ADAPTATIONS TO HIGH ALTITUDE

• VENTILATION• BICARBONATE IONS• 2,3-DIPHOSPHOGLYCERATE (2,3-DPG)

• RED BLOOD CELL (RBC) AND HEMOGLOBIN (Hb) CONCENTRATION

• CAPILLARIZATION AND CELLULAR ADAPTATIONS• SUBMAXIMAL AND MAXIMAL EXERCISE RESPONSES• BODY FLUIDS• BODY COMPOSITION• METABOLISM• NEUROHORMONAL ADAPTATIONS• PERCEPTUAL AND PSYCHOMOTOR FUNCTIONS• ALTITUDE TRAINING AND COMPETITION• GENDER DFFERENES

ABBREVIATIONS:

• VE = EXPIRED VENTILATION RATE• VO2 = OXYGEN UPTAKE RATE• VO2MAX = MAXIMAL OXYGEN UPTAKE RATE• Q = CARDIAC OUTPUT• SV = STROKE VOLUME• HR = HEART RATE• Hb = HEMOGLOBIN• RBC = RED BLOOD CELLS• OCC OR O.C.C = OXYGEN CARRYING CAPACITY OF BLOOD• A - V O2 DIFF = ARTERIAL - VENOUS OXYGEN DIFFERENCE (I.E., OXYGEN EXTRACTION)• O2 = OXYGEN• CO2 = CARBON DIOXIDE• PO2 = PARTIAL PRESSURE OF OXYGEN• PCO2 = PARTIAL PRESSURE OF CARBON DIOXIDE• H+ = HYDROGEN IONS• PIO2 = PARTIAL PRESSURE OF INSPIRED OXYGEN• PICO2 = PARTIAL PRESSURE OF INSPIRED CARBON DIOXIDE• PAO2 = PARTIAL PRESSURE OF OXYGEN IN THE ALVEOLI• PACO2 = PARTIAL PRESSURE OF CARBON DIOXIDE IN THE ALVEOLI• PaO2 = PARTIAL PRESSURE OF OXYGEN IN THE ARTERIAL BLOOD• PaCO2 = PARTIAL PRESSURE OF CARBON DIOXIDE IN THE ARTERIAL BLOOD• SaO2 = ARTERIAL SATURATION WITH OXYGEN• CaO2 = CEREBRAL ARTERIAL SATURATION WITH OXYGEN

RESTING VENTILATION (VE)

• VE INCREASES WITHIN A FEW HOURS AFTER ARRIVING AT HIGH ALTITUDE (FIG 13-1)

• THE INCREASED VE WILL:- INCREASE PAO2 AND HENCE SaO2

- DECREASE PACO2 AND PaCO2

- INCREASE pH

• THUS, AFTER ACCLIMATION FOR A GIVEN PI02, PAO2 IS HIGHER AND PACO2 IS LOWER(FIG 13-2)

• ALSO, NATIVE HIGHLANDERS HAVE AN INCREASED PULMONARY DIFFUSION CAPACITY (PDC) DUE TO FUNCTIONAL AND STRUCTURAL CHANGES (E.G., HIGHER PULMONARY CAPILLARY BLOOD FLOW AND SMALLER DEAD SPACE) THAT TEND TO OCCUR PRIMARILY DURING THE DEVELOPMENTAL YEARS

• NON-NATIVE HIGHLANDERS (ACCLIMATED LOWLANDERS) SHOW NO CHANGE IN PDC DURING REST OR EXERCISE

• THE INCREASE IN RESTING VE IS DUE TO MECHANISMS RELATED TO HYPOXIA AND HYPOXIC INDUCED HYPERCAPNIA AND REDUCED BLOOD pH

• BOTH CENTRAL (MEDULLA OBLONGATA) AND PERIPHERAL (CAROTID BODIES AND AORTIC ARCH) CHEMORECEPTORS ARE INVOLVED IN THE VENTILATORY ADAPTATION

