KAAP 430*- Final

homothermic

internal body temp regulated & kept nearly constant despite environmental temp changes

thermoregulation

regulation of body temp around a physiological set point

normal body temp

36.1-37.8 C | 97-100 F

ATP breakdown

25% -> cellular work (W)

75% -> metabolic heat (M)

types of dry heat exchange

\- conduction (K)

\- convection (C)

\- radiation (R)

conduction

heat transfer through direct molecular contact (negligible)

convection

heat transfer by movement of gas or liquid across a surface

radiation

heat loss in forms of infared rays

insulation

resistance to dry heat exchange

ideal insulator -> still layer of air

evaporation

heat loss via phase change from liquid to gas

primary heat loss during exercise (\~80%)

effect of humidity of heat loss

as humidity increases, evaporation decrease

(prolonged evaporation via sweat = dehydration)

heat balance equation

M-W ± R ± C ± K-E\=0

heat loss equation

M ± R ± C ± K - E < 0

heat gain equation

M ± R ± C ± K - E \> 0

can briefly withstand core temps of...

< 35 C

> 41 C

core temp greater than this inhibits physiological function

\> 40 C

preoptic-anterior hypothalamus (POAH)

\- body's thermostat

\- receives input from sensory thermoreceptors

\- activates thermoregulatory mechanisms

sensory receptors

\- peripheral: in skin

\- central: in brain & spinal cord

effectors

\- muscles & glands

\- respond to signals from the brain to regulate body temp

\- includes endocrine gland

effects of heat on cardiovascular function

\- skin arterioles VD to increase convection heat loss

\- POAH triggers SNS (increased cardiac output & VC in nonessential tissues)

\- blood volume decreases (sweating)

\- SV can't increase due to blood pooling

cardiovascular drift

\- occurs in prolonged exercise in hot conditions

\- heart rate increases to compensate for decreased blood volume

limitations to exercise in heat

\- cardiovascular system overload

\- critical temperature theory

cardiovascular system overload

\- heart can't provide sufficient blood flow to both exercising muscles and skin

\- especially in untrained / nonacclimated athletes

critical temperature theory

\- brain shuts down exercise at \~40-41C

\- limitation in trained / well acclimated athletes

only avenue of heat loss in hot conditions

evaporation (sweating)

sweat electrolyte content

\- duct reabsorbs Na+ and Cl-

\- light sweating: dilute sweat

training and sweat composition

\- more sensitive to aldosterone

\- reabsorb more Na+ and Cl-

sweat loss during exercise

\- can lose 1.6-2.0L (2.5-3.2% body weight) each hour

\- increased sweating -> decreased blood volume -> decreased cardiac output

hormonal control of fluid balance

\- adrenal cortex & posterior pituitary gland

\- loss of water & electrolytes triggers release of aldosterone & ADH

aldosterone

retains Na+ at kidneys

ADH

vasopressin; retains water at kidneys

risk factors for exercise in heat

1\. metabolic heat production

2\. air temperature

3\. humidity

4\. air velocity (convection)

5\. radiant heat sources

6\. clothing

wet-bulb globe temperature

\- reflects physiological stress

\- measures convection, evaporation, & radiation

severity of heat illness

lowest: heat cramps

mid: heat exhaustion

highest: heatstroke

heat cramps

\- severe painful cramping of large muscles

\- triggered by Na+ losses & dehydration

\- more common in heavy sweaters

\- treated by cooling down & dinking electrolytes

heat exhaustion

\- fatigue, dizziness, nausea, vomiting, fainting, weak rapid pulse

\- caused by severe dehydration from sweating

\- blood flow needs of muscle and skin cant be met (low BV)

\- thermoregulatory mechanisms functional but overwhelmed

\- more common in unfit or unacclimated people

\- treated by cooling person down

heatstroke

\- life threatening

\- thermoregulatory mechanism failure

\- core temp >40 C

\- mental decline: confusion, disorientation, unconsciousness

\- must cool whole body ASAP

acclimation

short term adaptation to environmental stressor (days / weeks)

acclimatization

long term adaptation to environmental stressor (months / years)

acclimation to heat

\- cardiovascular function optimized (decreased heart rate, increased cardiac output)

