Ch 12/23 Flashcards
Temp regulation
homeotherms
maintain constant body core temp
* humans are homeotherms
* heat loss must match heat gain - to avoid execessive core body temp - why heat balance is so important
Core temperatures above 45 degrees C can result in:
Core temps below 34 degrees C can result in:
- 45 degrees C can damage proteins and enzymes and lead to death
- 34 degrees C can result in decreased metabolism, neuron function, cardiac arrhythmias
Thermal gradient
exists between deep body core to skin surface
– Typical gradient is approximately 4°C
– In extreme cold, may be 20°C
how is deep body (core) temp measured
- Measured at rectum, ear, or esophagus (Usually in laboratory)
- Ingestible temperature sensor telemetry system
(Can be used in athletes during practice sessions)
How is skin (shell) temp measured
Thermistors at various locations
– Calculate mean skin temperature
Voluntary vs. involuntary heat production
- Voluntary: exercise - 70-80% energy expenditure released as heat (depends on efficiency)
- Involuntary: shivering (increases heat production by ~5x) & non-shivering thermogenesis (initiated by thyroxine - thyroid hormone - or catecholamines)
4 mechanisms of heat loss
- Evaporation (most important in hot environments)
- Radiation: heat lost ot nearby objexts without physically touching them
- Conduction: heat lost to nearby objects through direct physical touch
- Convection: heat lost to surrounding air, which becomes warmer, rises and is replaced with cooler air
Evaporation rate depends on
- temp and relative humidity
- the higher the temperature and/or humidity, the higher the water vapor pressure = lower rate of evaporation - convective currents around the body: fan or air blowing by you will increase evaporation
- amount of skin surface exposed: evaporation much be directly off skin (not clothes) to get the most cooling benefit
heat index
body’s perception of how hot it feels
* high relative humidity reduces evaporative heat loss = increased preception of how hot it feels
* relative humidity adds to both preceptions of heat and an actual increase in heat
which avenue of heat loss plays the most important role during exercise in a hot/dry enviornment
evaporation
note that evaporation does DECREASE in very hot evironments due to an increased vapor pressure. Though this mechanism will still play a crucial role
What is the body’s thermostat
the preoptic anterior hypothalamus (POAH)
how does the preoptic anterior hypothalamus (POAH) respond to heat load (+ its two mechanisms)
responds to increases in core temp by
1. stimulating sweat glands to increase evaporative heat loss
2. cutaneous vasodilation so more heat is lost from the skin
How does the preoptic anterior hypothalamus stimulate sweat glands
in eccrine sweat glands, Ach binds to mAchR (muscarinic receptor) which stimulates production of sweat
How does preoptic anterior hypothalamus stimulate cutaneous vasodilation
same as sweating - Ach binds mAchR causing vasodilation of blood vessels in the skin
not your body will also remove vasoconstricter tone to encourage vasodilation
What do we call the preoptic anterior hypothalamus’s control during increased core body temp
sympathetic cholinergic control
What determines heat production during steady state exercise
exercise intensity, not environmental temp
* its the intensity NOT the heat
as exercise intensity increases, heat production ____ due to
increases due to muscular contraction = increased metabolism generating energy = more heat
* linear increase in body temperature
Core temp increases proportional to what
active muscle mass - ie. doing bicep curls will produce less heat than a whole body exercise
Describe
Heat production does NOT change, what changes is how we lose heat
as room warms, they relied more on evaporation and less on radiation and convection
- negative radiation & convection = ** gaining heat**
Why is a hot/humid environment so dangerous for exercise
humidity/heat makes evaporation harder; environmental heat will result in a shift from radiation/convection mechanisms to evaporation. Radiation and convection can switch if hot enough and give heat back to the body
important to note that enviornmental temp does not determine heat production during exercise but rather can transfer heat back to the body
submax exercise in a hot/humid environment leads to risk of
heat illness (heat cramps, then heat exhaustion, then heatstroke) & hyperthermia
Main cardiovascular responses to exercise in heat
- upward drift in oxygen uptake (VO2) - cant maintain steady state
- cardiac output remains same (see below)
- HR increase (to compensate for decreased SV)
- Decrease in SV
- blood flow directed away from working muscles and nonessential areas to the skin
Sweat rates during exercise in heat
higher swear rate
* varies by size of individual (larger = more sweating)
* genetic variation
endocrine responses to exercise in heat
increased release of vasopressin and aldosterone to retain blood volume
3 pillars of impaired exercise performance in heat
accelerated muscle fatigue can also affect NS and decrease motivation
Ways to prevent exercise-related heat injuries since increases in core body temp with exercise is risky
- hydration
- less/more breathable clothin
- heat therapy - acclimating
- staying out of the heat
- Frequent rests/cool-down breaks
Acclimation vs acclimatization
What do they both require