• IN ADDITION, HYPOXIA (DECREASED CaO2) INCREASES BRAIN TISSUE LACTATE PRODUCTION RESULTING IN ACIDOTIC CEREBRAL INTERSTITIAL FLUID, WHICH STIMULATES MEDULLARY CHEMORECEPTORS

DETERMINANTS OF VENTILATORY RESPONSE

• GENETICS• MAGNITUDE OR SEVERITY OF HYPOXIA• YEARS OF ALTITUDE EXPOSURE• AGE AT ARRIVAL TO ALTITUDE (FIG 13-3: VE OF NON-NATIVE HIGHLANDERS ARE INTERMEDIATE TO LOWLANDERS AND NATIVE HIGHLANDERS)

• PHYSICAL ACTIVITY OR EXERCISE PATTERNS

• VENTILATORY ADAPTATION PROGRESSES THROUGH AN INTERMEDIATE HYPERVENTILATORY PHASE TO A PHASE WHERE HYPOXIC SENSITIVITY IS DECREASED; THIS REPRESENTS A HABITUATION RESPONSE

• NATIVE HIGHLANDERS HAVE LOWER VENTILATION THAN LOWLANDERS OR NON-NATIVE HIGHLANDERS

• INCREASE IN THE SEVERITY OF HIGH ALTITUDE EXPOSURE AND/OR YEARS OF ALTITUDE EXPOSURE, AS IN NATIVE HIGHLANDERS, WILL:

1. INCREASE PaCO2 SET POINT OR THRESHOLD FOR THE ONSET

OF VE

2. LOWER PaO2 SET POINT OR THRESHOLD FOR THE ONSET OF VE

EXERCISE VENTILATION RATE

• DURING SUBMAXIMAL EXERCISE, AN ACUTE RESPONSE TO HIGH ALTITUDE IS AN ELEVATED VENTILATORY RATE OVER AND ABOVE NORMOXIC CONDITIONS

• INITIAL STAGES OF ADAPTATION TO HIGH ALTITUDE FURTHER INCREASES THE VE DURING EXERCISE (FIG 13-4)

• AS INDICATED IN FIGURE 13-5, BOTH NATIVE HIGHLANDERS AND NON-NATIVE HIGHLANDERS (ACCLIMATED LOWLANDERS) SHOW A SIMILAR HYPER-VENTILATORY RESPONSE TO ALTITUDE DURING EXERCISE

BICARBONATE IONS

• DURING THE FIRST FEW DAYS AT HIGH ALTITUDE, THE INCREASE VE REDUCES THE HYDROGEN CONCENTRATION IN THE BLOOD AND HENCE, THE pH OF THE BLOOD INCREASES; THE INCREASE IN pH SHIFTS THE Hb-O2 DISSOCIATION CURVE TO THE LEFT INCREASING THE AFFINITY OF Hb FOR O2 AND HENCE, REDUCING THE BOHR EFFECT OR RELEASE OF OXYGEN TO MUSCLE TISSUE

• HOWEVER, WITHIN SEVERAL DAYS THE pH OF THE BLOOD IS STABILIZED NEAR NORMAL LEVELS DUE TO AN INCREASE IN THE ELIMINATION OF BICARBONATE IONS IN THE URINE; THE KIDNEYS INCREASE BICARBONATE ION EXCRETION TO NORMALIZE pH

ALTITUDE INCREASES CARBON DIOXIDE AND LACTATE PRODUCTION

2,3-DIPHOSPHOGLYCERATE(2,3-DPG)

• THE INCREASED VE DURING THE FIRST FEW DAYS OF HIGH ALTITUDE EXPOSURE ALSO STIMULATES RBC GLYCOLYSIS AND ALONG WITH THE DECREASE IN PO2 WHICH STIMULATES DPG MUTASE, 2,3-DPG LEVELS INCREASE

