Abstract
Regular resistance exercise induces skeletal muscle hypertrophy and improvement of glycemic control in type 2 diabetes patients. Administration of dehydroepiandrosterone (DHEA), a sex steroid hormone precursor, increases 5α-dihydrotestosterone (DHT) synthesis and is associated with improvements in fasting blood glucose level and skeletal muscle hypertrophy. Therefore, the aim of this study was to investigate whether increase in muscle DHT levels, induced by chronic resistance exercise, can contribute to skeletal muscle hypertrophy and concomitant improvement of muscular glucose metabolism in type 2 diabetic rats. Male 20-week-old type 2 diabetic rats (OLETF) were randomly divided into 3 groups: sedentary control, resistance training (3 times a week on alternate days for 8 weeks), or resistance training with continuous infusion of a 5α-reductase inhibitor (n = 8 each group). Age-matched, healthy nondiabetic Long-Evans Tokushima Otsuka (LETO) rats (n = 8) were used as controls. The results indicated that OLETF rats showed significant decrease in muscular DHEA, free testosterone, DHT levels, and protein expression of steroidogenic enzymes, with loss of skeletal muscle mass and hyperglycemia, compared to that of LETO rats. However, 8-week resistance training in OLETF rats significantly increased the levels of muscle sex steroid hormones and protein expression of steroidogenic enzymes with a concomitant increase in skeletal muscle mass, improved fasting glucose level, and insulin sensitivity index. Moreover, resistance training accelerated glucose transporter-4 (GLUT-4) translocation and protein kinase B and C-ζ/λ phosphorylation. Administering the 5α-reductase inhibitor in resistance-trained OLETF rats resulted in suppression of the exercise-induced effects on skeletal muscle mass, fasting glucose level, insulin sensitivity index, and GLUT-4 signaling, with a decline in muscular DHT levels. These findings suggest that resistance training-induced elevation of muscular DHT levels may contribute to improvement of hyperglycemia and skeletal muscle hypertrophy in type 2 diabetic rats.
Highlights
In 2014, 9% of adults 18 years and older around the world had diabetes, and diabetes was the direct cause of 1.5 million deaths [1, 2]
The results indicated that Otsuka Long-Evans Tokushima Fatty (OLETF) rats showed significant decrease in muscular DHEA, free testosterone, DHT levels, and protein expression of steroidogenic enzymes, with loss of skeletal muscle mass and hyperglycemia, compared to that of Long-Evans Tokushima Otsuka (LETO) rats
The results of this study demonstrated that chronic resistance training induced a significant increase in muscle tissue levels of DHEA, testosterone, and DHT; increased protein levels of steroidogenic enzymes; reduced fasting glucose level; improved insulin sensitivity index (QUICKI), and increased muscle mass and cross-sectional area in OLETF diabetic rats
Summary
In 2014, 9% of adults 18 years and older around the world had diabetes, and diabetes was the direct cause of 1.5 million deaths [1, 2]. Our recent study showed that chronic resistance exercise elevated muscular DHT levels, which correlated with traininginduced skeletal muscle hypertrophy in healthy older patients [15]. These steroid hormones may be a part of the mechanism through which resistance exercise leads to better glycemic control with skeletal muscle hypertrophy in patients with type 2 diabetes. It remains unclear whether chronic resistance exercise-induced increases in muscle sex steroid metabolism can contribute to improvement of muscular glucose metabolism and skeletal muscle hypertrophy in type 2 diabetics
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