关键词: 抗阻运动, 脂联素, 脂联素受体1, 骨骼肌, 衰老, 卫星细胞

Abstract: BACKGROUND: Muscle atrophy (sarcopenia) and muscle weakness caused by aging are becoming increasingly serious health problems, and there is currently a lack of effective drug treatments. Exercise training, especially resistance exercise, plays an important role in preventing muscle atrophy; however, its molecular mechanism is not yet fully understood.
OBJECTIVE: To explore the effects of regular resistance exercise on skeletal muscle satellite cells in aging rats and the possible mechanism.
METHODS: Forty-five 20-month-old male SD rats were randomly divided into old sedentary, old exercise, or old exercise inhibitor groups, and ten 6-month-old male SD rats were selected as young sedentary group. Rats in young sedentary and old sedentary groups were kept quietly in mouse cage, while those of old exercise group performed weight-bearing ladder training and old exercise inhibitor group was given administration with adiponectin receptor 1 inhibitor while exercising, in which the intervention period was lasting for 12 weeks. After the intervention, the endurance and strength levels were determined by grated treadmill exercise test and progressive tail-loaded ladder exercise test, respectively. The gastrocnemius was isolated, and the adiponectin content was detected by enzyme-linked immunosorbent assay. The cell cross-sectional area was measured by hematoxylin-eosin staining. The mitochondrial DNA copy number was examined by real-time fluorescence quantitative PCR. Cell proliferation was detected by proliferating cell nuclear antigen immunohistochemical staining. The number of activated skeletal muscle satellite cells was measured by paired box gene 7/myogenic differentiation antigen immunofluorescence staining. Immunoblotting was used to detect the expression of related proteins in skeletal muscle. Adiponectin receptor 1 agonist AdiopRon was co-incubated with satellite cells cultured in vitro for 24 hours. Paired box gene 7/myogenic differentiation antigen immunofluorescence staining was used to detect the number of activated satellite cells. Western blotting was used to detect the expression of AMP-activated protein kinase protein in satellite cells.
RESULTS AND CONCLUSION: (1) Compared with old sedentary group, endurance and strength level, gastrocnemius mass index, adiponectin content, cell cross-sectional area, mitochondrial DNA copy number, cell proliferation by proliferating cell nuclear antigen+ cell counts, and paired box gene 7+/myogenic differentiation antigen+ cell counts were increased (P < 0.05); total protein content and protein expression of adiponectin receptor 1, peroxisome proliferator-activated receptor γ coactivator 1-alpha, nuclear respiratory factor 1, mitochondrial transcription factor A, protein kinase B, mammalian target of rapamycin, P70 Ribosomal protein S6 kinase, paired box gene 7, myogenic differentiation antigen, myogenin, and myogenic factor 5 were upregulated (P < 0.05) in the old exercise group. (2) The above benefits of exercise on aging skeletal muscle were diminished after administration with adiponectin receptor 1 inhibitor (P < 0.05). (3) Cell culture experiments found that AdiopRon could increase the number of paired box gene 7+/myogenic differentiation antigen + cells and the expression of AMP-activated protein kinase protein in satellite cells. These findings indicate that regular resistance exercise activates satellite cells through adiponectin receptor 1 pathway, thereby promoting muscle cell proliferation and restoring skeletal muscle quality and function in aged rats. Adiponectin receptor 1 is a key target for regular exercise to protect against muscle mass loss and strength decline during aging.

Key words:  resistance exercise, adiponectin, adiponectin receptor 1, skeletal muscle, aging, satellite cell