• THE INCREASE IN 2,3-DPG LEVELS SHIFTS THE Hb-02 DISSOCIATION CURVE TO THE RIGHT

• THE SHIFT OF THE CURVE TO THE RIGHT DOES NOT AFFECT 02 LOADING IN THE LUNGS, BUT INCREASES O2 AVAILABILITY (UNLOADING) TO THE MUSCLE TISSUE BY 26-FOLD

THIS MAJOR ADAPTATION OCCURS WITHIN 48 HOURS

OF HIGH ALTITUDE EXPOSURE

• NOTE: EXERCISE DECREASES pH AND INCREASES TEMPERATURE AND PC02 THEREBY SHIFTING THE CURVE TO THE RIGHT, WHICH INCREASES OXYGEN AVAILABILITY TO THE MUSCLE TISSUE

PHYSICAL WORK CAPACITY (PWC) AT ALTITUDE

• PHYSICAL WORK CAPACITY (PWC) IS INCREASED WITHIN 2-3 WEEKS OF HIGH ALTITUDE EXPOSURE

• REASONS FOR THE INCREASE IN PWC

1. INCREASED RBC AND Hb CONCENTRATIONS- INCREASED OXYGEN CARRYING

CAPACITY OF THE BLOOD- INCREASED SaO2

• NOTE: HYPOXEMIA (LOW PO2 IN THE BLOOD) STIMULATES THE RELEASE OF ERYTHROPOIETIN FROM THE KIDNEYS THAT INCREASES RBC PRODUCTION IN THE RED BONE MARROW

• NOTE: LONG-TERM RESIDENTS AT 3,100 M SHOW AN INCREASE IN BLOOD VOLUME DUE TO BOTH AN INCREASE IN PLASMA VOLUME AND RBC LEVEL WITH NO CHANGE IN HEMATOCRIT; SINCE VASCULAR ANATOMY PROVIDES THE UPPER LIMIT FOR ANY INCREASE IN TOTAL BLOOD VOLUME, RESIDENTS AT 4,300 M SHOW AN INCREASE IN BLOOD VOLUME AND RBC LEVEL, BUT A DECREASE IN PLASMA VOLUME RESULTING IN AN INCREASE IN HEMATOCRIT AND BLOOD VISCOSITY

REASONS FOR INCREASD PWC (CONTINUED)

2. INCREASED CONTRIBUTION OF FAT METABOLISM TO ENERGY

PRODUCTION RESULTING IN GLYCOGEN SPARING

AND LOWER LACTATE LEVELS FOR A GIVEN WORKLOAD

3. DECREASE IN RELATIVE SUBMAXIMAL EXERCISE INTENSITY DUE TO THE INCREASE IN MAXIMAL OXYGEN

UPTAKE RATE (VO2MAX)???- NO CHANGE IN SUBMAXIMAL OXYGEN

UPTAKE RATE (VO2)

- INCREASE IN VO2MAX

EFFECTS OF HIGH ALTITUDE ON MAXIMAL OXYGEN UPTAKE RATE

(V02MAX)

• ALTITUDE INITIALLY DECREASES VO2MAX

WHICH INCREASES THE RELATIVE EXERCISE INTENSITY OF AN ABSOLUTE SUBMAXIMAL WORKLOAD

• WIDE INDIVIDUAL VARIABILITY EXISTS IN THE ACUTE DECREASE IN VO2MAX AT ALTITUDE

EFFECTS OF HIGH ALTITUDE ON MAXIMAL OXYGEN UPTAKE (V02MAX) (CONTINUED)

2. LONG-TERM EXPOSURE DOES NOT FURTHER DECREASE VO2MAX IF PHYSICAL ACTIVITY IS MAINTAINED

3. DETRAINING MAY BE ACCELERATED AT HIGH ALTITUDE DUE TO

- DECREASE IN LEAN BODY WEIGHT (LBW)- DEVELOPMENT OF PULMONARY OR

CEREBRAL EDEMA AT ELEVATIONS > 12,500 FEET- MOUNTAIN SICKNESS (HEADACHE, NAUSEA, VOMITING, ANOREXIA, INDIGESTION, FLATUS, CONSTIPATION,

