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KIN 269 > TRAINING PERFORMANCE > Flashcards

TRAINING PERFORMANCE Flashcards

1
Q

What is training overload?

A

Training effect occurs when a system is exercised at a level beyond which it is normally accustomed

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2
Q

What is training specificity?

A

Training effect is specific to:

Muscle fibers recruited during exercise.

Energy system involved (aerobic versus anaerobic).

Velocity of contraction.

Type of contraction (eccentric, concentric, isometric).

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3
Q

What is training reversibility?

A

Gains are lost when overload is removed

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4
Q

Research Designs to Study Training?

A

Cross-sectional studies

Longitudinal studies

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5
Q

What are the Cross-sectional studies of training?

A

Examine groups of differing physical activity at one time

Record differences between groups

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6
Q

What are the Longitudinal studies
of training?

A

Examine groups before and after training

Record changes over time in the groups

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7
Q

How do you perform Training to increase VO2 max?

A

Large muscle groups, dynamic activity

20–60 min, 3–5 times/week, 50–85% VO2 max

Intervals: 2-5 min, 95%, x 8-10 repeats

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8
Q

When training what are the Expected increases in VO2 max?

A

Average = 15 - 20%

2–3% in those with high initial VO2 max

Requires intensity of 95–100% VO2 max

30–50% in those with low initial VO2 max

Training intensity of 40–70% VO2 max

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9
Q

What is the genetic predisposition to increasing VO2 max?

A

Accounts for 40%–66% VO2 max

Prerequisite for VO2 max of 60–80 mLkg–1min–1

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10
Q

What is The HERITAGE Family Study?

A

Designed to study the role of genotype in cardiovascular, metabolic, and hormonal responses to exercise and training

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11
Q

What were the results of The HERITAGE Family Study?

A

Heritability of VO2 max is ~50%

Maternal contribution is ~30%

Large variation in change in VO2 max with training

Average improvement 15–20%

Ranged from slight decrease to 1 L/min increase

Heritability of change in VO2 max is 47%

Difference genes for sedentary VO2 max and change in VO2 max with training

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12
Q

What is the Product of maximal cardiac output and arteriovenous difference (Fick Equation)?

A

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

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13
Q

What are the Differences in VO2 max in different populations?

A

Primarily due to differences in SV max

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14
Q

What are the Improvements in VO2 max?

A

50% due to (up arrow) SV (central component)

50% due to (up arrow) a-vO2 (peripheral component)

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15
Q

Factors Increasing Stroke Volume?

A

Increased stroke volume

Increased end diastolic volume (“pre-load”)

Increased contractility

Increased plasma volume

Increased filling time and venous return

Increased ventricular volume

Decreased peripheral resistance (“afterload”)

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16
Q

What is stroke volume?

A

Increased maximal stroke volume

increased Preload (EDV)
increased Plasma volume
increased Venous return
increased Ventricular volume

decreased Afterload (TPR)
decreased Arterial constriction
increased Maximal muscle blood flow with no change in mean arterial pressure

increased Contractility

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17
Q

Changes occur rapidly in stroke volume when?

A

11% ↑ in plasma volume, 7% ↑ VO2 max, and 10% ↑ in stroke volume within first six days of endurance training.

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18
Q

Why Do Some Individuals Have High VO2 Max Values Without Training?

A

Some individuals have very high VO2 max values with no history of training

VO2 max = 65.3 mlkg–1min–1

Compared to 46.3 mlkg–1min–1 in sedentary with low VO2 max

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19
Q

Higher VO2 max is due to?

A

Higher maximal cardiac output, stroke volume, and lower total peripheral resistance

No difference in a-vO2 difference or maximal heart rate

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20
Q

Higher stroke volume linked to?

A

Higher blood volume and red cell volume

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21
Q

Arteriovenous O2 Difference?

A

increased Muscle blood flow

decreased SNS vasoconstriction

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22
Q

Improved ability of the muscle to extract oxygen from the blood causes?

A

increased Capillary density
increased Mitochondial number

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22
Q

Improved ability of the muscle to extract oxygen from the blood causes?

A

increased Capillary density
increased Mitochondial number

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23
Q

Explain The a-vO2 diff—Arterial O2 Content?

A

Hemoglobin (Hb)—1 molecule of Hb carries 4 molecules of O2, and 100 ml of blood contains ~14-18 g of Hb in men and ~12-14 in women (1 g of Hb combines with 1.34 ml of oxygen).

