peripheral fatigue Flashcards
fatigue
failure to maintain the required or expected force/power
stimulation of mucle in vivo- effects of fatigue
Not able to reach same force level
Increase in force is flattened- takes longer to reach plateau
Takes longer for muscle to relax
sites of fatigue
determining whether fatigue is located centrally or peripherally
electrical stimulation of a muscle
if individual can perform the movement with the stimulaton then it shows the brian is stopping the muscle from contracting
energy required duirng muscle work
excitation- contraction couple (ATP dependent)
myosin head force development
Na+ K+ ATPase to resting potential
calcium pump- ca2+ is released but also needs to come back into sarcoplasmic reticulum
in an energy crisis or if enzyme activties drop, these processes could impair performance
calcium release leads to contraction
ca2+ binds to troponin, moves tropomyosin out of the way
troponin is on actin
movement allows myosin head to attach
force and calcium
type 1 vs type 2 fibres
t2 fibres fatigue quickly
t1 fibres are almost unfatiguable
Ca conc much lower in in t2 after lower number of reps
ca2+ and caffiene
caffiene facilitates opening of ryanodine receptors in sacro reticulum membrane, releasing calcium
ca2+ release
inhibitory effects
- high AMP
- high ADP
- very low ATP - little effect in range of 2-8mmol/L
- Mg2+- conc doubles at fatigue as ADP, AMP + IMP have lower affinity for mg2+ than atp
reducing ATP conc (fatigue) - calcium release drops further
increasing AMP or IMP- calcium release drops further again
ca2+ reuptake
once released, must be taken back up into SR
quicker it is taken up, quicker muscle can relax
Na+K+
Na+K+ atpase acitivty is depressed at fatigue
this powers nak+ pump to restore the resting potential of a cell following an action potential
taking longer to establish resting potential will delay the time it takes to build up force again
pottasium
K gradient will affect action potentials
- fatigue= accumalation of K+ in extracellular space
- T tubular membrane- large surface
- T tubular network- small volume
- rapid K+ accumalation- due to small colume but large SA
- more difficult to induce action potential
inorganic phosphate
implicated/contributes to fatigue
Pi or H3PO4
pi rises with contraction time (as pcr is broken down), this increase is associated with a decline in force production
can form calcium phosphate (cahpo4) and reduce amount of free calcium
inorganic phosphate can bind calcium - taking calcium away from our use
pH
importance of physiological range
decrease in pH cannot explain fatigue alone
some studies show muscle fatigue at only moderate drops of pH
long lasting activity - little or no acidosis (marathon)
force typically recovers much faster than pH
activation of ca2+ release not noticeably inhibited even at 6.2pH
patients with McArdles disease dont accumalate H+ but do fatigue
pH can induce fatigue due to chainging the optimal range of enzymes but there are other components to consider
atp depletion
studies report that atp in a cell doesnt drop below 60% of resting levels (in whole muscle)
isolated fibres- down to 20%- atp concentrations are not the same as whole muscle
localised atp depletion possible in space between t tubule and SR
areas where most atp are being produced- pumps and myosin head
are ca+ and Na+K+ affected- cant tell exactly where ADP drops most
compartmentalisation
argument by many reseaerchers to explain apparent contradictions
metabolite concentrations vary within different compartments of the cell
ADP is tightly regulated and doesnt accumalate
ATP average levels do not fall far enough to affect cross bridge function
H+ does seem to play minor role in physiological conditions
