Diabetes. 2004;53(2):294-305.
Background: Aerobic endurance training increases insulin action in patients with type 2 diabetes, and results in improvement of glycemic control. However, it is very difficult to engage these patients in a regular sustained exercise regimen. Many patients with type 2 diabetes are overweight and have difficulty with the performance of endurance-type exercises. For some patients, resistance training represents an attractive exercise alternative. However, little is known regarding the effect of this type of training modality on insulin action and glucose metabolism in patients with type 2 diabetes.
Objective: This study aimed to investigate the effects of very low levels of strength training on insulin action in the skeletal muscle and glucose metabolism in patients with type 2 diabetes.
Methods: Ten subjects with type 2 diabetes and 7 healthy controls were recruited for the study. All subjects participated in a 6-week program, with one leg performing progressive strength training exercises (leg press, knee extension, and hamstring curl) while the other leg remained sedentary. Each session lasted no more than 30 minutes. During the last training session, leg volume and thigh circumference were measured. Muscle biopsies were obtained, and an isoglycemic-hyperinsulinemic clamp combined with arterio-femoral venous catheterization of both legs was performed.
Results: After the strength training program, muscle strength increased in all subjects. Leg volume was not different between the trained and untrained legs but thigh circumference slightly increased for the trained leg in diabetic subjects. Fasting glucose, insulin, and c-peptide concentrations in plasma were unaltered by training. During clamp step II, there was a significant training effect seen among diabetic subjects with regards to glucose clearance. Insulin-mediated leg blood flow was also higher in the trained leg compared to the untrained leg. Muscle biopsies showed no differences in the fraction of slow type I to fast type II fibers in the untrained and trained legs. Capillary density was also unchanged. However, in diabetics, there was a 40% increase in the subtype 4 glucose transporter (GLUT4) density in the trained muscle. In response to training, there was also an increase in the protein expression of the insulin receptor, upregulation of protein kinase B( (an enzyme involved in the insulin signaling pathway), glycogen synthase protein expression, and glycogen synthase total activity. There were no differences with regards to markers of oxidative capacity for both groups indicating that the predominant type of exercise obtained was indeed strength training.
Conclusions: In this study, the authors demonstrated that resistance type exercise training results in an increase in insulin action in skeletal muscles in patients with type 2 diabetes; this effect was likely not caused solely by an increase in muscle mass as supported by the muscle biopsy data. It appears that skeletal muscles adapt qualitatively to a strength-training program. Increases in insulin-mediated blood flow and glucose-clearance rates were also observed. A possible mechanism for this training effect may be related to changes in local contraction-mediated mechanisms involving key proteins in the insulin signaling pathway. These adaptations were seen in response to only minimal training effort.
Comments: Mechanistic studies are always generally very difficult to perform as isolating local effects entails several assumptions regarding the experimental set-up. Nevertheless, this study does demonstrate that strength training, like endurance training, enhances insulin action in skeletal muscles in patients with type 2 diabetes. This study adds to our knowledge of the benefits of resistance type exercises for diabetic patients. Such resistance-type training programs may be attractive alternatives for our deconditioned diabetic patients who would like to engage in some form of exercise, but are discouraged by their limited capacity to perform endurance-type exercises.