CH. 12 - Exercise in Hot and Cold Environments Flashcards
how do humans regulate temperature
humans are homeothermic
- > internal body temp is regulated by keeping a near constant, even when environmental temp changes
thermoregulation
regulation of body temp around a physiological set point
acclimation
short term adaptation to environmental stressor (days/weeks)
acclimatization
long term adaptation to environmental stressors (months/years)
in physiology, temperatures are expressed as ____
degrees Centigrade
°C = (°F-32)/1.8
°F= (°C X 1.8) +32
what are the main mechanisms of the transfers of body heat
Conduction (K)
Convection (C)
Radiation (R)
Evaporation (E)
Humidity and Heat loss
Cooling capacity of sweat
conduction (K)
heat transfer from one solid material through direct molecular contact
Convection (C)
- > heat transfer by movement of gas or liquid across a surface
- > increase movement across skin surface = increase heat exchange
- > major daily thermoregulatory factor
Radiation (R)
- > heat loss in form of infrared
- > body can give off or receive radiant heat
- > major daily thermoregulatory factor
avenues of dry heat exchange
avenues of dry heat exchange = C + K + R
- > insulation (I) is resistant to dry heat exchange
- > still layer of ideal insulator
Evaporation (E)
- > heat loss via phase change from liquid to gas
- > the primary heat loss mechanism during exercise (80%)
- > at rest, 10-20% of body heat is lost via E (process called insensible water loss)
- > clothing is resistant to E
humidity and heat loss
- > water vapour pressure (humidity) affects E
inc humidity = decreased E
dec humidity = increase E
- > high humidity limits evaporation via sweat, causes dehydration, and low humidity offers ideal sweat evap and heat loss
POAH
Peroptic-anterior-hypothalamus
- > body’s thermostat located in the brain
- > receives input from sensory thermo-receptors
- > when body temp deviates, POAH activates thermoregulatory mechanism
sensory receptors involved in thermoregulatory control
- > peripheral theromoreceptors in skin
- > central thermoreceptors in brain and spinal cord
- > POAH signals symp. NS effectors
thermoregulatory effectors
signals sent by POAH via symp NS are sent to 4 sets of effectors
- > skin arteriole effectors
- > eccrine sweat gland effectors
- > skeletal muscle effectors
- > endocrine gland effectors
what do skin arteriole effectors do
- > SNS vasocontriction (VC) will minimize heat loss
- > SNS vasodilation (VD) will enhance heat loss
how do eccrine sweat glands effectors affect temp
SNS stimulation of sweating = E heat loss
the primary neurotransmitter involved secretion of sweat onto the skin surface, is acetylcholine, thus we refer to sweat gland activation as sympathetic cholinergic stimulation
more responsive to changes in core temp than skin temp
how do skeletal muscle effectors aid in thermoregulation
help generate additional heat via shivering
- > involuntary cycle of contraction and relaxation
- > only heat production, no useful work
how do endocrine gland effectors affect thermoregulation
- > the effects of several hormones lead to inc metabolism which leads to inc heat production
- > cooling of the body stimulates the the release of thyroxin and catecholamines which then will inc metabolism
why does exercise disturb thermal homeostasis in mosts environments
- > increases metabolic heat load
effects of exercise in heat on cardiovascular function
- > skin arterioles VD to increase C heat loss, requires inc BF compared to exercise in the cold
- > POAH triggers SNS: cardiac output increases further via HR and contractility, increase VC to non-essential tissues
- > blood volume decreases (sweat), SV can’t increase (blood pooling), so HR increases further to compensate (cardiovascular drift)
limitations of exercising in heat
Cardiovascular Overload
- > consider going running on a hot day, this aerobic exercise increases metabolic heat production and the demand for in BF and O2 delivery to muscles
- > this excess heat can only be dissipated only if BF increases to the skin
- > the cardiovascular system cannot keep up with these demands and thus overloads the cardiovascular system and cannot provide sufficient BF to both exercising muscle and skin
- > interfered heat dissipation leads to impaired performance, inc risk of overheating
- > especially in untrained or non-acclimated athletes
Critical temperature theory
- > brain shuts down at exercise 40-41 deg celcius
- > helps explain limitations in trained, well-acclimated athletes
body fluid balance via sweating
its not uncommon for hot environment temps > skin, core temp
- > C, K, R are all avenues for heat gain, E only avenue of heat loss; increased dependance on evaporation means increased demand for sweating
- > eccrine sweat gland controlled by POAH
electrolyte composition during light sweating vs exercise
during light sweating, the filtrate sweat travels slowly enough through the sweat duct that there is enough time for Na and Cl reabsorption
- > when sweating rate increases during exercise, filtrate moves more quickly through the tubules, allowing for less time for reabsorption and Na Cl content of sweat is much higher
how does training affect sweat composition
- > training and repeated heat exposure (acclimation) allow for more Na and Cl to be absorbed, making sweat more diluted
- > this is caused because sweat glands become more sensitive to Aldosterone
- > K Ca Mg losses remain unchanged with aldosterone release
sweat loss during exercise
- > can lose 1.6 - 2.0L of sweat per hour; severe dehydration can occur and trigger the onset of heat related illness
increased sweating = decrease BV = decrease cardiac output
hormonal control of fluid balance
exercise and water loss stimulate adrenal cortex and posterior pituitary
- > loss of water, electrolytes trigger the release of aldosterone and ADH
