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Exercise Physiology > Chapter 13, 14, 20 > Flashcards

Chapter 13, 14, 20 Flashcards

1
Q

overload

A

the need to stress the body in order to create adaptations
increased capacity of a system in response to training above the level to which it is accustomed

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2
Q

what are the 3 key components of overload

A

intensity
duration
frequency

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3
Q

can you have too much overloading

A

yes which would lead to overtraining or overreaching

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4
Q

reversibility

A

when training is stopped, the training gains are lost quickly

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5
Q

specificity: training effect is specific to

A

muscle fibers recruited during exercise
type of contraction (eccentric or concentric)
energy system involved (aerobic vs anaerobic)

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6
Q

suppose you test the VO2 max of highly trained rowers, cyclists, skiers on uphill running on a treadmill and then during their sport specific activity. What changes in VO2 max would be observed?

A

VO2 max attained by all athletes during their SPORT specific activity was as high or higher than the values obtained on the treadmill

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7
Q

influence of sex on training

A

men and women respond similarly to training programs even though exercise training Rx should be personalized

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8
Q

how does fitness level relate to training improvement

A

training improvement is always greater in individuals with lower initial fitness

50% increase in VO2 max in sedentary adults
10-20% improvement in normal, active subjects
3-5% improvement in trained athletes

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9
Q

influence of genetics on training

A

genetics plays an important role in how people respond to training, however is not the only factor as variability still exists

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10
Q

high responders (genotype E)

A

individuals with the ideal genetic makeup required for champion endurance athletes
posses a relatively high untrained VO2 max

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11
Q

low responders (genotype A)

A

possess a relatively low untrained VO2 max
often exhibit limited exercise training response

such as McArdles patients

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12
Q

what is more genetically determined: aerobic or anaerobic capacity

A

anaerobic capacity is more genetically determined than aerobic capacity

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13
Q

can training improve anaerobic performance

A

only to a small degree

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14
Q

what anaerobic capacity largely dependent on

A

fast type IIx fibers which is determined early in development

even if you increase hypertrophy, if you don’t have a lot of these fibers it is hard to increase performance

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15
Q

3 main pillars of performance

A

VO2 max
economy
LT/VT - how close to VO2 max can I sustain HR for longer

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16
Q

adaptations in muscle as a result of endurance training

A

repeated excitation and contraction of muscle fibers during endurance training stimulate changes in their structure and function

changes seen in:
muscle fiber type
capillary density
Mb content
mitochondrial function
mitochondrial oxidative enzymes

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17
Q

as a result of endurance training what happens to muscle fiber type

A

fast to slow shift in muscle fiber type

reduction in the cross sectional area of fast fibers and increase in the number of slow fibers

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18
Q

magnitude of muscle fiber type change is determined by

A

duration, training, type of training, and genetics

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19
Q

as a result of endurance training what happens to capillary density

A

increased number of capillaries surrounding muscle fibers leading to enhanced diffusion of O2 (since moving blood as slowly as possible) and the improved removal of wastes

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20
Q

as a result of endurance training, what happens to Mb content

A

endurance training increases muscle Mb content by 75-80% which supports a muscles increased capacity for oxidative metabolism after training

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21
Q

time course of training mitochondrial changes

A

muscle mitochondria adapt quickly to training

the # of muscle mitochondria doubles within 5 weeks of training

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22
Q

endurance training effects of mitochondrial volume

A

endurance training increases the volume of both sarcolemmal (SS) and intermyofibrillar (IMF) mitochondria in muscle fibers

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23
Q

as a result of increased volume of SS and IMF mitochondria, what happens to oxidative capacity

A

improved oxidative capacity and ability to utilize fat as fuel

share workload across other mitochondria (1 mitochondria- use CHO, 2+ mitochondria, use FATs)

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24
Q

endurance training effects on mitochondrial turnover

A

increases mitochondrial turnover (which is the breakdown of damaged mitochondria and replacement with healthy mitochondria)

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25
Q

mitophagy

A

the breakdown of damaged mitochondria

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26
Q

significance of increased mitochondrial volume

A

increased mitochondrial volume results in greater capacity for oxidative phosphorylation meaning more energy
increased mitochondrial volume also decreases cytosolic [ADP] due to increased ADP transporters in mitochondrial membrane resulting in less lactate and H+ formation and less PC depletion

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27
Q

effects of endurance training on O2 deficit

A

reduces the O2 deficit at the onset of work
reach steady state faster

faster rise in O2 uptake = less lactate formation and less PC depletion

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28
Q

exercise induced signaling : primary and secondary signaling molecules

A

primary and secondary signaling molecules contribute to exercise induced adaptation to endurance training

