HPHE 6710: Section 06 - Exercise Training to Improve Performance (Chapter 21,22,23)
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Transcript of HPHE 6710: Section 05 - Exercise Performance and Environmental Stress (Chapter 25,24,26,27)
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Section 05:
Exercise Performance and
Environmental Stress
Chapter 25 Exercise and Thermal Stress
Chapter 24 Exercise at High and Medium Altitude
Chapter 26
Sport DivingChapter 27 Microgravity: The Final Frontier
HPHE 6710 Exercise Physiology II
Dr. Cheatham
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Chapter 25
Exercise and Thermal Stress
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Chapter Objectives
Understand the physiological mechanisms inresponse to heat and cold exposure
Understand the physiological responses during
exercise in the heat and the cold Understand heat and cold acclimatization
Understand the different types of heat illness
Understand factors that modify the responses
to heat and cold
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Introduction
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Part 1
Mechanisms of Thermoregulation
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Thermal Balance
E-RCCMS dV
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Hypothalamic Regulation of Temperature
Hypothalamus Central coordinating center for temperature
regulation
Activation of bodys heat-regulatingmechanisms
Thermal receptors in the skin
Changes in blood temperature perfusing thehypothalamus
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Hypothalamic Regulation of Temperature
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Hypothalamic Regulation of Temperature
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Hypothalamic Regulation of Temperature
23C, 74F
TCORE = 37.1C
TSET = 37.1C
0C, 32F
TCORE = 37.1C
36C, 97F
TCORE = 37.1C
Skin
Temp
Skin
Temp
TSET = 37.5CIm
cold!
TSET = 36.5C
Im
hot!
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Hypothalamic Regulation of Temperature
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Hypothalamic Regulation of Temperature
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Hypothalamic Regulation of Temperature
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Thermoregulation in Cold Stress: Heat Conservation
and Heat Production
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Thermoregulation in Cold Stress: Heat Conservation
and Heat Production
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Thermoregulation in Cold Stress: Heat Conservation
and Heat Production
h l i i ld i
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Thermoregulation in Cold Stress: Heat Conservation
and Heat Production
Vascular adjustments Cutaneous cold receptors constrict peripheral blood
vessels. 250 mL/min at thermoneutral; approaches zero with severe
cold stress
Begins when skin temperature < 35C and is maximal when skintemperature < 31C
Skin temperature declines
Muscular activity Shivering
Maximal rates have been shown to be around 46% VO2max
Hormonal output Epinephrine and norepinephrine (short term)
Thyroxine (long term)
Th l i i C ld S H C i
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Thermoregulation in Cold Stress: Heat Conservation
and Heat Production
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Individual Factors Modifying Responses to Cold
Anthropometric Characteristics
Surface area to mass ratio
Body Composition
Thermoregulation in Cold Stress: Heat Conservation
and Heat Production
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Thermoregulation in Heat Stress: Heat Loss
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Radiation
Electromagnetic heat waves
Conduction
Direct contact between molecules Convection
Movement of adjacent air or water molecules
Evaporation Vaporizing water
Evaporative heat loss at high ambient temperatures
Heat loss in high humidity
Thermoregulation in Heat Stress: Heat Loss
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Thermoregulation in Heat Stress: Heat Loss
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Thermoregulation in Heat Stress: Heat Loss
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Thermoregulation in Heat Stress: Heat Loss
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Integration of Heat Dissipating Mechanisms Circulation
Body can control dry heat loss by varying skin blood flow
and thus skin temperature
After sweating has begun, skin blood flow serves
primarily to deliver to the skin the heat that is being
removed by sweat evaporation.
Skin blood flow is affected by temperature in two ways:
Local effect on smooth muscle
Reflexes operating through the SNS
Thermoregulation in Heat Stress: Heat Loss
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Thermoregulation in Heat Stress: Heat Loss
36C (97F), 60% RH, 105 Watts
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Thermoregulation in Heat Stress: Heat Loss
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Integration of Heat Dissipating Mechanisms Evaporation
Sweating begins within several seconds of the start of vigorous
exercise.
