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Exercise Physiology > Exam 3 Review > Flashcards

Exam 3 Review Flashcards

1
Q

We are called homeotherms because we are so good at?

A

maintaining a consistent core body temp

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2
Q

In a cold environment, we regulate core temp by?

A

centralizing body heat

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3
Q

During intense exercise most heat loss will be through?

A

evaporation (sweat)

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4
Q

One of the first (within 3 days) adaptations to exercise in high heat environments, is marked as a increase in ?

A

increase in plasma volume

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5
Q

Where is heat load sensed?

A

receptors in/near skin, receptors in CNS, and hypothalamus

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6
Q
  1. Explain what an acid is. Now explain what a base is.
A

An acid is a molecule that releases H, while a base absorbs H

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7
Q
  1. What are the intracellular buffers? What is the most important?
A

cellular proteins (most important) , bicarbonate, and phosphate

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8
Q
  1. What are the extracellular buffers?
A

bicarbonate, hemoglobin, and blood protein

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9
Q
  1. Why are H+ ions damaging to performance?
A

inhibit enzymes used in energy production, mess with Calcium release and reuptake, compete with calcium and troponin and myosin sites, interfere with cross-bridge cycling

mess with muscle contraction, decreases force output as acidity goes up, and reduces effectiveness of energy systems

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10
Q
  1. How does body fat impact heat loss?
A

increased presence of adipose tissue reduces heat loss and increases the body’s ability to retain heat

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11
Q
  1. What are the common adaptations to training in heat?
A

expansion of plasma volume (blood volume), increased sweat rate, decrease in mineral loss in sweat

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12
Q

1.What is body temperature homeostatis and how is it maintained?

A

The stable human body temperature is 37C and is maintained by releasing or gaining heat or hormonal responses

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13
Q
  1. What are the responses to an increase in core temperature (2 big ones first)? (not CV or resp this time)
A

2 big ones: blood to skin and sweating

an increase in metabolism, blood pooling at skin to disperse heat, muscular activity, release of sympa hormones

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14
Q
  1. What are important factors that impact heat loss and evaporation?
A

skin exposed, temperature/humidity, convective currents

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15
Q
  1. How does heat impact fatigue?
A

diverting blood = higher loss of fluids, loss of blood volume (blood to skin instead of heart), increase in cardiac output, stroke volume, and heart rate but unable to sustain

force outputs drop because aerobic to anaerobic meaning more glucose use and more lactate

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16
Q
  1. How does sweat change as one becomes acclimated to training in the heat?
A

less salts, earlier onset, more profuse

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17
Q
  1. How does the body “balance” heat loss with heat production?
A

the body attempts to thermoregulate through two different means

when it’s cold we internalize heat and restrict blood flow

when its hot we disperse heat through convection, conduction, evaporation, and radiation

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18
Q
  1. How are cutaneous vessels impacted by increases/decreases in core temperature?
A

With heat loss there is vasodilation of cutaneous arterioles to allow more blood to reach the skin

temperature decrease leads to constriction

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19
Q
  1. What are the primary adaptations to training in heat?
A

increased blood volume, increased sweat rate, decrease mineral content of blood

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20
Q
  1. What role does the hypothalamus play in temperature regulation?
A

The hypothalamus controls sweating and vasodilation, which are key in heat loss

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21
Q
  1. What is the most serious form of heat illness?
A

heat stroke which leads to thermoregulatory failure

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22
Q
  1. What happens to the percentage of O2 at altitude? How about the concentration of O2? Why?
A

percentage of O2 stays the same

As altitude/volume increases the density of oxygen in the air decreases meaning less oxygen is available

The partial pressure of oxygen decreases as altitude increases making it harder to hold onto oxygen

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23
Q
  1. What is HR like during exercise at altitude when compared to exercise at sea level?
A

because there is less oxygen available at altitude, heart rate increases, cardiac output increases, and blood pressure increases

stroke volume decreases

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24
Q
  1. What are normal adaptations to living at altitude?
A

less bircarbonate, better buffering systems, lower stroke volume, higher HR,

long term = increased nitric oxide, increased red blood cells, increased hemoglobin, increased O2 transport, increased capillary density, increased aerobic enzyme concentrations

25
Q
  1. What are the short term responses to traveling to altitude? What are the causes for them?
A

elevated HR, reduced plasma volume, increased hemoglobin/red blood cells, increased ventilation, lower stroke volume=lower venous return

cross below hypoxic threshold, so oxygen becomes primary driver of oxygen, we blow off too much CO2

long term solution is to get rid of blood buffers (drop bicarbonate to drop blood volume)

26
Q
  1. How do CO2 and O2 have differential impacts on ventilation at altitude?
A

There is a decreased difference between output of CO2 and input of O2 because there is less O2 available and the body has to work harder (ventilation) to maintain

bad to have low CO2 because of changes in pH, need (central chemoreceptors brought about 70% change CO2, O2 deals with peropheral)

27
Q
  1. What is the oxygen cascade and where does it end? How does altitude change things?
A

The oxygen cascade is the transfer of oxygen from air to mitochondria

With altitude, the beginning of the process starts at a lower partial pressure and continues to lose oxygen at each stage because there is less oxygen available

28
Q
  1. Why are sprint performances improved at altitude?
A

Because of decreased partial pressure(less dense) there is decreased air resistance.

The athletes also run off of CP and anaerobic systems so oxygen isn’t needed

29
Q
  1. Why might athletes benefit more from training at sea level than training at altitude?
A

limited on maximum outputs, lower blood volume, can’t strain muscle and energy systems to potential

While altitude training does increase oxygen uptake and delivery once adapted to, the decreased blood volume can severely affect performance.

