Fatigue & Recovery Flashcards

1
Q

fatigue

A

“loss of capacity for developing force and/or velocity of muscle resulting in muscle activity underload, reversible by rest”
- depletion and accumulation of substances
- type, intensity, duration of exercise
- energy systems associated

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2
Q

CNS fatigue

A
  • malfunction of neurons
  • inhibition of voluntary effector (motor cortex)
  • psychological factors
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3
Q

PNS fatigue

A

-peripheral nerve (alpha motor neuron)
- neuromuscular junction (inhibition of axon terminal, depleted neurotransmitters, altered bind to receptors)
- muscle fiber
- t tubule (unable to release Ca or Ca not bind to troponin)
- contractile elements (depleted ATP, PC, GLY; accumulation of H, PO4, La)

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4
Q

ATP-PC depletion

A

after sprint training, HIIT workouts
- PCr can deplete to 15% of starting value
- ATP rarely goes below 40%

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5
Q

glycogen and glucose depletion

A

less muscle glycogen = less glyco(geno)lysis = less pyruvate and thus less acetyl-coA = less OAA = slower Krebs = less CHO/fat metabolism = less NADH and FADH2 made = less ETC function = less ATP

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6
Q

metabolite accumulation

A

accumulation in H, Ca, and Pi cause fatigue

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7
Q

H+ accumulation (during exercise)

A

since enzymes work at a certain pH level, increasing H can lower the pH and make it acidic, which is not workable for lots of enzymes in metabolism

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8
Q

Ca accumulation (during exercise)

A

Especially after eccentric muscle work.
Too much ca will cause:
-mito. to well and change in tissue molarity
- Pain (DOMS)
- local ischemia and more pain

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9
Q

Pi accumulation (during exercise)

A

(from breakdown of ATP) just as important as H accumulation
- decrease Ca released from SR and ability to bind at troponin

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10
Q

heat accumulation (in exercise)

A

Heat cause fatigue beacause inhibit enzymes to work and can denature them
-hypothalamus is incharge of heat regulation
- exertional heat illnessw

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11
Q

Free radicals

A

an atom that has lost or gained an electron

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12
Q

free radical accumulation

A

contracting skeletal muscles produce ROS (reactive oxygen species) and RNS, (reactive nitrogen species) which can damage proteins in dysfunction and fatigue
- can modulate gene expression
- trainable

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13
Q

impaired oxygen delivery

A

due to high intensity aerobic exercise, pollution or altitude there can be “desaturation” of Hb (less O2 attaching)
- exercise induced arterial hypoxemia
- less aerobic metabolism = more anaerobic metabolism = more H = fatigue

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14
Q

CNS neural fatigue

A

less blood glucose to the brain impairs ood and CNS
- less TRP (AA) across BBB, meaning less serotonin (bad mood)
- more plasma H means less motivation, drive, pain tolerance
- impair motor unit recruitment

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15
Q

PNS neural fatigue

A

regulation of acetylcholine (ACh) at motor end plate (NMJ) decreases muscle membrane excitability

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16
Q

traditional human model of fatigue

A

muscle fatigue&raquo_space; unable to continue
muscle fatigue&raquo_space; sense of effort

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17
Q

Psychobiological model of fatigue

A

muscle fatigue&raquo_space; sense of effort (including non physical ways )&raquo_space; decision to stop

18
Q

mental fatigue

A

mental exertion&raquo_space; increase cerebral adenosine (decrease dopamine and motivation)&raquo_space; increase perception of effort&raquo_space; decrease performance

19
Q

CHO mouth rinse

A

CHO mouth rinse can trick oral receptors in brain to think glucose is coming later, which stimulates reward and motivation areas of the brain

20
Q

factors influencing fatigue

A

hydration (too much or little)
environment (hot, cold, altitude, wind, pollution)
nutrition
trained state
muscle fiber type
equipment, technology, clothing
efficiency, technique
psychological factors