The onset time of thermoregulatory sweating is influenced by skin
temperature, acclimatization status, hydration status, and non-
thermal stimuli.
Sweating closely parallels increase in body temperature
First, recruitment of sweat glands increases
Second, sweat secretion per gland increases Chest and back sweat first, followed by limbs
Cooled blood returns to core to absorb additional heat.
Hormonal adjustments
Vasopressin and aldosterone help maintain blood volume.
Thermoregulation in Heat Stress: Heat Loss
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Thermoregulation in Heat Stress: Heat Loss
36C (97F), 60% RH, 105 Watts
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Effects of Clothing on Thermoregulation
Clothing Insulation (CLO Units) Index of thermal resistance
A clo unit of 1 maintains a sedentary person at 1MET indefinitely in an environment at 21C (68.8F)
and 50% RH
Factors: Wind speed
Body movements
Chimney effect baggy clothes Bellows effect movement increases ventilation of air
layers
Water vapor transfer
Permeation efficiency factor clothes absorb sweat
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Effects of Clothing on Thermoregulation
Cold-weather clothingLayers trap air
Moisture properties Warm-weather clothing
Light in color
Moisture properties
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Effects of Clothing on Thermoregulation
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Effects of Clothing on Thermoregulation
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Part 2
Thermoregulation and Environmental
Stress During Exercise
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Core Temperature During Exercise
Exercise in the Heat
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Exercise in the Heat
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Exercise in the Heat
36C (97F), 60% RH, 105 Watts
h
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Exercise in the Heat
i i h
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Exercise in the Heat
i i h
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Exercise in the Heat
Circulatory Adjustments Two competing cardiovascular demands:
Adequate muscle blood flow for metabolism
Adequate peripheral blood flow for thermoregulation
Also, maintenance of blood pressure
E i i h H
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Exercise in the Heat
E i i h H
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Exercise in the Heat
E i i h H
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Exercise in the Heat
Cardiovascular Responses
E i i th H t
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Exercise in the Heat
Cardiovascular Responses
E i i th H t
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Exercise in the HeatCardiovascular Responses
E i i th H t
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Exercise in the HeatCardiovascular Drift
E i i th H t
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HR Higher in heat
SV Lower in heat
Q At low intensity will increase
At higher intensities usually maintained
a-vO2 difference Usually higher in heat
Blood Pressure Lower in heat
TPR Usually lower in heat
Exercise in the Heat
E i i th H t
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Exercise Performance
Limitations
Performance Effects
VO2max is lower in hot
compared to temperateenvironments
0.25 L/min lower in 49C
compared to 21C
Why? Decrease in muscle blood flow
Decrease in central blood flow
and thus maximal CO
Exercise in the Heat
E i i th H t
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Exercise in the Heat
E ercise in the Heat
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Water Loss in the Heat: Dehydration Magnitude of fluid loss
The more prolonged or intense the exercise, the greaterthe loss.
Sweat rates can exceed 3 L/hour Significant consequences
Dehydration may threaten health.
Physiologic and performance decrements occur.
For every liter of sweat loss, HR can increase by 8 b/minwith a corresponding 1.0 L/min decrease in Q
Diuretics
Cause greater fluid loss from plasma than sweating
Exercise in the Heat
Exercise in the Heat
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Water Loss in the Heat: Dehydration Dehydration by more than 2% of body weight will
negatively impact endurance exercise
Increased hyperthermia
Core temperature elevations ~ 0.2C for every 1% decrease in
BW
Lowers the core temperature that can be tolerated before heat
exhaustion from heat strain
Sweating is reduced Increased cardiovascular strain
Altered metabolic function
Altered CNS function
Exercise in the Heat
Maintaining Fluid Balance
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Maintaining Fluid Balance
Maintaining Fluid Balance
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Maintaining Fluid Balance
Factors That Modify Heat Tolerance
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Factors That Modify Heat Tolerance
Acclimatization Physiologic changes that improve heat tolerance
Optimal acclimatization requires adequaterehydration.