30
Q
  1. What are the main neural adaptations to RT?
A

increased neural drive (better signals from brain, better muscle coordination, bigger motor units at brain, better control of golgi tendon, better muscle control) = suprasprinal input

increased synchronization of motor units (individually and as groups) = intra/intermuscular

decreased spinal excitability: decreased need for golgi tendon = better agonist activation, increased reciprocal inhibition (muscle spindle) = decreased activation of the antagonist

31
Q
  1. How do fiber types shift due to resistance training?
A

they become more fatigue resistance = shift from 2x down to 2a

32
Q
  1. How should one train to maximize neural adaptations?
A

High intensity training (90% of 1 RM or high weight/low reps)

Power training (40 to 60% of 1 RM and maximal velocities)

33
Q
  1. During the first 6 to 12 weeks of RT, most strength gains are due to?
A

These are due to neuromuscular adaptations

34
Q
  1. How are the energy systems impacted by RT?
A

THEY ALL GET BETTER = RT increases enzyme presence, lowers (aerobic enzymes, capillary and mitochondrial density), and increases substrate storage (CP, ATP, Glycogen)

The lowering issue is due to increased presence of muscle fibers and decreased use of aerobic means

35
Q
  1. What is protein dilution?
A

more mitochondria and more capillary as we train, but we expand our protein faster (opposite of aerobic training)

In this case protein isn’t as pure and easy to absorb because its been diluted (finding better sources)

36
Q
  1. What are the common adaptions to endurance training? (Protein, respiratory, ATP, Cardio, heart?)
A

heart is better (bigger walls, bigger chamber, better output, better ventricle (size and muscle combo is good) = lower HR and increased heart rate reserve at any given workrate

37
Q
  1. How does the structure of the heart change with ET?
A

eccentric hypertrophy (pump in/chamber size) = volume overload

concentric hypertrophy (pump out/wall thickness) = pressure overload

physiological hypertrophy (both) = exercise pregnancy

38
Q
  1. What is preload? Afterload?
A

Preload is ventricular filling (venous return) or pressure in ventricle because of more blood volume

Afterload is the force against the heart to contract, product of all resistance pushing back on the heart (resistance is derived from arteries and arterioles)

resistance training = high afterload, will go down with cardio = better at dilating and capillary beds (relieving pressure)

39
Q
  1. How are the energy substrates and energy pathways impacted by ET?
A

THEY ALL GET BETTER
increase in fat usage, increase in glycogen and triglyceride storage, so better utilization

more ATP and CP storage

40
Q

As one moves to higher altitudes, the air around them will?

A
  • Contain a lower partial pressure
41
Q

As you ascend to higher altitudes the air around you will?

A
  • Become less dense
42
Q

Immediately upon ascending to altitude one can expect?

A
  • Temporarily elevated ventilation
43
Q

How is cardiac output increased when we first go to altitude?

A
  • Increase in HR
44
Q

After several days at altitude, we would expect an athlete to have:?

A
  • Elevated HR, reduced plasma volumes, increased hemoglobin, increased minute ventilation
45
Q

What adaptations occur with muscle cells (endurance training specific)?

A

increased glycogen storage, increased presence of glycolytic enzymes (PFK), more lactate dehydrogenase

46
Q

What adaptations occur related to lactate (endurance training specific)?

A

accumulate less lactate, increased lactate clearance + increased threshold, increased lactate tolerance at Vo2 Max

47
Q

What adaptations occur with carb usage (endurance training specific)?

A

increased triglyceride and muscle/liver glycogen reserves, less glucose use, better usage at max work rates

48
Q

What adaptations occur with fat utilization (endurance training specific)?

A

use of fat at any workrate, better storage of triglyceride, better use of FFAs and increased Beta Oxidation

49
Q

What adaptations occur with protein utilization?(endurance training specific)

A

increased use of protein as substrate, being aerobically fit means better glucose and protein usage

50
Q

What are the resp adaptations (endurance training specific)?

A

better ventilation (decreased ventilation) to perfusion matching (limiter at lung

increased O2 exchange in lungs, better blood flow at lung

51
Q

What adaptations occur with ATP (endurance training specific)?

A

better storage/easier to restore, FFA availability, more fuels/substrates, oxygen deficit and EPOC decrease

52
Q

What are the CV adaptations (endurance training specific)?

A

lower HR, increased CO, increased SV, increased hemoglobin, increased peripheral vasodilation (reduced BP), increased BV, increased thermal regulation

53
Q

What adaptations impact heart health ((endurance training specific)?

A

volume overload –> larger ventricles–>increased stroke volume–> decreased heart rates

decreased blood pressure

improvements in blood lipids = increased HDL, decreased LDL

54
Q

What changes happen to the heart? (endurance training specific)

A
  • Eccentric hypertrophy/dilated heart = volume overload
    o Increase in chamber dimension
    o Pump more in
  • Concentric hypertrophy= pressure overload
    o Increase in wall thickness
    o Pump more out
  • Physiological hypertrophy = exercise pregnancy
    o Combines best of both
    o Pump more blood in and pump more out
55
Q

What changes occur to the vasculature of the heart?

A

additional collateral pathways open up and connect = tissue can still be feed in case of blockage

56
Q

What is Nitric Oxide in terms of vasodilator and more?

A

reduces superoxide radicals, dilates blood vessels, reduces oxidation of LDL cholesterol (not issue when healthy), helps with muscle shearing

57
Q

What is VLDL?

A

very low density lipid - energy delivery system, too much LDL creates excess leading to oxidaiton, oxidation means LDL becomes plaque

58
Q

What adaptations occur with O2 utilization?

A

structural changes increase BV and reduce HR

arteries = increased hemoglobin/capillaries/ventilation to perfusion matching

veins = increased myoglobin/mitochondria/enzymes

Exercise Physiology (11 decks)

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