PC@ (mmHa)
Breath Holdina Condition (FRCsw)
63.48 144 72 - 50
DAY ONE 22.40 144
Rate of Perceiveci Exertion 1 8 1 8 1 8 1
DAY TWO 23 -40 128
1 DAY ONE
DAY THREE 26-24 112
DAY 'IWO 29-00 120 64 15 47
Breath Hold Tme (s) initiai d - t i d d poZ (mmHg) F i end-tidal POr (mmHg) hihi d- t ida l PC&(mmHg) Fmai end-tidal PC& (mmHg)
56 30 5 1
60 -
50
DAY THREE 29-26 124 60 20 50
24.18 144 64 - 50
64 15 47
Breath Hotdina Condition (TLQ
Brieath Hold Time (s) initial end-tidal POz(mmHpr)
Rate of Perceiveci Exertion
Breath Holding Condition (FRC)
DAYTfiREE 37.60 144
DAYONE 45 -29
144
Breath Hold T i e (s) Initial end4dal Pû&nm&) Fiuai end-tidal P&(mmHg) Uiitini end-tidal P C a ( d g )
Final end-tidal PC@ (mmHg) Rate of Perceiveci Exertion
1 Rate of Perceived Exertion
DAYTWO 46.69 144
Breatb Holding Condition (FRCsw)
DAYTHREE ,
44.75 144 84 -
42 -
DAYONE 34-70
1 4 4 88
O
45 -
DAYTWO 44-54
144 88 -
44 -
DAY THREE 17.52
DAY ONE 14.27
DAY TWO 15.31
DAY ONE DAYTWO 1 DAYTHREE 1 B h Hold Tme (s) 22.62 17.0 t 1 13.20
BREATH HOLDING DATA
B r d H01dm~ Condition (TLQ
1 Rate of Percenred Exertion 1 - 1 8 1 8 1
Breath Holding Condition (TLCsw)
Breabi Hold TMe (s) lnitinl ead4dai P&(mmHg)
1 DAY ONE 1 DAY TWO f DAY THREE
DAY TWO 39.02 144
- DAY ONE 34.98 144
DAY THREE 35.5 1 144 88 Final end-tidal pOr (rnmtig)
Braith Holdina Condition FRC)
100 1 84
. . - - -
F ' i end-tidal tQ ( d g ) Initial endddal PC@(mmHg) F ' d end-tidai PC& (mmHg) Rate of Perçeived Exertion
initial enMdai PC~(mmHg) Fmal enckidal PC&(mmHg)
- - -
Breath Hold Time (s) initial end-tidai E Q (mmHg)
1 Raie of Perceived Exertim 1 - 1 8 1 7 1
38.94 140
51.14 144 88
O
39 -
Breath Holdmn Condition WRCsw)
35.08 144
DAY THREE 13.96 120
Br& Hold T i e (s) initial end-tidai Pa (rnmHg)
- 42
- 33
92 -
35 9
- 44
80 -
44 9
Fmal end-ti&l Ft&(mdig) Inih'nl end-tidal PC02(.IIIlH)JP)
- DAY 38.94
-
Breath Hold Tiie (s) hihial enCi.tidal po2 (mmHg) F i d&lal pO2(mmWg) hihi end-tidal PC@ (mmHg) F ' d ad-tidal PCa (mmHg) Rate of Pexwived Exerticm
- DAY TWO 26.3 1 112
- - 80 1 76
26 20
DAY'THREE ,
13.06 108
76 1
30 I
44 9
DAYONE 16.60 -
- O
- -
DAYTWO 2 1.53 140 84 6 38 9
BREATE HOLDING DATA
%ma& HoldMn Condition (TLQ
