Effect of resistance exercise training on expression of Hsp70 and inflammatory cytokines in skeletal muscle and adipose tissue of STZ-induced diabetic rats.

Impairment of adipose tissue and skeletal muscles accrued following type 1 diabetes is associated with protein misfolding and loss of adipose mass and skeletal muscle atrophy. Resistance training can maintain muscle mass by changing both inflammatory cytokines and stress factors in adipose tissue and skeletal muscle. The purpose of this study was to determine the effects of a 5-week ladder climbing resistance training program on the expression of Hsp70 and inflammatory cytokines in adipose tissue and fast-twitch flexor hallucis longus (FHL) and slow-twitch soleus muscles in healthy and streptozotocin-induced diabetic rats. Induction of diabetes reduced body mass, while resistance training preserved FHL muscle weight in diabetic rats without any changes in body mass. Diabetes increased Hsp70 protein content in skeletal muscles, adipose tissue, and serum. Hsp70 protein levels were decreased in normal and diabetic rats by resistance training in the FHL, but not soleus muscle. Furthermore, resistance training decreased inflammatory cytokines in FHL skeletal muscle. On the other hand, Hsp70 and inflammatory cytokine protein levels were increased by training in adipose tissue. Also, significant positive correlations between inflammatory cytokines in adipose tissue and skeletal muscles with Hsp70 protein levels were observed. In conclusion, we found that in diabetic rats, resistance training decreased inflammatory cytokines and Hsp70 protein levels in fast skeletal muscle, increased adipose tissue inflammatory cytokines and Hsp70, and preserved FHL muscle mass. These results suggest that resistance training can maintain skeletal muscle mass in diabetes by changing inflammatory cytokines and stress factors such as Hsp70 in skeletal muscle and adipose tissue.

Expression of interleukin-15 and inflammatory cytokines in skeletal muscles of STZ-induced diabetic rats: effect of resistance exercise training.

Skeletal muscle atrophy is associated with type-1 diabetes. Skeletal muscle is the source of pro- and anti-inflammatory cytokines that can mediate muscle hypertrophy and atrophy, while resistance exercise can modulate both muscle mass and muscle cytokine expression. This study determined the effects of a 5-week resistance exercise training regimen on the expression of muscle cytokines in healthy and streptozotocin-induced diabetic rats, with special emphasis on interleukin-15 (IL-15), a muscle-derived cytokine proposed to be involved in muscle hypertrophy or responses to stress. Induction of diabetes reduced muscle weight in both the fast flexor hallucis longus (FHL) and slow soleus muscles, while resistance training preserved FHL muscle weight in diabetic rats. IL-15 protein content was increased by training in both FHL and soleus muscles, as well as serum, in normal and diabetic rats. With regard to proinflammatory cytokines, muscle IL-6 levels were increased in diabetic rats, while training decreased muscle IL-6 levels in diabetic rats; training had no effect on FHL muscle IL-6 levels in healthy rats. Also, tumor necrosis factor-alpha (TNF-α) and IL-1ß levels were increased by diabetes, but not changed by training. In conclusion, we found that in diabetic rats, resistance training increased muscle and serum IL-15 levels, decreased muscle IL-6 levels, and preserved FHL muscle mass.

The effect of resistance training on plasma S1P level and gene expression of S1P1,2,3 receptors in male Wistar rats.

AIM: The purpose of present study was to study the effect of 8 weeks resistance training on plasma Sphingosine-1-phosphate (S1P) level and gene expression of S1P receptors in skeletal muscles of male Wistar rat. METHODS: In this study 24 (8 week-old) male Wistar rats (190-250 gr) were divided randomly to a control (N.=12) and a training (N.=12) group. Resistance ladder was 1 meter height with 2 cm grid ladder. The content of plasma S1P and relative mRNA expression of S1P receptors were determined by high pressure liquid chromatography (HPLC) and Real-time PCR, respectively. RESULTS: Resistance training increased the content of plasma S1P of exercised group compared to control group (P=0.001). Furthermore, Resistance exercise training increased the gene expression of S1P1 (P=0.001), S1P2 (P=0.000) and S1P3 receptors (P=0.021) in exercised flexor hallucis longus (FHL) compared to control group. In soleus (SOL) muscle, resistance training increased the gene expression of S1P1 (P=0.000), S1P2 (P=0.603) and S1P3 receptors (P=0.009). CONCLUSION: The key conclusion is that resistance training strongly caused to increase in plasma S1P content and its receptors in skeletal muscles of rat that might indicate to the involvement of S1P signalling in the molecular events controlling adaptations of resistance trained muscles which needs to be elucidated in future studies.

Increased activity in the form of endurance training increases calcitonin gene-related peptide content in lumbar motoneuron cell bodies and in sciatic nerve in the rat.

The relative content of calcitonin gene-related peptide in lumbar motoneuron cell bodies (semiquantitative immunohistochemistry) and sciatic nerve was examined in rats who had previously undergone a 16-week period of endurance training on a motor-driven treadmill. Soleus motoneurons were identified in the spinal cord by their fluorescence following injection of FluoroGold into the muscle one week before killing. In sedentary rats, calcitonin gene-related peptide was detectable in 76-90% of motoneurons, with no difference in the proportions of negative cells, or in the mean staining intensity of positive cells, between soleus and neighbouring (presumptive fast hindlimb muscle) unlabelled moto-neurons. In endurance-trained rats, the estimated content of calcitonin gene-related peptide was significantly increased (90%) in cell bodies of soleus and neighbouring motoneurons, with no training-induced alterations in the proportions of calcitonin gene-related peptide-positive cells in either sample. The content of the neuropeptide was also significantly higher (37%) in sciatic nerve of endurance-trained rats. Relative accumulation of calcitonin gene-related peptide proximal to a sciatic nerve ligature applied 4 h before, however, was unchanged. The increases in calcitonin gene-related peptide in motoneuron cell bodies and sciatic nerve axons following endurance training may indicate an up-regulation of the synthesis, transport and terminal release of this neuropeptide, which could play a significant role in other morphological and functional adaptations which are known to occur at the neuromuscular junction following this chronic change in activity level.