Antagonistic muscle prefatigue weakens the functional corticomuscular coupling during isometric elbow extension contraction.

OBJECTIVE: During muscle fatigue, acute changes in the interaction between the sensorimotor cortex and peripheral neurons have been widely studied. However, it is still unclear about the effect of antagonist muscle prefatigue on corticomuscular coupling and central modulation. The purpose of this study was to investigate the changes in the magnitude of electroencephalogram-electromyography (EEG-EMG) coherence and phase synchronization index (PSI) induced by antagonistic muscle prefatigue. METHODS: Twelve young male volunteers conducted a 30-s long, nonfatiguing isometric elbow extension with a target force level of 20% maximum voluntary contraction (MVC) before and after a fatiguing sustained elbow flexion contraction at 20% MVC until task failure. Coherence and PSI between the EEG recorded over the sensorimotor cortex and the surface EMG of the triceps brachii (TB) muscle were quantified for the pre- and post-fatigue elbow extension contractions. RESULTS: Coherence and PSI in the gamma frequency band (35-60 Hz) were found significantly decreased in the postfatigue elbow extension contraction than the prefatigue contraction. The power of the EEG in the beta and gamma band were significantly increased, while the EMG power showed no significant changes when the antagonistic muscle was prefatigued. PSI in the gamma frequency band between the EMG of the TB muscle and the EEG were found significantly decreased during postfatigue elbow extension contraction compared with prefatigue contraction. CONCLUSION: Antagonistic muscle prefatigue led to significantly lower gamma band corticomuscular coherence and phase coupling during an isometric elbow extension position task. The lower corticomuscular coupling may indicate a central modulation mechanism of antagonist muscle prefatigue that related to decreased descending common drive or joint instability compensation modulation mechanism.

Antagonist Muscle Prefatigue Increases the Intracortical Communication between Contralateral Motor Cortices during Elbow Extension Contraction.

To investigate the cortico-cortical coupling changes related to antagonist muscle prefatigue, we recorded EEG at FC3, C3, FC4, and C4 electrodes of twelve young male volunteers during a 30-second-long, nonfatiguing isometric elbow extension contraction with a target force level of 20% MVC before and after a sustained fatiguing elbow flexion contraction until task failure. EEG-EEG phase synchronization indices in alpha and beta frequency bands were calculated for the pre- and postfatigue elbow extension contractions. The phase synchronization index in the beta frequency band was found significantly increased between EEG of FC3-C3. The increased phase synchronization index may reflect an enhanced intracortical communication or integration of the signals between contralateral motor cortices with antagonist muscle prefatigue, which may be related to the central modulation so as to compensate for the antagonist muscle prefatigue-induced joint instability.

Fatigue-related electromyographic coherence and phase synchronization analysis between antagonistic elbow muscles.

The aim of this study was to examine coherence and phase synchronization between antagonistic elbow muscles and thus to explore the coupling and common neural inputs of antagonistic elbow muscles during sustained submaximal isometric fatiguing contraction. Fifteen healthy male subjects sustained an isometric elbow flexion at 20 % maximal level until exhaustion, while surface electromyographic signals (sEMG) were collected from biceps brachii (BB) and triceps brachii (TB). sEMG signals were divided into the first half (stage 1 with minimal fatigue) and second half (stage 2 with severe fatigue) of the contraction. Coherence and phase synchronization analysis was conducted between sEMG of BB and TB, and coherence value and phase synchronization index in alpha (8-12 Hz), beta (15-35 Hz) and gamma (35-60 Hz) frequency bands were obtained. Significant increase in EMG-EMG coherence and phase synchronization index in alpha and beta frequency bands between antagonistic elbow flexion muscles was observed all increased in stage 2 compared to stage 1. Coupling of EMG activities between antagonistic muscles increased as a result of fatigue caused by 20 % maximal level sustained isometric elbow flexion, indicating the increased interconnection between synchronized cortical neurons and the motoneuron pool of BB and TB, which may be cortical in origin. This increased coupling may help to maintain coactivation level so as to ensure joint stability on the basis of maintaining the joint force output.

[Effects of exercise and low-fat diet on the TNF-alpha expression of insulin resistance in rats].

OBJECTIVE: To investigate the effects of exercise (EX), low-fat diet (LFD) and their combination intervention on the tumor necrosis factor-alpha (TNF-alpha) expression of insulin resistance in rats. METHODS: One hundred and thirty male rats randomly assigned to 2 groups: Control (CON)-10 rats consuming a low-fat diet; HFD-120 rats consuming a high-fat diet (HFD). The dietary regimen was sustained for 8 wk, at which point the 40 HFD group rats gaining the most weight were referred to as the obese rats. Glucose tolerance was assessed by an oral glucose tolerance test (OGTT). During the procedure of OGTT, the blood was drawn for insulin assay (insulin release test). The whole body insulin resistance was assessed by glucose-insulin index. The obese HFD group rats were randomized into one of four intervention groups: HFD-sedentary (HFD-SED), HFD-exercise(HFD-EX), low fat diet-SED (LFD-SED), LFD-EX. Ex rats performed 8-wk exercise training on a motorized treadmill. The CON group had access to low-fat diet for another 8 wk. After 8 wk of exercise and low-fat diet intervention, the OGTT and insulin release test were performed again. To use ELISA technique for detecting TNF-alpha in soleus muscle and adipose tissue. RESULTS: After being fed high-fat diet for 8 wk, glucose-insulin index in the HFD group were significantly greater than that in CON group (P < 0.01). After 8-week exercise and low-fat diet intervention, glucose-insulin index in HFD-SED group was significantly greater than that in CON group (P < 0.01). The index in three intervention groups was significantly less than that in HFD-SED group (P < 0.01) . TNF-alpha content in adipose tissue and the soleus muscle for HFD-SED group was significantly greater than that in CON group (P < 0.01). Three intervention groups were significantly less than HFD-SED group (P < 0.01). CONCLUSION: Exercise and low-fat diet interventions can decrease the TNF-alpha expression in insulin resistance rat.

