Environmental Exercise Physiology Flashcards
What is body temperature regulation?
Stress of physical exertion complicated by
environmental thermal conditions
What is meant by humans being homeothermic?
Internal body temperature regulated, nearly constant
despite environmental temperature changes
What is thermoregulation?
Thermoregulation: regulation of body temperature
around a physiological set point
What is acclimation?
Acclimation: short-term adaptation to environmental stressor (days/weeks)
What is acclimatization?
Acclimatization: long-term adaptation to environmental stressor (months/years)
What are the conversion equations from celcius to fahrenheit?
° C = (° F – 32) / 1.8
° F = (° C x 1.8) + 32
State what percent of ATP breakdown in metabolic heat production is cellular work & how much is metabolic heat.
– <25% ATP breakdown - cellular work (W)
– >75% ATP breakdown - metabolic heat
What is the direction of heat transfer between the body and the external environment?
Heat moves from body core to periphery via blood
What is conduction?
Heat transfer from one solid material to another
through direct molecular contact (negligible)
– Sitting on chilly (or hot) metal bleachers
What is convection?
Heat transfer by movement of gas or liquid across a
surface
– Movement across skin = heat exchange
– Major daily thermoregulatory factor
What is radiation?
Heat loss in form of infrared rays
– Body can give off or receive radiant heat
– Major daily thermoregulatory factor
What is insulation?
– Insulation (I): resistance to dry heat exchange
– Still layer of air ideal insulator
What is evaporation?
Heat loss via phase change from liquid to gas
– Primary heat loss during exercise (~80%)
– Clothing = resistance to E
What is the heat balance equation?
– M – W ± R ± C ± C – E = 0 (Heat balance)
– If M – W ± R ± C ± C – E < 0 (Heat loss)
– If M – W ± R ± C ± C – E > 0 (Heat gain)
Describe the changes in humidity and heat loss in transfer of body heat.
Water vapor pressure (humidity) affects Evaporation
– increased Humidity = decreased E, decreased humidity = increased E
– Prolonged evaporation via sweat - dehydration
Describe the cooling capacity of sweat
Air temperature can become ≥ skin temperature
– 1.5 L sweat evaporated cools 400 W
What are the main thermoregulatory responses of the body?
Core temperature regulated around 37 °C
– Core temperature >40 °C inhibits physiological
function
What part of the brain is thermoregulatory function controlled by?
Thermoregulatory function controlled by POAH
preoptic anterior hypothalamus
How does the pre-optic anterior hypothalamus (POAH) work?
– Body’s thermostat located in the brain
– Receives input from sensory thermo-receptors
– When body temperature deviates, POAH activates
thermoregulatory mechanisms
What are sensory receptors?
– Peripheral thermoreceptors in skin
– Central thermoreceptors in brain, spinal cord
What is the role of skin arteriole effectors?
SNS vasoconstriction (VC) minimizes heat loss – SNS vasodilation (VD) enhances heat loss
What is the role of eccrine sweat gland effectors?
SNS stimulation of sweating
– Acetylcholine: sympathetic cholinergic stimulation
– More responsive to changes in core temperature
than skin temperature
What is the role of skeletal muscle effectors?
Help generate additional heat via shivering
– Involuntary cycle of contraction and relaxation
– Only heat production, no useful work
What is the role of endocrine gland effectors?
increased Metabolism = increased heat production
– Cooling - release of thyroxine, catecholamines
– Hormonal stimulation of heat production
What is the role of exercise in relation to heat load?
Exercise = increases heat load, disturbs thermal
homeostasis in most environments
What is the effect of heat load on cardiovascular function?
Skin arterioles VD to increase heat loss, requires increased blood flow compared to exercise in the cold
– POAH triggers SNS: cardiac output increases further via HR/contractility, increased VC to nonessential tissues
– Blood volume decreases (sweat), SV can’t increase (blood pooling),
so HR increases further to compensate (cardiovascular drift)
What are some physiological limitations to exercise in the heat?
Limitation: cardiovascular system overload
– Heart cannot provide sufficient blood flow to both
exercising muscle and skin
– Impaired performance, increased risk of overheating
– Especially in untrained or non-acclimated athletes
• Limitation: critical temperature theory
– Brain shuts down exercise at ~40 to 41 ° C
– Helps to explain limitations in trained, wellacclimated athletes
How does training affect sweat composition?
– More sensitive to aldosterone
– Reabsorb (i.e., conserve) more Na+
, Cl-
– K+, Ca2+, Mg2+ losses unchanged
How much sweat is lost during exercise?
