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Exercise Physiology > Chapter 13/14/20: The Physiology of Training > Flashcards

Chapter 13/14/20: The Physiology of Training Flashcards

1
Q

describe the principle of overload

A

increased capacity of a system in response to training above the level to which it is accustomed

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2
Q

what factors can contribute to overload?

A

intensity, duration and frequency

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3
Q

what does too much overload lead to? common issue in which group?

A

overtraining or overreaching, which is a common issue with elite athletes

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4
Q

describe the principle of reversibility

A

when training is stopped, the training effect is quickly lost

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5
Q

describe the principle of specificity

A

training effect is specific to:
1) muscle fibers recruited during exercise
2) type of contraction (eccentric, concentric, isometric)
3) energy system involved (aerobic vs. anaerobic)

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6
Q

how does the VO2 max for an athlete during their sport specific activity compare to their VO2 max on a treadmill?

A

VO2 max during sport specific activity were as high or higher than their VO2 max on a treadmill

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7
Q

is there a difference between men and women’s responses to training programs?

A

no, exercise prescriptions should be individualized

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8
Q

how does initial fitness level effect training improvement?

A

training improvement is always greater in individuals with lower initial fitness levels

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9
Q

how do genetics influence an individual’s response to training? evidence?

A

genetics play an important role, evidence with identical twin study: ten sets of identical twins went through the same training program- there was a similarity in the response of each pair, but improvement in VO2 max varied from 0-40%

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10
Q

how does training affect the VO2 max of high responders (genetically)?

A

high responders possess a relatively high untrained VO2 max which increases significantly with training

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11
Q

how does training effect the VO2 max of low responders (genetically)?

A

low responders possess a relatively low untrained VO2 max which does not increase significantly with training

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12
Q

how do genetics effect anaerobic training?

A

anaerobic training is more genetically determined, training can only improve anaerobic performance to a small degree

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13
Q

why is anaerobic capacity more genetically determined than aerobic capacity?

A

anaerobic capacity is largely dependent on fast (type IIx) fibers which are determined early in development

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14
Q

how does muscle fiber type change with aerobic training?

A

reduction in cross-sectional area of fast fibers and increase in cross-sectional area of slow fibers

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15
Q

how does capillary density change with aerobic training? consequence?

A

increased number of capillaries surrounding muscle fibers which enhances oxygen diffusion and improves removal of wastes

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16
Q

how does myoglobin content change during aerobic training? consequence?

A

increases muscle myoglobin content by 75-80% which supports the muscle’s increased capacity for oxidative metabolism after training

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17
Q

how does muscle mitochondria content change with aerobic training?

A

doubles within 5 weeks of training, then plateaus

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18
Q

what types of mitochondria are increased with endurance training?

A

both subsarcolemmal (SS) and intermyofibrillar (IMF) mitochondria

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19
Q

what does increasing volume of mitochondria in muscle fibers result in?

A

improved oxidative phosphorylation capacity and ability to utilize fat as fuel

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20
Q

how does aerobic training affect mitochondrial turnover?

A

training increases the breakdown of damaged mitochondria and replacement with healthy mitochondria (increases turnover)

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21
Q

term for breakdown of damaged mitochondrial

A

mitophagy

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22
Q

how does increased mitochondrial volume affect ADP levels? what does this result in?

A

increased mitochondrial volume decreases cytosolic [ADP] due to increased ADP transporters in mitochondrial membrane, which results in less lactate and H+ formation and less PC depletion

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23
Q

how does endurance training affect the O2 deficit at the onset of work? how?

A

endurance training reduces the O2 deficit at the onset of work; because more mitochondria can increase oxidative capacity

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24
Q

does aerobic training affect the absolute amount of oxygen consumed at a given work rate once steady state is reached?

A

no, does not change amount of oxygen consumed at a given workload once steady state is reached (still costs the same amount of oxygen)

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25
Q

how does low muscle glycogen influence endurance training-induced adaptations?

A

low muscle glycogen induces higher activation of PGC-1alpha (signaling molecule) which leads to increased protein synthesis and mitochondria formation

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26
Q

2 approaches to create low muscle glycogen, what may be a disadvantage to each?

A

1) restrict dietary carbs: may cause fatigue and limit training
2) train twice per day (every other day): second training session with lower muscle glycogen (lower performance)

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27
Q

effect of exercise duration on muscle fuel source

A

increased exercise duration increases fat utilization and decreases carb utilization

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28
Q

how do endurance trained athletes compare to untrained individuals with regards to fuel source?