21
Q

recovery from exercise

A

physiological process that returns an individual to resting state
- EPOC (excess post-exercise Oxygen consumption)
- VO2 is still high after ending exercise

22
Q

Exercise post oxygen consumption (EPOC)

A

amount of oxygen consumed after exercise stops in an effort to replace oxygen lost at beginning of exercise in oxygen deficit phase and usually lasts 2-3 minutes after exercise stops
- harder intensity of exercise = higher EPOC
- burn calories while EPOC is high
- aka recovery VO2

23
Q

oxygen deficit

A

period of time at start of exercise when aerobic system hasn’t caught up to anaerobic system and O2 takes a while to get to its steady state of consumption
- “inertia of metabolsim”
- trainable

24
Q

trained vs untrained

A

trained subjects have higher aerobic bioergenetic capacity (cardio and muscles)
- trained people have aerobic ATP production faster than untrained

25
EPOC phases
fast: oxygen consumption post exercise drops quickly (2-3 minutes) slow: o2 consumption post exercise tapers off (3-60 min)
26
Causes of EPOC
fast: restored intramuscular PCr (aerobic), restore O2 Mb and Hb, elevated cardio-respiratory functions slow: La removal, oxidation, GNG; shift from using CHO to fats; increased body temp and heat dissipation; elevated hormones (E, NE); elevated cardio-respiratory
27
ATP-PC recovery
half time of 10-20 sec, full recovery 2-8 minutes - need energy (ATP) from aerobic system (send ADP to ETC) - recover passively W:R of 1:3
28
Removal of H+ (Lactic System recovery)
half time 5-8 min in muscle pH (12-20 min)
29
Removal of La (Lactic System recovery)
half time 12-20 min in muscle La (1hr)
30
Blood Ph (Lactic System recovery)
half time 10-20 min, full 30-60 min
31
Blood La (Lactic System recovery)
half time 15-25 min, full 1hr
32
passive vs active recovery
- BLa decreases faster with active recovery, typically cardio at self selected pase - best for intermittent sports (hockey, soccer) who build up La and need to release it - light - moderate
33
aerobic system recovery
After heavy training muscle glycogen levels lower, want to restore it - T1/2 for glycogen recovery = 5-6 hrs. Full = 24-48 hrs best replenishers of glycogen: - need time to rest and recover - Adequate dietary intake (take simple CHO during and immediately after exercise, take complex carbs after every 2 hours until ~500 g are taken)
34
Training improving recovery
↑ enzymes (CK, LDH) ↑ capillarization (remove waste) ↑ oxidative capacity (lactate metabolism) ↑ buffering capacity (H+ removal) ↑ sensitivity of CNS and PNS sensitivity to phys. mech. less byproducts made for same exercise before
35
Relief Ratios (ATP-PC, Glycolysis, & Aerobic)
ATP-PC: WI = 1-10s W:R ratio = 1:3 - 1:20 Glycolysis: WI: 10-90s W:R ration: 1:2 - 1:5 Aerobic: WI: >90s W:R ratio: 1:1/2 - 1:3
36
Exercise-Induced Muscle Damage (EIMD) and Delayed Onset Muscle Soreness (DOMS)
unaccustomed exercise (often eccentric) that stimulates events that: - diminish performance - ultrastructural damage - initiates inflammatory reaction
37
Muscle damage and DOMS
EIMD leads to inflammation > pain, tender, stiff = DOMS - Creatine Kinase can leak into blood from muscles if they are damaged, good way to indicate damage
38
Muscle Repair
-inflammatory cells fill in gap at damaged muscle, send for satellite cells - satellite cells come when called by WBC and make myoblasts -Myoblasts turn into myotubes -myofibrillar synthesis and assembly - regenerate muscle fiber
39
Repeated bout effect
A bout of unfamiliar exercise result in DOMS - Following recovery, another bout of same exercise results in minimal injury - Addition of sarcomeres = less strain - More ST motor unit recruitment - cytoskeletal changes - limited proliferation after EIMD
40