1 DAY ONE 1 DAYTWO 1 DAY THREE 1 Breath Hdd The (s) lnitUl end-tidal P&(mmHg) Final end-tidal î&(mmWrr) W end-tidal P C a (mmHg) F i d mdddal eC~(mmHg) Rate ofperceived Exertim
Breatb Hold T i i (s) rnmai end-tidal Pa (mmHg) Fiual end-tidal Pa ( d g ) Initial end4dal ECO2 (mmHg) Final end-tidal PC& (-8) Rate of Perce id Exertion
89.50 144 72 - 45 8
Breath Hold Time (s) initial end-tidai Pa (rnmHg) F Ï end-tkw P ~ ( d g ) Initial enckidai PCû&mHg) Fmal end-tidal P C a (mmkIg) Rate of Perceived Exertion
B r d Hold Time (s) W end-tidal poZ (mmHg)
1
Final end-tidal pOr (mm)fg) Initial md-tidai PCCl&mH& Fimal end-tidal P C a (mmHg)
-
75 -85 144 80 -
48 6
DAY THREE 160.90
144 52 - 53 9
DAY ONE 96-43 144 56 - 47 8
143.12 144 52
O
52
9 L
DAY TWO 106.81
144 68
O
48
8
DAY THREE 49.50 120 56 33 47 8
DAY ONE 50.94 104 60 35 48 7
DAY TWO 40.80
144 60 6 48 8
DAYTHREE 60.39 116
Rate of Perceived Exertion 1 8
DAYONE 57.48 120
DAYTWO 52.73 144
60 35 47
8 8
60 1 52 - 48
24 48
BREATH HOLDING DATA
Breath Hold Tm (s) Initiai end-tidal P & ( d g ) Fmal endddal P02 (mmHg) M i a i en&dal PC@ (mmHg) Fimal end-tidal PC& (mmHg) Rate o f P ~ i v e d Exertiun
Breatù Hold T i e (s) hhl end-tidal pOr ( d g ) Fial end-tidal P ~ ( m m H g ) Inih'al end-tidal PC& (mmHg) F i end-tidal P C a (rnmHg) Rate of Perceived Exertiou
, Brest& Hold T h e (s) initial end-tidal poZ ( d g ) Final end+i&l pOr (mtRHg) Uhl end-tidal PC~(rnmHg) Final end-tidal PCG (mmHg)
DAY THREE ,
95 -95 148 68 - 48 7
DAYONE 109.23
148 60 -
53
DAV~NE~ DAYTWO
DAYTWO 99.2 1 144 64 - 53
120.06 148 64 -
53 9
8 1 8
99.60 144 64 - 50 8
DAY THREE 47.48 116 64 27 47
DAY ONE 57.79 124 64 20 48
8
DAY TWO 48.2 1
128 72 21 44 7 Rate ofPerceived w o n 8
BREATH HOLDING DATA
Breaîh Holdina Coaddim (TILQ
1 Rate of Perceived Exertion 1 7 f 9 1 9
Breath Holding Conditim (TLCSW)
Breaîh Hold T i (s) W end-tidal POL (mmHg) Fiai e n d 4 POz(mmHg) Initial end-tidal PC& (rnmHg)
Fiual end-tidal PCO? (mmHg)
- DAY ONE 71.81
1 4 4 80 - 48
DAYTWO ' DAY THREE
1 Rate of Perceived Exertion 1 9 1 10 1 9 1
65.84 148 84 -
50
- Breath Hold Thne (s) hihi eaddïdal Pa (mmHg) Finai end-tidal P&(mmHg) JniW end-tidal PCG ( d g ) Fiuai end-tidal PC& (mflzHg) ,
Breath Holding Condition (FRCJ
76.30 148 80 -
53
1 Rate of Perce id Exertion 1 9 1 8 1 9
. DAYTHREE
69.24 148 76 -
53 .
