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지구성 훈련이 노화 쥐 골격근의 자가포식 유동(flux)에 미치는 영향

Autophagy flux is decreased in response to endurance exercise training in aged mouse skeletal muscle.

이동원|오성희|주정선|홍용식
한국운동생리학회|2016.02|운동과학 (Exercise Science)|제25권 제1호|pp. 50-59|DOI 10.15857/ksep.2016.25.1.50

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키워드

AgingAutophagySkeletal MuscleAutophagic FluxEndurance Exercise

초록

PURPOSE: The aims of this study were to investigate if autophagy was up-regulated in skeletal muscle from old mice, and to determine if endurance exercise training can intervene the autophagy process in old mouse muscle tissue. METHODS: Two age groups (10-wk and 18-mo old) of mice were assigned either swimming exercise training or sedentary control group. Male wild-type ICR mice performed five daily bouts of one hour swimming per week for 8 weeks. To determine autophagic flux in mouse skeletal muscle, mice were treated with or without 2 days of 0.4 mg/kg/day colchicine (blocking the degradation of autophagosome) administration intraperitoneally following swimming exercise training. Triceps muscles were harvested, and autophagic marker proteins and autophagy-related proteins were analyzed by Western blot analysis. RESULTS: The autophagic flux assay demonstrated that swimming training increased the autophagic flux (~3-fold increase in LC3-II, P<.05) in young mice, yet exhibited ~2-fold increase in the autophagic flux in muscle of aged mice. The basal autophagy was also decreased in aged mice (LC3, p62, P<.05). Despite no changes in Beclin-1 proteins, other autophagy marker proteins (Bnip3, Lamp1 and HDAC6) were significantly decreased in aged mice compared with young mice (P<.05). CONCLUSIONS: It is concluded that both basal and induced autophagy activated by exercise training was decreased in aged mouse skeletal muscle. The inhibited autophagy in skeletal muscle of aged mice was not reversed by endurance exercise training which activates autophagy in skeletal muscle.

Abstract

PURPOSE: The aims of this study were to investigate if autophagy was up-regulated in skeletal muscle from old mice, and to determine if endurance exercise training can intervene the autophagy process in old mouse muscle tissue. METHODS: Two age groups (10-wk and 18-mo old) of mice were assigned either swimming exercise training or sedentary control group. Male wild-type ICR mice performed five daily bouts of one hour swimming per week for 8 weeks. To determine autophagic flux in mouse skeletal muscle, mice were treated with or without 2 days of 0.4 mg/kg/day colchicine (blocking the degradation of autophagosome) administration intraperitoneally following swimming exercise training. Triceps muscles were harvested, and autophagic marker proteins and autophagy-related proteins were analyzed by Western blot analysis. RESULTS: The autophagic flux assay demonstrated that swimming training increased the autophagic flux (~3-fold increase in LC3-II, P<.05) in young mice, yet exhibited ~2-fold increase in the autophagic flux in muscle of aged mice. The basal autophagy was also decreased in aged mice (LC3, p62, P<.05). Despite no changes in Beclin-1 proteins, other autophagy marker proteins (Bnip3, Lamp1 and HDAC6) were significantly decreased in aged mice compared with young mice (P<.05). CONCLUSIONS: It is concluded that both basal and induced autophagy activated by exercise training was decreased in aged mouse skeletal muscle. The inhibited autophagy in skeletal muscle of aged mice was not reversed by endurance exercise training which activates autophagy in skeletal muscle.

참고문헌 (34)

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