chapter 12/23 Flashcards
what are homeotherms
- maintain constant body core temperature - rely on unefficiencies to produce heat to maintain body temperature
- heat loss must match heat gain
what is the normal core temperature
37 degrees C
at what temperatures is hyperthermia and hypothermia
hyperthermia = above 45 degrees C – can damage proteins and enzymes and lead to death (denaturing of protein and enzymes)
hypothermia = below 34 decrees C – can result in decreased metabolism and cardiac arrhythmias and neural function
what is the thermal gradient
difference between deep body core to skin surface temperature
* typical is about 4 degrees – in extreme cold may be 20 degrees C
How do you measure deep body (core) temperature
- rectum, ear, or esophagus
- ingestible temperature sensor telemetry system
what is an example of voluntary heat production
exercise – b/c not efficient = release more heat
- 70-80% energy expenditure released by heat
what is an example of involuntary heat production
- shivering = increases heat production by about 5%
- nonshivering thermogenesis = thyroxine (thyroid hormone, catecholamines – in brown adipose tissue produce heat without releasing more E)
what are the 4 mechanisms of heat loss
- evaporation: primary mechanism in hot environments
- radiation
- conduction
- convection
explain what evaporation is
body heat causes pirspiration which is lost from the body surface when changed from liquid to vapro
explain what radiation is
body heat is lost to nearby objects wihtout physically touching them
explain what conduction is
body heat is lost ot nearby objects through direct physical contact
explain what convection is
body heat is lost to surrounding air which becomes warmer, rises and is replaced with cooler air
* similar to a fan
evaporation rate depends on what 3 things
- temparature and relative humidity
- convective currents around the body – if sweating and have fan = more conduction
- amount of skin surface exposed
a high relative humidity decreases or increases the vapor pressure gradient between the skin and environment why?
decreases vapor pressure gradient – decreases rate of evaporation
what is heat index? how does it effect evaporative heat loss
measure of body’s perception of how hot it feels
* high relative humididty reduces evaporative heat loss –> increased perception of how hot it feels
what temperature increases evaporation
high temperatures
what anatomical location is the body’s thermostat
preoptic anterior hypothalamus (POAH)
what does the preoptic anterior hypothalamus do for body temperature
- responds to increased core temeprature
- stimulation of sweat glands - evaporative heat loss
- cutaneous vasodilation (release heat)
explain the sympathetic cholinergic control of sweat glands and cutaneous vasculature
SNS – cutaneous vasculature
* preganglionic neuron releases ACh to nicotinic receptors on postganglionic neuron
* postganglionic neuron releases Norepi onto adrenegic receptors on effector cells
SNS – sweat glands
*preganglionic neuron releases ACh to nicotinic receptors on postganglionic neuron
* postganglionic neuron releases Ach onto muscarininc receptors on cells of sweat gland
in eccrine sweat glands stimulation is caused by what and what does it bind to
stimulation occurs via activation by Ach which binds to the glands mAchR == production of sweat
Ach acting on mAchR causes what in the blood vessels in the skin at the periphery
causes vasodilation of blood vessels
removal of vasoconstriction tone = increase vasodilation
Explain the physiological response to heat load
include thermal receptors, integrators, and effectors
heat load –> thermal receptors: core, skin –> integration: preoptic-anterior hypothalamus –> effectors: cutaneous vasodilation, sweating
As exercise intensity increase describe the thermal events that occur
- heat production increases due to musclular contraction - heat increase b/c metabolism = production of E
- linear increase in body temperature – core temp increases proportional to active muscle mass
What happens to muscle temperature vs skin temperature with increasing exercise intensity
muscle temperature increases, mean skin temperature decreases (vasodilation)
What determines heat production during steady state exercise
exercise intensity
* and NOT environmental temperature
at same work rate = same amount of heat and rely on convection and radiation to change temperature
with negative radiation and convection you are gaining heat
in a humid/hot environment during submax exercise what happens to core temperature
higher core temperature
* risk of hyperthermia and heat injury – cannot rely on evaporation
(vs. in cool environment you can rely on evaporation, vonduction, radiation for decrease in heat)
explain the cardiovascular response to exercise in the heat
upward drive in VO2 during prolonged exercise in hot and humid environment – cannot reach steady state
To maintain cardiac output what happens to compensate for the decrease in SV
HR that gradually creeps upward to compensate for decrease in SV
- HR increases with heat
what happens to blood flow in different locations of the body in response to exercise in heat
blood flow is shunted away from working muscle and nonessential areas (gut, liver, kidneys –> to skin (more blood to periphery to decrease temp)
