ABSTRACT
Objective To explore the effects of excise-induced fatigue on the microloop plasticity of prefrontal cortex through observing the expression of parvalbumin positive neurons in prefrontal cortexes of rats induced by exhaustive exercise,so as to find out the possible mechanism of the central regulation of exercise-induced fatigue by measuring the expression of NMDAR2B receptors.Methods Thirty-six Wistar rats were randomly divided into an exhausted group (E),a repeated exhaustion group (RE) and a control group (CG),each of 12.For group E,the adjusted Bedford incremental load of treadmill exercise program was employed:the initial treadmill speed was 8.2 m/min,lasting for 15 minutes,then increased to 15 m/min for another 15 minutes,and finally increased to 20 m/min till exhaustion.For RE group,they were given continuous treadmill exercises to exhaustion for consecutive 7 days.The immunofluorescence technique was used to observe the expression of PV+ interneurons after exhausted treadmill running.The Western blotting technique was used to determine the expression of NMDAR2B in the tissue of the prefrontal cortex.Results After the exhausted treadmill running,the expression of PV+ interneurons in the prefrontal cortexes of both E and RE groups increased significantly compared with the control group(P＜0.01).The immunofluorescence results indicated that NMDAR2B positive neurons were seen in group E,but not obviously in group CG and RE.The Western blotting showed that compared with CG group the protein expression of NMDAR2B in prefrontal cortexes of group E was relatively high,and that of group RE was relatively low,but without significant difference (P＞0.05).The running distance and prefrontal cortex NMDAR2B expression were found negatively correlated (P＜ 0.01).Conclusions Exhaustive exercises have an impact on the plasticity in rats' prefrontal cortex neural network through regulating the local loop of PV positive neurons.This plasticity of the prefrontal cortex is involved in the regulation of central fatigue.The present study might provide morphological basis for the research of central mechanism of the exercise-induced fatigue.
ABSTRACT
Objective To investigate the effect of acute exhausted exercise in high temperature environment on the expression of myocardial HSP70 and plasma ANP level of in rats. Methods Forty eight male Sprague-Dawley rats was randomly and equally assigned to the following six groups:control group(C),exercise group(E),one-hour heat exposure group (H), heat exposure and exercise group (HE), exercise and 24 hours after exercise group(E'),heat exposure and 24 hours after exercise(HE'). Each group consisted of 8 rats. Rats in E,HE,E' and HE' ran on a treadmill until exhaustion, while rats in H and H' were exposed in a high temperature environment (33℃ ,50%RH) for one hour. Rats in C,E,HE and H were killed immediately after exercise or heat exposure. Rats in HE' and E' were killed 24 hours after exercise. Samples from myocardium and serum were collected for determining HSP70,ANP and CK-MB. Results(1) HSP70 levels in groups E and E' are significantly higher than that in group C(P<0.05 and P<0.01,respectively),and the level in group HE' is significantly higher than that in groups H and E'(P<0.01 );The HSP70 level in group H is significantly higher than that in group C. (2) The ANP and CK-MB levels in group E are Significantly higher than that in group C.and in group HE is higher than in group H (P<0.05);The HSP70 levels in group E' and HE' significantly decrease comparing to that in groups E and HE (P<0.01). Conclusions(1)Both heat exposure and exercise can induce the increased expression of myocardial HSP70 in rats and the peak expression is seen 24 hours after exercise. The increased expression of HSP70 may have protective effects on the heat-induced myocardial injury. (2) The increased ANP levels in plasma immediately after exhausted exercise improves the blood circulation in myocardium and hints the potential possibility of myocardial damage. However,the high temperature environment does not strengthen the increase of plasma ANP level that caused by exhaustive exercise.