3 primary signals and 6 secondary signals

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29
Q

what is the main secondary signal

A

PGC-1a

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30
Q

why is low muscle glycogen a positive influence on endurance training induced adaptations

A

low muscle glycogen activates PGC-1a and promotes increased protein synthesis and mitochondria formation

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31
Q

two approaches to the increase in PGC-1a

A

1) restrict dietary CHO - but this may cause fatigue and limit training
2) train twice per day (every other day) which should lead to the second training session having lower muscle glycogen

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32
Q

as exercise duration increases what happens to substrate utilization

A

decrease in CHO and an increase in FAT utilization due to low muscle glycogen stores

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33
Q

endurance trained athletes: substrate utilization

A

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

shifts relative fat oxidation graph up and left

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34
Q

training effects on lactate threshold

A

in a trained state, one can exercise at a higher % of one’s VO2 max before lactate begins to accumulate in the blood
shifts LT to the right

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35
Q

cardiovascular adaptations that occur in response to endurance training

A

changes in
VO2 max
Q
heart size
HR (resting, submax, max, and recovery)
SV
Blood volume
(a-v)O2 difference

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36
Q

effects of training on VO2 max

A

VO2 max is increased with 12 months of endurance training

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37
Q

what exercise intensities show the greatest improvement in VO2 max

A

intensities ~80% VO2 max

38
Q

what is the most important factor in improving VO2 max?

A

intensity NOT duration

39
Q

what can be used as an estimate of an athletes relative training intensity

A

measurement of exercise HR

40
Q

calculation of VO2 max

A

product of max Q and (a-v)O2 difference

VO2 max= HRmax x SVmax x max(a-v)O2 difference

or VO2 max= Qmax x (a-v)O2 difference

41
Q

effects of training on cardiac output

A

increases with training

42
Q

effects of endurance training on heart size

A

as an adaptation to increased work demand, cardiac muscle mass and ventricular volume increase with endurance training
(increase in chamber radius and left ventricular hypertophy)

43
Q

effects of endurance training on resting heart rate

A

decreases markedly as a result of endurance training

can be as low as 30-40 bpm in highly conditioned endurance athletes (bradycardia)

44
Q

effects of aerobic training on HR

A

aerobic training results in a lower HR at any given absolute exercise intensity

45
Q

effects of aerobic training on maxHR

A

maxHR typically remains relatively unchanged (or may slightly decrease) after training

46
Q

effects of endurance training on recovery HR

A

after endurance training, HR returns to resting level much more quickly after an exercise bout than it does before training

47
Q

increases in VO2 max depend on adaptations in

A

SV max and max (a-v)O2 difference

not HRmax because it stays the same or decreases

48
Q

improvements in VO2 max during short duration (4 months) training is due to

A

increase in SV

49
Q

the improvements in VO2 max after a longer duration of training (~28 months) is due to

A

increases in SV and (a-v)O2 difference

50
Q

effects of endurance training on SV

A

SV will plateau at a much higher workload if trained

51
Q

endurance training effects on blood volume

A

increases total blood volume and this effect is larger at higher training intensities

increase plasma volume, increase volume of RBCs, decrease hematocrit

52
Q

why is an increase in plasma volume a good thing

A

prevents decreases in SV due to loss of fluids due to sweat

increase blood volume= increase in SV in longer duration exercises

53
Q

why is there an increased SV at rest in endurance athletes

A

improved ventricular filling due to bradycardia

54
Q

why might SV not plateau in elite athletes

A

improved ventricular filling
increase in EDV and SV at a high HR

55
Q

(a-v)O2 difference

A

amount of O2 delivered as you go from arteries to veins

arteries deliver O2 to capillaries and remaining O2 in veins goes back to the heart

56
Q

factors increasing (a-v)O2 difference

A

increased muscle blood flow due to decreases SNS vasoconstriction at the same work load

improved ability of the muscle to extract O2 from the blood

57
Q

what is involved in the improved ability of muscle to extract O2 from the blood

A

increased capillary density (slowed blood flow through muscle)
increased mitochondrial number (more O2 molecules dropped off at mitochondria which increases the drive for O2 to be delivered from Hb to Mb)

58
Q

does the respiratory system limit performance

A

the respiratory system does NOT limit performance because ventilation can be increased to a much greater extent than cardiovascular function

59
Q

training effects on lung structure and function

A

no effect at rest

60
Q

effects of training on pulmonary ventilation

A

ventilation is lower during submaximal exercise following training
max pulmonary ventilation is substantially increased

