Fatigue Flashcards
Factors effecting performance
event
genetics - strength/skill
energy demand
environ
diet
psychology
Fatigue
inability to maintain power output or force during repeated muscle contraction
reversible with rest
Central fatigue
CNS
reduction in motor units activated/firing frequency
CNS arousal = facilitate motor unit recruitment - increase motivation/physical or mental diversion
Overtraining - reduced performance, prolonged fatigue - related to brain serotonin activity/ratio to dopamine
Peripheral fatigue
neural factors
mechanical factors
energetics of contraction
Central Governor model
Noakes
conscious and subconscious brain
not spinal cord or motor unit
Psycho-biological model
Marcora
fatigue is conscious process
exercise persist if motivation greater than perceived exertion
Neural factors
neuromuscular junction - not site of fatigue
sarcolemma and transverse tubules - altered muscle membrane to conduction and action potentials
inability of Na+/K+ pump to maintain action potential amplitude/frequency - improved by training
action potential block in transverse tubules - reduced sarcoplasmic reticulum Ca2+ release
Mechanical factors - crossbridge cycling/tension
cross-bridge cycling and tension development depends on:
arrangement of actin and myosin
Ca2+ binding to troponin
ATP availability
Mechanical factors - H+ conc
high H+ conc contribute to fatigue
reduce force per crossbridge
reduce force generated at given Ca2+ conc
inhibit Ca2+ release from SR
Mechanical factors - end result
relaxation time longer
due to slower cross-bridge cycling
important in fast twitch fibres
Energetics of contraction - ATP
imbalance ATP requirements/ATP generating capacity
accumulation Pi = inhibit max force, reduce crossbridge binding to actin, inhibit Ca2+ release from SR
rate ATP utilization slowed faster than rate of ATP generation
maintain ATP conc
cell not run out of ATP
Energetics of contraction - muscle fibre
muscle fibre recruitment increasing intensities of exercise
type 1 –> type 2a –> type 2x
40% VO2max type 1 fibres recruited
type 2a fibres recruited at 40-75% VO2max
exercise >75% VO2max requires 2x fibres = increased lactate and H+ production
Radical production fatigue
exercise promotes free radical production
damage contractile proteins (myosin and troponin) = limit number cross-bridges in strong binding state
depress sodium/potassium pump activity = disruption potassium homeostasis
Antioxidant supplement
high antioxidant doses not impair muscle performance
N-actetyl-cytenine = delay exercise-induced muscle fatigue
high doses may depress adaptation in skeletal muscle
Ultra short-term performance
recruitment type 2 muscle fibres - generate great force
motivation, skill, arousal important
anaerobic energy source - ATP-PC system/glycolysis
creatine supplementation may improve performance
Short-term performance
anaerobic (70% at 10s) to aerobic (60% at 180s) metabolism
anaerobic glycolysis fuel = elevated lactate and H+ levels
interferes with Ca2+ binding with troponin
interferes with glycolytic ATP production
ingestion of buffers may improve performance
10-60s = fast twitch
60-180s = mix fast and slow
Moderate-duration performance
60% ATP generated aerobically 3m
90% ATP supplied aerobically 20m
high volume VO2max
high max SV
high arterial O2 content - haemoglobin content/inspired O2
requires energy expenditure near VO2max
type 2x fibres recruited
high levels lactate and H+ accumulation
Intermediate-duration performance
aerobic
<90% VO2max (high VO2max important)
running economy - high % type 1 fibres
environ- heat/hummidity
state hydration
lactate threshold
Long-term performances
aerobic
enviorn - heat/hummidity
maintain rate carb utilization - muscle/liver glycogen decline, ingest carb = maintain carb oxidation by muscles
consume fluids/electrolytes
VO2max maintain - depend on lactate threshold
running eceonomy - % type 1 fibres
Ultra-endurance events
VO2max
%VO2max that can be sustained
metabolic responses - increase fat oxidation, 50% reduction muscle glycogen stores
hyponatremia
foot management
