Department of Physical Education, Faculty of Shahid Chamran, Kerman Branch, Technical and Vocational University (YVU), Tehran, Iran.
Neuroscience Research Center, Institute of Neuropharmacology, Kerman University of Medical Sciences, Kerman, Iran; Physiology Research Center, Institute of Neuropharmacology, Kerman University of Medical Sciences, Kerman, Iran; Cardiovascular Research Center, Institute of Basic and Clinical Physiology Sciences, Kerman University of Medical Science, Kerman, Iran; Department of Physiology and Pharmacology, School of Medicine, Kerman University of Medical Sciences, Kerman, Iran.
Life Sci. 2018 Jun 1;202:103-109. doi: 10.1016/j.lfs.2018.03.051. Epub 2018 Mar 28.
Existing evidence emphasize the role of mitochondrial dysfunction in sarcopenia which is revealed as loss of skeletal muscle mass and neuromuscular junction remodeling. We assessed the effect of low-intensity aerobic training along with blood flow restriction on muscle hypertrophy index, muscle-specific kinase (MuSK), a pivotal protein of the neuromuscular junction and Peroxisome proliferator-activated receptor gamma co-activator 1-alpha (PGC-1α) in aged male rats.
Animals groups were control (CTL), sham (Sh), leg blood flow restriction (BFR), exercise (Ex), sham + exercise (Sh + Ex), and BFR plus exercise (BFR + Ex) groups. The exercise groups were trained with low intensity exercise for 10 weeks. 48 h after the last training session, animals were sacrificed under anesthesia. Soleus and EDL muscles were isolated, hypertrophy index was estimated and MuSK and PGC-1α were measured by western blot method.
Hypertrophy index enhanced in soleus and Extensor digitorum longus (EDL) muscles of BFR + Ex group (P < 0.01 versus CTL and Sh groups, and P < 0.001 versus other groups). The MuSK protein of soleus and EDL muscles increased in BFR + Ex group (P < 0.01 and P < 0.001, respectively) in comparison with CTL and Sh groups. In BFR + Ex group, the PGC-1α protein increased in both soleus and EDL (P < 0.001 compared to other groups). Also the PGC-1α of soleus muscle was higher in Ex and Sh + Ex groups versus CTL and Sh groups (P < 0.05).
Findings suggest that low endurance exercise plus BFR improves the MuSK and hypertrophy index of both slow and fast muscles of elderly rats probably through the rise of PGC-1α expression.
现有证据强调了线粒体功能障碍在肌肉减少症中的作用，肌肉减少症表现为骨骼肌质量和运动终板重塑的丧失。我们评估了低强度有氧运动结合血流限制对老年雄性大鼠肌肉肥大指数、肌肉特异性激酶（MuSK）、运动终板的关键蛋白和过氧化物酶体增殖物激活受体γ共激活因子 1-α（PGC-1α）的影响。
动物分为对照组（CTL）、假手术组（Sh）、腿部血流限制组（BFR）、运动组（Ex）、假手术加运动组（Sh+Ex）和血流限制加运动组（BFR+Ex）。运动组进行 10 周低强度运动训练。最后一次训练结束后 48 小时，动物在麻醉下处死。分离比目鱼肌和伸趾长肌，通过 Western blot 法测定肌肉肥大指数和 MuSK、PGC-1α。
BFR+Ex 组比目鱼肌和伸趾长肌的肌肉肥大指数增加（与 CTL 和 Sh 组相比，P<0.01；与其他组相比，P<0.001）。BFR+Ex 组比目鱼肌和伸趾长肌的 MuSK 蛋白增加（分别为 P<0.01 和 P<0.001）与 CTL 和 Sh 组相比。BFR+Ex 组比目鱼肌和伸趾长肌的 PGC-1α 蛋白增加（与其他组相比，P<0.001）。此外，与 CTL 和 Sh 组相比，Ex 和 Sh+Ex 组比目鱼肌的 PGC-1α 更高（P<0.05）。
研究结果表明，低耐力运动加血流限制可改善老年大鼠慢肌和快肌的 MuSK 和肥大指数，可能是通过增加 PGC-1α 的表达。
