Morphometric analysis of aging skeletal muscle following endurance training

Abstract

Aging of skeletal muscle in the hindleg of the mouse is accompanied by a progressive increase in the amount of the interstitial tissue and especially that of lipid cells and fibroblasts. Quantitative analysis indicates that there was a nonsignificant increase in the total number of muscle fibers per unit area, perhaps due to a splitting process. The proportion of high oxidative fibers was decreased to a nonsignificant degree, and the remaining high oxidative fibers underwent a significant compensatory hypertrophy. Concomitantly, the number of low oxidative fibers increased significantly. This study revealed that endurance training in young animals induced morphometric changes very similar to those noticed in intact aging animals (i.e., splitting phenomenon, hypertrophy of high oxidative fibers, and an increased proportion of low oxidative fibers). It also became apparent that the skeletal muscle of old animals lacks the capacity to respond to enforced training, except for a further increase in the proportion of low oxidative fibers. It appears that aging muscle is unable to adapt to changing environmental circumstances.

Differential expression of caveolins and myosin heavy chains in response to forced exercise in rats

“…Depending on the muscle type and the nature of the exercise, different studies have reported increases in oxidative capacity [8], the number and size of mitochondria [9], muscle weight [10], the appearance of split muscle fibers [11], and an altered distribution of muscle fiber types [4]. …”

Distribution of the Macromolecular Components of Masticatory Muscles during Differentiation of the Muscle Fibers in the Postnatal Rat

“…Immunochemical methods using monoclonal antibodies can differentiate between the heavy and light chains of myosin in the fast-oxidative muscle fibers (Zhang et al, 1989). In general, muscle fibers change their properties, with type I fibers being transformed into type II (Tauchi et al, 1971;Silberman et al, 1983;Fujimoto et al , 1994), and type II being transformed into type I during aging (Eddinger et al, 1985), and the activities of certain enzymes decrease. By contrast , various isoforms of myosin gradually replace each other during the postnatal development of rapidly contracting muscles (Hoh and Yeoh, 1979;Whalen et al, 1981;D'Albis et al, 1985).…”

Effects of Aging and Physical Training on the Neuromuscular Junction of the Mouse

“…The regimen of training employed did not further reduce CAT and AChE activities beyond the age-dependent changes observed. It is quite possible though that the age-associated decrement in enzyme activities can account for the reduced adapt ability of the muscle to exercise in old age.Physical exercise is known to induce mus cle hypertrophy in young mice, while in old mice it leads to atrophy and degeneration of muscle tissue [13]. Previous studies showed that skeletal muscle of old C57BL/6J mice, subjected to a regimen of 10 weeks of daily 30-min running sessions at a speed of 3.5 m/min, undergoes structural and bio chemical changes.…”