61
Q

detraining: first 12 days

A

initial decrease in VO2max due to decrease SV max (12 days)
HR and (a-vO2) difference remained the same or increased

62
Q

detraining: after 12 days (later effect)

A

later decrease in VO2 max due to decrease in (a-vO2) max
due to a decrease in mitochondria but no change in capillary density

63
Q

time course of detraining mitochondrial changes

A

mitochondrial changes are lost quickly with detraining
requires 3-4 weeks of retraining to regain mitochondrial adaptations

64
Q

lack of transfer: endurance events

A

if I train one leg, no ability to transfer training to another leg

65
Q

muscular strength

A

maximal force a muscle or muscle group can generate
1 repetition max (1-RM)

66
Q

muscular endurance

A

ability to make repeated contractions against a submaximal load

67
Q

strength training

A

high resistance training (6-10 reps till fatigue)
low resistance training (35 to 40 reps till fatigue)

68
Q

high resistance training results in

A

strength increases

69
Q

low resistance training results in

A

endurance

70
Q

transfer : resistance training

A

unlike endurance training, when one arm is exposed to resistance training, a portion of the training is “transferred” to the other arm due to neuromodulation that occurs with strength training

71
Q

what is responsible for early gains in strength due to resistance training

A

neural adaptations for initial 8-20 weeks

72
Q

adaptations in initial 8-20 weeks as a result of resistance training

A

increased neural drive
- increased number of motor units recruited
- increased firing rate of motor units
-increased motor unit synchronization
-improved neural transmission across neuromuscular junction

changes in rate of agonist/antagonist activation

73
Q

hyperplasia

A

increase in the number of muscle fibers
does not occur in humans

74
Q

hypertrophy

A

increase in cross sectional area of muscle fibers
due to increased muscle proteins (actin and myosin) which increases cross bridges and increases force production

(adding sarcomeres in parallel)

75
Q

what is the dominant factor in resistance training induced increases in muscle mass

A

hypertrophy

76
Q

resistance training effect on muscle fiber type

A

fast to slow shift in fiber type (from type IIx to IIa) due to increased oxidative capacity which increases ATP available to muscles

5-11% change following 20 weeks of training

77
Q

mTOR activation

A

resistance training
downstream effect
activate mTOR
protein synthesis
hypertrophy

**just stacking muscle fibers in parallel and increasing numbers of myonuclei not changing the number of fibers themselves

78
Q

consequences of ingesting proteins

A

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

plan protein intake around workouts (amount and timing)

79
Q

genetic influence on resistance training induced hypertrophy

A

approx 80% of differences in muscle mass between individuals is due to genetic variation

80
Q

why does inactivity induced muscle atrophy occur

A

due to decreased protein synthesis and increased protein breakdown

81
Q

cessation of resistance training results in

A

muscle atrophy and loss of strength

82
Q

compared to endurance training, the rate of strength loss (detraining) in resistance training is

A

slower

83
Q

compared to endurance training, the recovery of dynamic strength loss can occur ___ with resistance retraining

A

rapidly (within 6 weeks)

84
Q

what types of training may reduce strength gains

A

combined strength and endurance training may limit strength gains vs strength training alone

  • depends on training state of subject, volume and frequency of training, and integration of methods
  • endurance training >3 days/week and 40-40 min/day
85
Q

why does a combination of endurance and strength training decrease gains

A

1) neural factors - fatigue
2) overtraining = fatigue
3) depressed protein synthesis

86
Q

depressed protein synthesis as a result of endurance and strength training together

A

endurance training interferes with protein synthesis via inhibition of mTOR by activation of AMPK

AMPK activated during exercise which inhibits mTOR which inhibits protein synthesis and muscle hypertrophy decreasing strength

87
Q

recommendations for concurrent strength and endurance training

A
  • perform strength and endurance training on alternate days for optimal STRENGTH gains
  • athletes whose sport requires maximal strength should avoid concurrent training

*the performance of combined strength and endurance training does NOT impair training induced increases in ENDURANCE

88
Q

periodized training programs

A

varies the training load over time to achieve acute overload and some overreaching while avoiding overtraining

89
Q

10% rule for increasing training load

A

increasing intensity or duration < 10% / week

90
Q

what indicates optimal psychological adaptations and performance

A

overreaching

91
Q

tapering

A

short term reduction in training load prior to competition
allows muscles to resynthesize glycogen and heal from training induced damage
improves performance in both strength and endurance events (athletes can reduce training load by 60% without a reduction in performance)

Exercise Physiology (8 decks)

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