A

endurance trained athletes use more fat and less carb than less-fit athletes during prolonged exercise at the same intensity

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29
Q

2 methods by which endurance training affect free-fatty acid and glucose utilization?

A

1) increased mitochondrial number —> increased beta oxidation enzymes
2) increased capillary density —> slows blood flow in muscle and increased FFA transporters —> increased uptake and utilization of FFA —> spares plasma glucose

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30
Q

how does increased mitochondrial volume with endurance training improve acid-based balance during exercise? (2 ways)

A

1) increased mitochondrial number —> increased FFA oxidation and decreased PFK activity —> decreased pyruvate —> decreased lactate and H+ formation —> blood pH maintained
2) increased mitochondrial number —> increased mitochondrial uptake of pyruvate and NADH —> decreased lactate and H+ formation —> blood pH maintained

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31
Q

how does endurance training affect the lactate threshold?

A

with endurance training, the lactate threshold occurs at a higher percentage of one’s VO2 max

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32
Q

which is more important in improving VO2 max: intensity or duration?

A

intensity

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33
Q

ideal exercise intensity that shows the greatest improvement in VO2 max

A

80% of VO2 max

34
Q

what factors determine VO2 max? what equation?

A

VO2 max is the product of maximal cardiac output and arteriovenous difference (Fick equation)

VO2 max = HR max x SV max x max(a-vO2) diff

35
Q

how does cardiac output change with endurance training?

A

max cardiac output increases with endurance training

36
Q

how does endurance training affect heart size?

A

cardiac muscle mass and ventricular volume increase as an adaptation to the increased work demand

37
Q

how does endurance training affect resting heart rate?

A

resting heart rate decreases markedly (bradycardia)

38
Q

how does endurance training affect submaximal and maximal heart rate?

A

heart rate is lower at any given absolute exercise intensity, but max heart rate typically remains unchanged (or may slightly decrease)

39
Q

how does endurance training affect recovery heart rate?

A

heart rate returns to resting level much more quickly after an exercise bout than it does before training

40
Q

because heart rate max does not change or decreases, how can there be an increase in VO2 max? (Fick equation)

A

adaptations in stroke volume max and (a-vO2) difference max

41
Q

how do short duration training programs (approx. 4 months) compare to longer duration training programs (approx. 28 months) in terms of improvements in VO2 max?

A

with short duration training, the dominant factor in increasing VO2 max is an increase in stroke volume

with longer duration training, both stroke volume and a-vO2 increase to improve VO2 max

42
Q

how does aerobic training affect stroke volume?

A

stroke volume plateaus at a higher workload after training (and may not plateau with elite athletes)

43
Q

3 factors increasing stroke volume

A

1) increased preload (EDV)
2) increased contractility
3) decreased afterload

44
Q

3 factors increasing end diastolic volume

A

1) increased plasma volume
2) increased filling time and venous return
3) increased ventricular volume

45
Q

what factor does endurance training specifically change that leads to an increase in stroke volume? when does this effect have a larger influence?

A

increases total blood volume –> increased plasma volume and increased volume of red blood cells
(this effect is larger at higher training intensities)

46
Q

what happens if the change in plasma volume & number of red blood cells isn’t exactly proportional?

A

decreased hematocrit (pseudoanemia) - it looks like the number of red blood cells decreased, but they didn’t, the increase in plasma volume was just slightly larger

47
Q

how does endurance training affect ventricular filling?

A

improves ventricular filling due to bradycardia

48
Q

2 mechanisms of how endurance training affects the max (a-vO2) difference

A

1) increased muscle blood flow (decreased SNS vasoconstriction at same absolute workload)
2) improved ability of the muscle to extract oxygen from the blood (increased capillary density and increased mitochondrial number)

49
Q

why does the respiratory system NOT usually limit performance?

A

ventilation can be increased to a much greater extent than cardiovascular function

50
Q

how does endurance training affect lung structure and function at rest? what adaptations does the respiratory system undergo?

A

no effect on lung structure and function at rest; pulmonary ventilation changes to maximize efficiency

51
Q

how does endurance training affect pulmonary ventilation?

A

pulmonary ventilation is lower during submaximal exercises and maximal pulmonary ventilation is substantially increased

52
Q

how do females and males compare in max pulmonary ventilation?

A

males typically have a higher max pulmonary ventilation (they have bigger lungs)

53
Q

during detraining, what is the initial decrease in VO2 max (12 days) due to? do HR and a-vO2 diff change?

A

decreased max stroke volume; HR and a-vO2 diff remain unchanged

54
Q

during detraining, what is the later decrease in VO2 due to?

