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. 2012 Sep;28(3):171-9.
doi: 10.5625/lar.2012.28.3.171. Epub 2012 Sep 26.

Prophylactic effects of swimming exercise on autophagy-induced muscle atrophy in diabetic rats

Youngjeon Lee  1 , Joo-Heon Kim, Yunkyung Hong, Sang-Rae Lee, Kyu-Tae Chang, Yonggeun Hong
Affiliations

Prophylactic effects of swimming exercise on autophagy-induced muscle atrophy in diabetic rats

Youngjeon Lee et al. Lab Anim Res. 2012 Sep.

Abstract

Diabetes decreases skeletal muscle mass and induces atrophy. However, the mechanisms by which hyperglycemia and insulin deficiency modify muscle mass are not well defined. In this study, we evaluated the effects of swimming exercise on muscle mass and intracellular protein degradation in diabetic rats, and proposed that autophagy inhibition induced by swimming exercise serves as a hypercatabolic mechanism in the skeletal muscles of diabetic rats, supporting a notion that swimming exercise could efficiently reverse the reduced skeletal muscle mass caused by diabetes. Adult male Sprague-Dawley rats were injected intraperitoneally with streptozotocin (60 mg/kg body weight) to induce diabetes and then submitted to 1 hr per day of forced swimming exercise, 5 days per week for 4 weeks. We conducted an intraperitoneal glucose tolerance test on the animals and measured body weight, skeletal muscle mass, and protein degradation and examined the level of autophagy in the isolated extensor digitorum longus, plantaris, and soleus muscles. Body weight and muscle tissue mass were higher in the exercising diabetic rats than in control diabetic rats that remained sedentary. Compared to control rats, exercising diabetic rats had lower blood glucose levels, increased intracellular contractile protein expression, and decreased autophagic protein expression. We conclude that swimming exercise improves muscle mass in diabetes-induced skeletal muscle atrophy, suggesting the activation of autophagy in diabetes contributes to muscle atrophy through hypercatabolic metabolism and that aerobic exercise, by suppressing autophagy, may modify or reverse skeletal muscle wasting in diabetic patients.

Keywords: Autophagy; diabetes; muscle atrophy; prophylactic effect; swimming exercise.

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Figures

Figure 1
Figure 1
Schematic view of the experimental design. Con=control, DM=diabetes mellitus, Adaptation=adaptation to the water.
Figure 2
Figure 2
Changes of blood glucose after streptozotocin (STZ) injection and intraperitoneal glucose tolerance after 4-week exercise treatment. A, Blood glucose levels following STZ injection. B, Intraperitoneal glucose tolerance test in experimental animals. The exercised diabetic group (DM+Ex) performed 4 weeks of swimming training. Data are shown as the mean±SEM. *P<0.05, **P<0.001 (compared to Con or Con+Ex). Groups; Con=control; Con+Ex=exercised control; DM=diabetic; DM+Ex=exercised diabetic. C, Effect of 4 weeks of exercise training on body mass. Values are provided as mean±SEM for each group (n=4). *P<0.05 between control and diabetic animals. Groups: Con=control; Con+Ex=exercised control; DM=diabetic; DM+Ex=exercised diabetic.
Figure 3
Figure 3
Prophylactic effect of swimming exercise on diabetic skeletal muscle atrophy. A, Appearance of skeletal muscles in diabetic (DM), control (Con), exercised diabetic (DM+Ex), and exercised control (Con+Ex) rats. SOL=soleus; EDL=extensor digitorum longus; PLT=plantaris, Scale bar=0.5 cm. B, Final muscle mass in all experimental groups. C, Muscle mass data were expressed as % of body weight. Values are provided as mean±SEM for each group (n=4). *P<0.05 vs. Con, **P<0.001 vs. Con, †P<0.05 vs. DM, ††P<0.001 vs. DM. D, Hematoxylin-eosin stained sections of the extensor digitorum longus muscle. Cross section of control (a), diabetic (b), and exercised-diabetic (c) rats. Longitudinal section of control (d), diabetic (e), and exercised-diabetic (f) rats. Magnification ×400, scale bars=50 µm.
Figure 4
Figure 4
Effect of diabetes and swimming training on expression of microtubule-associated protein-1 light chain-3 (LC3) and actin protein. A, Western blot analysis, immunoblotted with a monoclonal anti-LC3 and anti-actin antibody. **P<0.01, ***P<0.001. B, Western blot analysis, immunoblotted with a monoclonal anti-LC3 antibody. Results are representative of the mean±SEM. *P<0.05. Relative intensity of LC3 includes LC3-I and LC3-II.
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