\- widespread sweating earlier, more dilute

\- lower core temp during exercise

\- plasma volume increases due to increase oncotic P

sex differences in heat

\- lower sweat rate in women

\- more active sweat glands but less sweat production per gland

\- women have advantage in humid climates, disadvantage in hot, dry climates

cold stress

any environmental condition causing loss of body heat

effects of cold

\- POAH triggers peripheral VC

\- nonshivering thermogenesis

\- skeletal muscle shivering

\- cerebral cortex triggers behavioral adaptations

cold habituation

\- occurs after repeated cold exposures without significant heat loss

\- VC & shivering blunted

\- core temp allowed to decrease more

metabolic acclimation

\- occurs after repeated cold exposures with heat loss

\- enhanced metabolic & shivering heat productions

insulative acclimation

\- when increased metabolism cant prevent heat loss

\- enhanced skin VC ( increased peripheral tissue insulation)

overdressing in cold climates

\- can be dangerous

\- causes sweating which increases evaporation

how body composition increases insulation

\- increased inactive peripheral muscle

\- increased subcutaneous fat

\- decreased surface area:mass ratio (bigger person)

windchill

\- refers to speed not temp

\- based on cooling effect of wind

\- increases convection heat loss

\- higher windchill increases risk of freezing tissues

cooling effects of liquid vs air

\- heat loss 4x faster in cold water

\- core temp constant until water temp < 32 C / 89.6 F

\- core temp drops 2.1 C per hour in 15 C water

\- heat loss is faster in moving water & slower with exercise

muscle function in cold

\- decreases

\- altered fiber recruitment -> lower contractile force

\- shortened velocity and decreased power

\- affects superficial muscles

fatigue in the cold

\- metabolic heat production decreases

\- energy reserve is depleted with endurance exercise

\- potential for hypothermia

FFA in cold

\- increased catecholamine secretion but no increase in FFA

\- VC in subcutaneous fat decreases FFA mobilization

glucose metabolism in cold

\- blood glucose maintained well during cold exercise

\- muscle glycogen utilization increased

\- hypoglycemia suppresses shivering

hypothermia

\- core temp 29.5-34.5: thermoregulatory function compromised

\- core temp

cardiorespiratory effects of cold

\- low core temp leads to slow HR (SA node)

\- may cause arrhythmia

\- doesn't damage ventilatory tissues

\- may decrease ventilation rate and volume

treatment for mild hypothermia

\- remove from cold

\- dry clothing, blankets

\- warm drink

treatment for severe hypothermia

\- gentle handling to avoid arrhythmias

\- gradual rewarming

\- may require medical supervision

frostbite

\- excessive VC > lack of O2 & nutrients > tissue death

\- gradual rewarm (no risk of refreezing)

exercise-induced asthma (cold)

\- affects 50% of winter sport athletes

\- excessive airway drying

partial pressure of oxygen

\- portion of barometric pressure exerted my oxygen

\- reduced PO2 at altitude limits performance

hypobaria

\- reduced Pb seen at altitude

\- results in hypoxia & hypoxemia

hypoxia

low oxygen saturation / supply of the tissues

hypoxemia

low oxygen content in the blood

change of PO2

\- percent of O2 in air doesn't change

\- change results from decrease Pb at higher altitudes

humidity at altitude

\- cold holds very little water

\- air at altitude is very cold & dry

\- faster dehydration via skin & lungs

altitude

> 1,500 m

few physiological effects below that

low altitude

\- 500-2,000 m

\- no effects on well being

\- performance may be lower, but restored by acclimation

moderate altitude

\- 2,000-3,000 m

\- effects unacclimated people

\- performance and aerobic capacity declines

\- performance may or may not be restored by acclimation

high altitude

\- 3,000-5,500 m

\- acute mountain sickness

\- performance declines, not restored by acclimation

extreme high altitude

\- >5,500

\- severe hypoxic effects

pulmonary response to acute altitude (rest & submaximal)

