The functional and bioenergetics impact of regular physical activity upon type-2 diabetic skeletal muscle independently of confounding factors of overweight remains undocumented. Here, gastrocnemius muscle energy fluxes, mitochondrial capacity and mechanical performance were assessed noninvasively and longitudinally in non-obese diabetic Goto-Kakizaki rats using magnetic resonance (MR) imaging and dynamic 31-phosphorus MR spectroscopy (³¹P-MRS) throughout a 6-min fatiguing bout of exercise performed before, in the middle (4-week) and at the end of an 8-week training protocol consisting in 60-min daily run on a treadmill. The training protocol reduced plasmatic insulin level (−61%) whereas blood glucose and non-esterified fatty acids levels remained unaffected, thereby indicating an improvement of insulin sensitivity. It also increased muscle mitochondrial citrate synthase activity (+45%) but this increase did not enhance oxidative ATP synthesis capacity in working muscle in vivo while glycolytic ATP production was increased (+33%). On the other hand, the training protocol impaired maximal force-generating capacity (−9%), total amount of force produced (−12%) and increased ATP cost of contraction (+32%) during the fatiguing exercise. Importantly, these deleterious effects were transiently worsened in the middle of the 8-week period, in association with reduced oxidative capacity and increased basal [P_i]/[PCr] ratio (an in vivo biomarker of muscle damage). These data demonstrate that the beneficial effect of regular training on insulin sensitivity in non-obese diabetic rat occurs separately from any improvement in muscle mitochondrial function and might be linked to an increased capacity for metabolizing glucose through anaerobic process in exercising muscle.

有规律的体育锻炼对2型糖尿病骨骼肌的功能和生物能影响，与超重的混杂因素无关，尚无记录。在这里，使用磁共振（MR）成像和动态31磷MR光谱对非肥胖型糖尿病Goto-Kakizaki大鼠进行无创和纵向评估腓肠肌能量通量，线粒体容量和机械性能（³¹P-MRS）在整个8分钟训练方案的之前，之中（4周）和结束（包括每天在跑步机上跑步60分钟）进行的6分钟疲劳训练期间。训练方案可降低血浆胰岛素水平（-61％），而血糖和非酯化脂肪酸水平仍不受影响，从而表明胰岛素敏感性得到改善。它也增加了肌肉线粒体柠檬酸合酶的活性（+ 45％），但是这种增加并没有增强体内工作肌肉的氧化ATP合成能力，而糖酵解ATP的产量却增加了（+ 33％）。另一方面，在疲劳锻炼过程中，训练方案会削弱最大力量生成能力（-9％），产生的总力量（-12％）和增加的ATP收缩成本（+ 32％）。重要的，_i ] / [PCr]比（肌肉损伤的体内生物标志物）。这些数据表明，常规训练对非肥胖糖尿病大鼠胰岛素敏感性的有益效果与肌肉线粒体功能的任何改善是分开发生的，并且可能与通过锻炼肌肉的无氧过程增加了代谢葡萄糖的能力有关。