耐力運動訓練對誘發骨骼肌細胞凋亡之粒腺體訊息傳遞路徑的影響

The effect of endurance exercise training on the mitochondria signaling pathway of apoptosis in skeletal muscle

目的：探討經十二週之耐力運動訓練後，單次衰竭運動對誘發骨骼肌細胞凋亡之粒腺體訊息傳遞路徑的影響。方法：以雄鼠（Wistar）為本研究之受試對象，將實驗動物隨機分成訓練組及控制組，訓練組利用動物跑步機進行十二週之運動訓練，每週五天；控制組正常飼養十二週。經一週休息後，於第十四週將訓練組及控制組分別再次分為運動前犧牲組（pre-exercise；PRE）、運動結束後第0小時犧牲組（post-exercise0h；PE0）及運動結束後第48小時犧牲組（post-exercise48h；PE48）。動物犧牲後取出後腿之比目魚肌（soleus muscle；SM）及腓腸肌（gastrocnemius muscle；GM）進行後續之分析。結果：訓練組SM之檸檬酸合成酶於PRE,PE0及PE48均顯著高於控制組（p<.05）。訓練組之GM／體重及SM／體重之比值顯著高於控制組（p<.05）。Bcl-2的表現量，訓練組之GM及SM在PE0均高於控制組（p<.05），而在PE48均低於控制組（p<.05）。Bax的表現量，訓練組之GM與SM在PE0及PE48均低於控制組（p<.05）。在PE48骨骼肌之細胞凋亡現象，訓練組GM及SM之表現量均顯著低於控制組（p<.05）。結論：骨骼肌在運動訓練後，可能經由改變細胞內Bcl-2與Bax之細胞凋亡訊息傳遞分子的表現及粒腺體的氧化能力，而達到縮短骨骼肌細胞凋亡作用之時間或抑制骨骼肌細胞凋亡的現象，進而可能導致骨骼肌肥大的現象。

Purpose: This study is to investigate the influence of exercise training on skeletal muscle apoptosis induced by mitochondrial pathway. Methods: Animals, male Wistar rats, were randomly assigned to either a control group or an exercise group. Exercise group were trained for 5 days weekly for 12 weeks on treadmill. An exhausted exercise test was performed after a rest period of 7 days after 12 weeks exercise training. Rats were sacrificed at pre-exercise (PRE), post-exercise 0 hour (PE0) and post-exercise 48 hour (PE48), respectively. The soleus and gastrocnemius were dissected out and frozen in liquid nitrogen rapidly. Results: The citrate synthesis activity of soleus of trained was significantly higher than untrained at PRE, PE0 and PE48 (p < .05), respectively. Both the muscle weight-to-body weight ratio of gastrocnemius and soleus of trained were significantly higher than untrained (p < .05). In Bcl-2 expression, both of the gastrocnemius and soleus of trained were significantly higher than untrained at PE0 (p < .05) and significantly lower than untrained at PE48 (p < .05). In Bax expression, both of the gastrocnemius and soleus of trained were significantly lower than untrained at PE0 and PE48 (p < .05), respectively. Both the apoptosis index of gastrocnemius and soleus of trained were significantly lower than untrained after PE48 (p < .05). Conclusion: These findings suggest that skeletal muscle may modulate their Bcl-2 and Bax apoptotic signals expression and the oxidative activity of mitochondria after exercise training, lead to attenuating the time of skeletal muscle apoptosis or inhibiting the apoptotic signals expression, and then the probability of hypertrophy occurred.