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HES 403 > chapter 13: effects of aerobic and anaerobic trainings > Flashcards

chapter 13: effects of aerobic and anaerobic trainings Flashcards

1
Q

principles of training: overload

A

must be stressed beyond which it is accustomed to achieve training adaptation.

  • continual progression results in improved function over time (manipulating intensity, duration, and frequency)
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2
Q

reversibility

A

gains achieved from overload can be quickly lost if you stop

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3
Q

specificity

A

specific to the muscles involved in activity, fiber types recruited, principal energy system (aerobic vs. anaerobic), velocity of contraction, type of muscle contraction

  • types of adaptation occurring in muscle (aerobic = increased capillaries and mitochondria volume & resistance training = increase quantity of contractile proteins)
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4
Q

what does training do to VO2max?

A

increased max cardiac output
and difference of how much O2 is removed from arteries and used by tissues

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5
Q

in untrained individuals over a short duration what physiological parameters are changed?

A
  • Vo2 max, max cardiac output, no sig fig in max Vo2 difference (arterial and tissue use of O2)
  • all training improvement is due to max cardiac output increases
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6
Q

what are the long term changes seen with endurance training

A

all parts increase (Vo2 max, cardiac output, and tissue use of O2)

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7
Q

How does EDV increase stroke volume

A
  • higher end diastolic volume increased stretch of left ventricle (frank-starling)
  • plasma increased (can occur rapidly)
  • over the years can increase left ventricle with little change in wall thickness
  • increased filling time associated with slower heart rate at rest
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8
Q

cardiac contractility

A

increase force of ventricular contraction

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9
Q

afterload

A

the pressure the heart has to overcome to pump blood out
- decreases after max exercise due to reduced vasoconstriction activity (SNS)
- mean arterial blood pressure remains unchanged

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10
Q

why does endurance training increase ateriovenous O2 difference

A

increase in O2 extraction from blood due to increase capillary density, decreases diffusion distance, slows blood flood rate to allow time for O2 diffusion.

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11
Q

endurance training changes to muscle fibers & capillaries

A
  • this type of training does not shift all fast to slow muscle fibers and is dependent on the years you have been endurance training (intensity as well)
  • increase capillaries it allow shorter distance for O2 and nutrients to travel (and removal of metabolic waste)
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12
Q

where are the two subpopulations of mitochondira?

A

subsarcolemmal & 80% is intermyofibrillar

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13
Q

where are intermyofibrillar mitochondria found?

A

around contractile proteins

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14
Q

what types and how fast can mitochondrial increase after working out?

A

both will increase within 1-5 days after in active skeletal muscle

primarily due to increased size not amount

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15
Q

how much can endurance training increase muscle mitochondrial volume

A

50-100% in first 6 weeks (dependent on duration and intensity of sessions)

  • increased endurance performance due to muscle metabolism changes
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16
Q

why is the increased ability to use fats as fuel source over carbs a good quality in mitochondria ?

A

prevents limited carb depletion

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17
Q

mitophagy

A

removal of damaged or old mitochondria by lysosome. this keeps the population healthy and large compared to untrained muscle fibers

  • helps keep oxidative capacity and metabolism of fats high
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18
Q

why is lower ADP in endurance athletes advantageous?

A

less stimulation of glycolysis (anaerobic glycolysis which creates lactate)
- higher phosphocreatine
- less disruption to homeostasis

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19
Q

blood glucose and endurance training

A

rely more on fat than carbs for fuel source which allows better maintenance of blood glucose

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20
Q

fat metabolism during exercise

A

increase fat metabolism and delivery of fat

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21
Q

what are the three training-induce adaptation to increase fat delivery

A
  1. increased capillary density to deliver fatty acids
  2. increase ability to transport fatty acids across sarcolemma
  3. improvement to moving fatty acids from cytoplasm into mitochondria (also increase number of mitochondria to metabolize)
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22
Q

why can trained individuals use more free fatty acids as fuel?

A

-increased fatty acid binding protein
- and (FAT translocase) that transports across sarcolemma into fiber & mitochondria (CPT-I &FAT)

22
Q

where does fat come from when using to exercise?

A

50% intramuscular and the rest is plasma free fatty acids

23
Q

how does enzymes of fatty acid cycle increase AcetylCoA?

A

allows us to go right into beta oxiation (FFA->citrate) spares carbs for liver and muscle

24
Q

what are free radicals?

A

chemical species with unpaired e- in outer orbital making them reactive with other cellular components usually produced from muscular contraction

  • antioxidants protect us against these
25
Q

where do you get antioxidents

A

endogenous antioxidents (made in body)
exogenous (get from diet)

26
Q

what is pH of arterial blood (7.40)

A
27
Q

how do you increase muscle buffering capacity?

