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1

rest exercise transision

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

2

2 Portions of EPOC

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

3

Redistribution of blood flow during ex

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

4

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

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

5

What 2 things determine magnitude of adaptation following ex

1. genetics
2. initial training status

6

Cardiac adaptations w exercise

1. cardiac remodeling- increase ventricular chamber size (fillable volume)

2. Complience of heart wall increases (increase EDV and SV)

3. Cardiac hypertrophy

7

Stims that trigger adaptation

Stretch (preload)
Afterload ( concentric hypertrophy)
Neurohumoral
metabolic

8

Endurance training effect on vasculature

Angiogenesis
- increase # of capillaries
-increase # of capillaries in parallel w eachother
- Increase potential to decrease resistance when there is appropriate vasodialation

2. Improved control of vaso dialation and recruitment of capillary netwroks

9

Effects of having more capillaries

-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

10

Sarcolemma

outer surface membrane that surrounds entire muscle cell (excitable)

11

T-Tubules

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

12

Sarcoplasmic reticulum

-extensive muscle membrane system surrounding myofibril
- plays key role in regulation of intracellular ca (stores and releases)

13

Steps in excitation contraction coupling

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

14

Mitocondrial bigenesis after endurance training

-size and number of mitochondria increase
- more triglyceride storage in muscle
-enhanced FFA delievery to muscle during ex

15

increase in mitochondral biogenesis after endurance training leads to

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

16

Tight vs loose metabolic control

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

resistance training neural adaptation

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

What is hypertrophy due to

translational capacity + # of myonuclei
-increase in ribosomal translation= produce more pro
- satellite cells can become myonuclei= more ribosomes= more translation of pro

19

Mitochondrial biogenesis pathway

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

20

3 key players on mitochondrial biogenesis

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

21

moderate and exessive amounds of ROS effects

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

Exess
-muscle damgage (activated neutrophils)
-ischemia reprofusion

22

Calcium as a signiling molecule

ca--> calcineurin--> hypertrophy, IL6
--> too much--> calpain--> pro breakdown

23

Moderate levels of IL6

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

24

Irisin

increase UCP-1, fat cell browning

25

UCP-1

decreases hydrogen gradient producing heat instead

26

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

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

Metabolic syndrom what do you need

3 OF-
-high BP
-high blood glucose
- excess body fat around waist
-high blood triglyceride
-reduce HDC