There are ~20.1 ml of O2 per 100 ml of arterial blood (15 g of Hb  1.34 ml of O2/g of Hb) in men and ~17.4 ml of O2 per 100 ml of arterial blood (13 g x 1.34) in women.

Low iron leads to iron-deficiency anemia, reducing the body’s capacity to transport oxygen—this is more of a problem in women than men.

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24
Q

The ability to perform prolonged, submaximal exercise is dependent on the ability to maintain homeostasis, how is this possible?

A

Endurance exercise training results in numerous adaptations in muscle fibers that assist in maintaining homeostasis.

Shift in muscle fiber type (fast-to-slow) and increased number of capillaries.

Increased mitochondrial volume.

Training-induced changes in fuel utilization.

Increased antioxidant capacity.

Improved acid-base regulation.

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25
Q

What happens during a Fast-to-slow shift in muscle fiber type?

A

Reduction in fast fibers and increase in number of slow fibers.

Magnitude of fiber type change determined by duration of training, type of training, and genetics.

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26
Q

Increased number of capillaries surrounding muscle fibers causess?

A

Enhanced diffusion of oxygen.

Improved removal of wastes.

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27
Q

How does endurance training increases the volume of both subsarcolemmal and intermyofibrillar mitochondria in muscle fibers?

A

Results in improved oxidative capacity and ability to utilize fat as fuel.

Training also increases mitochondrial turnover (that is, breakdown of damaged mitochondria and replacement with healthy mitochondria).

Breakdown of damaged mitochondrial is termed “mitophagy.”

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28
Q

What is the Significance of Increased Mitochondrial Volume?

A

Increased mitochondrial volume results in greater capacity for oxidative phosphorylation.

However, during submaximal exercise, the steady-state VO2 is not influenced by endurance training.

Increased mitochondrial volume also decreases cytosolic [ADP] due to increased ADP transporters in mitochondrial membrane-results in:

Less lactate and H+ formation.

Less PC depletion.

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29
Q

What is the Influence of Mitochondrial Volume on Cytosolic ADP Concentration during Submaximal Exercise?

A

Increases in the number of ADP transporters in mitochondrial membrane = faster ADP uptake into mitochondria and lower cytosolic [ADP]

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30
Q

What is Citrate synthase (CS)?

A

Marker of mitochondrial oxidative capacity

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31
Q

What is the effect of exercise intensity with Citrate synthase (CS)?

A

55%, 65%, or 75% VO2 max

Increased CS in oxidative (IIa) fibers with all training intensities

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32
Q

What is the Effect of exercise duration with Citrate synthase (CS)?

A

30, 60, or 90 minutes

No difference between durations on CS activity in IIa fibers

Increase in CS activity in IIx fibers with higher-intensity, longer-duration training

33
Q

What does Endurance Training-Induced Changes in Fuel Utilization do?

A

Increased utilization of fat and sparing of plasma glucose and muscle glycogen.

Increased transport of FFA into the muscle.

Increased capillary density.

Increased fatty acid binding protein and fatty acid translocase (FAT).

34
Q

Transport of FFA from the cytoplasm to the mitochondria causess?

A

Higher levels of carnitine palmitoyltransferase and FAT

35
Q

What does Mitochondrial oxidation of FFA do?

A

Increased enzymes of β-oxidation.

Increased rate of acetyl-CoA formation.

High citrate level inhibits PFK and glycolysis.

36
Q

What does Contracting skeletal muscles produce free radicals promote?

A

Radicals promote oxidative damage and muscle fatigue

37
Q

Training increases endogenous antioxidant enzymes by?

A

Improves the fibers ability to remove radicals.

Protects against exercise-induced oxidative damage and muscle fatigue.

38
Q

Lactate production during exercise equation?

A

pyruvate + NADH —-> lactate + NAD

—-> (LDH)

39
Q

Training adaptations include?

A

Increased mitochondrial number.

Less carbohydrate utilization = less pyruvate formed.

Increased NADH shuttles.

Less NADH available for lactic acid formation.

Change in LDH isoform.

Heart form (H4) has lower affinity for pyruvate = less lactic acid formation.

40
Q

Endurance and resistance exercise training promotes what?

A

protein synthesis in fibers.

Exercise “stress” activates gene transcription

41
Q

Process of training-induced muscle adaptation causes?

A

Muscle contraction activates primary and secondary messengers.

