Gordon P L, Vannier E, Hamada K, Layne J, Hurley B F, Roubenoff R, Castaneda-Sceppa C
Nutrition, Exercise Physiology and Sarcopenia Laboratory, Jean Mayer USDA Human Nutrition Research Center on Aging at Tufts University, Boston, MA, USA.
Int J Immunopathol Pharmacol. 2006 Oct-Dec;19(4):739-49. doi: 10.1177/039463200601900404.
Resistance training results in muscle hypertrophy and improves glycemic control in patients with type 2 diabetes. Whether resistance training modulates inflammation in muscles of diabetic patients remains unknown. We examined the expression of genes encoding the cytokines, tumor necrosis factor-alpha (TNF-alpha), interleukin-1beta (IL-1beta) and transforming growth factor-beta1 (TGF-beta1) as well as the pan-leukocyte marker CD18. Thirty men and women (67+/-7 years) were randomized to either 16 weeks of resistance training and usual diabetes care (EX) or to usual diabetes care only (CON). Muscle biopsies were obtained from the vastus lateralis muscle prior to the 16-week intervention, and 72 h following the maximal strength test post-intervention. Fiber cross-sectional area (CSA) was determined following ATPase staining. Cytokine and CD18 transcript levels were assessed by real-time PCR. Resistance training increased CSA of type I and II fibers (both P <0.05) and IL-1beta transcript levels (P = 0.05). TNF-alpha (P<0.05) and TGF-beta1 transcripts (P<0.05) increased over time in the EX group, but these increases did not differ from those in the CON group. In both groups, the increase in CD18 transcripts remained minimal. The two groups differ by the relationship between changes in CD18 and changes in cytokine transcripts, suggesting that resistance training affects the source of cytokines in muscle. Our studies establish that resistance training in older adults with type 2 diabetes results in muscle fiber hypertrophy, despite a greater accumulation of inflammatory cytokine transcripts in muscle.
抗阻训练可导致肌肉肥大,并改善2型糖尿病患者的血糖控制。抗阻训练是否能调节糖尿病患者肌肉中的炎症尚不清楚。我们检测了编码细胞因子、肿瘤坏死因子-α(TNF-α)、白细胞介素-1β(IL-1β)和转化生长因子-β1(TGF-β1)的基因以及全白细胞标志物CD18的表达。30名男性和女性(67±7岁)被随机分为两组,一组进行16周的抗阻训练并接受常规糖尿病护理(EX组),另一组仅接受常规糖尿病护理(CON组)。在为期16周的干预前,以及干预后最大力量测试72小时后,从股外侧肌获取肌肉活检样本。通过ATP酶染色测定肌纤维横截面积(CSA)。通过实时PCR评估细胞因子和CD18转录水平。抗阻训练增加了I型和II型肌纤维的CSA(均P<0.05)以及IL-1β转录水平(P = 0.05)。EX组中TNF-α(P<0.05)和TGF-β1转录本(P<0.05)随时间增加,但这些增加与CON组无差异。在两组中,CD18转录本的增加均保持在最低水平。两组在CD18变化与细胞因子转录本变化之间的关系上存在差异,这表明抗阻训练会影响肌肉中细胞因子的来源。我们的研究表明,2型糖尿病老年患者进行抗阻训练可导致肌纤维肥大,尽管肌肉中炎症细胞因子转录本的积累更多。