acclimation: Rapid physiological adaptation that occurs within days to a few weeks, or is artificially induced in a climatic chamber
acclimatization: Gradual, long-term adaptation that occurs within months to years of exposure to the environmental stress (i.e., climate)
BOTH require exercise in hot environment: elevated core temp promotes adaptation (larger response from exercising than just sitting in heat - sauna)
End result of heat acclimation
lower heart rate and core temp during submaximal exercise
Note theres a larger improvement to core body temp but will decrease both
5 adaptations from heat acclimation
-
increased plasma volume (10-12%): maintains blood volume, stoke volume, and sweating capacity
- also dependent on fluid consumption after exercise - Earlier onset of sweating/higher sweat rate: less heat storage, maintain lower body temp
- Reduced sodium chloride loss in sweat: reduced risk of electrolyte disturbances
- Reduced skin blood flow: able to maintain core body temp better at same intensity
- Increased cellular heat shock proteins: prevent cellular damage due to heat
how does the body reduce sodium loss in sweat during heat acclimation
different composition of sweat - enhanced aldosterone release causes eccrine gland to reabsorb electrolytes
After heat acclimation and individual will start sweating at a ____ core body temp
lower - sweating much earlier
how does synthesis of heat shock proteins reduce risk of heat injury
protect cells from thermal injury by stabilizing, refolding, and resynthesizing important damaged proteins
Number of days required for each component of heat acclimation (HR, plasma volume, precieved exertion, and sweat rate)
- Heart rate decrease & Plasma volume increase: quickest adaptation (within 3-6 days) - because these are linked - if we have a plasma volume increase we no longer need higher HR to conteract
- Perceived exertion decrease: 5-8 days
- Sweat rate: slowest - 7-14 day (1-2 weeks)
Sex and age differences in thermoregulation and heat tolerance
- when matched for body composition and level of acclimiation, there are sex differences but they are small
- Aging results in reduced ability to lose heat: skin blood flow redution with age (> 60 years)
How fast is heat acclimation lost? why?
lost within a few days of no heat exposure
* significant decline in 7 days; complete loss in 28 days
* because maintaining high blood volume is difficult/problematic for the body if not constantly maintaining heat exposure
How does the preoptic anterior hypothalamus (POAH) respond to cold
responds to decreased core temperature (receptors in the skin/core) by stimulating shivering, cutaneous vasoconstriction, and non-shivering thermogenesis
identify the mechanism of heat loss where the body exchanges heat with an object thru physical contact
conduction
Adaptations during heat acclimatization are important for defending against heat stress. Which of the following is not an adaptation
* increased plasma volume
* earlier onset of sweating
* increased skin blood flow
* increased heat shock proteins
* all of the above are adaptation
- increased skin blood flow: skin blood flow DECREASES due to lower core body temp
Mechanism of shivering
somatic motor neurons stimulate skeletal muscle contraction = heat production
mechanism of non-shivering thermogenesis
POAH initiates the release of norepinephrine (catecholamines) and thyroxine which bind to brown adipocyte
* causes increase in rate of cellular metabolism and since mitochondria are inefficient they create a lot of heat
How does the POAH induce cutaneous vasoconstriction in the cold
release of NE acts on alpha1 adrenergic receptors (a1-ADR) causing vasoconstriction of blood vessels in the skin
name the different ligand and receptors involved in vasodilation vs vasocontriction
- vasodilation: Ach binding to mAchR
- Vasoconstriction: NE binding to a1-ADR
Exercise in a cold environment causes (consequences)
- enhanced heat loss
- may result in hypothermia: loss of judgment and risk of further cold injury
Insulating factors
- subcutaneous fat: especially effective in cold water; primary fuel for shivering in well-fed individuals
- clothing: colder weather = need for more layers/insulation
- wet vs. dry
winchill index
similar concept to heat index - windier it is, the colder it feels
water immersion on heat loss
rate of heat loss = 25x greater than in air of same temperatue - water will disapate heat much faster
main cardiovascular response to exercise in cold
Cutaneous vasoconstriction - blood flow shunted away from the skin and to the core
why is muscle function impared in a cold environment
blood flow is shunted away from the skin = reduced blood flow and depressed rate of neural transmission
* results in loss of dexterity and negatively impacts motor skills
* especially in hands and feet
Endocrine response to exercising in the cold
increased release of NE, E, and thyroxine for metabolic heath production (non-shivering thermo)
compared to cold water, exercise in cold air presents less risk of developing
hypothermia
* However breathing cold air can trigger exercise-induced asthma because of cooling and drying of airways
3 adaptations from cold acclimation
- lower skin temp at which shivering begins due to increased non-shivering thermogenesis (with less regular shivering)
- can maintain higher hand and foot temp due to improved peripheral blood flow (cold-induced vasodilation)