AND SLEEP DISTURBANCES)

4. ALTITUDE'S ABILITY TO DECREASE VO2MAX MAY OR MAY BE NOT ALTERED BY SHORT-TERM ALTITUDE

ACCLIMATION OF 3-5 WEEKS

NOTE: THE TWO BEST STUDIES REPORT CONFLICTING RESULTS (HORSTMAN REPORTED AN INCREASE WHEN EXPRESSED IN ML/KG/MIN; YOUNG REPORTED NO CHANGE

WHEN EXPRESSED IN L/MIN)

• IF VO2MAX IS INCREASED, IT IS PROBABLY DUE TO A DECREASE IN BODY WEIGHT, PRIMARILY FROM A DECREASE IN FAT WEIGHT OR DIURESIS (DECREASE IN TOTAL BODY WATER) AS A DECREASE IN LEAN BODY WEIGHT WOULD DECREASE VO2MAX; IF LEAN BODY WEIGHT IS DECREASED, APPARENTLY AN INCREASE RBC AND Hb LEVELS OFFSET THE POTENTIAL LOSS OF OXIDATIVE CAPABILITIES THAT MAY BE ASSOCIATED WITH THE DECREASE IN LBM

SYSTEMATIC O2 TRANSPORT AND DELIVERYFICK EQUATION: VO2 = Q X O2 EXTRACTION

OR VO2 = SV X HR X A - V O2 DIFFERENCE

ACUTE EXPOSURE

• DECREASE IN SaO2 AND CaO2 WILL STIMULATE SNS WHICH INCREASES HR AND HENCE Q AT A GIVEN SUBMAXIMAL WORKLOAD; CONSEQUENTLY VO2 AT AN ABSOLUTE WORKLOAD IS MAINTAINED

• INCREASED CARDIAC OUTPUT (Q) DUE TO INCREASED HR TO MAINTAIN VO2 AT A GIVEN SUBMAXIMAL WORKLOAD

HIGH ALTITUDE ADAPTATION

RELATED TO:

• CHANGES IN CARDIAC OUTPUT(SV X HR)

• CHANGES IN OXYGEN EXTRACTION (I.E., ARTERIAL - VENOUS OXYGEN DIFFERENCE)

HIGH ALTITUDE ADPATATION

• DECREASED CARDIAC OUTPUT (FIG 13-8) DUE TO A DECREASE IN STROKE VOLUME

• DECREASE IN Q APPEARS AFTER 48 HOURS AND CONTINUES TO DECREASE FOR 8-9 DAYS

• NATIVE HIGHLANDERS (NH) AND ACCLIMATED LOWLANDERS (AL) BOTH HAVE A SIMILARLY REDUCED Q

DECREASE IN CARDIAC OUTPUT IS DUE TO:

• DECREASE IN RESTING, SUBMAXIMAL, AND MAXIMAL SV

• DURING FIRST TWO WEEKS OF ALTITUDE ADAPTATION, PLASMA VOLUME DECREASES; BECAUSE OF THE INCREASE IN RBC LEVELS AND THE DECREASE IN PLASMA VOLUME, HEMATOCRIT AND BLOOD VISCOSITY INCREASES; THIS WOULD POTENTIALLY DECREASE CARDIAC OUTPUT DUE TO AN INCREASE IN PERIPHERAL RESISTANCE (Q = P/R)

REASONS FOR A DECREASE IN SV:

• DECREASED CARDIAC FILLING (I.E., EDV), POSSIBLY DUE TO TACHYCARDIA, INCREASED VENTILATION RATE, DECREASED PLASMA VOLUME, AND/OR INCREASED BLOOD VISCOSITY; THE INCREASED VISCOSITY AND DECREASED PLASMA VOLUME MAY DECREASE VENOUS RETURN OF BLOOD FLOW TO THE HEART

