The aging process (AKA 30 years of age onwards), in the presence of high ROS (reactive oxygen species) and/or damaged mitochondrial DNA, can induce widespred mitochondrial dysfunction. In the healthy cell, mitophagy results in the removal of dysfunctional mitochondria and related material. In the abscence of functional removal of unwanted mitochondrial material, a retrograde and anterograde signalling process is potentially instigated, which results in both motor neuronal and muscle fibre apoptosis (death) (Alway, Mohamed, Myers 2017, Ex Sp Sc Rev, 45, 2, 58-69). This process is irreversible. Investigations in healthy populations, have shown that regular exercise improves the ability to cope with regular oxidative stress by the buffering and 'mopping up' of ROS agents which are induced as a result of exercise. It is plausible and highly probable that regular exercise throughout life can mitigate against muscle fibre death (Sarcopenia). Importantly, this process of muscle fibre death can commence in the 4th decade of life. and be as much as 1% per year. Reduction of muscle mass can result in immune and metabolic compromise, including subclinical inflammation, type II diabetes as well as the obvious reduction in functional capacity for activities of daily living.
See : Sarcopenia and Aging
Published 11 July 2017