Three classical signs:
Lower HR
Lower core temperature
Higher sweat rate
After acclimatization, the threshold for sweatingoccurs at a lower core temperature
Lower skin temperatures decrease cutaneous BFrequirements for heat balance
Factors That Modify Heat Tolerance
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Factors That Modify Heat Tolerance
Factors That Modify Heat Tolerance
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Factors That Modify Heat Tolerance
Factors That Modify Heat Tolerance
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Factors That Modify Heat Tolerance
Factors That Modify Heat Tolerance
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Factors That Modify Heat Tolerance
Factors That Modify Heat Tolerance
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Training status Increased sensitivity and capacity of sweating response
Plasma volume increases
Greater skin and GI blood flow
Larger volumes of more dilute sweat Age
Age-related differences in heat tolerance
Some age-related factors affect thermoregulatory
dynamics. Children
Lower sweating rate and higher core temperature
Sweat is more concentrated.
Factors That Modify Heat Tolerance
Factors That Modify Heat Tolerance
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Gender When studies control for fitness level and relative
exercise intensity, no gender differences are observed.
Sweating Women Sweat less prolifically than men despite having more heat-activated
sweat glands
Sweat smaller volumes
Begin sweating at higher skin and core temperatures
Compared to men, women tend to cool faster. Menstrual cycle alters skin blood flow and sweating response.
Body fat insulates body, retards heat dissipation, and adds to
metabolic cost of weight-bearing activities.
Factors That Modify Heat Tolerance
Complications from Excessive Heat Stress
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Complications from Excessive Heat Stress
Heat Cramps (Involuntary Muscle Spasms) Core temperature typically in normal range
Due to an imbalance in fluid levels and electrolyte
concentrations
Those at risk tend to have high sweat rate and high
sweat sodium concentrations
Prevention
Adequate fluid and electrolyte intake before and during
exercise
Complications from Excessive Heat Stress
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Heat Exhaustion Ineffective circulatory adjustments, depletion of extracellularvolume (especially PV)
Peripheral pooling occurs, central blood volume decreases,cardiac output usually decreases
Symptoms: Weak, rapid pulse
Low blood pressure
Dizziness, headache, overall weakness
Possible decrease in sweat rate
Core temperature is elevated but not to dangerous levels (i.e.> 40C or 104F)
Treatment Move to cooler location, rapid body cooling, fluids (possibly
intravenously)
Complications from Excessive Heat Stress
Complications from Excessive Heat Stress
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Heat Stroke The failure of the heat-regulating mechanisms from
an excessively high core temperature
Classic Form:
Environmental heat overloads the bodys heat dissipatingmechanisms.
Symptoms:
Core temp > 105F, altered mental status, absence of sweating,multisystem organ dysfunction.
Exertional Heat Stroke:
Extreme hyperthermia from:
Metabolic heat load in exercise
Challenge in heat dissipation from a hot-humid environment
Complications from Excessive Heat Stress
Complications from Excessive Heat Stress
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Heat Stroke (contd) ExertionalHeat Stroke (contd):
Symptoms:
Core temp > 41.5C
Sweating diminishes, skin becomes dry and hot
Inordinate strain on the CV system
Rapid breathing
Altered mental status
Treatment: Rapid cooling: ice packs, alcohol rubs, whole-body immersion in
cold water or ice, intravenous fluids, EMS medical attention,
drug treatment (endotoxins)
Complications from Excessive Heat Stress
Complications from Excessive Heat Stress
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Complications from Excessive Heat Stress
Exercise in the Cold
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Exercise in the Cold
Cardiovascular Responses At Rest:
Higher Q
Higher SV
No change in HR
Higher BP and TPR
a-vO2 diff
Lower if muscle temp decreases Similar between cold and neutral if muscle temp remains the
same
Exercise in the Cold
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Cardiovascular
Responses
During Exercise:
Increased Q
Increased SV
No change or slight
decrease in HR
Increased BP and TPR
Exercise in the Cold
Note to self: Get better figure for this slide
Exercise in the Cold
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Oxygen Uptake andSystemic OxygenTransport
Man in the cold is not
necessarily a cold man If cold stress is sufficient
to decrease coretemperature or muscle
temperature, then: VO2max may be reduced
Impairment of myocardialcontractility
Exercise in the Cold
Exercise in the Cold
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Exercise in the Cold
Exercise in the Cold
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VO2max in the Cold Matsui et al. (1978)
Acute exposures to 5C, 18C, and 35C
No differences in VO2max
Astrand and Saltin (1961)
20C and -5C
No difference in VO2max
Bergh (1980)
5 to 6% decrease for every 1C drop in core
Probably related to decrease in max HR and thus
maximum Q
Exercise in the Cold
