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PHYL2730 > Environmental Exercise Physiology > Flashcards

Environmental Exercise Physiology Flashcards

1
Q

What is body temperature regulation?

A

Stress of physical exertion complicated by

environmental thermal conditions

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2
Q

What is meant by humans being homeothermic?

A

Internal body temperature regulated, nearly constant

despite environmental temperature changes

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3
Q

What is thermoregulation?

A

Thermoregulation: regulation of body temperature

around a physiological set point

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4
Q

What is acclimation?

A 
Acclimation: short-term adaptation to
environmental stressor (days/weeks)
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5
Q

What is acclimatization?

A 
Acclimatization: long-term adaptation to
environmental stressor (months/years)
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6
Q

What are the conversion equations from celcius to fahrenheit?

A

° C = (° F – 32) / 1.8

° F = (° C x 1.8) + 32

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7
Q

State what percent of ATP breakdown in metabolic heat production is cellular work & how much is metabolic heat.

A

– <25% ATP breakdown - cellular work (W)

– >75% ATP breakdown - metabolic heat

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8
Q

What is the direction of heat transfer between the body and the external environment?

A

Heat moves from body core to periphery via blood

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9
Q

What is conduction?

A

Heat transfer from one solid material to another
through direct molecular contact (negligible)
– Sitting on chilly (or hot) metal bleachers

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10
Q

What is convection?

A

Heat transfer by movement of gas or liquid across a
surface
–  Movement across skin =  heat exchange
– Major daily thermoregulatory factor

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11
Q

What is radiation?

A

Heat loss in form of infrared rays
– Body can give off or receive radiant heat
– Major daily thermoregulatory factor

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12
Q

What is insulation?

A

– Insulation (I): resistance to dry heat exchange

– Still layer of air ideal insulator

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13
Q

What is evaporation?

A

Heat loss via phase change from liquid to gas
– Primary heat loss during exercise (~80%)
– Clothing = resistance to E

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14
Q

What is the heat balance equation?

A

– 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)

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15
Q

Describe the changes in humidity and heat loss in transfer of body heat.

A

Water vapor pressure (humidity) affects Evaporation
– increased Humidity = decreased E, decreased humidity = increased E
– Prolonged evaporation via sweat - dehydration

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16
Q

Describe the cooling capacity of sweat

A

Air temperature can become ≥ skin temperature

– 1.5 L sweat evaporated cools 400 W

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17
Q

What are the main thermoregulatory responses of the body?

A

Core temperature regulated around 37 °C
– Core temperature >40 °C inhibits physiological
function

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18
Q

What part of the brain is thermoregulatory function controlled by?

A

Thermoregulatory function controlled by POAH

preoptic anterior hypothalamus

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19
Q

How does the pre-optic anterior hypothalamus (POAH) work?

A

– Body’s thermostat located in the brain
– Receives input from sensory thermo-receptors
– When body temperature deviates, POAH activates
thermoregulatory mechanisms

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20
Q

What are sensory receptors?

A

– Peripheral thermoreceptors in skin

– Central thermoreceptors in brain, spinal cord

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21
Q

What is the role of skin arteriole effectors?

A 
SNS vasoconstriction (VC) minimizes heat loss
– SNS vasodilation (VD) enhances heat loss
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22
Q

What is the role of eccrine sweat gland effectors?

A

SNS stimulation of sweating
– Acetylcholine: sympathetic cholinergic stimulation
– More responsive to changes in core temperature
than skin temperature

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23
Q

What is the role of skeletal muscle effectors?

A

Help generate additional heat via shivering
– Involuntary cycle of contraction and relaxation
– Only heat production, no useful work

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24
Q

What is the role of endocrine gland effectors?

A

increased Metabolism = increased heat production
– Cooling - release of thyroxine, catecholamines
– Hormonal stimulation of heat production

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25
Q

What is the role of exercise in relation to heat load?