DAYONE 79.61
144 72 -
51
r
Breath HoId Tme (s) rnirial aid4dd Pû&nmHg)
DAYTWO 8 1.59 148 76 -
51
DAY ONE 16.16 138
' DAY ONE
1 Final end-tidal PC&(rr.uxH& 1 51 1 53 1 53
, Fmal enckidal P&(mmWg) 1 72 Jnitial end-tidal PCG(mmH@ 8 Fmal end-ti&i P C a (mmHg) 1 51
hitd ad4dal ~ ( m m H g ) Fmal end-tidal P@(mmH&
DAY TWO 15.22 120
[ Bresth Hold Ti (O) 15.19 13.39 13.82 DAY 'IWO
DAY THREE 18-95 136
72 23 53
DAY THREE
ïdiü end4idd PC@(mmH& 8 3 1 18 1
L
136 68
72 9 53
148 1 128 72 68
BREATH HOLDING DATA
Breath Holding Con&- CIZQ
DAYONE
--
Rate of Perceived Exerticm I 8 I 7 9 I
Uimai end-tidal Pa (nimtlg) Final end-tidal P&(rmnHrr) lnitisl adddpi PC4(mmH@ Fimal end-tiM PC&(rrrmHg)
Breath Holding Condition (TLCsw)
[ Breath HoId T i e (s) 68.10 73.74 86.8 1 DAYTWO
~ D A Y 0- 1 DAYTWO 1 DAYTHREE ]
DAYTHREE
194 76 -
44
1 SrCam Hold Time (s) 1 65 -75 1 70.02 1 72.65 1
144 76
B d Holding Condition (FRCI
148 76
Idid end-tidal PC& (mmEig)
Fmal end-tidal PCO&mH& Rate of Perceived Exertion
- 42
- 42 9
Breaîh Hold Tiie (s) uiitial end-tidal Pa (mmHg) FinaI end-tidal POz (mm&)
Breath Holding Condition mCsw1
- 44
hitiai end-tidal PC@ (mmH& Finai end-ti&l PC4 (mmHg) ~ a t e of Perceived Exertian
DAY THREE 21.15
- 42 9
DAYONE 30.83 144 68
- 42 9
DAYTWO 2 1.42 100 68
4 -
42 33 42
Breath Hold Tme (s) Initiai end-tidal pol(mmHg) Fiiend-tidalpoZ(mmHg) rnitisi end-tidal PC&(mmH&
9 I 9
DAY ONE 22.98 104 72 33
DAYTWO 16.67 IO0 -
30
DAYTHREE 20.09 120 80 18
BREATH HOLDING DATA
Breath Hold Time (s) Uiitiai etid-bdal P&(~funHg) Finai end-tidal poZ (rnrnHg) Initial end-tidal EC& ( d g )
Fmal endddal PC&(mmHg) Rate of Perceiveci Exertion
Breath Hofdinn Condition @RC)
B r d Hold T i e (s) Uiitiai end4dal IQ (mmHg) F M end-tidai Pa ( M d Initial end-tidai PCOz (mmtIg) Final end-tidd PCO?,(mmH& Rate of Perceived Exertion
Breaîh Hold T i e (s)
DAY THREE 65.80
144 72 -
DAY ONE 72.77
144 76 -
42 -
-
Initial end4dal Po2 ~ I ~ I H Q )
( DAY TWO 68.01 144 80 - 44 -
DAY THREE 68.30 144 68 -
47 7
DAY ONE 1 DAY TWO 69.83 1 77.86
Breath Holdinn Condition ERCsw)
45 5
144 84 -
38 -
DAYONE -
144 80
O
45 O
DAYTWO 20.62
Breath Hold Tune (s) Fnmnr ead4dal P@(mmHg)
. F i emd-tidal p4(- InïW end-tidal PCa (mmHg) Finai end-tidal PCOr (mmHg) Rate of Perceived Exertion
DAYTHREE 18.86 '
DAY T'HREE 25 -53
- - O
- - O
DAY ONE - - - - - -
DAY TWO 29.28 IO8 88 33 36
6
BREATH HOLDING DATA
B d Holding Condition (TLC)
Breath Holdina Condition CTLCsw)
Breath Hold Tirne (s) Initial endtidai PQL(mmHg) Finai end-tidal PO&m.Hg) W end-tidal PC@ (mmHg) Final end-tidal PC~(mmfig) Rate ofPerceived Exertion
*
1 DAY ONE 1 DAY TWO 1 DAY THREE 1 - -
[ b a t h Hold T i e (s) 1 62.50 1 50.44 1 - 1
1 DAY ONE 55.61 144 84 -