• INCREASED ESV DUE TO DECREASED MYOCARDIAL CONTRACTILITY (FRANK-STARLING LAW

NOTE: NATIVE HIGHLANDERS (NH) AND ACCLIMATED LOWLANDERS (AL) BOTHHAVE A SIMILARLY REDUCED Q AS SHOWN PREVIOUSLY IN FIG 13-9

- NATIVE HIGHLANDERS HAVE GREATER SV AND LOWER HR THAN THE ACCLIMATED LOWLANDERS

- ACCLIMATED LOWLANDERS HAVE A HIGHER HR AND LOWER SV THAN THE NATIVE HIGHLANDERS

ARTERIAL - VENOUS OXYGEN DIFFERENCE (I.E., OXYGEN EXTRACTION)

• MAXIMAL EXERCISE: A -V O2 DIFFERENCE IS THE SAME OR SLIGHTLY GREATER IF TISSUE ADAPTATIONS HAVE OCCURRED

TISSUE ADAPTATIONS OF LONG-TERM RESIDENTS AT HIGH ALTITUDE, WHICH WOULD INCREASE SUBMAXIMAL AND MAXIMAL OXYGEN EXTRACTION CAPABILITIES, INCLUDE:

• INCREASED CAPILLARIZATION

• INCREASED MYOGLOBIN CONCENTRATION

• INCREASED MITOCHONDRIAL DENSITY

• INCREASED OXIDATIVE ENZYME LEVELS

THEREFORE, IF VO2MAX CONTINUES TO BE REDUCED AFTER ADAPTATION TO ALTITUDE, IT IS PROBABLY DUE TO A DECREASE IN Q THAT IS GREATER THAN THE INCREASE IN OXYGEN EXTRACTION

A - V O2 DIFF IS INCREASED DURING SUBMAXIMAL EXERCISE AT THE SAME ABSOLUTE WORKLOAD THEREBY OFFSETTING THE SUBMAXIMAL EXERCISE DECREASE IN Q; HENCE, SUBMAXIMAL VO2 WHEN PERFORMING THE SAME ABSOLUTE SUBMAXIMAL WORKLOAD IS UNCHANGED

REASONS FOR THE INCREASE IN SUBMAXIMAL A - V 02 DIFFERENCE:

• INCREASE IN VE

• INCREASE IN 2,3-DPG LEVELS

• INCREASE IN RBC AND Hb LEVELS

• LONG-TERM TISSUE ADAPTATIONS

BODY FLUIDSADAPTATIONS TO HIGH ALTITUDE DURING THE FIRST TWO WEEKS INCLUDE:

• NO CHANGE IN TOTAL BODY WATER• DECREASE IN PLASMA VOLUME• DECREASE IN EXTRACELLULAR AND INTERSTITIAL VOLUMES

• INCREASE IN INTRACELLULAR VOLUME• INCREASE IN BLOOD HEMATOCRIT AND BLOOD VISCOSITY DUE TO THE DECREASE IN PLASMA VOLUME AND INCREASE IN RBC

• REVIEW FIG 13-11 AND TABLE 5-2

LONG-TERM ADAPTATION TO HIGH ALTITUDE

• LONG-TERM RESIDENTS AT 3,100 M SHOW AN INCREASE IN PLASMA VOLUME AND RBC LEVEL WITH NO CHANGE IN HEMATOCRIT

• SINCE VASCULAR ANATOMY PROVIDES THE UPPER LIMIT FOR ANY INCREASE IN TOTAL BLOOD VOLUME, LONG-TERM RESIDENTS AT 4,300 M SHOW AN INCREASE IN BLOOD VOLUME AND RBC LEVEL, BUT A DECREASE IN PLASMA VOLUME RESULTING IN AN INCREASE IN HEMATOCRIT AND BLOOD VISCOSITY; THE INCREASE IN BLOOD VISCOSITY WILL DECREASE CARDIAC OUTPUT AS CARDIAC OUTPUT IS EQUAL TO THE PRESSURE GRADIENT (I.E., MEAN ARTERIAL BLOOD PRESSURE) DIVIDED BY THE RESISTANCE TO BLOOD FLOW

