The purpose of this study was to examine whether exercise training can prevent microangiopathy of skeletal muscles in rats with type 2 diabetes and if succinate dehydrogenase (SDH) activity, an indicator of mitochondrial oxidative enzyme activity, is involved in the prevention of microangiopathy. Six-week-old male Goto-Kakizaki (GK) rats and age-matched male Wistar rats (control group (Con)) were used. GK rats were randomly assigned to nonexercise (DB) and exercise (DBEx) groups. The DBEx group was trained on a treadmill 5 times a week for 3 weeks. No significant differences in the capillary-to-fibre ratio or the capillary density were observed between the 3 groups. The luminal capillary diameter of the DB group was significantly lower than that of the Con group, whereas the capillary diameter of the DBEx group was significantly higher than that of the DB group. In addition, SDH activity was significantly higher in the DBEx group than in the Con and DB groups. Microangiopathy of skeletal muscles in type 2 diabetes was correlated with a decrease in the luminal capillary diameter, which was prevented by exercise training. Thus, the mitochondrial oxidative capacity appears to be involved in the overall mechanism by which exercise prevents microangiopathy.

This study aimed to clarify the effects of a combined treatment comprising blood flow restriction and low-current electrical stimulation on skeletal muscle hypertrophy in rats. Male Wistar rats were divided into control (Cont), blood flow restriction (Bfr), electrical stimulation (Es), or Bfr with Es (Bfr + Es) groups. Pressure cuffs (80 mmHg) were placed around the thighs of Bfr and Bfr + Es rats. Low-current Es was applied to calf muscles in the Es and Bfr + Es rats. In experiment 1, a 1-day treatment regimen (5-min stimulation, followed by 5-min rest) was delivered four times to study the acute effects. In experiment 2, the same treatment regimen was delivered three times/wk for 8 wk. Body weight, muscle mass, changes in maximal isometric contraction, fiber cross-sectional area of the soleus muscle, expression of phosphorylated and total-ERK1/2, phosphorylated-rpS6 Ser235/236, phosphorylated and total Akt, and phosphorylated-rpS6 Ser240/244 were measured. Bfr and Es treatment alone failed to induce muscle hypertrophy and increase the expression of phosphorylated rpS6 Ser240/244. Combined Bfr + Es upregulated muscle mass, increased the fiber cross-sectional area, and increased phosphorylated rpS6 Ser240/244 expression and phosphorylated rpS6 Ser235/236 expression compared with controls. Combined treatment with Bfr and low-current Es can induce muscle hypertrophy via activation of two protein synthesis signaling pathways. This treatment should be introduced for older patients with sarcopenia and others with muscle weakness. NEW & NOTEWORTHY We investigated the acute and chronic effect of low-current electrical stimulation with blood flow restriction on skeletal muscle hypertrophy and the mechanisms controlling the hypertrophic response. Low-current electrical stimulation could not induce skeletal muscle hypertrophy, but a combination treatment did. Blood lactate and growth hormone levels were increased in the early response. Moreover, activation of ERK1/2 and mTOR pathways were observed in both the acute and chronic response, which contribute to muscle hypertrophy.

Combination treatment with Bfr and ES may prevent diabetes-associated muscle atrophy by upregulating inhibition of AGEs, which leads to the activation of protein synthesis.