Exercise Training Induced Regulation of Muscle Mitochondrial Dynamics
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IntroductionExercise training is a potent stimulator of muscle oxidative metabolism, which is tightly coupled to mitochondrial biogenesis, dynamics, and mitophagy. Mitochondrial dynamics involves the coordinated processes of fission and fusion. The IL6 family of cytokines can activate intracellular signaling pathways, such as STAT3, through the binding of their receptor complexes involving glycoprotein 130 (gp130). While systemic IL6 signaling can alter the expression of proteins related to mitochondrial dynamics, gp130 regulation of mitochondrial dynamic protein expression by exercise requires further investigation. The purpose of this study is to examine exercise training induced regulation of skeletal muscle mitochondrial dynamics.MethodsMale, C57BL/6 (B6; N=18) and skeletal musclespecific gp130 knockout (skmgp130 KO; N=12) mice were assigned to either cage control (CC) or treadmill exercise training (EX) beginning at 6 weeks of age. EX mice performed 6 weeks of treadmill exercise (5% incline, 18 m/min, 55 min/d, 6 d/wk) and were sacrificed 48 hours after the last training session. Gastrocnemius protein expression of mitochondrial dynamics and mitophagy by Western blot.ResultsExerciseinduced improvements in oxidative capacity were accompanied by increased muscle gp130 protein expression regardless of genotype. In B6 mice, EX training increased Fis1 protein expression and decreased Mfn1 protein expression. Interestingly, skmgp130 KO increased Fis1 protein expression and decreased Mfn1 protein expression. There were no further effects of EX on Fis1 or Mfn1 protein expression in skmgp130 KO mice. EX and and skmgp130 KO increased Beclin1 protein expression, and was further increased by exercise in skmgp130 KO.ConclusionsOur results demonstrate that skeletal muscle gp130 knockout did not block the induction of muscle oxidative capacity by treadmill exercise training. We found that the deletion of skeletal muscle gp130 altered protein expression related to mitochondrial fission, fusion, and mitophagy. These findings indicate that the gp130 receptor may be involved in the regulation of mitochondrial dynamics. Future studies are required to establish a mechanistic role of gp130 in the regulation of mitochondrial dynamics.
