Assessment of acute neuromuscular fatigue manifestations and functional performances after heavy resistance exercise.

BACKGROUND: This study aimed to assess neuromuscular fatigue after heavy resistance exercise in rugby players. METHODS: Twelve male rugby players performed five sets of knee extension exercise lifting 80% of their one repetition maximum until failure, with 3min of rest in-between. Maximal voluntary contraction (MVC) and surface electromyographic activity from quadriceps muscles, as well as ions (i.e., Na+, K+, and Cl-) and metabolic responses (i.e., blood lactate and ammonia concentrations) were measured before and after exercise. Maximum repetitions performance and both peripheral (RPEp) and overall body (RPEo) rating of perceived exertion were recorded following each set. RESULTS: The number of maximum repetitions decreased significantly across sets (P<0.001). Both RPEp and RPEo increased significantly across sets (P<0.001) with higher RPEp values after each set (P<0.001). Both RPEp (r=-0.98, P<0.01) and RPEo (r=-0.99, P<0.001) were negatively correlated with the changes in the number of maximum repetitions. MVC (P<0.001), root mean square (P<0.05), and neuromuscular efficiency (P<0.01) as well as Na+ (P<0.01), Cl- (P<0.001) and blood concentrations of lactate (P<0.001) and ammonia (P<0.001) increased significantly after the exercise. However, K+ (P<0.001) increased after the resistance exercise. CONCLUSIONS: Heavy resistance exercise affected both objective (i.e., neuromuscular and biochemical parameters) and subjective (i.e., RPE) aspects of neuromuscular fatigue.

Oxidative damage induced by chromium (VI) in rat erythrocytes: protective effect of selenium.

Excess chromium (Cr) exposure is associated with various pathological conditions including hematological dysfunction. The generation of oxidative stress is one of the plausible mechanisms behind Cr-induced cellular deteriorations. The efficacy of selenium (Se) to combat Cr-induced oxidative damage in the erythrocytes of adult rats was investigated in the current study. Female Wistar rats were randomly divided into four groups of six each: group I served as controls which received standard diet, group II received in drinking water K(2)Cr(2)O(7) alone (700 ppm), group III received both K(2)Cr(2)O(7) and Se (0.5 Na(2)SeO(3) mg/kg of diet), and group IV received Se (0.5 mg/kg of diet) for 3 weeks. Rats exposed to K(2)Cr(2)O(7) showed an increase of malondialdehyde and protein carbonyl levels and a decrease of sulfhydryl content, glutathione, non-protein thiol, and vitamin C levels. A decrease of enzyme activities like catalase, glutathione peroxidase, and superoxide dismutase activities was also noted. Co-administration of Se with K(2)Cr(2)O(7) restored the parameters cited above to near-normal values. Therefore, our investigation revealed that Se was a useful element preventing K(2)Cr(2)O(7)-induced erythrocyte damages.

Cobalt chloride induces hepatotoxicity in adult rats and their suckling pups.

To assess liver damages in pregnant and lactating rats and in their suckling pups, wistar female rats were given through drinking water 350 ppm of CoCl(2) (157 ppm Co(2+)) from the 14th day of pregnancy until day 14 after delivery. The effects of cobalt chloride on lipid peroxidation levels, antioxidant enzyme activities, lipid profile and histopathology aspects of liver were evaluated. Biochemical results showed that lipid peroxidation increased significantly in Co-treated rats, as evidenced by high liver thiobarbituric acid-reactive substance (TBARS) levels. Alteration of the antioxidant system in treated group was confirmed by the significant decline of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx) activities and reduced glutathione (GSH) content in liver of suckling pups and their mothers. Moreover, CoCl(2) exposure induced an increase in the activities of the aspartate transaminase (AST), alanine transaminase (ALT), lactate deshydrogenase (LDH) and bilirubin levels in pups and their mothers while liver LDH activity and plasma albumin level were significantly decreased. On the other hand, cobalt chloride induced a marked hypoglycemia, a significant decline in triglycerides and total cholesterol levels. Histological studies showed an infiltration of mononuclear cells and vascular congestion in liver of pups and their mothers. Based on the present findings, exposure of rats to CoCl(2) during late pregnancy and early postnatal period affects antioxidant enzyme activities and lipid peroxidation indicating liver damage in mothers and their offspring.