43 5
Innial end-tidai (armHg) 144 148 - Finai end-tidai Pû&mHg) 80 92 - \
f Rate of Perceived Exertion 1 7 7 1 - 1
DAY TIHO 55 -40 148 92 -
47 5
Breath Holding Condition (FRC)
DAY THREE - - - - - O
1 B d Hold Tirne (SI
1 Rate of Perceiveci Exerticm 1 6 1 5 1 - 1
Fmal end-tidai Pa (rmnHg) Initiai end-tidal PC@ (mmHg)
Breath Hoidina Condition (FRCSW)
DAY ONE 1 DAY TWO 33.30 1 29.84
DAY TEiREE -
I
72 35
Breaîh Hold Tme (s) hiid end-tidal po2(mmH& Final en&&l poZ(nunH& J & d end4dal P C ~ ( m m W g ) Final end-tidai PC& (mmHg) ]Rate of Perceived Exertion
80 33
- O
DAY ONE 33.30 108 76 33 45 7
DAYTWO 34.55 116 72 32 50 7
DAY THREE ,
O
- - - - -
BREATE HOLDING DATA
Breaîh Holdma Condition (TLCI
B d Holdina Condition (TLCswl
Brearh Hold T i e (s) Miai end-tidai Pa (mmHg)
1 Rate of Perceived Exertion 1 10 1 10 10 1
DAY ONE 1 12. Id 144
B m t h Hold T i e (s) rnitial end-tidai Pa (mmHg) Final end-tidal Pa (mmHg) initiai end-tidd PC@ ( d g )
F i end-tidal PC& (mmHg)
Breath Holdina Condition WRC)
DAYTWO [ DAYTHREE ,
Fmal end-tidai Pa (rrrmHg) initiai ad-tidd PCa (mrdg) Fmal end-tidal PC@ (mmHg)
DAY ONE 162.43 144 56
13 1.89 148 72 - 72 -
45
Breath Hold rime (s) hhl wd-tidal poZ ( d g ) Final end-tidal P02 (rnmHs) initial end-tidai fC02 (mmHg)
B& Holdina Condition (FRCsw)
167.12 144 40 -
DAY TWO 164.47
148 52
Finai end-tidal PC&(&&~ Rate of Perceived Exertion
1 DAY ONE 1 DAY TFVO 1 DAY THREE 1
47 1 52 1
DAY THREE 157.38
144 40
DAYONE 53.77 120 56 15
- 50
- 47
39 9
- 50
DAYTWO 54-88 136 72 Il
DAYTHREE 94.69 128 52 12
38 9
Breath Hold Ti (s) 1 99.4 1
42 9
78.55 132 52 15 45 9
Tnitinl end-tidal poZ(mmIig) Final e n c i = t i M p 0 2 ( ~ W end-tidai PC& (mm&) Fmal end-tidal PCO&mHg) Rate of Perceived Exertion
94.27 132 40 1 t 45
9
120 -
33 - 10
BREATH HOLDING DATA
Breath Hold Ti (s) hritial end4dd l'oz(-) F i end-tidal poL(mmHg) I n h i ad-tidd PCOz (mm&)
50 8
~ ~ L d t i d a . 1 PC&(mdi& -
Rate of Perceived Exertion
1 Breath Hold Time (SI
1 Rate of Perceived EY,+CZ 1 9 1 8 1 8 1
DAYTHREE 5 8.23 144 76 -
DAYONE 60.73 148 84 -
initiai end-tidal P G (mmHa) F'mal end-bdal Pa (&g) W end-tidal PCOz (mmHa)
DAYTWO 79.10 144 64 -
47 6
50 8
DAY THREE 70.62
DAY ONE 59-40
148 76 -
Breath Hold T m e (s) Tnitial end-tidai POr(mmH8)
1 Final endQdal PC&(mmHg) 1 47 1 48 1 48 1
DAY TWO 91.86
1 Rate of Perceived Exerhon 1 7 1 8 1 8 1
1
68 1 76 36 36
-
Final end-tidal Pa (mmHg) rnitinl end-tidal PCOz (mmtig)
144 64 -
DAY THREE A
24.86 DAY ONE
17.88
76 38
1 Rate of Perceived Exertion I
1 7 1 7 1 8 1
144 72 -
104 1 100 1 108 A
DAY TWO 23 -20
Breath Hold Time (s) Initiai end-tidal POr(mmHg) Final md-tidal poZ(mmH& Initiai end-tidd PCOr (mmHg) FÏÏ end4da.l PC& (mmtIg)