A

Exercise = increases heat load, disturbs thermal

homeostasis in most environments

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26
Q

What is the effect of heat load on cardiovascular function?

A

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)

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27
Q

What are some physiological limitations to exercise in the heat?

A

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

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28
Q

How does training affect sweat composition?

A

– More sensitive to aldosterone
– Reabsorb (i.e., conserve) more Na+
, Cl-
– K+, Ca2+, Mg2+ losses unchanged

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29
Q

How much sweat is lost during exercise?

A

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

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30
Q

What are the 6 risk factors that must be considered prior to exercising in the heat?

A 
Metabolic heat production
– Air temperature
– Ambient water vapor pressure (humidity)
– Air velocity
– Radiant heat sources
– Clothing
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31
Q

What are the symptoms of heat exhaustion?

A 
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
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32
Q

What are the symptoms of heat stroke?

A

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)

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33
Q

What are the guidelines for practicing and competing in the heat?

A

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

34
Q

What are the effects of acclimation?

A

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

35
Q

What are some sex differences to acclimation in the heat?

A 
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
36
Q

What is cold stress?

A

any environmental condition

causing loss of body heat

37
Q

What are some physiological and behavioural responses to cold stress?

A

– POAH triggers peripheral VC
– POAH triggers nonshivering thermogenesis
– POAH triggers skeletal muscle shivering
– Cerebral cortex triggers behavioral adaptations

38
Q

What is cold habituation?

A

– Occurs after repeated cold exposures without
significant heat loss
– VC, shivering blunted; core temperature allowed to ↓
more

39
Q

What is metabolic acclimation?

A

Occurs after repeated cold exposures with heat loss

– Enhanced metabolic, shivering heat production

40
Q

What is insulative acclimation?

A

When ↑ metabolism cannot prevent heat loss

– Enhanced skin VC (↑ peripheral tissue insulation)

41
Q

How does body composition affect heat loss?

A

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

42
Q

How does windchill affect heat loss?

A

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

43
Q

How does cold water vs. cold air affect heat loss?

A

– 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

44
Q

What is the muscle function response to exercise in the cold?

A

– Altered fiber recruitment = decreased contractile force
– Shortening velocity and power decreased
– Affects superficial muscles (deep muscle spared)

45
Q

What is the response of metabolic heat function to exercise in the cold?

A

As fatigue increased, metabolic heat production decreased
– Energy reserve depletion with endurance exercise =
increased potential for hypothermia

46
Q

What are some FFA metabolic responses to exercise in the cold?

A

Normally, increased catecholamines = increased FFA oxidation
– Cold = increased catecholamine secretion but no certain increase of FFA
– VC in subcutaneous fat = decreased FFA mobilization

47
Q

What are glucose metabolic responses to exercise in the cold?

A

Blood glucose maintained well during cold exposure
– Muscle glycogen utilization increased
– Hypoglycemia suppresses shivering

48
Q

What is hypothermia?

A

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

49
Q

What are the cardiorespiratory effects of the cold?

A

Low core temperature = slow HR (SA node effects)

– Cold may decrease ventilation (rate and volume)

50
Q

What is treatment for mild hypothermia?

A

Remove individual from cold

– Provide dry clothing, blankets, warm beverages

51
Q

What is treatment for severe hypothermia?

A

– Gentle handling to avoid arrhythmias
– Gradual rewarming
– May require hospital facilities, medical care

52
Q

What is frostbite?

A

– 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

53
Q

What is exercise-induced asthma?

