Chapter 12 & 23 Flashcards
humans are
homeotherms
*maintain constant body core temperature through metabolic heat production
*heat loss must match heat gain so that we avoid increases in body temperature
normal core temperature
37C
temperatures above 45C
can damage proteins and enzymes can lead to death
temperatures below 34C
can result in decreased metabolism and cardiac arrythmias
thermal gradients
exists between deep body core to skin surface
- typical gradient is 4C
-in extreme cold may be 20C
what measures deep body (core) temperature
ingestible temperature pill
what measures skin (shell) temperature
thermistors at various locations and can calculate mean skin temperature
voluntary heat production
exercise
70-80% EE released as heat (metabolism) dependent on efficiency
involuntary heat production
shivering - increases heat production by ~5x
non-shivering thermogenesis - in brown adipose tissue (mediated by thyroxine and catecholamines)
mechanisms of heat loss/transfer
evaporation
radiation
conduction
convection
evaporation
primary mechanism in hot environments
body heat causes sweating which is lost from the body surface when changed from a liquid to a vapor
radiation
body heat loss to nearby objects without physically touching them
convection
body heat is lost to convection which becomes warmer, rises and is replaced with cooler air
conduction
body heat is lost to nearby objets through direct physical touch
evaporation rate depends on
temperature and relative humidity
convective currents around the body (fan vs no fan)
amount of skin surface exposed
high relative humidity decreases the vapor pressure gradient between the skin and the environment leading to
less evaporation
- the warmer = increased vapor pressure = less evaporation
- the more humid = increased water molecules in the air = decreased evaporation
heat index
measurement of body’s perception of how hot it feels
high relative humidity does what to evaporative heat loss
decreases it and increases the perception of how hot it feels
POAH (preoptic anterior hypothalamus)
body’s thermostat
* responds to increased core temperature
increased core body temperature causes
the POAH to stimulate the sweat glands for evaporative heat loss as well as cutaneous vasodilation to the periphery
how does the POAH stimulate sweat glands and cutaneous vasodilation
via sympathetic cholinergic control of sweat glands and cutaneous vasculature
stimulation of sweating mechanism
in eccrine sweat glands, stimulation occurs via activation by ACh, which binds to mACHR
ACh binding to mACHR causes vasodilation of blood vessels in the skin
as exercise intensity increases, what thermal events occur
heat production increases due to muscular contraction (metabolism)
linear increase in body temperature (core body temperature increases proportional to active muscle mass)
what determines heat production during steady state exercise
EXERCISE INTENSITY
NOT environmental temperature
different work rates = different heat production
submaximal exercise in a hot/humid environment causes
higher core temperature which increases risk for hyperthermia and heat injury because no longer can rely on evaporation
heat illnesses : severity
heat cramps (1st) - thirst, sweating, etc
heat exhaustion (2nd) - headache, nausea, chills
heat stroke (3rd) - no sweating, confusion, loss of consciousness
cardiovascular responses to exercise in the heat
upward drift in VO2 during prolonged exercise in a hot and humid environment
how is cardiac output maintained in hot and humid environments
heart rate gradually increases to help compensate for the decrease in SV
what happens to blood flow in hot and humid environments
blood flow is shunted AWAY from working muscle and nonessential areas (gut, liver, and kidneys) and goes to the skin
sweat rates during exercise
higher sweat rate - 4/5 L per hour (larger individuals will sweat more and genetics)
endocrine responses to exercise in the heat
loss of blood volume causes increased release of vasopressin and aldosterone which helps retain blood volume
* this is easier at rest and harder during exercise
factors that contribute to impaired exercise performance in the heat
1) CNS dysfunction
2) Cardiovascular dysfunction
3) accelerated muscle fatigue
CNS dysfunction that leads to impaired exercise performance in the heat
decreased motivation
reduced voluntary activation of motor units
cardiovascular dysfunction that leads to impaired exercise performance in the heat
reduced SV
decreased Q during high intensity exercise
decreased muscle blood flow
accelerated muscle fatigue leading to impaired exercise performance in the heat
increased radical production
decreased muscle pH
muscle glycogen depletion
acclimation
rapid biological adaption that occurs within days to a few weeks or is artificially induced in a climactic chamber
in a lab
acclimitization
gradual LONG TERM adaptation that occurs within months to years of exposure to environmental stress *climate
