Flashcards in background Deck (27)
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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