\- ventilation increases immediately

\- decrease PO2 stimulates chemoreceptors in aortic arch & carotids

\- increased tidal volume and respiration rate for several hours-days

hyperventilation

\- increase ventilation at altitude

\- alveolar PCO2 decreases, so gradient increases and there is an increased loss

\- respiratory alkalosis

respiratory alkalosis

\- high blood pH

\- oxyhemoglobin curve shifts left

\- prevents hypoxia-driven hyperventilation- kidneys excrete more bicarbonate to decrease buffering and reverse alkalosis

pulmonary diffusion at altitude

\- at rest, does not limit gas exchange

\- hypoxemia is a direct reflection of low alveolar PO2

oxygen transport at altitude

\- decreased alveolar PO2 causes decreased hemoglobin saturation

\- curve shifts left to minimize desaturation

O2 diffusion at altitude

\- 15 mmHg diffusion gradient

\- significant reduction in diffusion into muscles

left shift of oxyhemoglobin curve

\- higher saturation at lower pressures

\- adaptation to combat desaturation at lower PO2 at altitude

vascular system at altitude (short term)

\- plasma volume decreases (up to 25%) within a few hours

\- respiratory water loss & increased urination

\- short term increase in hematocrit

vascular system at altitude (long term)

\- red blood cell count increases

\- hypoxemia triggers EPO release from kidneys

\- increased RBC production in bone marrow

\- long term increase in hematocrit

cardiac system at altitude (short term)

\- cardiac output increases (despite decrease in plasma & stroke volume)

\- increased SNS activity > increase in HR

\- inefficient

cardiac system at altitude (muscles)

\- after a few days muscles extract more O2

\- increases a-v O2 difference

\- reduces demand for cardiac output

cardiac system at altitude (long term)

\- decreased stroke volume due to decrease plasma volume

\- decreased HR due to decreased SNS responsiveness

\- decreased VO2 max due to decreased cardiac output & decreased PO2 gradient

metabolic rate at altitude

\- basal metabolic rate increases (increased thyroxine and catecholamine secretion)

\- decreased appetite but must increase food intake to maintain body mass

\- increased anaerobic metabolism

glucose vs fat

at altitude, glucose (carbs) provide more energy per liter of oxygen

effects of increase anaerobic metabolism

\- increase lactic acid

\- production decreases over time (dk why)

VO2max at altitude

\- VO2max decreases as altitude increases

\- due to decreased arterial PO2 and cardiac output

\- decreases as a percentage of sea level VO2max

\- lower sea-level VO2max > higher perceived effort (even though task has same absolute O2 requirement)

Mt. Everest ascent study

\- climbers' VO2max decrease from 62 to 15

\- if sea level VO2 is

anaerobic performance at altitude

\- unaffected

\- ATP-PCr and anaerobic glycolytic metabolism not affected by lower PO2 (minimal oxygen requirements)

\- thinner air > less resistance

\- can have improved swim & run times (

acclimation to altitude

\- improves performance, but not to that of sea level

\- takes 3 weeks at moderate altitude (+1 week for every additional 600m)

\- lost within 1 month at sea level

changes from chronic exposure to high altitude

\- ventilation increases & stays elevated

\- stroke volume drops & recovers slightly

\- heart rate drops immediately & then rises (receptors not as sensitive to SNS)

\- cardiac output drops & remains lower

\- VO2 max drops and stays lower

strategies for sea-level athletes competing at altitude

1. compete immediately

2. train high for 2 weeks

(1) compete ASAP

\- doesn't give benefits of acclimation

\- too soon for adverse effects

(2) train high for 2 weeks

\- worst adverse effects of altitude over

\- aerobic training at altitude not as effective (train at lower intensity)

“live high, train low”

\- best of both worlds

\- permits passive acclimation to altitude

\- training intensity not compromised by low PO2

\- shows significant improvement in 5k trial

\- aerobic performance and VO2max improved

artificial altitude training

\- attempt to gain benefits of hypoxia at sea level

\- breath hypoxic air 1-2 hours a day, train normally

\- no improvements

natural vs artificial live high train low

\- natural best for elite athletes

\- nonelite athletes may benefit from artificial

acute altitude (mountain) sickness

\- onset 6-48h after arrival (most severe days 2-3)

\- headache, nausea / vomiting, dyspnea, insomnia

\- can develop into more lethal conditions

\- incidence increases with altitude, rate of ascent, and susceptibility

\- causes: low ventilatory response, CO2 accumulates & causes acidosis

headache in altitude sickness

\- most common symptom

\- worse in morning & after exercise

\- hypoxia causes cerebral vasodilation which leads to stretching of pain receptors

altitude sickness insomnia

\- interruption of sleep stages

\- Cheyne-Stokes breathing prevents sleep

\- incidence of irregular breathing increases with altitude