[Effects of exercise and diet intervention on oxidative stress in insulin resistant rat].

OBJECTIVE: To investigate the effects of exercise, diet and their combination intervention on oxidative stress of insulin resistance rat. METHODS: Establish obesity-induced insulin resistance rat models. Obesity was assessed by the body weight and lipid ratio. Glucose tolerance was assessed by the integrated area under the curve for glucose (AUCg) during an oral glucose tolerance test (OGTT), then 8 weeks of exercise, diet, and combination interventions, respectively. To analyze serum free fatty acids (FFA) content, superoxide dismutase (SOD) and maleic dialdehyde (MDA) content in liver, adipose tissue and soleus muscle by biochemical method. Judge oxidative stressby FFA content and SOD/MDA. RESULTS: Three kinds of intervention reduced the body weight (P < 0.01), lipid ratio (P < 0.01) and AUCg (P < 0.01). Dietary and combination intervention lowered serum free fatty acid concentration (P < 0.01), separate exercise intervention had not such effect. Three kinds of intervention increased SOD/MDA in the liver and adipose tissue, exercise and combination intervention improved SOD/MDA in soleus muscle, dietary intervention alone had not the effect. CONCLUSION: Exercise and dietary intervention may improve the overall insulin resistance by alleviating oxidative stress.

Nandrolone attenuates aortic adaptation to exercise in rats.

AIMS: In this study, we investigated the interaction between exercise-induced mitochondrial adaptation of large vessels and the effects of chronic anabolic androgenic steroids (AASs). METHODS AND RESULTS: Four groups of Sprague-Dawley rats were studied: (i) sedentary, (ii) sedentary + nandrolone-treated, (iii) aerobic exercise trained, and (iv) trained + nandrolone-treated. Aerobic training increased the levels of aortic endothelial nitric oxide synthase (eNOS) and heme oxygenase-1 (HO-1) in accordance with improved acetylcholine-induced vascular relaxation. These beneficial effects were associated with induction of mitochondrial complexes I and V, increased mitochondrial DNA copy number, and greater expression of transcription factors involved in mitochondrial biogenesis/fusion. We also observed enhanced mitochondrial autophagy pathway activity, including increased conversion of LC3-I to LC3-II and greater expression of beclin1 and autophagy-related protein-7 (ATG7). The levels of thiobarbituric acid-reactive substances and protein carbonyls remained unchanged, whereas significant increases in catalase and mitochondrial manganese superoxide dismutase (MnSOD) levels were observed in the aortas of trained animals, when compared with sedentary controls. Nandrolone increased oxidative stress biomarkers and inhibited exercise-induced increases of eNOS, HO-1, catalase, and MnSOD expression. In addition, it also attenuated elevated peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α) and mitofusin-2 expression, and further up-regulated LC3II conversion, beclin1, ATG7, and dynamin-related protein-1 expression. CONCLUSION: These results demonstrate that nandrolone attenuates aortic adaptations to exercise by regulating mitochondrial dynamic remodelling, including down-regulation of mitochondrial biogenesis and intensive autophagy.

Low-intensity voluntary running lowers blood pressure with simultaneous improvement in endothelium-dependent vasodilatation and insulin sensitivity in aged spontaneously hypertensive rats.

Our objective is to examine the effects of voluntary running at different intensity levels on blood pressure, endothelium-dependent vessel dysfunction and insulin resistance in aged spontaneously hypertensive rats (SHR) with severe hypertension. Ten-month-old male and female SHR with severe hypertension were assigned to voluntary running at either low intensity (30% of maximal aerobic velocity) or moderate intensity (60% of maximal aerobic velocity) on a motor-driven treadmill for 6 weeks, 20 min per day and 7 days per week. Age-matched Wistar-Kyoto rats and SHR were kept under sedentary conditions as controls. Blood pressure and heart rate were measured by the tail-cuff method. At the end of the exercise training, blood samples were collected for glucose, insulin and lipids assay, and aortae were isolated to examine their function in vitro. Low-intensity but not moderate-intensity running significantly lowered blood pressure in both male and female SHR (p<0.01). There was significant impairment in acetylcholine-induced vasorelaxation in SHR (p<0.01), which was improved by low-intensity training (p<0.05). Nitric oxide synthase blockade abrogated the improvement in endothelium-dependent relaxation. Hypertensive rats had elevated blood glucose and insulin levels with lowered insulin sensitivity that was ameliorated by low-intensity running. A significant increase in blood high-density lipoprotein (HDL)-cholesterol and a significant decrease in triglycerides were found in exercised SHR. In conclusion, low-intensity voluntary exercise lowers hypertension in aged SHR with severe hypertension. Exercise-induced simultaneous improvement in endothelium-dependent vessel relaxation and insulin sensitivity may act concomitantly in attenuating cardiovascular risk factors in aged hypertensive rats with significantly high blood pressure.