Accompanying to increasing number of aged people, the progressive loss of muscle strength and muscle mass, as sarcopenia, due to reduced physical activity, has resulted in a series of influence on the
quality of life for these aged people and highly economic burden. The quality and mass control of skeletal muscle during the lifetime is the requirement for the delayed decline of the function with
aging. The autophagy is a major cellular pathway to regulate protein and organelle turnover in skeletal muscle. Since the basal autophagy is regarded as the attenuation with the extension of age,
appropriate exercise training has revealed the enhanced autophagic signaling in aged mice. Furthermore, spermidine is a natural polyamine involved in many important cellular functions for the
extension of lifespan and improvement of life quality through the induction of autophagy.
In the present study, the effect of spermidine and exercise on the mass maintenance of skeletal muscle in D-galactose (D-gal) induced aging rat model. Sub-acute aging was induced in male SD rats by
subcutaneous injection of D-gal (200 mg/kg•d), and the rats were treated with spermidine (5 mg/kg•d, intraperitoneally) or/and swimming (60 min/d, 5d/wk) for 42 days. After sacrificed, the
gastrocnemius muscle samples were surgically harvested, and fixed with 10% neutral-buffered formalin. Other samples were stored at -80 ℃ for western blot assay.
In order to understand the skeletal muscle loss caused by D-gal exposure, we examined the ratio of gastrocnemius and body weight. In our study, the gastrocnemius of D-gal-treated rats exhibited
significantly decline when compared with that in the control group (t-test, n = 5; P < 0.001), suggesting that D-gal induces the loss of skeletal muscle mass in rats. The combinatorial intervention of
spermidine and exercise could accomplish the obvious protective effect on gal-induced impairments although the single intervention could not produce the satisfactory result. To characterize the
internal structure of muscle fibers, the morphology of the gastrocnemius after 6 weeks of exercise training and spermidine intervention, the structure of myofilament was improved. The expression level
of LC3B and Beclin-1 revealed an obvious increase due to the combinatorial intervention of exercise and spermidine. Therefore, the D-gal-induced decline of skeletal muscle mass could be slowed down
through the activated autophagy by exercise and spermidine.
Autophapy, as an important physiological process, can be activated by exercise and spermidine, which can ameliorate the D-gal-induced detrimental aging of skeletal muscle and can provide the reference
for the prevention and rehabilitation of sarcopenia.