Exercise in the Cold
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Individual Factors Modifying Responses to Cold Anthropometric Characteristics
Surface area to mass ratio
Body Composition
Exercise in the Cold
Acclimatization to Cold
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Acclimatization to Cold
Acclimatization to Cold
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Acclimatization to Cold
Acclimatization to Cold
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Acclimatization to Cold
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Chapter 24
Exercise at Medium and High Altitude
Chapter Objectives
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Chapter Objectives
Fill in
The Stress of Altitude
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The Stress of Altitude
Reduced PO2 creates a metabolic challenge. Oxygen transport cascade
Progressive change in environments oxygen
pressure and in various body areas Acclimatization
Adaptations occurring due to a change in the
natural environment
Acclimation
Adaptations produced in a controlled laboratory
setting
The Stress of Altitude
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e St ess of t tude
The Stress of Altitude
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f
The Stress of Altitude
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f
The Stress of Altitude
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149
104
9640
23
40
84
53
40
25
159 94Sea Level 4300 m
f
The Stress of Altitude
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Oxygen Loading at Altitude No meaningful change in Hb saturation until an
elevation of 3048 m
Examples At 1981 m (6500 feet)
PAO2 at sea level = 100 mmHg (97.2% saturated)
PAO2 at 6500 feet = 78 mmHg (~ 94% saturated)
Mexico City Olympics (1968) (2300 m, 7546 feet) PaO2 = 120 mmHg (80% saturated)
Performance decrement
Sudden exposure to 4300 m VO2max decreases by 32%
Mt. Everest VO
2max
decrease of 70%
f
The Stress of Altitude
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f
The Stress of Altitude
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f
The Stress of Altitude
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f
Acclimatization
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Acclimatization
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Immediate Response to Altitude Increase in respiratory drive to produce hyperventilation
Increase in blood flow during rest and submaximal exercise
Hyperventilation Low PaO2 sensed by peripheral chemoreceptors
When PIO2 drops below 110 (normal = 150) or PaO2 is less than60 (normal = 96) ventilation increases
Beyond these levels, ventilation increases in proportion tolevel of hypoxia
Increase in ventilation increases PAO2 and decreases PACO2
What happens during rapid exposure to low O2 First few minutes = dramatic increase in VE After initial minutes = slight blunting of VE but still more than
normal
Why? Ventilation induced hypocapnia
Acclimatization
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Acclimatization
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Immediate Response to Altitude (contd) Increased cardiovascular response
Resting SBP increases
Submaximal exercise heart rate and cardiac output can rise to50% above sea level values (no change in SV)
At a given absolute workload:
Q is increased at altitude
HR is increased at altitude
SV is the same
Compensation for lower a-vO2 difference
However, a given absolute workload is a greater relativeworkload because VO2max is reduced at altitude
If same relative workload is performed, no difference betweennormoxia and hypoxia
Acclimatization
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Catecholamine Response Plasma and urine catecholamines are higher at
altitude
Mostly due to increase in NE not E
During first few minutes, no difference in NE
Production is increased, but removal is also increased
Within 14-18 hours, an increase in NE is observed
Production is increased, but removal is decreased Splanchnic removal is proportional to arterial
concentration
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Acclimatization
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Longer-Term Adjustments to Altitude Regulation of acid-base balance altered by
hyperventilation
Synthesis of hemoglobin and red blood cells
Elevated sympathetic neurohormonal activity
Acid-Base Readjustment
Hyperventilation causes a decrease in PCO2 Increase in pH
Kidneys begin to excrete bicarbonate
Acclimatization
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Longer-Term Adjustments to Altitude (contd) Hematologic Changes
Initial plasma volume decrease
Shift from intravascular space to interstitial and intracellular
space Increases red blood cell and hemoglobin concentration
Diuresis
Maintains fluid balance between the compartments even
though total body water is reduced
Red blood cell mass increases
Acclimatization
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Longer-Term
Adjustments toAltitude (contd)
Cellular Changes
Capillaryadjustments
Increasedmyoglobin
Increased
mitochondrialdensity
Increased 2,3-DPGlevels
Altitude Training and Sea-Level Performance
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Performance upon return is not improved if usingVO2max as the criteria
Altitude acclimatization improves ability to perform at
altitude.