BODY COMPOSITION

• DECREASE IN BODY WEIGHT DUE TO A DECREASE IN BOTH LEAN BODY WEIGHT AND FAT WEIGHT; WEIGHT LOSS APPEARS TO BE INVERSELY RELATED TO FAT WEIGHT AS LEANER SUBJECTS SHOW A GREATER WEIGHT LOSS THAN HEAVIER, MORE FAT SUBJECTS

• DECREASE IN LEAN BODY WEIGHT (LBW)

• DECREASE POTENTIALLY IN FAT WEIGHT (FW)

• INCREASE IN PERCENT BODY FAT AS THE DECREASE IN LEAN BODY WEIGHT TENDS TO BE GREATER THAN THE DECREASE IN FAT WEIGHT

• THE DECREASE IN BODY WEIGHT, LEAN BODY WEIGHT, AND FAT WEIGHT ARE DUE INPART TO A DECREASE IN CALORIC INTAKE AS APPETITE TENDS TO BE SUPPRESSED DURING THE INITIAL STAGES OF ALTITUDE ACCLIMATION

METABOLISM• INCREASED RESTING PLASMA FFA CONCENTRATION AFTER 14-18 DAYS AT 4,300 METERS INDICATES INCREASED FAT METABOLISM

• INCREASED FFA METABOLISM TENDS TO INCREASE PWC AND ENDURANCE TIME TO EXHAUSTION DUE TO GLYCOGEN SPARING AS EVIDENCED BY- DECREASED BLOOD LACTATE- BETTER MAINTENANCE OF MUSCLE

GLYCOGEN LEVELSREVIEW FIGURE 13-12

MECHANISMS FOR DECREASED MUSCLE GLYCOGENOLYSIS AND INCREASED LIPOLYSIS

• LOW CHO AND/OR HYPOCALORIC DIET INCREASES FAT METABOLISM

• SNS STIMULATION INCREASES CIRCULATING NOREPRINEPHRINE (NEPI) LEVELS THEREBY INCREASING FAT MOBILIZATION AND LIPOLYSIS

• THE BREAKDOWN OF CARBOHYDRATES SLOWS DOWN DUE TO DECREASED PFK ENZYME ACTIVITY (PHOSPHOFRUCTOKINASE IS THE RATE LIMITING ENZYME OF GLYCOLYSIS); PYRUVATE THAT IS FORMED FROM GLYCOGENOLYSIS IS CONVERTED INTO ACETYL CoA AND ENTERS THE KREBS CYCLE RATHER THAN INTO LACTIC ACID

• DECREASED BLOOD LACTIC LEVELS WHICH INCREASES FAT MOBILIZATION, AS INCREASED BLOOD LACTATE LEVELS INHIBITS FAT MOBILIZATION

NEUROHORMONAL RESPONSES

• INCREASED SYMPATHETIC NERVOUS SYSTEM (SNS) STIMULATION AND HENCE CIRCULATING NOREPINEPHRINE (NEPI) LEVELS WITHIN 3-5 DAYS WHICH TEND TO PLATEAU AFTER ONE WEEK; SNS ACTIVITY TENDS TO DIMINISH AFTER 1 MONTH DUE TO A DECREASE IN RECEPTORS AT THE BETA ADRENERGIC SITES; INCREASED NOREPINEPHRINE LEVELS WILL

