ADAPTATIONS TO HIGH
ALTITUDE
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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:
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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
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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 NONNATIVE 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
HYPERVENTILATORY
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 DELIVERY
FICK 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
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 (FRANKSTARLING LAW
NOTE: NATIVE HIGHLANDERS (NH) AND
ACCLIMATED LOWLANDERS (AL) BOTH
HAVE 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 FLUIDS
ADAPTATIONS 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 LEVELS
REVIEW 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 LIPOLYSIS
C. 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 LEVEL
B. 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-TERM
ADAPTATIONS 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??