Insulin resistance is associated with cardiometabolic risk factors, and exercise training can improve insulin-mediated glucose uptake. However, few studies have demonstrated the reversibility of exercise-induced benefits. Thus, the authors examine the time–response effects of exercise training and detraining on glucose transporter 4 (GLUT4) content, insulin-dependent and insulin-independent pathways in cardiac and gastrocnemius muscle tissues of spontaneously hypertensive rats. Thirty-two male spontaneously hypertensive rats, 4 months old, were assigned to (n = 8/group): T (exercise training: 10-week treadmill exercise, 50–70% maximum effort capacity, 1 hr/day, 5 days/week); D2 (exercise training + 2-day detraining), D4 (exercise training + 4-day detraining); and S (no exercise). The authors evaluated insulin resistance, maximum effort capacity, GLUT4 content, p-IRS-1^Tyr1179, p-AS160^Ser588, p-AMPKα1^Thr172, and p-CaMKII^Thr286 in cardiac and gastrocnemius muscle tissues (Western blot). In response to exercise training, there were improvements in insulin resistance (15.4%; p = .010), increased GLUT4 content (microsomal, 29.4%; p = .012; plasma membrane, 27.1%; p < .001), p-IRS-1 (42.2%; p < .001), p-AS160 (60.0%; p < .001) in cardiac tissue, and increased GLUT4 content (microsomal, 29.4%; p = .009; plasma membrane, 55.5%; p < .001), p-IRS-1 (28.1%; p = .018), p-AS160 (76.0%; p < .001), p-AMPK-α1 (37.5%; p = .026), and p-CaMKII (30.0%; p = .040) in the gastrocnemius tissue. In D4 group, the exercise-induced increase in GLUT4 was reversed (plasma membrane, −21.3%; p = .027), p-IRS1 (−37.1%; p = .008), and p-AS160 (−82.6%; p < .001) in the cardiac tissue; p-AS160 expression (−35.7%; p = .034) was reduced in the gastrocnemius. In conclusion, the cardiac tissue is more susceptible to exercise adaptations in the GLUT4 content and signaling pathways than the gastrocnemius muscle. This finding may be explained by particular characteristics of insulin-dependent and insulin-independent pathways in the muscle tissues studied.

胰岛素抵抗与心脏代谢危险因素有关，运动训练可以改善胰岛素介导的葡萄糖摄取。然而，很少有研究证明运动带来的益处是可逆的。因此，作者检查了运动训练和去训练对自发性高血压大鼠心脏和腓肠肌组织中葡萄糖转运蛋白 4 (GLUT4) 含量、胰岛素依赖性和胰岛素非依赖性通路的时间反应影响。32 只雄性自发性高血压大鼠，4 个月大，被分配到（n = 8/组）：T（运动训练：10 周跑步机运动，50-70% 最大努力能力，1 小时/天，5 天/周）；D2（运动训练+2天退训），D4（运动训练+4天退训）；和 S（不运动）。作者评估了心脏和腓肠肌组织中的胰岛素抵抗、最大努力能力、GLUT4 含量、p-IRS-1 ^Tyr1179、p-AS160 ^Ser588、p-AMPKα1 ^Thr172和 p-CaMKII ^Thr286（蛋白质印迹）。运动训练后，胰岛素抵抗得到改善（15.4%；p  = .010），GLUT4 含量增加（微粒体，29.4%；p  = .012；质膜，27.1%；p  < .001），p- IRS-1 (42.2%; p < .001)， 心脏组织中的p-AS160 (60.0%；p < .001)，以及 GLUT4 含量增加（微粒体，29.4%；p  = .009；质膜，55.5%；p  < .001），p- IRS-1 (28.1%; p  = .018)、p-AS160 (76.0%; p  < .001)、p-AMPK-α1 (37.5%; p  = .026) 和 p-CaMKII (30.0%; p  = .040) 在腓肠肌组织中。在 D4 组中，运动诱导的 GLUT4 增加被逆转（质膜，-21.3%；p  = .027）、p-IRS1（-37.1%；p  = .008 ）和 p-AS160（-82.6%；p  < .001) 在心脏组织中；p-AS160 表达 (-35.7%; p = .034) 在腓肠肌中减少。总之，心脏组织比腓肠肌更容易受到 GLUT4 含量和信号通路的运动适应的影响。这一发现可以通过所研究的肌肉组织中胰岛素依赖和胰岛素非依赖途径的特定特征来解释。