A

HIIT

28
Q

how does endurance training cause less disruption to blood pH

A

produce less lactate and H+ ions

(less pyruvate from oxidation in Krebs cycle increase of being converted to lactate)

29
Q

how does endurance training decrease H+ amount

A

increase mitochondrial volume creates more “shuttles” to transport electrons (NADH) from cytoplasm into mitchondria

30
Q

what are the five isozymes of LDH present in muscle cells

A

M4,M3H, M3H2, MH3, and H4

endurance shifts LDH to H4 form which is less likely to produce pyruvate

31
Q

training adaptations “ big picture”

A

stress of exercise (regular bouts) causes increased production of mRNA and subsequent proteins to improve muscle function. have greatest increase in muscle proteins in first couple weeks than decreases as training accumulates

32
Q

what are the four primary signals for muscle adaptation during exercise

A
  1. mechanical stimuli
  2. increases in cellular Ca2+
  3. elevated free radicals
  4. decreases in muscle phosphate/energy levels
33
Q

mechanical stimuli

A

muscles can sense the different stress of endurance vs resistance training and when lifting weights you signal the mechanical stretch and it promotes contractile protein synthesis which results in hypertrophy

34
Q

calcium

A

neural activation of skeletal muscle results in release of Ca2+ from SR and depending on activity it will stay in cytoplasm for longer (endurance) or shorter (resistance) time and can lead to specific muscle protein creation

35
Q

free radicals

A

signal to create NFkB and p38 that promote expression of antioxidant enzymes that protect your muscle fibers against exercise induced oxidative stress

36
Q

what is AMPK

A

senses energy state of muscle that can be activated by HIIT or prolonged endurance training that leads to muscle adaptation
- stimulates glucose uptake and fatty acid oxidation during exercise
- activates transcription factors related to fatty acid oxidation and mitochondrial biogenesis

37
Q

PGC-1a

A
  • promotes mitochondrial biogenesis
    -regulates formation of new capillaries, shift from fast to slow muscle fibers, and antioxidant enzymes
  • muscle’s ability to metabolize fat and take up glucose
38
Q

how is CaMK activated?

A

increase CA2+ in cytoplasm
this kinase can activate PGC-1a

39
Q

what is a phosphatase

A

enzyme that removes phosphate group from molecules

40
Q

calciuneurin function

A

fiber growth & switch to slow muscle type

41
Q

what is mTOR

A

protein kinase that regulated protein synthesis and muscle size.

it is activated by mechanoreceptors on sarcolemma of muscle

42
Q

what is the function of primary signaling

A

signal exercise induced muscle adaptation and than signal secondary pathways to promote gene expression

43
Q

how much can VO2 max be changed through endurance trianing?

A

20-50%

44
Q

what primary and secondary signaling pathways have important role in exercise-induced fast to low fiber transformation?

A

PGC-1a & calcineurin

45
Q

what activates PGC-1a?

A

CaMK, AMPK, and p38

46
Q

what signals contribute to increased muscle antioxidants

A

PGC-1a & NFkB

47
Q

how does endurance training decrease heart rate and ventilation during exercise through peripheral feedback?

A

more mitochondria dont create as much waste product (lactate and H+ ions) so this reduced the peripheral feedback to the brain and does not stimulate increased HR and ventilation

48
Q

how does central command influence heart rate and ventilation?

A

higher areas in brain send AP to lower parts to influence cardiorespiratory response to exercise

49
Q

how does endurance training impact central command control (2 things) which results in lower sympathetic NS stimulation

A
  1. training improvements in muscle require lower motor unit recruitment so less drive from cardiorespiratory control is needed
  2. reduced central command to cardioresp centers
50
Q

what is the timeline for decrease in VO2 max (physiological differences that occur when training is stopped)

A
  1. first 12 days: decrease in stroke volume (decrease in plasma levels )
  2. day 21-84th: decrease in avO2 difference (lower mitochondria - but capillary density unchanged)
  3. oxidative capacity reduced and slow twitch changed back to fast twitch
51
Q

how does detraining impact endurance training?

A
  • decreased mitochondria amount (rapid onset but can drop by 50% within one week of no training)
52
Q

can you regain training level after stopping?

A

YES you will produce mitochondria quicker when retraining than start

53
Q

what is the percent decline in Vo2max after stopping training for 12 days? 84 days?

A
  1. 8%
    2.20%

HES 403 (5 decks)

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