what do heat adaptations such as acclimation and acclimitization require
requires exercise in hot environments to elicit a response
*elevated core temperature promotes adaptations
impact of heat acclimation/acclimitization
lower heart rate and core temperature during submaximal exercise
adaptations during heat acclimation
1) increased plasma volume (10-12%)
2) earlier onset of sweating and higher sweat rate
3) reduced sodium chloride loss in sweat
4) reduced skin blood flow
5) increased HSP
increased plasma volume results in
maintains blood volume, SV, and sweating capacity
earlier onset of sweating and higher sweat rate results in
less heat storage, maintain lower body temperature
reduced sodium loss in sweat results in
reduced risk of electrolyte disturbance via enhanced aldosterone release
reduced skin blood flow helps
body sweat earlier and cool down faster
better equipped to handle core body temperature
increased cellular HSP results in
prevention of cellular damage due to heat
protects cells from thermal injury by stabilizing and refolding damaged proteins
number of days required for heat acclimation
HR decrease and plasma volume increase happens quickly (within 6-8 days)
then RPE decrease
last== sweat rate adaptation
sex and age differences in thermoregulation
sex differences are small when matched for body composition and level of acclimation
aging results in reduced ability to lose heat during exercise because skin blood flow is reduced in older individuals (ability to vasodilate decreases as we age)
loss of acclimation
lost within a few days of inactivity (no heat exposure)
- significant decline in 7 days (hard to maintain high blood volume if not constantly stressed)
- complete loss of adaptations in 28 days
PAOH role in cold weather
responds to DECREASED core temperature
causing:
shivering and decreased skin blood flow (shunting heat to the core)
shivering
if core temperature drops significantly, involuntary shivering begins
somatic motor neurons release ACh and stimulates skeletal muscle contraction which helps in heat production
non-shivering thermogenesis
the POAH initiates the release of NE/thyroxine which increases the rate of cellular metabolism to create heat and increase body temperature
how does NE cause vasoconstriction of the blood vessels in the skin
acts on alpa-1 ADR
exercise in the cold environment results in
enhanced heat LOSS to the environment
may result in hypothermia which causes loss of judgment and risk of further cold injury
insulating factors that help maintain body heat
subcutaneous fat
- especially effective in cold water
- fat is the primary fuel for shivering in well fed individuals
changes in insulation required during exercise
lower insulation is needed during exercise
rate of heat loss is influenced by what environmental factor
windchill index
effect of water temperature on survival
water immersion causes a rate of heat loss 25x greater than air of the same temperature
*heat dissipates in water fast
cardiovascular responses to exercise in the cold
blood flow is shunted AWAY from the SKIN and towards the core via cutaneous vascoCONSTRICTION
muscle function in a cold environment
impaired
hands exposed to cold temps often become numb due to reduced blood flow and depressed rate of neural transmission (because all heat kept in core)
reduction in neural transmission and blood flow to hands results in loss of dexterity and negatively impacts motor skills
endocrine responses to exercise in the cold
in response to the cold there is an increased release of NE/E and thyroxine for metabolic heat production via increased non-shivering thermogenesis
health risks during exercise in the cold
individuals immersed in cold water (15C and below) are at risk for hypothermia
** when body temperature declines from 37C to 25C or lower, this level of hypothermia is associated with life threatening cardiac arrhythmias
exercise in cold water vs cold air
cold water = increased risk for hypothermia
cold air= less risk
exercise in cold air:
- exposed skin is at risk for frostbite when air temps below freezing
- breathing cold air during exercise DOES NOT pose a risk to respiratory tract or lungs because the air is rapidly warmed before entering the lungs
- breathing cold air can trigger exercise induced asthma in some individuals because of cooling and drying of airways
cold acclimation
1) results in lower skin temperature at which shivering begins
2) maintain higher hand and foot temperature
3) improved ability to sleep in the cold
lower skin temperature at which shivering begins due to
increased non-shivering thermogenesis
maintain higher hand and foot temperature due to
improved peripheral blood flow
improved ability to sleep in the cold due to
reduced shivering
how do cold-acclimatized people maintain body heat with less shivering
by increasing non-shivering thermogenesis
sex responses to cold exposure : at rest
women show a faster reduction in body temperature than men
sex responses to cold exposure : in cold water