Can lose 1.6 to 2.0 L (2.5-3.2% body weight) each
hour
– increased Sweating = decreased blood volume + decreased cardiac output
– Severe dehydration = onset of heat-related illness
What are the 6 risk factors that must be considered prior to exercising in the heat?
Metabolic heat production – Air temperature – Ambient water vapor pressure (humidity) – Air velocity – Radiant heat sources – Clothing
What are the symptoms of heat exhaustion?
Accompanied by fatigue; dizziness; nausea; vomiting; fainting; weak, rapid pulse • Caused by severe dehydration from sweating • Simultaneous blood flow needs of muscle and skin not met due to low blood volume • Thermoregulatory mechanisms functional but overwhelmed
What are the symptoms of heat stroke?
Life threatening, most dangerous
• Thermoregulatory mechanism failure
• Characterized by
– Core temp >40 ° C
– Confusion, disorientation, unconsciousness
• If untreated, results in coma and death
• Must cool whole body ASAP (e.g., ice bath)
What are the guidelines for practicing and competing in the heat?
Events should not take place during hottest
time of day, avoid WBGT >28 ° C
• Adequate supply of palatable fluids
• Customize fluid intake based on fluid losses
(1 L sweat loss = 1 kg weight loss)
• Be aware of signs of heat illness
• Organizers get final call on stopping events,
excluding athletes who have heat illness
What are the effects of acclimation?
Cardiovascular function optimized
– Sweating rate, sweat distribution, and sweat content
change
– Results in a lower core temperature during exercise
Plasma volume increases due to increased oncotic (protein)
pressure, drawing water into circulation
– Temporary (back to normal after 10 days)
– Buys time for other adaptations to occur
• decreased Heart rate, increased cardiac output
– Supports increased skin blood flow
– Greater heat loss, decreased core temperature
• Widespread sweating earlier, more dilute
– Prevents dangerous Na+
loss
– Optimized E heat loss
What are some sex differences to acclimation in the heat?
Women have the same capacity for exercising in the heat as men at the same relative exercise intensity • Lower sweat rates in women • Women have more active sweat glands but less sweat production per gland – Advantage in humid climates – Disadvantage in hot, dry climates
What is cold stress?
any environmental condition
causing loss of body heat
What are some physiological and behavioural responses to cold stress?
– POAH triggers peripheral VC
– POAH triggers nonshivering thermogenesis
– POAH triggers skeletal muscle shivering
– Cerebral cortex triggers behavioral adaptations
What is cold habituation?
– Occurs after repeated cold exposures without
significant heat loss
– VC, shivering blunted; core temperature allowed to ↓
more
What is metabolic acclimation?
Occurs after repeated cold exposures with heat loss
– Enhanced metabolic, shivering heat production
What is insulative acclimation?
When ↑ metabolism cannot prevent heat loss
– Enhanced skin VC (↑ peripheral tissue insulation)
How does body composition affect heat loss?
increased Inactive peripheral muscle = increased insulation
– increased Subcutaneous fat = increased insulation
– decreased Body surface area:mass ratio = decreased heat loss
– Child versus adult versus elderly
– Men versus women
• Women have more subcutaneous fat which is an
advantage but less active muscle, which is a disadvantage
How does windchill affect heat loss?
Often misunderstood: air movement, not air
temperature
– Index based on cooling effect of wind
– Increases C heat loss
– Refers to cooling power of environment
– increased Windchill = increased risk of freezing tissues
How does cold water vs. cold air affect heat loss?
– When C + C + E + R is considered, heat loss 4 times
faster in cold water versus cold air
– Core temperature constant until water temp <32 ° C
– Core temperature lower than 2.1 ° C per h in 15 ° C water
– Heat loss increases in moving water, decreases with exercise
– Hypothermia from cold water occurs well above 0 °
C
What is the muscle function response to exercise in the cold?
– Altered fiber recruitment = decreased contractile force
– Shortening velocity and power decreased
– Affects superficial muscles (deep muscle spared)
What is the response of metabolic heat function to exercise in the cold?
As fatigue increased, metabolic heat production decreased
– Energy reserve depletion with endurance exercise =
increased potential for hypothermia
What are some FFA metabolic responses to exercise in the cold?
Normally, increased catecholamines = increased FFA oxidation
– Cold = increased catecholamine secretion but no certain increase of FFA
– VC in subcutaneous fat = decreased FFA mobilization
What are glucose metabolic responses to exercise in the cold?
Blood glucose maintained well during cold exposure
– Muscle glycogen utilization increased
– Hypoglycemia suppresses shivering
What is hypothermia?
Core temp 34.5 to 29.5 C: POAH function compromised
– Core temp <29.5°C: POAH thermoregulation
completely lost, metabolism slows, drowsiness, lethargy,
coma
What are the cardiorespiratory effects of the cold?