Results in expression of genes and synthesis of new proteins.

mRNA levels typically peak in 4 to 8 hours, back to baseline within 24 hours.

Daily exercise required for training-induced adaptation.

42
Q

Explain how m i RNAs are small molecules that decrease protein synthesis by blockade of mRNA.

A

More than 700 m i RNAs exist in humans.

Endurance training and resistance training results in decreases in the levels of several different m i RNAs.

Exercise-induced decreases in specific m i RNAs likely contribute to the exercise-induced training response to both endurance exercise and resistance exercise.

43
Q

Primary and secondary signals lead to muscle adaptations lead to?

A

Increased protein synthesis.

44
Q

Specific muscle adaptive responses depends on?

A

exercise stimulus.

Resistance vs. endurance training.

Intensity and duration of training.

45
Q

Primary signals responsible for exercise-induced adaptation cause?

A

Mechanical stretch (resistance training).

Calcium (endurance training).

A M P/A T P (endurance training).

Free radicals (endurance training).

46
Q

What are the Secondary Messengers in Skeletal Muscle?

A

AMP kinase (AMPK).

Mitogen-activated kinase (p38).

PGC-1α.

47
Q

What is AMP kinase (AMPK)?

A

Important signaling molecule activated during endurance exercise; promotes glucose uptake and linked to gene expression by activation of transcriptional activating factors.

48
Q

What is Mitogen-activated kinase (p38)?

A

Important for signaling.

49
Q

What is PGC-1α?

A

Master regulator of mitochondrial biogenesis; promotes angiogenesis (that is, increased capillarization) and synthesis of antioxidant enzymes.
Activated by p38 and CaMK.

50
Q

What is Calmodulin-dependent kinases (CaMK)?

A

Activated by increases in cytosolic calcium-promotes activation of PGC-1α.

51
Q

What is Calcineurin (phosphatase)?

A

Participates in numerous adaptive responses of muscle including fiber regeneration and a fast-to-slow shift in fiber type.

52
Q

What is Nuclear factor kappa B (NFκB)?

A

Activated by radicals-promotes synthesis of antioxidant enzymes.

53
Q

What is mTOR?

A

Protein kinase-major regulator of protein synthesis and muscle size.

54
Q

What are the Biochemical adaptations to training influence the physiological response to exercise?

A

Sympathetic nervous system (decreased E/NE)

Cardiorespiratory system (decreased HR, decreased ventilation)

55
Q

Biochemical adaptations to training influence the physiological response to exercise is due to?

A

Reduction in “feedback” from muscle chemoreceptors

Reduced number of motor units recruited

56
Q

Biochemical adaptations to training influence the physiological response to exercise demonstrated in one-leg training studies. How was this possible?

A

Lack of transfer of training effect to untrained leg

More recent research has shown increased adaptations in the other non-exercised leg

57
Q

Training-induced reductions in HR and ventilation due to?

A

Training results in improved muscle homeostasis during exercise and reduced “feedback” from muscle chemoreceptors to cardiovascular control center.

Less feedback to cardiovascular control center from group 3 and group 4 nerve fibers (responsive to temperature and biochemical changes).

Reduced number of motor units recruited.

58
Q

Training-induced reductions in HR and ventilation due to?

A

Training results in improved muscle homeostasis during exercise and reduced “feedback” from muscle chemoreceptors to cardiovascular control center.

Less feedback to cardiovascular control center from group 3 and group 4 nerve fibers (responsive to temperature and biochemical changes).

Reduced number of motor units recruited.

59
Q

Decrease in VO2 max with cessation of training causes?

A

decreased SV max
Rapid loss of plasma volume

decreased Maximal a-vO2 difference
decreased Mitochondria
decreased Oxidative capacity of muscle
decreased Type IIa fibers and  type IIx fibers

Initial decrease (12 days) due to decreased SV max

Later decrease due to decreased a-vO2 max

60
Q

What happens to mitochondria during training?

A

Mitochondria double with five weeks of training

61
Q

What happens to mitochondria during detraining?

A

About 50% of the increase in mitochondrial content was lost after one week of detraining

All of the adaptations were lost after five weeks of detraining

It took four weeks of retraining to regain the adaptations lost in the first week of detraining

62
Q

How long does Muscle mitochondria adapt quickly to training?

A

Double within 5 weeks of training.

63
Q

How fast does Mitochondrial adaptations lost quickly with detraining?