A. INCREASE EXPIRED VENTILATION RATE B. INCREASE LIPOLYSISC. INCREASE HEART RATE

REVIEW FIGURE 13-13

• ADAPTATION HAS NO EFFECT ON PARASYMPATHERIC NERVOUS SYSTEM (PNS) ACTIVITY

• TRANSIENT INCREASE IN THYROXIN DURING FIRST FEW DAYS WHICH MAY INCREASE BASAL VO2 AND WEIGHT LOSS

• LONG-TERM RESIDENTS HAVE HIGHER PLASMA INSULIN LEVELS AND/OR INCREASED INSULIN SENSITIVITY AS THEY HAVE FASTER GLUCOSE CLEARANCE AND HENCE, BETTER GLUCOSE TOLERANCE

• INCREASED CIRCULATING CORTISOL LEVELS DURING THE FIRST WEEK OF HIGH ALTITUDE WHICH EVENTUALLY RETURN BACK TOWARD BASELINE

A. THE INCREASED CORTISOL LEVELS WILL HAVE A CATABOLIC EFFECT ON TISSUES TO PROVIDE AMINO ACIDS FOR

GLUCONEOGENESIS, WHICH MAY CONTRIBUTE TO THE DECREASE IN LEAN

BODY WEIGHT

B. ALSO IN CONJUNCTION WITH NOREPINEPHRINE, CORTISOL STIMULATES LIPOLYSIS

• LONG-TERM RESIDENTS HAVE HIGHER PLASMA GROWTH HORMONE (GH) LEVELS DURING EXERCISE DUE TO A HIGHER SET POINT FOR GROWTH HORMONE LEVELS IN THE HYPOTHALAMUS AND HENCE, DECREASED HEPATIC CLEARANCE; THE HIGHER CIRCULATING GROWTH HORMONE LEVELS

A. MAY HAVE AN ANABOLIC EFFECT THAT MAY OFFSET THE DECREASE IN LEAN BODY

WEIGHT OBSERVED DURING THE EARLY STAGES OF ADAPTATION

B. WILL STIMULATE FAT MOBILIZATION AND LIPOLYSIS THEREBY INCREASING AEROBIC METABOLISM AND REDUCING OXYGEN DEFICIT AND LACTATE ACCUMULATION

• DECREASED CIRCULATING ALDOSTERONE LEVELS MAY CONTRIBUTE TO THE OBSERVED DECREASES IN PLASMA VOLUME DURING THE INITIAL STAGES OF ADAPTATION AS ALDOSTERONE INCREASES WATER RETENTION BY THE KIDNEYS

PERCEPTUAL AND PSYCHOMOTOR FUNCTIONS

• AFFECTS OF ALTITUDE ACCLIMATION ON CNS FUNCTION IS UNCLEAR AND NEEDS MORE RESEARCH

• DURING SUBMAXIMAL EXERCISE (85% OF VO2MAX), LOCAL FACTORS DOMINANT THE RPE AT SEA LEVEL AND ACUTE HIGH ALTITUDE WHEREAS CENTRAL FACTORS DOMINANT RPE AT CHRONIC ALTITUDE AS LACTATE LEVELS TEND TO BE LOWER

TRAINING AND COMPETITION AT HIGH ALTITUDE

• TRAINING AT HIGH ALTITUDE MAY BE DETRIMENTAL TO COMPETITION AT SEA LEVEL AS ABSOLUTE TRAINING INTENSITY IS LOWERED AS VO2MAX IS DECREASED; MOTOR UNIT SPECIFICITY IS COMPRISED

• INTERVAL TRAINING IS NOT DETRIMENTALLY AFFECTED BY HIGH ALTITUDE AND MAY EVEN BE ENHANCED; DURING THE EARLY STAGES OF ACCLIMATION INTERVAL TRAINING MAY ALSO HELP MAINTAIN MUSCLE POWER AND HELP OFFSET REDUCTIONS IN ENDURANCE PERFORMANCE

