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Exercise Physiology > Exam 3- Lecture 17 & 18 > Flashcards

Exam 3- Lecture 17 & 18 Flashcards

1
Q

2 major factors that influence endurance performance

A
  • maximal capacity to utilize oxygen (reflected by VO2max, sets upper limit)
  • Exercise intensity at lactate threshold (approximates max work-rate that can be maintained for prolonged periods)
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2
Q

Enhancement of maximal exercise capacity

A
  • enhancement of VO2max in healthy persons primarily due to increased cardiovascular capacity
  • improved ability to deliver oxygen to the active muscle
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3
Q

Submaximal exercise capacity

A
  • enhanced capacity for prolonged submaximal exercise strongly related to factors inhaling aerobic capacity of trained muscle
  • A consequence of structural and metabolic adaptations in muscle
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4
Q

Degree of VO2max improvement is inversely linked to…

A

initial fitness level

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5
Q

VO2 max =

A

maximal CO x max a-v O2 difference

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6
Q

enhance VO2max with training is due to increases in

A
  • max CO

- max a-v O2 difference

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7
Q

how does max CO increase?

A
  • max HR does not change with exercise training

- rise in max CO is completely due to augmented max SV

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8
Q

HR response to training

A
  • At rest: decreases due to greater vagal tone
  • Max HR doesn’t change much –> allows for more ventricular filling time
  • HR at any submax VO2 is less
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9
Q

SV response to training

A
  • Rest: higher after training
  • Max SV is higher
  • SV at any given submax VO2 is higher
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10
Q

What factors contribute to augmented max SV?

A
  • Increased ventricular chamber volumes results in increased EDV and eccentric hypertrophy (greater left ventricular muscle mass)
  • Enhanced blood volume (preload factor)
  • Time course - BV, PV, and RBC
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11
Q

Athlete’s Heart

A

Increased heart mass
Normal cardiac function
Reversible

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12
Q

Failing Heart

A

Increase heart mass
Reduced cardiac function
Irreversible cell death and fibrosis
Increased mortality

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13
Q

Endurance athlete’s heart

A
  • thickening of LV walls

- LV dilation

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14
Q

Practical implications of changes in HR-VO2 relationship after training

A
  • When a person endurance trains, HR after any given absolute workload will decrease after training
  • Fall in HR at submax workload is a common marker for a training effect
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15
Q

When HR at absolute workload decreases due to training, how can you continue to achieve training HR?

A

adjust absolute workload upwards

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16
Q

What occurs to myocardial oxygen consumption after training?

A
  • it is likely reduced at rest and at any submaximal exercise intensity
    (indexed by RPP)
  • HR x SBP
  • Beneficial for patients with exertion anginal symptoms
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17
Q

Is cardiac output affected by exercise training?

A
  • No

SV increases but HR decreases

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18
Q

factors that contribute to increased max a-v O2 difference with training

A
  1. greater delivery of blood to the active muscle at max exercise
  2. enhanced diffusion capacity for oxygen at the active muscle (increased surface area available for exchange and capillary density)
  3. increased aerobic capacity of the active muscle
  4. increased vasodilation in active muscle and redistribution of blood flow
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19
Q

What is the primary reason why the ability of the heart to pump is believed to be the limiting factor in VO2 max?

A
  • Sympathetic activity to muscle vasculature is still present at maximal exercise
  • brain must limit vasodilation of the active muscles or blood pressure would fall because the heart couldn’t keep up with fall in vascular resistance
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20
Q

CV Adaptation to exercise training summary- At a given absolute submaximal workload:

A
  • same CO
  • Same a-v O2 difference
  • lower HR
  • increased SV
  • Same VO2 (assuming the economy of movement hasn’t changed)
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21
Q

CV Adaptation to exercise training summary- At a given relative % of VO2max intensity

A
  • Increased CO
  • Increased a-v O2 difference
  • Same HR
  • Increased SV
  • Working at a higher VO2
22
Q

How does regular aerobic exercise change resting blood pressure?

A

May lower it
Relatively small effect
- In hypertensive individuals, lowers SBP 8 and DBP 6

23
Q

Postexercise Hypotension

A
  • Blood pressure decreases immediately following acute exercise (~5mmHg decrease SBP)
24
Q

Why does post exercise hypotension occur?

A

persistent vasodilation in skeletal muscle:

  • centrally: resetting of arterial baroreflex
  • peripheral: less responsive SNS; histamine induced vasodilation
25
Q

Why does histamine release increase with exercise?

A

increase mast cell degeneration and HDC expression

26
Q

What does histamine post exercise change?

A
  • vascular function
  • cellular maintenance
  • metabolism
  • inflammation
27
Q

What happens to SBP during submaximal exercise for those with normal blood pressure?

A

it is either unaltered or shows a mild decrease (<10mmHg) after training

28
Q

What occurs to SBP during submaximal exercise in patients with heart disease?