- > aldosterone: retains Na at kidneys
- > ADH (vasopressin): retains water by kidneys
6 main risk factors with exercising in heat
- > metabolic heat production
- > air temp
- > ambient water vapour pressure (humidity)
- > air velocity
- > radiant heat sources
- > clothing
how do we measure external heat stress
- > heat index does not reflect physiological stress
- > wet-bulb globe temperature (WBGT) includes C, E, and R
*reflects the physiological heat stress on an individual devised to account for convection, evaporation and radiation
3 main heat related disorders
- > heat cramps
- > heat exhaustion
- > heatstroke
heat cramps
- > least serious of the 3 disorders
- > triggered by Na losses and dehydration
- > prevented by liberal intake of Na and water
heat exhaustion
- > accompanied by fatigue, dizziness, nausea, vomiting, fainting, weak rapid pulse
- > caused by severe dehydration from sweating
- > simultaneous BF needs of muscle and skin not met due to low BV
- > thermoregulation mechanisms functional but are overwhelmed
heat stroke
- > life threatening
- > thermoregulatory mechanism failure
characterized by…
- > body core temp >40
- > confusion
- > disorientation
- > unconsciousness
- must cool body down ASAP*
preventing hyperthermia
no outdoor activities when WBGT > 28 deg
- > never restrict fluid intake
*fluids readily available to replace sweat loss
*drinks every 15-30mins
*minimize rise in HR and core temp
- > minimize clothing
acclimation vs acclimatization to exercise in heat
repeated exercise in heat = rapid change for better performance in hot conditions
acclimation: short term (9-14 days)
acclimatization: long term (months/years)
effects of heat acclimation
- > cardiovascular function optimized
- > sweating rate, sweat distribution, and sweat content change
- > results in lower core temp during exercise
physiological effects of acclimation to exercising in the heat
plasma vol increases due to increased oncotic pressure
- > this is temporary (back to normal after 10 days)
- > buys time for other adaptations to occur
decrease HR, increase cardiac output
- > supports inc skin BF
- > greater heat loss, decrease core temp
widespread sweating earlier, more dilute
- > prevents dangerous Na loss
- > optimize E heat loss
cold stress
any environmental condition causing loss of body heat
a decrease in core or skin temperature (in the cold) triggers which physiological + behavioural mechanisms
- > POAH triggers peripheral VC
- > POAH triggers non-shivering thermogenesis
- > POAH triggers skeletal muscle shivering
- > cerebral cortex triggers behavioural adaptation
cold habituation
- > occurs after repeated cold exposure without significant heat loss
- > VC, shivering blunted, core temp allowed to decrease moe
describe metabolic and insulative acclimation
Metabolic acclimation
- > occurs after repeated cold exposure with heat loss
- > enhanced metabolic shivering heat production
Insulative acclamation
- > when increase metabolism cannot prevent heat loss
- > enhanced skin VS (increased peripheral insulation)
____________ conditions are hard to define
dangerous (hypothermia-inducting) environmental
how does body composition affect heat loss
- > increase inactive peripheral muscle = increased isolation
- > increase subcutaneous fat = increased insulation
- > decrease body surface area: mass ration = decrease heat loss
- > differs between children, adults and elderly
Men vs Women
- > women have more subcutaneous fat which is advantageous but have less active muscles which is disadvantage
how does windchill affect heat loss
- as with heat, air temp alone is not valid index of heat loss*
- > often misunderstood: air movement, not air temp
- > index based on cooling effect of wind
- > increase C heat loss
- > refers to cooling power of environment
- > increase windchill = increase risk of freezing tissues
cold water vs air affects heat loss
when C + K + E + R is considered, heat loss 4X faster in cold water vs cold air
- > core temp constant until water temp <32 deg
- > core temp decreases 21 deg C per h in 15 deg C
- > heat losses increase in moving water, decrease with exercise
- > hypothermia from cold water occurs well above 0deg
physiological response to exercise in the cold
Muscle function decreases
- > altered fiber recruitment = decrease contractile force
- > shortening velocity and power decreases
- > affects superficial muscles (deep muscles spared)
as fatigue increases, metabolic heat production decreases
- > energy reserves depletion with endurance exercise = potential for hypothermia
FFA metabolic responses
- > normally, increase in catecholamines = FFA oxidation
- > cold = increase catecholamine secretion but no increase in FFA mobilisation
- > VC in subsutaneous fat = decrease FFA mobilization
glucose metabolic responses
- > blood glucose maintained well during cold exposure
- > muscle glycogen utilization increases
- > hypoglycaemia suppresses shivering
hypothermia
- > core temp 34.5-29.5: POAH fuction compromised
- > core temp <29.5: POAH thermoregulation completely lost, metabolism slows, drowsiness, coma
cardiorespiratory effects of cold
- > low core temp = slows HR (SA Node effects)
- > cold air dones not damage ventilatory tissues
- > cold may decrease ventilation (rate and volume)
treatment for mild hypothermia
- > remove individual from cold
- > provide dry clothing, blankets, warm beverages
treatment for severe hypothermia
- > gentle handling to avoid arrhythmia’s
- > slow rewarming
frostbite
- > peripheral tissue freezing
- > excessive VC - lack O2 nutrients = leads to tissue death
- > untreated frostbite leads to tissue loss and gangrene
- > gradual rewarm when there is no risk of refreezing
exercise induced asthma
affects 5% of winter sports athletes
- > excessive airway drying
- > treated with beta-agonists, steroid inhalers