DAYTHREE , 22.77 108 68 38 50
DAY ONE 30.03 120 72 12 50
DAY 'IWO 31.31 108 68 33 48
BREATE HOLDING DATA
Breath Holdina Condition (TLC)
Breaîh Holding Condition (TLCsw)
Breath Hold Time (s)
Breath Holdma Condition WRC)
Breath Hold Tme (s) Initial end-tidal PQ&mHg) Fnial ad-ti&l Pû&nrnHg) initial end-tidd P C a ( d g )
DAY THREE 63 -37
DAYONE 57.30
1 Raie of Perceived Exertim 1 7 1 8 1 5 1
144 84 -
42 4
5
DAY TWO 69-16
Breath Hold T i e (s) initial end-tidal P02 (mmHg)
, Final ad-tidal poZ (mmHg) h W end3idai PCa (mmHg) Final end4dd PC&(lfunHg)
Breatb Holdina Condition @RCsw)
144 76 O
44
Jkim end-tidal POr(mmHg) I 144
DAY THREE 68.09 144 80 -
DAY ONE 1 DAY TWO 73 -40 1 67.3 1
, Final end-tidai poZ (mmH@
42 7
144 76 -
Rate ofperceived Exextian 1 7 1 7 1 7
72
Rate of Perceived Exertion
144 80
O
44 7
F'mal end-ti&l PC& (mmHg) Rate of Perceived Exertion
DAY ONE 24.08 108 88 30 36
Breath Hold T i e (s) m;t;ar end-tidal POz (&g) F i end-tidal poZ (mmHg) lnihai end4dal PCOr(mmng) F i a i d a Pm(mmHg)
6 1 6
44 7
DAY TWO 25 .O5 108 84 32 38
DAY THREE 23 -72 108 88 30 38
h&id end-tidal PC@ ( m m . Fial end-tidal PC@ (mmHg)
Y
DAY~NË 3 1 -46 108 80 30 39
- 45
DAYTWO 24.18 Il2 76 26 42
DAYTHREE 28.61 128 80 14 39
BREATH HOLDING DATA
Breath Holding Condition (TLC)
Br& Hold Thne (s) Inih'nl end-tidal Pa (mmHgj Fmal end3idal poZ(mmHg) hiîiai end-tidal PC& (mmHg) Final aid-tidal PC@(mmHg) Rate of Perceived Exertim
Final end-tidd f Oz ( d g , ) 80 68 - W end-tidal PCOz (mmHg) - - -
Rate of ~e&ved Exertion 1 7 1 7 1 - 1
. Breath Hold Thne (s) Initiai endiidal Pa (mmHg)
B d Hotdina Condition WRC)
DAYTHREE , - - O
- - -
DAYONE 35.85 144 84 - 42 7
DAY TWO 40.16 144 76 - 45 7
F i end-tidal poi(mmHlt) 64 76 1 O
Initiai end-tidal PCOz (mm&) 32 30 -
DAY THREE - O
DAY ONE 45 -58 144
Breath Hold T'me (s) Initiai end-tidal Pa (rnmHg)
1 Rate of Perceived Exertion 1 7 1 IO 1 -
DAY TWO 49.75 144
1 Rate of Perceived Exertion 1 8 1 10 1 O
DAY THREE - -
DAY ONE 18.10 104
Brieath Hold Trme (s) Miai ead4dd POz(mmtfg)
DAY TWO 23.5 1 112
DAY ONE 19.73 100
Fmal eadtidal P%(mmfilrÙ 1 - hïtbi endddai Pcîk<mmHQ) 33 Fmal enckidal P C C M e 1 O
DAY TWO 30.49 108
DAY THREE - -
64 30 42
- - O
BREATH HOLDING DATA
Breath Hotdinn Condhion (TLQ
1 Rate o f P e r ~ ~ i v e d Exertion 1 8 1 9 1 9 1
Breadh Hdd E u e (s) Initial endhdal poZ (mmHg) Final end-tid;rl PQ (mmHg) k t d end-tidai PCOr(mmHg) Fmal enckidai PCO&mHg)
Bmath Hold Time (SI
DAY ONE 107.65
144 68 -
45
Breath Hoid Time (s) Initial ad-tidal Fa2 <=lmE?g) Finai end-tidal E Q (rmnHg) Initiai end-tidai P C a (mrnHg)
Final end4dal POz (mmHg) Iaitial end-tiW K a (mmHg) Finai end-tidal PCCMrmHrù Rate of Perceiveci Exertiou
DAY TWO 104.08