- improved ability to sleep in the cold due to reduced shovering
Why does cold acclimation cause less shivering
heat production is maintained due to increased non-shivering thermogenesis (core temp stays relatively the same)
Sex and age differences when responding to cold
- Women show faster reduction in body temp (body composition)
- similar decrease in body temp between men and women during cold water exposure (properties of disipation)
- Older (>60) = less tolerant to cold due to decrease in lean muscle mass
- children body temp falls faster
Dalton’s law
The total pressure of a gas mixture is equal to the sum of the pressure that each gas would exert independently (PO2 + PCO2 + PN2)
What causes differences in atmospheric conditions
partial pressure of Oxygen changes - %O2 in the air does NOT change(20.93%), # of total molecules does
Things you could do to prevent altitude sickness
- Hydrate
- Acclimate
Describe the changes in atmospheric pressure and PO2 with increasing altitude
at altitude atmospheric pressure decreases and PO2 decreases; diffusion gradient is much smaller ~15 mmHg
Effect of hypoxia (altitude) vs. hyperoxia on the hemoglobin-oxygen dissociation curve
- hypoxia/altitude (low PO2) = left shift - to help make it easier to deliver O2
- hyperoxia (high PO2) = right shift
3 things that influence arterial oxygen content (CaO2)
- Saturation
- hemoglobin concentration
- Partial pressure of oxygen in arteries (minor contribution since thats what influence dissolved oxygen in the plasma)
Physiological responses to exercise at altitude
- decreased VO2max at higher altitude: lower PO2 = lower PaO2 = lower PAO2 and less overall oxygen delivery to muscles
- Heart rate increases
- Ventilation increases
do trained or untrained individuals have a larger decline in VO2max at alitude
Trained
* larger capacity to start with
* higher stroke volume = less transit time
Describe the figure that shows the decline in VO2max (capillary PO2 vs capillary transit time)
decline in partial pressure with altitude reduces the driving force so that even if transit time is reduced, we wont have full saturation
Besides training status, what other factor plays into percent decline in VO2max
individual variablility in how we respond to altitude - some respond better to altitude and can maintain a higher % hemoglobin saturation
How does HR increase at altitude
decreased PIO2 and PaO2 causes adrenals to release epinephrine which
* increases HR, SV, and Q
* Increased vasodilation in the periphery
Why does ventilation increase at altitude
peripheral chemoreceptors sense lower PaO2
how altitude (low PO2) affects sprint and distance running performance
Sprints (short-term anaerobic performance): no effect on performance
* relying on non-oxidative sources: O2 transport to muscle does not limit performance
* Lower air resistance may improve performance
Distance (long-term aerobic performance): lower PO2 results in poorer aerobic performance
* Why? Cuz theyre heavily reliant on oxygen for energy production
adaptations that happen with acclimatization to high altitude (longer term)
- Production of more red blood cells: kidneys release EPO = red blood cell production
* linear increase with altitude - Greater oxygen saturation due to increase in blood flow to lungs
- Hyperventilation: increased sensitivity of carotid chemoreceptor
Acute cardiovascular response to altitude
Decreased plasma volume upon initial
arrival to altitude → decreased SV
* Due to respiratory water loss and increased
urine production → increased hematocrit (no actual change in RBC count, just dehyration)
* normal after a few weeks if adequate fluid is ingestion
Describe the physiological processes by which high altitude residents in the Andes adapt to
altitude compared to those who live in Tibet
- Andeans: producing more red blood cells to counter the desaturation caused
by lower PO2 (hematocrit ~50-65%) - Tibetan (Sherpas): increased the oxygen saturation of the existing hemoglobin - high nitric oxide = vasodilation = more blood flow to the lungs
Does being born in altitude effect adaptations
- lifetime altitude residents have complete adaptations in arterial O2 content and VO2 max
– Adaptations are less complete in those arriving at altitude later
What can athletes do to most effectively prepare for competition at altitude?
* compete within 24 hrs upon arrival to altitude
* breather hypoxic gases (1-2 hrs per day, 3-5 days) before competing at altitude
* All of the above
* A and C
All of the above
* minimizing altitude exposure
* intermittent acute hypoxia - induce helpful physiological changes
* get acclimitized
Live high, train low
At rest (living) we want to increase altitude response (RBC mass via EPO) and during exercise we want to maintain high interval training velocity (at low altitude)
- traditionally increase RBC mass leads to increased VO2max
Some athletes have higher VO2max upon return to low altitude, while other do not- why?
could be due to “detraining effect”
- cannot train as intensely at altitude
Live low, train high
- avoids negative effects of prolonged alititude exposure
- No real changes in VO2max or hemoglobin concentration
Dealing with problems from training at altitude
artifical “altitude” training
- altitude tent
- Simulated altitude training pool
While there may be no “gold standard” for altitude training, what does each method try to promote
increase in blood volume/RBC mass while maintaining training intensity