A

decreased max a-vO2 diff

55
Q

why does max a-vO2 diff decrease later in detraining?

A

due to decreased mitochondria (no change in capillary density)

56
Q

time course of mitochondrial changes during detraining

A

mitochondrial adaptations lost very quickly, requires 3-4 weeks of retraining to regain mitochondrial adaptations

57
Q

describe the lack of transfer of training effect

A

the responses of the cardiovascular, pulmonary, and sympathetic nervous systems are more dependent on the trained state of the muscles involved in the activity than on some specific adaptations in those systems (endurance training on one leg does not transfer to the other)

58
Q

define muscular endurance

A

ability to make repeated contractions against a submaximal load

58
Q

define muscular strength

A

maximal force a muscle or muscle group can generate (1 rep max)

59
Q

difference between high-resistance training and low-resistance training

A

high-resistance (6-10 reps until fatigue): results in strength increases
low-resistance (35-40 reps until fatigue): results in increases in endurance

60
Q

unlike endurance training, when one arm is exposed to resistance training, a portion of the training is “transferred” to the other arm, why?

A

neural adaptations

61
Q

2 changes in skeletal muscle size with resistance training

A

1) hyperplasia: increase in muscle fiber number
2) hypertrophy: increase in cross-sectional area of muscle fibers (due to increased muscle proteins - actin and myosin)

62
Q

what is responsible for early gains (8-20 weeks) in strength?

A

neural adaptations including:
1) increased number of motor units recruited
2) increased firing rate of motor units
3) increased motor unit synchronization
4) improved neural transmission across neuromuscular junctions
5) increased agonist activity, decreased antagonist activity

63
Q

does hyperplasia occur in humans?

A

probably not

64
Q

how does resistance training change muscle fiber type?

A

increase in cross sectional area of all fiber types but there is a shift from fast fibers to slow fibers (shift in cross-sectional area from type IIx to type IIa)

65
Q

why would muscle fiber types shift from type IIx to type IIa during strength training?

A

increased oxidative capacity allows more energy production over long periods of time (multiple reps for multiple sets - in every sport, even the gym)

66
Q

how does resistance training lead to muscle hypertrophy?

A

resistance training –> mTOR activation –> protein synthesis –> muscle hypertrophy

67
Q

how does ingesting protein influence muscle protein synthesis?

A

ingesting protein increases the rate of protein synthesis for both endurance and resistance training

68
Q

how do genetics influence the magnitude of resistance training-induced hypertrophy?

A

genetics account for 80% of the difference in muscle mass between individuals

69
Q

how does detraining after resistance training affect the muscles?

A

muscle atrophy due to decreased protein synthesis and increased protein breakdown (muscle takes a lot of energy to maintain)

70
Q

how does the rate of decline of detraining with resistance training compare to that of endurance training?

A

rate of detraining (strength loss) is slower and recovery of dynamic strength loss can occur more rapidly with retraining

71
Q

why does retraining with resistance training happen much faster than endurance training?

A

because of muscle myonuclei (stick around)

72
Q

how does combining strength and endurance training affect strength gains?

A

combining strength and endurance training limits strength gains

73
Q

3 potential mechanisms of why strength gains are limited when you combine endurance and strength training (one with strong evidence)

A

1) neural factors: impaired neural unit recruitment (limited evidence)
2) overtraining: no direct evidence
3) depressed protein synthesis: endurance training cell signaling can interfere with protein synthesis (strongest evidence)

74
Q

how does endurance training cell signaling interfere with protein synthesis?

A

endurance training –> increases AMPK –> AMPK inhibits mTOR –> inhibits protein synthesis

75
Q

does concurrent training impair training-induced increases in endurance?

A

no

76
Q

what should athletes do to avoid decreases in strength with concurrent training?

A

perform strength and endurance training on alternate days for optimal strength gains, or avoid concurrent training if your sport requires maximal strength

77
Q

describe the “ten percent rule.” what does this strategy mitigate?

A

increase intensity or duration less then or equal to 10% per week; mitigates overtraining

78
Q

symptoms of overtraining

A

decrease in performance, chronic fatigue, weight loss, increased infections, elevated heart rate and blood lactate levels during exercise

79
Q

how does heart rate change with overtraining in comparison to untrained

A

heart rate will be higher than their trained heart rate, but not as high as untrained heart rate

80
Q

describe the concept of tapering

A

short-term reduction in training load prior to competition which allows muscles to resynthesize glycogen and heal from training-induced damage

Exercise Physiology (25 decks)

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