ABSTRACT
There has been much debate about mitochondrial function in muscle fibers with different oxidative capacity, and interaction between mitochondrial and contractile apparatus. Loss of energy is related to mitochondrial dysfunction and diminished production of ATP in muscle fibers results fatigue and exertion. The decline of muscle mass in elderly people is caused by type II fibers atrophy and loss in the number of fast-twitch muscle fibers. The efficiency of interaction between contractile apparatus and mitochondria depends on the oxidative capacity of muscle fibers. Hypoxia disturbs the connections between mitochondria and sarcomeres, sarcomeric structures disintegrate the muscle fiber structure and cause destruction and cell death. Apoptosis is one of the reasons of the intensive protein degradation, loss of muscle nuclei associated with atrophy of fibers. The intensive development of the mitochondrial apparatus, as a result of regular moderate muscle activity, is covered the increased energy requirements of muscle fibers, mainly fibers with higher oxidative capacity as a result of efficacy of ATP synthesis.