A

Loss of 50% of training gain within 1 week of detraining.
Majority of adaptation lost in two weeks.

Requires 3 to 4 weeks of retraining to regain mitochondrial adaptations.

64
Q

What is Anaerobic exercise?

A

Refers to short-duration (that is, 10 to 30 S) all-out exercise (sprint training).

Recruits both type 1 and 2 muscle fibers.

During exercise <10 seconds, energy is primarily supplied by ATP-PC system.

During exercise lasting 20 to 30 seconds, 80% of energy needed is provided anaerobically whereas remaining 20% is provided aerobically.

65
Q

How does Anaerobic training increase performance? How long does it take?

A

4 to 10 weeks of sprint training can increase peak anaerobic power by 3 to 28% across individuals.

Sprint training improves muscle buffering capacity by increasing both intracellular buffers and hydrogen ion transporters.

Sprint training also results in hypertrophy of type 2 muscle fibers and elevates enzymes involved in both the ATP-PC system and glycolysis.

High intensity interval training >30 seconds (at near or above VO2 max) promotes mitochondrial biogenesis.

65
Q

How does Anaerobic training increase performance? How long does it take?

A

4 to 10 weeks of sprint training can increase peak anaerobic power by 3 to 28% across individuals.

Sprint training improves muscle buffering capacity by increasing both intracellular buffers and hydrogen ion transporters.

Sprint training also results in hypertrophy of type 2 muscle fibers and elevates enzymes involved in both the ATP-PC system and glycolysis.

High intensity interval training >30 seconds (at near or above VO2 max) promotes mitochondrial biogenesis.

66
Q

How do Marathon run alters immune system?

A

Elevated neutrophils, reduced lymphocytes and natural killer cells

Decreases in NK and T-cell function

Decreases in nasal neutrophil activity

Decreases in nasal and salivary IgA concentrations

Increases in pro-inflammatory cytokines

67
Q

What is the “Open window” hypothesis?

A

Immune suppression following marathon increases risk of infection

68
Q

What is the “Open window” hypothesis?

A

Immune suppression following marathon increases risk of infection

69
Q

What is Muscular strength?

A

Maximal force a muscle or muscle group can generate

1 repetition maximum (1-RM)

70
Q

What is Muscular endurance?

A

Ability to make repeated contractions against a submaximal load

71
Q

What is Strength training?

A

Percent gain inversely proportional to initial strength

Genetic limitation to gains in strength

High-resistance (2–10 RM) training

Gains in strength

Low-resistance training (20+ RM)

Gains in endurance

72
Q

Why does Strength training results in increased muscle size and strength?

A

Initial 6-12 weeks
Neural adaptations
Improved ability to recruit motor units
Learning, Coordination

Long-term training (12+ weeks)
Muscle hypertrophy
High-intensity training can result in hypertrophy with 10 sessions

73
Q

What is hypertrophy?

A

Enlargement of both type I and II fibers

Low-intensity (high RM), high-volume training results in smaller type II fibers

Heavy resistance (low RM) results in larger type II fibers

No increase in capillary density

74
Q

What is Hyperplasia?

A

Increase in muscle fiber number

Mainly seen in long-term strength training

Not as much evidence as muscle hypertrophy

75
Q

How does the Decline in strength after age 50?

A

Loss of muscle mass (sarcopenia)

Loss of both type I and II fibers

Atrophy of type II fibers

Loss of intramuscular fat and connective tissue

Loss of motor units

Reorganization of motor units

76
Q

What is Progressive resistance training?

A

Causes muscle hypertrophy and strength gains

Important for activities of daily living, balance, and reduced risk of falls

77
Q

What are Traditional training programs?

A

Variations in intensity (RM), sets, and repetitions

78
Q

What is Periodization?

A

Also includes variation of:
Rest periods, type of exercise, number of training sessions, and training volume

Develop workouts to achieve optimal gains in:
Strength, power, motor performance, and/or hypertrophy

Linear and undulating programs
Variations in volume/intensity over time

More effective than non-periodized training for improving strength and endurance

79
Q

What are the Potential for interference of adaptations?

A

Endurance training increases mitochondrial protein

Strength training increases contractile protein

Depends on intensity, volume, and frequency of training

80
Q

Why do the Studies show conflicting results?

A

Depends on intensity, volume, and frequency of training

Strength is compromised

KIN 269 (4 decks)

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