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exercise is med > background > Flashcards

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1
Q

rest exercise transision

A
  1. Oxygen uptake increases rapidly (steady within 1-4mins)
  2. Oxygen deficit- lag in oxygen uptake at begining of ex.
    - Suggests anaerobic pathways contribute to total ATP prod
    - after steady state is reached ATP requirement is met thru aerobic ATP prod
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2
Q

2 Portions of EPOC

A 
FAST
- 20%
- resynthesis of stored PC
-replenishing muscle + blood O2 stores
SLOW
-80%
-elevated body temp and catecholamines
-conversion of lactate and glucose
elevated HR and ventilation
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3
Q

Redistribution of blood flow during ex

A

larger % to muslces
withdrawl of sympathetic vasoconstriction
decrease O2 tension + PH
- increase capillary recruitment

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4
Q

Cardio changes during ex (SBP, SV, CO, HR, AVO2)

A

SBP - increases
SV- goes up then levels off at 40% because it cant fill w enough blood when pumping fast
CO, HR, AVO2- increases

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5
Q

What 2 things determine magnitude of adaptation following ex

A
  1. genetics

2. initial training status

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6
Q

Cardiac adaptations w exercise

A
  1. cardiac remodeling- increase ventricular chamber size (fillable volume)
  2. Complience of heart wall increases (increase EDV and SV)
  3. Cardiac hypertrophy
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7
Q

Stims that trigger adaptation

A

Stretch (preload)
Afterload ( concentric hypertrophy)
Neurohumoral
metabolic

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8
Q

Endurance training effect on vasculature

A

Angiogenesis

  • increase # of capillaries
  • increase # of capillaries in parallel w eachother
  • Increase potential to decrease resistance when there is appropriate vasodialation
  1. Improved control of vaso dialation and recruitment of capillary netwroks
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9
Q

Effects of having more capillaries

A
  • increase in max skeletal BF
  • Increase in surface area for diffusional exchange (increase twists and turns)
  • increase in twists + turns help prevent very fast travel of RBC and time for diffusion is maintained
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10
Q

Sarcolemma

A

outer surface membrane that surrounds entire muscle cell (excitable)

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11
Q

T-Tubules

A

Invagination of the sarcolemma into the fibres interior along a line vertical to fibre axis

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12
Q

Sarcoplasmic reticulum

A
  • extensive muscle membrane system surrounding myofibril

- plays key role in regulation of intracellular ca (stores and releases)

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13
Q

Steps in excitation contraction coupling

A
  1. AP is generated
  2. Ach is released @ neuromuscular junction
  3. AP conducted along sarcolemma + into T tubules
  4. Triggers Ca release from SR
  5. Ca binds to troponin removing tropomyosin from myosin binding cite on actin
  6. Power stroke of myosin moves actin
  7. Excitation stops + Ca is pumped from cytosol back into SR, Ca disociates from troponin
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14
Q

Mitocondrial bigenesis after endurance training

A
  • size and number of mitochondria increase
  • more triglyceride storage in muscle
  • enhanced FFA delievery to muscle during ex
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15
Q

increase in mitochondral biogenesis after endurance training leads to

A

increase fat oxidation

-decrease in glycolosys, CHO utalization, PCr hydrolysis, blood lactate accumulation

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16
Q

Tight vs loose metabolic control

A

tight- over broad range of metablic and work rates PCR, P, ATP, ADP show very minmal changes despite large increases in ATPase and mitocondrial ATP synthesis

17
Q

resistance training neural adaptation

A
  1. increased activation of agonist (possible to increase firing rates too)
  2. reduced antagonist coactivation
  3. muscle training provides strong stim that activates neuroendocrine system ( GH, IGF1, Test)
18
Q

What is hypertrophy due to

A

translational capacity + # of myonuclei

  • increase in ribosomal translation= produce more pro
  • satellite cells can become myonuclei= more ribosomes= more translation of pro
19
Q

Mitochondrial biogenesis pathway

A

exercise–> increase AMP–> AMPK—> PGC1a–> FA oxidation, mitochondrial biogenesis, angiogenesis

20
Q

3 key players on mitochondrial biogenesis

A

NRF1/2- increase transcription, Activates tFam
Tfam- increas mtDNA transcription, coordinate mRNA response
PGC1a- coactivate NRF

21
Q

moderate and exessive amounds of ROS effects

A

mod

  • signaling molecule for body
  • upregulates HSP
  • PGC1a upregulation (mitochondriagenesis, muscle hypertrophy)

Exess

  • muscle damgage (activated neutrophils)
  • ischemia reprofusion
22
Q

Calcium as a signiling molecule

A

ca–> calcineurin–> hypertrophy, IL6

–> too much–> calpain–> pro breakdown

23
Q

Moderate levels of IL6

A

decrease TNFa, increase neurtraphils + macrophages activates AMPK path, antinflammatory, angiogenesis

24
Q

Irisin

A

increase UCP-1, fat cell browning

25
Q

UCP-1

A

decreases hydrogen gradient producing heat instead

26
Q

changes that occur with transision to physical inactivity (skeletal muscle + adipose tissue)

A

mucle- decreased fatty acid oxidation, decrease muscle mass, decrease insulin signaling

adipose- increase adipose mass, increase cell volume, increase FFA traficking to triglyceride storage

27
Q

Metabolic syndrom what do you need

A

3 OF-

  • high BP
  • high blood glucose
  • excess body fat around waist
  • high blood triglyceride
  • reduce HDC

exercise is med (5 decks)

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