Crosstalk between Mitochondria and Myofibrils in Adult and Aging Striated Muscle Tissue: Effect of Increased Functional Activity

There has been much debate about changes of oxidative capacity in aging skeletal and heart muscle,
and endurance capacity. Physiological changes during aging are associated with a decline in muscle
mass, strength and endurance capacity. These changes in muscle structure and function are leading
to disability in the aging population. The purpose of the present review is to discuss about decrease of
oxidative capacity in adult and aging striated muscle tissue, changes in interaction between
mitochondria and myofibrils and loss in life quality; describe the effect of increased functional activity
(endurance exercise) on the oxidative metabolism. Decrease of endurance capacity (ability to keeo
moving for longer time) during aging is related with reduced oxidative capacity of skeletal muscle due
to decrease of mitochondrial biogenesis. Striated muscle cells with high oxidative capacity during
endurance exercise hypertrophy. Muscle fibres with lower and low oxidative capacity do not
hypertrophy during endurance type of exercise. Skeletal muscle respond to endurance exercise
training by increasing the fibre composition towards increase of fibres with higher oxidative capacity at
the expense of proportion of fibres with low oxidative capacity. Decease of oxidative capacity in
muscle tissue lead to the decrease of muscle quality, cause disability and loss in life quality of aging
population. Endurance exercise training is the effective way to increase the oxidative and endurance
capacity.