What happens to sweat rate during exercise
sweat rate inreases
- increases with body mass and genetic variations
what are the two major endocrine responses to exercise in the heat
increased release of vasopressin and aldosterone
explain what vasopressin and aldosterone do for the body with exercise in the heat
- vasopressin acts on kidneys increasing H2O permeability of renal tubules = increased reabsorption of water = minimize body fluid loss
- aldosterone acts on the kidney to increase Na+ absorbtion –> urine volume decreases b/c water goes back into body maintaining BP/plasma volume
What three factors contribute to impaired exercise performance in the heat
- CNS dysfunction
- cardiovascular dysfunction
- accelerated muscle fatigue
Explain how the CNS dysfunction contributes to impaired exercise performance in the heat
- decreased motivation
- reduced voluntary activation of motor units
Explain how the cardiovascular dysfunction contributes to impaired exercise performance in the heat
- reduced SV
- decreased cardiac output during high-intensity exercise
- decreased muscle blood flow
Explain how the accelerated muscle fatigue contributes to impaired exercise performance in the heat
- increased radical production
- decreased muscle pH
- muscle glycogen depletion
How does CNS dysfunction, cardiovascular dysfunction, and accelerated muscle fatigue relate to each other
- accelerated muscle fatigue effects motivation b/c if low glycogen = low motivation
- if have cardiovascular dysfunction with decreased muscle blood flow –> decrease muscle pH with accelerated muscle fatigue
what is acclimation
rapid physiological adaptation that occurs within days to a few weeks, or is artifically induced in a climatic chamber in a lab
what is acclimatization
gradual, long-term adaptation that occurs within months to years of exposure to the environmental stress (ie. climate)
what is the impact of heat acclimation on HR and core temp
the end result of acclimation is lower HR and core temperature during submax exercise
to get the largest response the body requires what change to the environment
requires exercise in hot environment
* elevated core temperature promotes adaptations
what are the 5 major adaptations during heat acclimation
- increased plasma volume (10-12%)
- earlier onset of sweating and higher sweat rate
- reduced sodium chloride loss in sweat
- reduced skin blood flow
- increased cellular heat shock proteins
Explain why plasma voluma increases during heat acclimation
maintains blood volume, SV, and sweating capacity
* replace fluids/hydration
Explain why reduced sodium chloride loss in sweat is an adaptation during heat acclimation
reduced risk of electrolyte (loss) disturbance
Explain why earlier onset of sweating and higher sweat rate occurs during heat acclimation
less heat storage, maintin lower body temperature
* sweating more = storing less heat
* more sweating = heat adaptation better in heat
what happens to the sweat rate in someone with microgravity exposure or bed rest threshold
dont sweat – sweat threshold increased
why is it beneficial to have low sodium chloride loss in sweat
becuase sodium chloride is needed along with the release of aldosterone to bring water back into the body to maintain blood volume
Explain why reduced skin blood flow is an adaptation during heat acclimation
because you are able to maintain core body temperature better
Explain why increased cellular heat shock proteins is an adaptation during heat acclimation
becuase it prevents cellular damage due to heat and it helps us with heat injuries
What is the effect of heat acclimation on heat injury
heat acclimation reduces risk of heat injury
* in response to exposure of heat stress
What is the effect of heat acclimation on heat shock proteins
increased heat exposure increases the synthesis of heat shock proteins
* protect cells from thermal injury
* stabilizing and refolding damaged proteins
With the number of days required for heat acclimation what two factors are linked
HR decrease and increase in plasma volume
explain the sex and age difference in thermoregulation
- small difference in SEX variablity in thermoregulation and heat tolerance
- aging results in reduced availability to lose heat during exercise – skin blood flow is reduced in older individuals = decrease thermoregulation
What happens to acclimation with inactivity
- what happens physiologically
acclimation lost within few days of inactivity (no hear exposure)
- body begins to decrease plasma volume to avoid high BP putting pressure on organ systems
Explain what 2 things happen in shivering
- if core temperature drop significantly involuntary shivering begins – create heat
- somatic motor neurons stimulate skeletal muscle contraction
What anatomy responds to a decrease in core temperature
reoptic anterior hypothalamus
* shivering (generate heat)
* decreased skin blood flow (vasoconstriction)
in shivering explain what the neurons do to produce shivering
somatic motor neuron from the spinal chord releases Ach to the skeletal muscle to begin shivering
Explain the process of non-shivering thermogenesis (NST)
POAH initiates the release of NE and throxine –> increases the rate of cellular metabolism –> nonshivering thermogenesis
