Fatigue & Recovery Flashcards
fatigue
“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
CNS fatigue
- malfunction of neurons
- inhibition of voluntary effector (motor cortex)
- psychological factors
PNS fatigue
-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)
ATP-PC depletion
after sprint training, HIIT workouts
- PCr can deplete to 15% of starting value
- ATP rarely goes below 40%
glycogen and glucose depletion
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
metabolite accumulation
accumulation in H, Ca, and Pi cause fatigue
H+ accumulation (during exercise)
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
Ca accumulation (during exercise)
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
Pi accumulation (during exercise)
(from breakdown of ATP) just as important as H accumulation
- decrease Ca released from SR and ability to bind at troponin
heat accumulation (in exercise)
Heat cause fatigue beacause inhibit enzymes to work and can denature them
-hypothalamus is incharge of heat regulation
- exertional heat illnessw
Free radicals
an atom that has lost or gained an electron
free radical accumulation
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
impaired oxygen delivery
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
CNS neural fatigue
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
PNS neural fatigue
regulation of acetylcholine (ACh) at motor end plate (NMJ) decreases muscle membrane excitability
traditional human model of fatigue
muscle fatigue»_space; unable to continue
muscle fatigue»_space; sense of effort
Psychobiological model of fatigue
muscle fatigue»_space; sense of effort (including non physical ways )»_space; decision to stop
mental fatigue
mental exertion»_space; increase cerebral adenosine (decrease dopamine and motivation)»_space; increase perception of effort»_space; decrease performance
CHO mouth rinse
CHO mouth rinse can trick oral receptors in brain to think glucose is coming later, which stimulates reward and motivation areas of the brain
factors influencing fatigue
hydration (too much or little)
environment (hot, cold, altitude, wind, pollution)
nutrition
trained state
muscle fiber type
equipment, technology, clothing
efficiency, technique
psychological factors
recovery from exercise
physiological process that returns an individual to resting state
- EPOC (excess post-exercise Oxygen consumption)
- VO2 is still high after ending exercise
Exercise post oxygen consumption (EPOC)
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
oxygen deficit
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
trained vs untrained
trained subjects have higher aerobic bioergenetic capacity (cardio and muscles)
- trained people have aerobic ATP production faster than untrained
EPOC phases
fast: oxygen consumption post exercise drops quickly (2-3 minutes)
slow: o2 consumption post exercise tapers off (3-60 min)
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
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
Removal of H+ (Lactic System recovery)
half time 5-8 min in muscle pH (12-20 min)
Removal of La (Lactic System recovery)
half time 12-20 min in muscle La (1hr)
Blood Ph (Lactic System recovery)
half time 10-20 min, full 30-60 min
Blood La (Lactic System recovery)
half time 15-25 min, full 1hr
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
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)
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
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
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
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
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
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