Low core temperature = slow HR (SA node effects)
– Cold may decrease ventilation (rate and volume)
What is treatment for mild hypothermia?
Remove individual from cold
– Provide dry clothing, blankets, warm beverages
What is treatment for severe hypothermia?
– Gentle handling to avoid arrhythmias
– Gradual rewarming
– May require hospital facilities, medical care
What is frostbite?
– Peripheral tissue freezing (air temperature
~−29 ° C)
– Excess VC = lack of O2 & nutrients = tissue death
– Untreated frostbite = gangrene, tissue loss
– Gradually rewarm only when no risk of refreezing
What is exercise-induced asthma?
– Affects up to 50% of winter-sport athletes
– Excessive airway drying
– Treated with e.g. steroid inhalers
Effects of low altitude (500-2000m) on bodily function
– No effects on well-being
– Performance may be decreased, restored by
acclimation
Effects of Moderate altitude (2,000-3,000 m) on bodily function
– Effects on well-being in un-acclimated people
– Performance and aerobic capacity
– Performance may or may not be restored by
acclimation
Effects of High altitude (3,000-5,500 m) on bodily function
– Acute mountain sickness
– Performance decreased, not restored by acclimation
Effects of Extreme high altitude (>5,500 m) on bodily function
– Severe hypoxic effects
– Highest settlements: 5,200 to 5,800 m
Outline the air temperature conditions at altitude
Temperature decreases 1 °C per 150 m ascent
– Contributes to risk of cold-related disorders
Outline the humidity conditions at altitude
– Cold air holds very little water
– Air at altitude very cold and very dry
– Dry air - quick dehydration via skin and lungs
Outline any other conditions that occur at altitude
• Solar radiation increases at high altitude
• UV rays travel through less atmosphere
• Water normally absorbs sun radiation, but
low water vapor at altitude can’t do so
• Snow reflects/amplifies solar radiation
Outline the physiological responses to acute altitude exposure
Pulmonary ventilation increases immediately
– At rest and submaximal exercise (but not maximal
exercise)
– decreased PO2 stimulates chemoreceptors
– increased Tidal volume for several hours, days
– Hyperventilation
• Respiratory alkalosis = high blood pH
– Oxyhemoglobin curve shifts left (↓ O2 saturation of Hb)
– Prevents further hypoxia-driven hyperventilation
• Kidneys excrete more bicarbonate
– Minimizes blood buffering capacity
– Reverses alkalosis, blood pH decreases to normal
• Gas exchange at muscles decreases
– PO2 gradient at muscle decreases
– Sea level: 100 – 40 = 60 mmHg gradient
– 4,300 m altitude: 42 – 27 = 15 mmHg gradient
– O2 diffusion into muscle significantly reduced
• Location of gradient change critical
– Hemoglobin desaturation at lungs - little/no effect
– decreased PO2 gradient at muscle decreases exercise capacity
Outline the physiological responses of the CV system to acute altitude exposure
• Short term: plasma volume decreases in a few hours
– Respiratory water loss, increased urine production
– Lose up to 25% plasma volume
– Short-term increase in hematocrit
• Red blood cell count increases after weeks/months
– Hypoxemia triggers EPO release from kidneys
– increased Red blood cell production in bone marrow
– Long-term increase
• Cardiac output increase (despite decreased plasma
volume, stroke volume)
– At rest and submaximal exercise (not maximal)
– Delivers more O2
to tissues per minute
– increased Sympathetic nervous system activity to increase HR
– Inefficient, short-term adaptation (6-10 days)
• After few days, muscles extract more O2
– increased (A-V O2 difference; increased diffusion gradient)
– Reduces demand for cardiac output in hematocrit
• Q•max = decreased SVmax x decreased HRmax
• decreased SVmax due to decreased PV
• decreased HRmax due to decreased Sympathetic Nervous System responsiveness
Outline the physiological responses of hunger and dehydration associated with acute altitude exposure
• Dehydration occurs faster – Water loss through skin, kidneys/urine – Exacerbated by sweating with exercise – Must consume ~3 to 5 L fluid/day • Appetite declines at altitude – Paired with ↑ metabolism, upward of 500 kcal/day deficit – Athletes/climbers must be educated about eating at altitude
Explain the mechanisms of exercise and sport performance at altitude
• V•O2max decreases as altitude increases past 1,500 m
– Atmospheric PO2 <131 mmHg
– Due to decreased arterial PO2 and Q•max
– Drops 8 to 11% per 1,000 m ascent
• Mt. Everest ascent study, 1981
– V•O2max decrease from 62 to 15 ml/kg/min
– If sea level V•O2max <50 ml/kg/min, could not climb
without supplemental oxygen
• Aerobic exercise performance affected most
