exercise induced muscle damage Flashcards
what causes muscle soreness
pain sensitive receptors (afferent neurons) are repsonsive to mech deformation and intramuscular metabolic disturbance
- fibres project to the CNS and promote the sensation of pain
what does eccentric exercise cause
decreased force output
highest soreness after first bout
- second bout = less soreness and less decrease in force output
what is the benefit of RBE
ability of the muscle to rapidly adapt to the damage from eccentric exercise to prevent further damage
what are the events leading to muscle damage from eccentric exercise
- overstretch of a muscle
- disrupted sarcomeres
- EC coupling disruption
- local contracture (increase in passive tension)
- swelling and soreness
what is sarcomere inhomogeneity
weaker sarcomeres are stretched beyond myofilament overlap
most of the length is taken by weakest half sarcomeres in myofilament
what is the popping sarcomere hypothesis
uncontrolled extension of individual half sarcomeres in each myofibril
- occurs one at a time - weakest to strongest
each sarcomere is stretched until half sarcomere is popped
- passive tension (titin) is able to support the sarcomere integrity until further stretch damages the titin as well
what is EC coupling disruption
t-tubule rupture releases calcium
torn tubule ends leads to inactivation of some sarcomeres
results in fall in muscle tension and force output
- entire EC coupling is disrupted due to muscle damage ((t-tubules and SR)
what is involved in local contracture (increase in passive tension)
rise in passive tension after eccentric exercise
muscle length is shorter and becomes stiff
increased stiffness = reduced ROM = reduced joint angle
peaks around 48-72 hours after exercise
what are the potential mechanisms for increase in passive tension
- increases in resting Ca2+ levels in muscle fibres due to damage
- shortening of parallel, non contractile elements in the muscle (titin)
what is the pain experienced during muscle contraction after eccentric exercise related to
- damage and shortening of the non contractile elements (muscle mechanical stiffness)
- damage to muscle fibre membranes (shown by an increase in CK enzyme)
- can be measured by blood draw
- shows a huge spike in CK around 48-72 hours - activation of group III/IV afferents
what is RBE
magnitude of muscle damage is attenuated in a subsequent exercise bout after performing a single bout of exercise
- less swelling of muscle
- smaller increases in CK
- less abnormalities in muscle structure in imaging
what is responsible for RBE
adaptations of muscle fibres and/or connective tissue
- neural adaptations are not totally discarded
how long does RBE last
literature - 6-9 months based on the magnitude of muscle damage in initial bout
- doesn’t make sense in real life
what are the mechansims underlying RBE
neural
mechanical
cellular - longitudinal addition of sarcomeres
how does the increase in sarcomeres in parallel occur
- eccentric contraction results in muscle damage
- contractions at longer muscle length = mroe damage + more symptoms
- addititonal sarcomeres in series created during the repair