Decrement in absolute training level at altitude
Athletes cannot train as intensely while at altitude.
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Live hightrain low appears to be
the best scenario for improvingperformance.
Capitalize on stress of altitude andacclimatization
Train lower so intensity can bemaintained
At-Home Acclimatization
Methods of simulating hypobaricconditions
Cause altitude-induced physiologicadaptations
Gamow hypobaric chamber
Wallace altitude tent
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Chapter 26
Sport Diving (Hyperbaria)
Chapter Objectives
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Introduction
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Pressure-Volume Relationships and Diving Depth
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Diving Depth and Pressure Hyperbaria
Water is noncompressible.
As a diver descends, the pressure increases.
Two forces produce this external pressure Weight of the column of water above the diver
Weight of the atmosphere at the waters surface
Every 33 feet of sea water represents anotheratmosphere of pressure.
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Diving Depth and Gas Volume Boyles law
At a given temperature, the volume of a gas
varies inversely with its pressure.
Greater pressure compresses the gas into a
smaller volume. So, volume of air underwater is less than that same amount of
air measured at sea level
P1V1 = P2V2
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Diving Depth and
Gas Volume(contd)
Example:
What is thevolume of 1 liter
of gas (measured
at sea level) at a
depth of 100 feet(4 ATM)?
(1)(1) = (4)(X)
X = 1/4 Liter
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Diving Depth and Gas Volume (contd) If a rigid container was submersed underwater, the
pressure in the container would not change
But, the human body is not a rigid container
Therefore, the contents of the human body will
compress as the pressure increases as water depth
increases
Water cannot compress (but the pressure of watercan increase), so the air spaces within the body will
compress
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Diving Depth and Gas Volume (contd) Which air spaces are susceptible to damage?
Natural Air Spaces
Lungs
Middle Ear Sinuses
Gastrointestinal Tract
Artificial Spaces
Cavities within teeth Face Mask
Air spaces within diving suit
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Diving Depth and Gas Volume (contd) What happens to the lungs?
A breath hold diver with a TLC of 6L and a RV of 1.5L
takes a full inspiration and dives downward
At 100 feet, pressure equals 4 ATM and lung volumeequals:
(6L)(1ATM) = (X)(4ATM)
X = 1.5 L
Residual volume has been reached and lung volume can
decrease no further
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Diving Depth and Gas Volume (contd) What happens if the diver goes deeper?
Pulmonary capillary and venous congestion displaces air
in thorax decreasing RV and equalizing pressure
Problem with this:
The increase in vascular pressures may lead to ruptures of the
microvasculature
Pulmonary edema and hemorrhage
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Diving Depth and Gas Volume (contd) What happens to diver during ascent?
At 100 feet, diver is running out of air
He fills his lungs with air from the tank
As he ascends, pressure decreases Volume of air expands because pressure is decreasing
Volume of air is too large to occupy lung space
Lung bursts
Only happens if breath holding during ascent
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Snorkeling and Breath-Hold Diving
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Limits to Snorkel Size Inspiratory capacity and diving depth
Pressure of water reduces lung expansion
Snorkel size and pulmonary dead space
The snorkel adds to the dead space.
Larger snorkel sizes are not effective due to too much
dead space, which limits alveolar ventilation.