decreased body temperature is similar in men and women (due to heat dissipation properties in water)
sex responses to cold exposure differences can be explained by
body composition and anthropometry
(decreased in lean muscle mass and body size)
age responses to cold exposure
older than 60 years less tolerant to cold
children experience faster fall in body temperature
dalton’s law
the total pressure of a gas mixture is = to the sum of the pressure that each gas would exert independently
basically partial pressure (sum of all gasses pressure in air)
as we increase in altitude, what happens
the % of O2 stays the SAME
the total # of O2 molecules is different
going from sea level to pikes peak
decreased diffusion gradient of O2
= cant drive O2 into tissues since PO2 is lower
effects of altitude on Hb-O2 curve
hypoxia = shift left (low O2/altitude)
hyperoxia- shift right (high PO2)
arterial O2 content is made of
SaO2
[Hb]
partial pressure of O2 in arteries
what happens to VO2 max at altitude
decreased
trained vs untrained VO2 at altitude
trained individuals have a LARGER decline because they have a larger capacity (VO2 max) and increase in SV, decrease in PaO2, and capillary transit time decreases
HR responses to altitude during submaximal exercise
HR increases
Ve response to submaximal exercise at altitude
Ve increases due to peripheral chemoreceptors sensing lower PO2
- at altitude, ventilatory drive is primarily induced by changes in PO2 whereas at rest it is normally controlled by PCO2 and pH
Lower PO2 (altitude) effects on short term anaerobic performance
should have no effect on performance because for short term exercises we are normally relying on non-oxidative sources so O2 transport to muscle would NOT limit performance
*lower air resistance may improve performance
lower PO2 (altitude) effects on long term aerobic performance
Lower PO2 results in poorer aerobic performance because long duration exercises mostly reliant on O2 sources and are dependent on O2 delivery to muscle
cardiovascular responses to altitude
decreased plasma volume upon initial arrival to altitude which decreases SV due to increased RWL and UWL which increases hematocrit
after a few weeks at altitude what is the CV response
diminished plasma volume will return to normal if adequate fluid ingested
acclimatization to altitude
1) production of more red blood cells
2) greater O2 saturation
3) hyperventilation
how are more RBC’s produced via EPO
higher RBC concentration via EPO from the kidneys
what is greater O2 saturation due to
an increase in blood flow to the lungs
what population produces more RBCs in response to high altitude
andeans adapt to high altitude by producing more RBCs to counter the desaturation caused by lower PO2
*they have an average hematocrit of 60-65% when normally we have 45%
function of EPO
decreased blood O2 stimulates the kidneys to release EPO which targets the red bone marrow causing increased RBC production which overall increases blood O2
what is hyperventilation due to at altitude
increased sensitivity of carotid chemoreceptor which responses to changes in CO2 (pH) and O2 (ventilation)
what populations exhibit greater O2 saturation due to altitude
tibetan high altitude residents (Sherpas) have NO increase in hematocrit but adapt by INCREASING THE O2 SATURATION of existing Hb via increased blood flow to the lungs due to high NO
NO (nitric oxide) = vasodilation = increased blood flow to lungs = increases V/Q relationship
lifetime altitude residents
have complete adaptations in arterial O2 content and VO2 max
- adaptations are less complete in those arriving at altitude later (sea level = decreased adaptations)
- moderate/high altitude = increased adaptations which could lead to increased NO or hematocrit
if you live at high altitude how should you train
at low altitude
which helps maintain high interval training velocity
* some athletes may still experience Hb desaturation
living at high altitude results in
an increase in RBC mass via EPO = increase in VO2max
>22 hr/day at 2,000-2,500 m required or do intermittent hypobaric hypoxia
improvement in race times in runners due to change in altitude in which they lived
sea level residents lived at 2,500 (altitude) and trained at altitude for 27 days
their 3000 m time trial performance increased by 1.1% and VO2 max increased by 3.2% as a result of intervention
if a sea level athlete moves to altitude to train and moves back to sea level what happens
some athletes will have a higher VO2 max upon return to low altitude while others will not
* could be due to detraining effect - cannot train as intensely at altitude
increased RBC mass leads to
increased VO2 max
can you have an improved VO2 max without increased RBC mass
controversial but some studies show an increased RBC mass is necessary but not sufficient for improved performance
effects of living Low, and training high
avoids negative effects of prolonged altitude exposure
no real changes in VO2 max or Hb concentration