- cuase the mitochondria to be more active and produce more heat to increase core temperature
Explain what causes cutaneous vasoconstriction
Norepi acts on α1-ADR –> cuase vasoconstriction of blood vessels in the skin
Explain the whole process of response to cold stress
*include receptors, integrators, and effectors
cold –> receptors: skin, core –> integrator: preoptic-anterior hypothalamus –> effectors: shivering, cutaneous vasoconstriction, catecholamine release (norepi), throxin release
Explains what happens when exercise in cold environment and hypothermia
- enhanced cold loss
- can result in hypothermia – loss of judgment and risk of further cold injury
explain the 4 factors that influence hypothermia
- insulating factors: subcutaneous fat, clothing (wet vs. dry)
- environmental factors: temperature, water vs. air, water-vapor pressure, wind
- descriptive characteristics: age, gender
- heat production
What is subcutaneous fat
- very effective in cold water for insulatin
- fat is primary fuel for shivering (in thermogenesis ) in well fed individuals
** just below skin but closer to skin than visceral fat**
what happens to heat loss with increased wind speed
with higher wind speed causes temperatures to feel colder
what is the effect of water temperature on heat loss
w/ water immersion the rate of heat loss in 25x greater than air of same temperature
Explain what happens to blood flow in response to exercise in the cold
blood flow shunted away from the skin –> to the core
- cutaneous vasoconstriction
explain how muscle function is impaired in a cold environment
(ie. hands)
- hands = numb b/c reduced blood flow and depressed rate of neural transmission
- reduction in neural transmission and blood flow = loss in dexterity and loss of motor skills
what are the endocrine responses to exercise in the cold
* what three things release more
increased release of norepi, epi, and thyroxine (thyroid hormone) for metabolic heat production –> non shivering thermogenesis
what temperature is associated with hypothermia
when decline from 37 to 25 or lower – life threatening cardiac arrhythmias
explain the difference in health risks in exercise in cold air vs. water
- exercise in cold air presents less risk of developing hypothermia than cold water
- in air skin at risk for frostbite if temp blow freezing
- breathign cold air doesnt pose risk to respiratory tract or lung b/c air rapidly warmed
- breathing cold air can trigger exercise induced asthma
Explain the 3 results of cold acclimation
- result in lower skin temperature at which shivering begins
- maintian higher hand and food temperature
- improved ability to sleep in the cold
Explain why in cold acclimation it results in lower skin temperature at which shivering begins
b/c there is increased non-shivering thermogenesis
Explain why in cold acclimation individuals maintian higher hand and food temperature
because there is imporved peripheral blood flow
Explain why in cold acclimation improved ability to sleep in the cold
due to reduced shiver – less wakefulness
explain how cold-acclimatized poeple maintain heat production with both types of shivering
with involuntary heat production
* decreased shivering – somatic neurons no longer send signal
* nonshivering thermogenesis – maintain heat (rely on this more)
How does Hunter’s phenomenon relate to cold acclimation
have cold endued vasodilation — to keep dexterity
explain the sex difference in response to cold exposure
- women show faster reduction in body temp than men – body mass
- in water, decrease in body temp similar in men and women
explain the age difference in response to cold exposure
- older (>60) less tolerant to cold
- children experience faster fall in body temp
explain Dalton’s law
total pressure of a gas mixture is euqual to the sum of the pressure that each gas would exert independently
how do you calculate the partial pressure of air? what is the equation?
Pair = PO2 + PCO2 + PN2
PO2 = (% in air - fraction = 0.2093)(Barometric pressure)
what value always remains constant in atmospheric condidiotns at any elevation
% of O2 in the air
always 20.93
- only the number of molecules change
explain the comparison of PO2 at sea level and altitude
at sea level:
* greater PO2 entering lungs –> reduced amount actually going through alveoli –> more muscle O2 absorbtion
* diffusion gradient = 100 (arterial) - 40 (venous) = 60 mmHg
at altitude
* much less PO2 entering lungs –> reduced amount actually going through alveoli –> less muscle O2 absorbtion
* diffusion gradient = 42 (arterial) - 27 (venous) = 15 mmHg
What are the effects of altitude on oxygen-hemoglobin dissociation curve
- hypoxia == shift left and drop off O2 even more – low PO2
- normoxia = normal PO2
- hyperoxia == shift right and dropp off less O2 to tissues – high PO2
what are the 4 effects of altitude on oxygen content
- arterial O2 content
- saturation
- hemoglobin concentration
- partial pressure of oxygen in the arteries (minor)
what is the euqaiton for arterial O2 content (CaO2)
CaO2 = (SaO2 * [Hb] * 1.37) + (PaO2 * 0.003)
Explain how max aerobic power is effected by altitude
there is decreased VO2 max at higher altitude – less O2 delivered to the muscles
explain the change in percent decline in VO2 max
* in trained? why?