by hypoxic conditions at altitude
• V•O2max decreases as a % of sea level V•O2max
– Given task still has same absolute O2
requirement
– Higher sea-level V•O2max - easier perceived effort
– Lower sea-level V•O2max - harder perceived effort
• Anaerobic performance unaffected
– For example, 100 to 400 m track sprints
– ATP-PCr and anaerobic glycolytic metabolism
– Minimal O2 requirements
• Thinner air - less air resistance
– Improved swim and run times
– Improved jump distances
– Throwing events, varied effects
– Mexico Summer Olympics, 1968
Explain the mechanisms of Acclimatization in relation to chronic exposure to altitude
• Acclimation affords improved performance, but performance may never match that at sea level • Pulmonary, cardiovascular, skeletal muscle changes • Takes 3 weeks at moderate altitude – Add 1 week for every additional 600 m – Lost within 1 month at sea level
Explain the pulmonary adaptations of chronic acclimatization to altitude
– increased Ventilation at rest and during submaximal
exercise
– Resting ventilation rate 40% higher than at sea level
(over 3-4 days)
– Submaximal rate 50% higher (longer time frame)
Explain the blood adaptations of chronic acclimatization to altitude
– EPO release increases from 2 to 3 days
– Stimulates polycythemia (increased red blood cell count,
hematocrit)
– Elevated red blood cell count for 3+ months
Explain the consequences of polycythemia in relation to chronic acclimatization to altitude
– Hematocrit at sea level: ~45%
– Hematocrit at 4,500 m: ~60%
– Hemoglobin ↑ proportional to elevation
How to optimise training and performance at altitude?
• Hypoxia at altitude prevents high-intensity
aerobic training
• Living and training high leads to dehydration, low blood volume, low muscle mass
• Value of altitude training for sea-level
performance not validated
• Value of live high, train low?
Explain the 2 strategies for sea level athletes who must compete at high altitudes
- Compete ASAP after arriving at altitude
• Does not confer benefits of acclimation
• Too soon for adverse effects of altitude - Train high for 2 weeks before competing
• Worst adverse effects of altitude over
• Aerobic training at altitude not as effective
What is artificial altitude training?
– Attempt to gain benefits of hypoxia at sea level
– Breathe hypoxic air 1 to 2 h per day, train normally
– No improvements
What is alternating train high, train low?
– Training high stimulates altitude acclimation
– Training low doesn’t lose altitude acclimation
– Training low permits maximal aerobic training
Explain the concept of live high, train low at sea level
– Sleep and live in hypoxic apartment – Train normally – Not scientifically validated yet – Best for elite athletes – Non elite exercisers may benefit from artificial approaches
What is acute altitude (mountain) sickness?
– Onset 6 to 48 h after arrival, most severe days 2 to 3
– Headache, nausea/vomiting, dyspnea, insomnia
– Can develop into more lethal conditions
What is the incidence of altitude sickness?
• Incidence of altitude sickness varies widely
– ↑ with altitude, rate of ascent, susceptibility
– Frequency: 7 to 22% at 2,500 to 3,500 m
– Women have higher incidence than men
What are some possible causes of altitude sickness?
– Low ventilatory response to altitude – CO2 accumulates, acidosis • Headache most common symptom – Mostly experienced >3,600 m – Continuous and throbbing – Worse in morning and after exercise – Hypoxia -> cerebral vasodilation -> stretch pain receptors
What is altitude sickness insomnia?
– Interruption of sleep stages
– Cheyne-Stokes breathing prevents sleep
– Incidence of irregular breathing ↑ with altitude
What is some prevention/treatment for altitude sickness?
– Gradual ascent to altitude
– Medication (+ steroids)
What are the two life-threatening conditions associated with altitude?
– High-altitude pulmonary edema (HAPE)
– High-altitude cerebral edema (HACE)
Explain the causes, symptoms and treatment of high altitude pulmonary edema (HAPE)
• HAPE causes
– Likely related to hypoxic pulmonary vasoconstriction
– Clot formation in pulmonary circulation
• HAPE symptoms
– Shortness of breath, cough, tightness, fatigue
– decreased Blood O2
, cyanosis, confusion, unconsciousness
• HAPE treatment
– Supplemental oxygen
– Immediate descent to lower altitude
Explain the causes, symptoms and treatment of high altitude cerebral edema (HACE)
• HACE causes – Complication of HAPE, >4,300 m – Edemic pressure buildup in intracranial space • HACE symptoms – Confusion, lethargy, ataxia – Unconsciousness, death • HACE treatment – Supplemental oxygen, hyperbaric bag – Immediate descent to lower altitude
