Changes in biomarker levels and myofiber constitution in rat soleus muscle at different exercise intensities.

Although exercise affects the function and structure of skeletal muscle, our knowledge regarding the biomedical alterations induced by different intensities of exercise is incomplete. Here we report on the changes in biomarker levels and myofiber constitution in the rat soleus muscle induced by exercise intensity. Male adult rats at 7 weeks of age were divided into 3 groups by exercise intensity, which was set based on the accumulated lactate levels in the blood using a treadmill: stationary control (0 m/min), aerobic exercise (15 m/min), and anaerobic exercise (25 m/min). The rats underwent 30 min/day treadmill training at different exercise intensities for 14 days. Immediately after the last training session, the soleus muscle was dissected out in order to measure the muscle biomarker levels and evaluate the changes in the myofibers. The mRNA expression of citrate synthase, glucose-6-phosphate dehydrogenase, and Myo D increased with aerobic exercise, while the mRNA expression of myosin heavy-chain I and Myo D increased in anaerobic exercise. These results suggest that muscle biomarkers can be used as parameters for the muscle adaptation process in aerobic/anaerobic exercise. Interestingly, by 14 days after the anaerobic exercise, the number of type II (fast-twitch) myofibers had decreased by about 20%. Furthermore, many macrophages and regenerated fibers were observed in addition to the injured fibers 14 days after the anaerobic exercise. Constitutional changes in myofibers due to damage incurred during anaerobic exercise are necessary for at least about 2 weeks. These results indicate that the changes in the biomarker levels and myofiber constitution by exercise intensity are extremely important for understanding the metabolic adaptations of skeletal muscle during physical exercise.

Effect of angiotensin II receptor blocker on TGF-ß1, MMP-1, and collagen type I and type III concentration in New Zealand rabbit urethral stricture model.

INTRODUCTION: Urethral stricture is a disease with a high recurrence rate. Angiotensin II via AT1 receptor increases collagen formation through its effects on TGF-ß1 and inhibition of collagenase activity. In this study, we evaluated the antifibrotic effect of angiotensin II receptor blocker on urethral stricture formation by creating a urethral stricture model in a male rabbit. MATERIAL AND METHODS: Thirty three male adult rabbits were separated into 3 groups (control, treatment, and sham). Group I consisted of 15 rabbits with urethral stricture that did not undergo any treatment, group II consisted of 15 rabbits with urethral stricture that were treated with a daily dose of 15 mg/kg losartan, given orally. Group III consisted of 3 rabbits with normal urethra and without any treatment. After 1, 2, and 4 weeks, the urethral tissues were collected, processed, and examined for TGF-ß1, MMP-1, collagen type I, and collagen type III using enzyme-linked immunosorbent assay. Data were analyzed using 2-way analysis of variance using SPSS version 20.0. RESULTS: Urethral TGF-ß1 concentration in the treatment group was significantly lower during the 2nd and 4th week of observation (p<0.0001), MMP-1 was significantly higher in the 1st, 2nd, and 4th week of observation (p<0.0001), collagen type I was significantly lower during the 2nd (p=0.001) and 4th week (p<0.0001), and collagen type III concentration was significantly lower in the 2nd and 4th week of observation (p<0.0001). CONCLUSION: Angiotensin II receptor blocker could limit the progression of urethral stricture. The mechanism may be related to the AT1 blockage that leads to a decrease in TGF-ß1 concentration, eventually resulting in lower collagen concentration due to increased MMP-1 activity.

Alterations of biochemical marker levels and myonuclear numbers in rat skeletal muscle after ischemia-reperfusion.

Prolonged ischemia-reperfusion results in various damages in skeletal muscle. Following reperfusion, although the damaged muscles undergo regeneration, the precise process and mechanism of regeneration have not yet been fully understood. Here, we show the altered levels of plasma biochemical markers of muscle damage, and the change in myonuclear numbers in adult rat skeletal muscle by ischemia-reperfusion. Male Wistar rats were subjected to unilateral hindlimb ischemia by clamping the anterior tibial artery for 2 h before reperfusion. Both plasma creatine kinase activity and C-reactive protein levels in plasma were increased significantly at 0.5 h of reperfusion and returned to the control level at 24 h. The transverse sectional area of muscle belly of the anterior tibial muscles in ischemic side was significantly decreased by 20 % compared with those in sham-ischemic (control) side at 2 days, and returned to the control level at 5 days of reperfusion. Moreover, the number of interstitial nuclei in the ischemic side were significantly increased at 5-14 days and returned to the control level at 21 days of reperfusion. Central nuclei that are specifically observed in regenerating muscle, appeared at 5 days, reached a peak at 14 days, and disappeared at 28 days of reperfusion. Furthermore, MyoD, a regulatory factor for myogenesis, showed a transient expression at 5 days of reperfusion. These results indicate that, although the size of muscle seems to be recovered by 5 days of reperfusion, the most active muscle regeneration occurs much later, as shown by the increase in central nuclei.