144 64 -
48
DAYONE 112.40
144 64 -
DAY THREE 137.78
148 56 -
57 I
Breath Hoidma Condition (FRCsw)
DAYTWO 1 16.85
Finai eud-tidal P C a (&g)
DAYTHREE 117.5 1
47 9
47
DAYTHREE 57.75
DAYONE 33 -70
53 9 ~ a t e ofperceived Exertion I 9
DAYTWO 55.26
~ r e a t h HOM r i e (s) W end-tidal P& (mmFTg) Fmat en- poZ(mmHg)
144 64 -
I 248 64 -
DAYONE 38.00 108 72
DAYTWO 67.36 112 60
DAYTHREE ,
55 -78 116 60
BREATH HOLDING DATA
Breath Holdma Ccmditim (TLC)
DAYONE
Breath Holding Condition (TLCsw)
initial end-tïdal P % ( e FinaI end-tidal (mmH& hiiniai enchidai PCû&mHg)
1 DAY ONE 1 DAY TWO 1 DAY THREE 1
1 Bnaai Hold T o i (s) 55.35 51.00 39.7 1 T
DAYTWO DAYTHREE
4
144 92 -
DAYONE DAYTWO DAYTHREE 29.75 29.57 30.86 116 120 116
144 96 -
Breath Hold T h e (s) Tnih‘nl end-tidal Pa (mmHg) Finai end-tidal Pa ( m g ) Inih'al end-tidal PC&(mmHg) Final end-tidal PCOz (mmHg) Rate of Perceived Exertioa
144 100 -
53.10 144 84 - 42 7
64.03 144 88 -
42 7
1 DAY ONE
58.48 144 96 - 39 7
DAY TWO ,
- Breath Hold Time (s) DAY THREE ,
24.09 22.20 116 100 26 33
5
initiai end3ida.l P&(mmHg) Final end-tidal Pa (mm&) Initial end-tidal PC& (mm.Hg) Fiual end-tidal PC@ (mmHg) Rate ofperceivexi Exertion
120 - 24 - 5
- - - - -
BREATH HOLDING DATA
DAYONE DAYTWO DAY THREE ' Breaîh Hoid Tme (s) 66.47 63.60 54.59 Idkd end4dal Pa (mmHg) 148 148 148
Breath Hold Time (s) InitialenMdal Po&nmHg) F i aibtidal Po&nmHg) lnitinl end4dal PC&(mmHg) Final end-tidal P C a (mmHg)
Rate of Perceived Exertion 1 9 1 9 1 9 1
B r d Holding Condition F R 0
Fnial end-tidal POr(mmHg) initial end-tidal PCOz (mmHg)
DAYTHREE 59.85 148 76 -
47
DAYONE 47.5 1 148 68 -
47
Rate of Perceived Exertion
DAYTWO 52.45 148 72 - 48
Breath Holding Coudhion FRCsw)
Breath Hold 1"- (s) Init;nl ead-tidai Pa (mmHg) Final end-tidai P&(Wg) Fnitial end4dal PCOi (mmH8)
DAYONE 23.18
84 - 41
DAYTWO 20.88 100 52 38
DAYTEiREE 22.34 104 52 36
Breath Hoidma Ccmddion (TLCsw)
Breath Hdd Ti (s) FniW endîidal Pa (mm.&) Fmal end-tidal poZ (mmHg) iaitinr end-tidal PC@(mmHg) Final end-tidaI PC@ ( d g )
r
DAY ONE DAY TWO DAY THREE 108.45 139.76 139.6 1
DAYONE 102.40
140 72 - 45
Breaîh Holding Condition (FRC)
Rate of Perceived Itertion 1 9
-i&i aid-tidd P C o 2 ( d s ) Rate of Perceived Exertian
DAYTWO 144.94
144 60 - 44
Breaîh Holdm~ Condition (FRCsw)
DAY-E 109.77
148 72 -
45 9 9
- -
45 9
42 9
DAYTHREE ,
63.81 DAYONE
- --
45 9
DAYTWO
Breath Hold T ï e (s) btbl end4dd poZ(mmHg) Fmale~d-tjdaIPOz(nmiHg) W end4dal Pc&(mmHg) Finai aid-tidal PC~(mniHg) Rate of Perceived Exertian
1 Breath Hoid Tme (s) 55.60 29.36
- DAY ONE
56.73 104 56 30 45 9
DAY TWO 34.33
92 60 35 47 9
DAY THREE 80.05 120 45 24 45 9
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