In this talk, I will focus on apoptotic pathways that have been
shown to be active in skeletal muscle during periods of muscle loss.
Apoptosis in skeletal muscle occurs under
various conditions and in pathological and non-pathological perturbations.
This include but are not limited to muscle loading,
aging, muscle disuse, and denervation.
Conditions of extreme muscle loading and bulky apoptotic signaling,
perhaps in part, a result of
muscle damage or increases in oxidative stress to the muscle.
Although resistance exercise has been used to offset muscle loss with aging,
sarcopenia or muscle wasting with age is inevitable.
Apoptosis has a role in regulating sarcopenic loss of muscle fiber number,
controlling atrophy of the existing muscle fibers,
and regulating at least in part the degree
to which hypertrophy can occur in loaded muscles.
Unloading and disuse, whether by prolonged bed rest or experimentally
in animals reduces muscle mass and invokes apoptotic signaling.
Denervation by loss of the motor nerve to the muscle,
whether by directly severing the nerve or by
spinal cord injury results in massive muscle loss,
and this is accompanied by increased apoptotic signaling in the muscle.
Apoptosis in skeletal muscle is more precisely described as nuclear apoptosis.
Why this distinction for nuclear apoptosis?
Muscle fibers are multinucleated and consisted both post-mitotic myonuclei,
and Dorman's satellite cells,
so they're capable of proliferation.
Unlike single-cell systems, which die if the nucleus is eliminated by apoptosis,
the elimination of a single nucleus may make muscle fiber a little bit smaller,
but it will not result in the death of the multinucleated muscle fiber.
Many nuclei must die and be eliminated before the entire muscle cell dies.