- trained individuals have a larger decline in VO2 max from sea level
- b/c they have a higher VO2 max b/c of the pulmonary-capillary transit time (less time)
explain the decline in VO2 max from sea level to altitude
- at sea level the blood isnt moving too fast and aple to keep up with fast capillary time
- at altitude the PO2 is Low and there is a small change in capillary transit time which effects O2 uptake –> reducing driving force of O2 into blood
explains why there are individual variability in % decline of VO2max from sealevel to altitude
climitize over time and variablity with how people respond
* mutations in p50 and Hb-O2 affinity
* intrapulmonary arteriovenous anastamosis (IPAVA) - deal w/ high pressure – not fully oxygenated blood: dont go through capillary bed
what is the effect of altitude on the HR response to submax exercise
HR increases
- acute hypoxia (altitude) –> increase epinephrine –> increase HR, SV, and Q
What is the effect of altitude on ventilation response to submax exercise
ventilation increases
* peripheral chemoreceptors sense lower PaO2
–> ventilatory drive switch @ high altitude to be sensitive to O2
explain the influence of short-term anaerobic performance with altitude
lower PO2 at altitude = no effect on performance
* O2 transport to muscle does not limit performance (anaerobic)
* lower air resistance may improve performance
be careful for the exam
explain the influence of long-term aerobic performance with altitude
lower PO2 results in poorer aerobic performance
* dependent on O2 delivery to the muscle
What happens to plasma volume upon initital arrival to altitude? why?
decreased plasma volume upon initital arrival to altitude –> lower SV
* b/c humidifying air through ventilation and more urine output = increased hematocrit
* fluid shift: decrease in PO2 –> physiological response = fluid shift from bloodstream into intersitital spaces surrounding cells –> incrase concentration of RBC and hemoglobin in blood – increase carrying capacity
What happens to plasma volume after a few weeks at altitude
diminished plasma volume returns to normal if adequate fluid is ingested
What are the two acclimatizations to high altitude and what type of breathing does this cause
- production of more RBCs
- greater O2 saturation
- hyperventilation
Why is there production of more RBCs with acclimatization to high altitude? What creates RBCs?
higher RBC concentration via EPO
* counter the desaturation cuased by lower PO2 == able to maintain high hematocrit
Why is there greater O2 saturation with acclimatization to high altitude
due to an increase in blood flow to the lungs – everyone has strong vasoconstriction in the lungs
*at high altitude – vasoconstrict vasculature –> increase pulmonary artery pressures –> force more O2 into blood
Explain how more RBCs are produced. Explain the pathway
decreased blood O2 –> sensor: kidney –> increased erythropoietin (EPO) –> red bone marrow increases RBC production –> increase blood O2 –> increase hematocrit
What happens to hemoglobin concentration with altitude
at higher altitudes there will be a higher hemoglobin concentration – to increase O2 delivery and absorbance
Explain how hyperventilation is an acclimatization to hgih altitude
increased sensititvity of carotid chemoreceptor
* respond quickly in change in CO2 then pH at sea level or low altidue with O2
* greater change in partial pressure = greater change in ventilation
what are the negative consequences of carotid chemoreceptor sensitization
- hyperventilation: extreme dsypena, increase work to breathe, blood flow disruption, hypertension
- sleep disruption
- decrease in plasma volume
- HAPE and HASE
how do tibetan sherpas adapt to high altitude
increase O2 saturation of the existing hemoglobin –> larger release of nitric oxide == greater vasodilation
with those who live at high altitude what is the adaptation to altitude
more nitric oxide released and higher hematocrit
- if move after childhood = less complete adaptation
What are the benefits of living at high altitude
decrease PO2 –> increase EPO –> increase plasma volume
* elicit an increase in RBC mass via EPO – increase VO2max
- greater then 22 hr/day at altitude requried
- intermittent hypobaric hypoxia = need greater stimulus for effects
explain why you train at low altitude
so you can maintain high interval training velocity
* some athletes still experience hemoglobin desaturation
What happesn to race time in athletes that lived at altitude and trained at low altitude
performance increased 1.1% and VO2 max increased 3.2%
Explain the change in VO2 in athletes that trained for competition at atltitude
some have higher VO2 max upon reutrn to low altitude and some do not
* could be “detraining” effect – cannot train as intensely at altitude
what are the effects in living at high altitude and training at low
- increased RBC mass leads to increased VO2 max in some individuals
- avoid negative effects of prolonged altitude exposure
- no real change in VO2 max or hemoglobin
