Lecture 16 Flashcards
(22 cards)
Importance of ATP
needed for binding capacity, releasing energy hat gets myosin into cocked position, restoring intracellular Ca2+ in SR and maintaining electrochemical gradients of ions across sarcolemma
ATP sources
1) Free ATP (exhausts quickly)
2) Creatine phosphate is dephosphorylated, forming ATP (short duration exercise). Anaerobic lasts ~1min
3) Glycolysis (aerobic and anaerobic)
Isotonic contraction
constant level of tension. muscle changes length and movement is produced
isometric contraction
muscle length remains the same, movement produced, resists gravity/forces
Concentric contraction
muscle shortens, movement is produced
eccentric contraction
muscle is contracting but lengthening, controlled movement is produced
time to reach maximum tension
muscles with more fast twitch fibres will reach maximum length quicker than those with more slow fibres
factors influencing force
when sarcomeres are parallel (akin with fast twitch) and large diameter, increase capacity for force production while increasing amount of sarcomeres in series, increasing velocity but, does not increase capacity for greater tension or force produced. Intracellular Ca2+, O2 and ATP availability can be trained to increase capacity to generate tension. Muscle length determines amount of active force and passive force generation and fatigue.
Factors influencing fatigue
continuous exercise that decreases capacity for cross-bridge formation due to the build up of metabolites in the cellular environment. This may be extracellular K+ accumulation (when opening nicotinic cation channels, influx of Na+ and efflux of K+ occurs). Na/K/ATPase pump restores balance and allows you to take Ca2+ out of the cell, sacrificing extracellular buildup of K which will contribute to depolarisation and decrease capacity for firing. Decreases ability for Ca to be released from SR.
muscle acidosis
Buildup of lactic acid
Pi accumulation
when using lots of ATP, you accumulate lots of inorganic phosphate which can interfere with cross bridge cycling (less efficient release) and less efficient capacity to release Ca from SR.
ROS and RNS
Produced through ETC. React with proteins to decrease capacity of proteins to undergo necessary process for muscle contraction
Depletion of glycogen during glycolytic respiration
Lose capacity to generate glucose
summation
frequency of stim and Ca2+ release > Ca2+ clearance = summed AP to produce greater force than single twitch.
tetanus
when peak force is generated through summation
active motor neurons and fatigue
not until max. tension is reached that you lose capacity for cross bridge cycling and muscle fatigue
active motor neurons
more motor neurons = increase force size = increase depolarisation/hyperpolarisation events = increase muscle activity on EMG.
EMG
takes absolute value of depolarisation as it’s negative and it’s a tool to measure muscle activity, not APs
motor neuron innervation
motor neurons come down from motor cortex and can excite 3 branching motor neurons that innervate same muscle. Recruitment of motor unit is regulated by soma size. Smaller size = more likely to be depolarised at an amount that will engage voltage-gated Ca2+ channels at the Axon Hillock = response from smaller neuron. larger stimulus= increased AP fired (temporal summation) = activation of larger and larger motor units in series
load
decrease load = faster velocity that muscle can shorten
increase load = increases time to reach movement that is achievable (slower muscle contraction)
parallel elastic components
incl muscle cell membrane and titan. Supplies resistance when passively stretched.
series elastic components
tendons and titan. Acts as spring to store elastic energy. When a tensed muscle is stretched.