A
  • decrease SBP is accompanied by decrease HR, which favorably decreases myocardial oxygen consumption at a given absolute intensity
29
Q

Exercise prescription for people with hypertension:

A

F: aerobic exercise on most or all days of week; resistance 2-3 days
I: mod aerobic (40-60% HRR, RPE 12-13); resistance training at 60-70 then 80% 1RM
T: >20-30 mins a day to total greater than 90-150 min per wk; resistance 2-4 sets of 8-12 reps of 8-10 exercises
T: emphasize rhythmic activities using large muscle groups; resistance training using major muscle groups

30
Q

Does pulmonary function at rest change after exercise training?

A

no

31
Q

does max exercise ventilation (Vemax) post-training?

A

yes but the effect is small

  • increases in tidal volume and frequency
  • not from changes in vital capacity (due to training of respiratory muscles)
32
Q

what occurs to Ve at submax exercise?

A
  • it is less at a given VO2
  • oxygen cost of exercise from breathing decreases
  • fall of respiratory rate results in tidal volume maintained or greater
  • probably due to less metabolic feedback from periphery because of greater mitochondrial respiration capacity
33
Q

how does exercise training change respiratory muscles?

A
  • increases the endurance

- result in delayed respiratory muscle fatigue

34
Q

what contributes to delayed fatigue?

A
  • increased oxidative capacity of respiratory muscles

- lower Ve/VO2 at submaximal exercise

35
Q

what is the shift in lactate threshold primarily due to?

A

peripheral adaptations

36
Q

what is increased VO2 max primarily due to?

A

central adaptations

37
Q

training induced adaptation allows a trained person to…

A

perform steady state exercise at a greater % of VO2max

38
Q

Major training-induced metabolic adaptations at the level of skeletal muscle:

A

increased oxidative capacity of mitochondria in the trained muscle:

  • increased number and size of mitochondria
  • increased oxidative enzyme activity
  • increase in total amount of enzyme protein
  • increase in enzymes that deal with fat, CHO, and protein metabolism (mitochondrial respiration)
39
Q

which type of fiber has the greatest change in oxidative enzymes?

A
  • slow Type I muscle in response to continuous training

- fast Type II muscle in response to interval training

40
Q

increase in mitochondria number and size leads to:

A

increased oxidative enzyme activity –> increased oxidative capacity

41
Q

Major adaptations in substrate mobilization and storage:

A
  • increased lipid: glycogen utilization
  • increased glycogen storage in trained muscle
  • decreased PFK activity:
    lower cell ADP
    higher cell FFA
    increased capillary density (enhances FFA and O2 delivery to muscle)
42
Q

what does trained muscle mass have more of?

A

intramuscular lipid –> better able to mobilize it for energy

43
Q

Glycogen sparing effect: Decreased rate of glycolysis

A
  • smaller rise in ADP in trained skeletal muscle

- high FFA in muscle cell

44
Q

glycogen sparing effect: enhanced lipid usage

A
  • increased oxidative capacity
  • less active acid:
    promotes FFA release from adipose tissue
    enhanced delivery of muscle FFA and O2
    trained muscles store more lipid –> better mobilizes this for energy
45
Q

endurance training structural adaptations in skeletal muscle

A
  • increased capillary density –> increases substrate delivery –> increases surface area for diffusion and reduces diffusion distance
  • increased fiber size –> selective hypertrophy of fibers used in the exercise; degree of hypertrophy <
46
Q

summary of muscle adaptations to endurance training

A
  • increased number and size of mitochondria
  • increased oxidative enzyme activity
  • increase in muscle glycogen storage
  • enhanced lipid oxidation with less glycogen utilization during submax exercise
  • increased capillary density
  • increased fiber size
47
Q

muscle adaptations to anaerobic training

A
  • increases in ATP, CP, creatinine, glycogen
  • increase in enzymes regulating glycogen/glucose breakdown during glycolysis –> especially in type II fibers
  • increased capacity for lactate production during max exercise
48
Q

training and oxygen deficit a the onset of exercise:

A

training results in a faster rise in oxygen uptake at the onset of exercise, resulting in less metabolic acidosis and creatine phosphate depletion –> achieve steady state faster and thus there will be less perturbation of cellular homeostasis

49
Q

good performance predictors:

A

exercise intensity at OBLA

lactate threshold

50
Q

how does anaerobic training affect OBLA?

A
  • progressive decrease in blood lactate for a given absolute workload
  • increases absolute exercise intensity at with OBLA occurs
  • can increase the relative exercise intensity at which OBLA or lactate threshold occurs
51
Q

what is that ability to exercise for long periods using primarily aerobic metabolism primarily due to?

A

factors relating to structural and metabolic capacity of muscles engages in the exercise

52
Q

See responses to acute exercise chart

A

pg 238

Exercise Physiology (17 decks)

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