Physical exercise generates several benefits in a short time in patients with diabetes mellitus. However, it can increase the chances of muscle damage, a serious problem for diabetic patients. Nonsteroidal anti-inflammatory drugs (NSAIDs) are widely used to treat these injuries, despite the serious adverse effects. In this way, photobiomodulation therapy (PBMT) with low-level laser therapy (LLLT) and/or light emitting diode therapy (LEDT) can be used as an alternative in this case. However, its efficacy in tissue repair of trauma injuries in diabetes mellitus until now is unknown, as well as the combination between PBMT and NSAIDs. The objective of the present study was to evaluate the effects of NSAIDs and PBMT applied alone or combined on functional and biochemical aspects, in an experimental model of muscle injury through controlled trauma in diabetic rats. Muscle injury was induced by means of a single trauma to the animals' anterior tibialis muscle. After 1 h, the rats were treated with PBMT (830 nm; continuous mode, with a power output of 100 mW; 3.57 W/cm; 3 J; 107.1 J/cm, 30 s), diclofenac sodium for topical use (1 g), or combination of them. Our results demonstrated that PBMT + diclofenac, and PBMT alone reduced the gene expression of cyclooxygenase-2 (COX-2) at all assessed times as compared to the injury and diclofenac groups (p < 0.05 and p < 0.01 respectively). The diclofenac alone showed reduced levels of COX-2 only in relation to the injury group (p < 0.05). Prostaglandin E levels in blood plasma demonstrated similar results to COX2. In addition, we observed that PBMT + diclofenac and PBMT alone showed significant improvement compared with injury and diclofenac groups in functional analysis at all time points. The results indicate that PBMT alone or in combination with diclofenac reduces levels of inflammatory markers and improves gait of diabetic rats in the acute phase of muscle injury.
ABSTRACT:The aim of the present study was to investigate the effects of different doses of oral creatine supplementation on tibial muscle resistance and fatigue in Wistar rats. The treatment protocols included swimming exercises, supplementation alone (different doses), and supplementation (different doses) + swimming exercises. Analysis of the effect of creatine supplementation on skeletal muscle fatigue was performed using the intensity of muscle contraction to electrical stimulation to evaluate the intensity of muscle contraction, decay time of muscle tetanic contraction to 50% of maximum tension (fatigue), and the area under the curve for the intensity x time ratio, besides AST, LDH, and urea plasmatic analysis. Our results suggest that creatine supplementation seems to be able to produce ergogenic effects on contractile metabolism in the group treated with the dose of 280 mg/kg + swim exercise. This creatine dose presented a statistically significant increase in decay time of muscle tetanic contraction (C280+swim (119±13.1), C500+swim (110±23.6) and C1000+swim (87±15.1)), area under the curve between tetanic contractions, and plasma LDH decrease, when compared to the other doses. These data clearly demonstrate that high doses do not lead to any additional ergogenic effects. We conclude that the dose of 280 mg/kg+swim exercise obtained the best ergogenic effects on tibial muscle resistance and fatigue in Wistar rats.
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