• FOR COMPETITION AT HIGH ALTITUDE, LOWLANDERS SHOULD ALLOW 3 WEEKS TO ADAPT

• ALTHOUGH ACCLIMATED LOWLANDERS (AL) MAY HAVE AN EDGE OVER UNACCLIMATED LOWLANDERS (UL) AT ALTITUDE COMPETITIONS, THIS APPEARS TO BE ELIMINATED AT SEA LEVEL COMPETITIONS AS:A. AL AND UL EXPERIENCE SIMILAR INCREASES IN VO2MAX WHEN COMING DOWN TO SEA LEVELB. AL HAVE MORE ERYTHROCYTES AND

OXYGEN CARRYING CAPACITY (WHICH DECREASE WITHIN 10 DAYS), UL HAVE HAVE A HIGHER CARDIAC OUTPUT

• HOWEVER, NATIVE HIGHLANDERS WHO HAVE EXPERIENCED LONG-TERMADAPTATIONS SUCH AS INCREASED CAPILLARIZATION, INCREASED PLASMA VOLUME, AND SUBCELLUAR TISSUE CHANGES (E.G., INCREASED MYOGLOBIN, MITOCHODRIA, AND OXIDATIVE ENZYME LEVELS) MAY HAVE AN ADVANTAGE IN SEA LEVEL COMPETITIONS AS WELL AS COMPETITIONS AT HIGH ALTITUDE

LIVE HIGH (2,000-2,700 M/6,560-8,855 FT) -TRAIN LOW (< 1,000 M/3,280 FT)!

• LIVING HIGH• INCREASES RBC MASS AND

HEMOGLOBIN CONCENTRATION• TRAINING LOW

• TRAINING CAN BE AT SEA LEVEL TRAINING INTENSITY/VELOCITY THEREBY INDUCING PERIPHERAL AND NEUROMUSCULAR ADAPTATIONS

LIVE HIGH (2,000-2,700 M/6,560-8,855 FT) -TRAIN LOW (< 1,000 M/3,280 FT)!

• IMPROVES SEA LEVEL MAXIMAL OXYGEN UPTAKE RATE AND ENDURANCE PERFORMANCE

• BENEFITS MAY LAST UP TO 3-WEEKS, PERHAPS LONGER, WHEN RETURNING TO SEA LEVEL LIVING AND TRAINING

ALTERNATIVE STRATEGIES TO LIVE HIGH, TRAIN LOW

SIMULATES HIGH ALTITUDE WHEN LIVING AND TRAINING AT LOW ALTITUDE:

• NORMOBARIC HYPOXIA VIA NITROGEN DILUTION (NITROGREN APARTMENTS)

• HYPOXIC SLEEPING UNITS/TENTS• MAY NOT HAVE THE SAME EFFECTS AS A

HYPOBARIC ENVIRONMENT

SIMULTATES SEA LEVEL TRAINING WHEN LIVING AND TRAINING AT HIGH ALTITUDE:

• OXYGEN SUPPLEMENTATION

GENDER DIFFERENCES IN HIGH ALTITUDE ADAPTATIONS

• NO MAJOR GENDER DIFFERENCES EXIST IN THE ADAPTATIVE PROCESSES AT HIGH ALTITUDE

• HOWEVER WHEN RETURNING TO SEA LEVEL, MEN TEND TO RETAIN INCREASED RBC CONCENTRATIONS LONGER (ERYTHROPOIETIC RESPONSE) THAN WOMEN AS MEN'S RBC LEVELS RETURN TO NORMAL SEA LEVEL VALUES MORE SLOWLY EVEN THOUGH THEIR PLASMA VOLUME RETURNS TO NORMAL SEA LEVEL VALUES MORE RAPIDLY THAN WOMEN;THEREFORE, CHANGES IN BLOOD VISCOSITY FOLLOW A SIMILAR TREND IN MEN AND WOMEN WHEN RETURNING TO SEA LEVEL FROM HIGH ALTITUDE

QUESTIONS??