Dubé John J, Amati Francesca, Stefanovic-Racic Maja, Toledo Frederico G S, Sauers Sarah E, Goodpaster Bret H
Division of Endocrinology and Metabolism, Department of Medicine, University of Pittsburgh School of Medicine, Pittsburgh, PA, USA.
Am J Physiol Endocrinol Metab. 2008 May;294(5):E882-8. doi: 10.1152/ajpendo.00769.2007. Epub 2008 Mar 4.
We previously reported an "athlete's paradox" in which endurance-trained athletes, who possess a high oxidative capacity and enhanced insulin sensitivity, also have higher intramyocellular lipid (IMCL) content. The purpose of this study was to determine whether moderate exercise training would increase IMCL, oxidative capacity of muscle, and insulin sensitivity in previously sedentary overweight to obese, insulin-resistant, older subjects. Twenty-five older (66.4 +/- 0.8 yr) obese (BMI = 30.3 +/- 0.7 kg/m2) men (n = 9) and women (n = 16) completed a 16-wk moderate but progressive exercise training program. Body weight and fat mass modestly but significantly (P < 0.01) decreased. Insulin sensitivity, measured using the euglycemic hyperinsulinemic clamp, was increased (21%, P = 0.02), with modest improvements (7%, P = 0.04) in aerobic fitness (Vo2peak). Histochemical analyses of IMCL (Oil Red O staining), oxidative capacity [succinate dehydrogenase activity (SDH)], glycogen content, capillary density, and fiber type were performed on skeletal muscle biopsies. Exercise training increased IMCL by 21%. In contrast, diacylglycerol and ceramide, measured by mass spectroscopy, were decreased (n = 13; -29% and -24%, respectively, P < 0.05) with exercise training. SDH (19%), glycogen content (15%), capillary density (7%), and the percentage of type I slow oxidative fibers (from 50.8 to 55.7%), all P < or = 0.05, were increased after exercise. In summary, these results extend the athlete's paradox by demonstrating that chronic exercise in overweight to obese older adults improves insulin sensitivity in conjunction with favorable alterations in lipid partitioning and an enhanced oxidative capacity within muscle. Therefore, several key deleterious effects of aging and/or obesity on the metabolic profile of skeletal muscle can be reversed with only moderate increases in physical activity.
我们之前报道过一种“运动员悖论”，即耐力训练的运动员虽具有高氧化能力和增强的胰岛素敏感性，但肌内脂质（IMCL）含量也更高。本研究的目的是确定适度运动训练是否会增加久坐不动的超重至肥胖、胰岛素抵抗的老年受试者的IMCL、肌肉氧化能力和胰岛素敏感性。25名年龄较大（66.4±0.8岁）的肥胖（BMI = 30.3±0.7 kg/m2）男性（n = 9）和女性（n = 16）完成了一项为期16周的适度但渐进式运动训练计划。体重和脂肪量适度但显著下降（P < 0.01）。使用正常血糖高胰岛素钳夹法测量的胰岛素敏感性增加（21%，P = 0.02），有氧适能（峰值摄氧量）有适度改善（7%，P = 0.04）。对骨骼肌活检组织进行IMCL的组织化学分析（油红O染色）、氧化能力[琥珀酸脱氢酶活性（SDH）]、糖原含量、毛细血管密度和纤维类型分析。运动训练使IMCL增加了21%。相比之下，通过质谱法测量的二酰甘油和神经酰胺在运动训练后下降（n = 13；分别下降29%和24%，P < 0.05）。运动后SDH（19%）、糖原含量（15%）、毛细血管密度（7%）以及I型慢氧化纤维的百分比（从50.8%增至55.7%）均增加，P均≤0.05。总之，这些结果扩展了运动员悖论，表明超重至肥胖的老年人进行长期运动可改善胰岛素敏感性，同时伴有脂质分配的有利改变和肌肉氧化能力增强。因此，仅适度增加身体活动就能逆转衰老和/或肥胖对骨骼肌代谢特征的几个关键有害影响。