A

– Affects up to 50% of winter-sport athletes
– Excessive airway drying
– Treated with e.g. steroid inhalers

54
Q

Effects of low altitude (500-2000m) on bodily function

A

– No effects on well-being
– Performance may be decreased, restored by
acclimation

55
Q

Effects of Moderate altitude (2,000-3,000 m) on bodily function

A

– Effects on well-being in un-acclimated people
– Performance and aerobic capacity
– Performance may or may not be restored by
acclimation

56
Q

Effects of High altitude (3,000-5,500 m) on bodily function

A

– Acute mountain sickness

– Performance decreased, not restored by acclimation

57
Q

Effects of Extreme high altitude (>5,500 m) on bodily function

A

– Severe hypoxic effects

– Highest settlements: 5,200 to 5,800 m

58
Q

Outline the air temperature conditions at altitude

A

Temperature decreases 1 °C per 150 m ascent

– Contributes to risk of cold-related disorders

59
Q

Outline the humidity conditions at altitude

A

– Cold air holds very little water
– Air at altitude very cold and very dry
– Dry air - quick dehydration via skin and lungs

60
Q

Outline any other conditions that occur at altitude

A

• 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

61
Q

Outline the physiological responses to acute altitude exposure

A

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

62
Q

Outline the physiological responses of the CV system to acute altitude exposure

A

• 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

63
Q

Outline the physiological responses of hunger and dehydration associated with acute altitude exposure

A 
• 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
64
Q

Explain the mechanisms of exercise and sport performance at altitude

A

• 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

65
Q

Explain the mechanisms of Acclimatization in relation to chronic exposure to altitude

A 
• 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
66
Q

Explain the pulmonary adaptations of chronic acclimatization to altitude

A

– 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)

67
Q

Explain the blood adaptations of chronic acclimatization to altitude

A

– EPO release increases from 2 to 3 days
– Stimulates polycythemia (increased red blood cell count,
hematocrit)
– Elevated red blood cell count for 3+ months

68
Q

Explain the consequences of polycythemia in relation to chronic acclimatization to altitude

A

– Hematocrit at sea level: ~45%
– Hematocrit at 4,500 m: ~60%
– Hemoglobin ↑ proportional to elevation

69
Q

How to optimise training and performance at altitude?

A

• 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?

70
Q

Explain the 2 strategies for sea level athletes who must compete at high altitudes

A
  1. Compete ASAP after arriving at altitude
    • Does not confer benefits of acclimation
    • Too soon for adverse effects of altitude
  2. Train high for 2 weeks before competing
    • Worst adverse effects of altitude over
    • Aerobic training at altitude not as effective
71
Q

What is artificial altitude training?

A

– Attempt to gain benefits of hypoxia at sea level
– Breathe hypoxic air 1 to 2 h per day, train normally
– No improvements

72
Q

What is alternating train high, train low?

A

– Training high stimulates altitude acclimation
– Training low doesn’t lose altitude acclimation
– Training low permits maximal aerobic training

73
Q

Explain the concept of live high, train low at sea level

A 
– Sleep and live in hypoxic apartment
– Train normally
– Not scientifically validated yet
– Best for elite athletes
– Non elite exercisers may benefit from artificial
approaches
74
Q

What is acute altitude (mountain) sickness?

A

– Onset 6 to 48 h after arrival, most severe days 2 to 3
– Headache, nausea/vomiting, dyspnea, insomnia
– Can develop into more lethal conditions

75
Q

What is the incidence of altitude sickness?

A

• 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

76
Q

What are some possible causes of altitude sickness?

A 
– 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
77
Q

What is altitude sickness insomnia?

A

– Interruption of sleep stages
– Cheyne-Stokes breathing prevents sleep
– Incidence of irregular breathing ↑ with altitude

78
Q

What is some prevention/treatment for altitude sickness?

A

– Gradual ascent to altitude

– Medication (+ steroids)

79
Q

What are the two life-threatening conditions associated with altitude?

A

– High-altitude pulmonary edema (HAPE)

– High-altitude cerebral edema (HACE)

80
Q

Explain the causes, symptoms and treatment of high altitude pulmonary edema (HAPE)

A

• 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

81
Q

Explain the causes, symptoms and treatment of high altitude cerebral edema (HACE)

A 
• 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

PHYL2730 (6 decks)

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