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Breath-Hold Diving Duration depends on
Time to CO2 build-up reaches breath-hold breakpoint(PCO2 ~ 50 mmHg)
Relationship between divers TLC and RLV Hyperventilation
Decreases PCO2, increases breath-hold time
Increases susceptibility to blackout
Thoracic squeeze Limits depth of breath-hold diving to about 100 FSW
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A Diving Reflex in Humans? Physiologic responses to water immersion
Bradycardia
Decreased cardiac output
Increased peripheral vasoconstriction
Lactate accumulation
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Scuba Diving
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Open vs. Closed Circuit Scuba
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Henrys law Gas dissolved in a liquid at a given temperature
depends upon pressure differences between the
gas and liquid and gas solubility in the liquid.
Air must be delivered at sufficient pressure toovercome force of water against divers thorax.
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The Bends At high pressures, the partial pressure of all gases
increases
The partial pressure of Nitrogen especially increases
Nitrogen is fat soluble and thus enters the fattytissues
Upon ascent, the pressure decreases and thus thegases must be released
The lungs cannot get rid of the nitrogen quicklyenough
Thus, the nitrogen begins to bubble out of thetissues and the nitrogen content of the bodyincreases
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The Bends (contd) Treatment
Recompression allows
the nitrogen to enter
into solution again
The pressure is then
gradually decreased
This allows time forthe nitrogen to escape
through the
respiratory system
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Oxygen Poisoning
Exposure to a high partial pressure of oxygen can
have severe effects on the lungs and the CNS
A high PO2 causes much oxygen to be dissolved insolution
The O2 dissolved in solution is the first O2 to be
used by the tissues Because the dissolved O2 is high, it is sufficient to
supply the tissues with O2
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Oxygen Poisoning (contd) Thus, O2 does not have to dissociate from
hemoglobin
Hemoglobin in venous blood contains high amountof O2
What problem does this cause?
Hemoglobin normally binds CO2 in the venous circulation
CO2 builds up since it cannot bind to hemoglobin
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Oxygen Poisoning (contd) Symptoms of O2 poisoning
The high PO2 can cause cerebral blood vessels to constrict
Visual distortion Rapid and shallow breathing
Convulsions
Irritation of the respiratory tract leading to pneumonia
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Nitrogen Narcosis Nitrogen is not metabolically active
Can act like an anesthetic gas
Diver develops symptoms similar to alcohol
intoxication
Every 15 meter descent is equal to the consumption of
one martini on an empty stomach
Impairment of judgment and diver may not recognize aproblem exists
Divers who dive below 30 meters will use a helium
mixture
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Chapter 27
Microgravity: The Last Fronteir
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Microgravity and Weightlessness
Microgravity: Gravitational forces acting on the
long axis of the body are minimized.
Gravity depends on the:
Persons mass, earth mass, and distance from the centerof the earth (increases 5% during spaceflight)
So, gravity is only slightly decreased in space
Weightlessness:
Caused in space due to the fact that the spacecraft is in
free fall.
The crafts centrifugal force counterbalances the force of gravity.
Therefore, the perception is weightlessness
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Space Flight
Microgravity unloads body tissues and
redistributes body fluids
Light and dark cycles are altered
Very little ultraviolet radiation
Carbon dioxide levels are elevated
Psychological stress
Vigorous physical activity
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Simulated Microgravity
Bed Rest
Loss of muscle mass and strengthwithin 2 weeks
Decrease in bone mineral density(~12 weeks)
Decrease in cardiac mass (~6weeks)
Exercise impairment (~ few days)
Decrease in maximal exercisecapacity (~ few weeks)
Immersion
Suspension and Immobilization
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Cardiovascular System
Decrease in plasma volume
Lower resting heart volume
Cardiac atrophy
May actually be negative caloric balance and body weight
Cardiac contractility probably not affected
Increases in cardiac compliance
But, these decrease after two weeks of bed rest
Increased venous compliance (decrease VR)
Decreased PNS, increased HR, increased SNS
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Musculoskeletal adaptations
Increased calcium loss
Skeletal muscle adaptations
Concentric and eccentric strength
Muscle ultrastructural changes Altered muscular coordination
Delayed-onset muscle soreness
General weakness and fatigue
Max explosive leg power decreases.
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