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Cardiac remodeling is a physiological adaptation to aerobic exercise and which is characterized by increases in ventricular volume and the number of cardiomyocytes. The mitochondrial derived peptide MOTS-c functions as an important regulator in physical capacity and performance. Exercise elevates levels of endogenous MOTS-c in circulation and in myocardium, while MOTS-c can significantly enhance exercise capacity. However, the effects of aerobic exercise combined with MOTS-c on cardiac structure and function are unclear. We used pressure–volume conductance catheter technique to examine cardiac function in exercised rats with and without treatment with MOTS-c. Surprisingly, MOTS-c improved myocardial mechanical efficiency, enhanced cardiac systolic function, and had a tendency to improve the diastolic function. The findings suggest that using exercise supplements could be used to modulate the cardiovascular benefits of athletic training.

Objective: Exercise-induced muscle fatigue is a complex physiological phenomenon involving the central and peripheral nervous systems, and fatigue tolerance varies across individuals. Various studies have emphasized the close relationships between muscle fatigue and the brain. However, the relationships between the resting-state electroencephalogram (rsEEG) brain network and individual muscle fatigue tolerance remain unexplored. Approach: Eighteen elite water polo athletes took part in our experiment. Five-minute before- and after-fatigue-exercise rsEEG and fatiguing task (i.e., elbow flexion and extension) electromyography (EMG) data were recorded. Based on the graph theory, we constructed the before- and after-task rsEEG coherence network and compared the network differences between them. Then, the correlation between the before-fatigue rsEEG network properties and the EMG fatigue indexes when a subject cannot keep on exercising anymore was profiled. Finally, a prediction model based on the before-fatigue rsEEG network properties was established to predict fatigue tolerance. Main Results: Results of this study revealed the significant differences between the before- and after-exercise rsEEG brain network and found significant high correlations between before-exercise rsEEG network properties in the beta band and individual muscle fatigue tolerance. Finally, an efficient support vector regression (SVR) model based on the before-exercise rsEEG network properties in the beta band was constructed and achieved the accurate prediction of individual fatigue tolerance. Similar results were also revealed on another thirty-subject swimmer data set further demonstrating the reliability of predicting fatigue tolerance based on the rsEEG network. Significance: Our study investigates the relationship between the rsEEG brain network and individual muscle fatigue tolerance and provides a potential objective physiological biomarker for tolerance prediction and the regulation of muscle fatigue.

Exercise mimetics are bioactive compounds that activate signaling pathways to simulate exercise-like benefits. Physical exercise activates peroxisome proliferator-activated receptor δ (PPAR δ), a master transcriptional regulator of skeletal muscle oxidative metabolism, and also stimulates AMP-activated protein kinase, a regulator of skeletal muscle glucose uptake, fat oxidation, and mitochondrial biogenesis. Exercise mimetics have therapeutic potential by activating pathways that regulate metabolic endurance, but our knowledge of these compounds is based almost entirely on preclinical findings in rodents.

Pathologic cardiac remodeling and dysfunction are the most common complications of type 2 diabetes. Physical exercise is important in inhibiting myocardial pathologic remodeling and restoring cardiac function in diabetes. The mitochondrial-derived peptide MOTS-c has exercise-like effects by improving insulin resistance, combatting hyperglycemia, and reducing lipid accumulation. We investigated the effects and transcriptomic profiling of MOTS-c and aerobic exercise on cardiac properties in a rat model of type 2 diabetes which was induced by feeding a high fat high sugar diet combined with an injection of a low dose of streptozotocin. Both aerobic exercise and MOTS-c treatment reduced abnormalities in cardiac structure and function. Transcriptomic function enrichment analysis revealed that MOTS-c had exercise-like effects on inflammation, myocardial apoptosis, angiogenesis and endothelial cell proliferation and migration, and showed that the NRG1-ErbB4 pathway might be an important component in both MOTS-c and exercise induced attenuation of cardiac dysfunction in diabetes. Moreover, our findings suggest that MOTS-c activates NRG1-ErbB4 signaling and mimics exercise-induced cardio-protection in diabetes.

As a cathode material for thermal batteries, WS 2 has high thermal decomposition temperature and large specific capacity, but it is an intermittent semiconductor, with relatively low conductivity. This low conductivity can prolong the activation time and reduce the discharge specific capacity of thermal batteries. Here, we prepared WS 2 with sulfur vacancies through a simple hightemperature annealing method and used electron paramagnetic resonance spectroscopy and X-ray photoelectron spectroscopy to detect the presence of sulfur vacancies. The result shows that sulfur vacancies were successfully introduced in WS 2 , and the existence of sulfur vacancies can effectively improve the discharge performance of thermal batteries. While maintaining the nanostructure, the thermal decomposition temperature still exceeds 1000 °C, which is far beyond the traditional FeS 2 (550 °C) and CoS 2 (650 °C) cathodes. The Li-B/LiF-LiBr-LiCl/WS 2 with sulfur vacancies (treated at 500 °C) couple has higher discharge specific capacity (when the cut-off voltage is 0.5 V, it is 380.58 mAh g −1 , which is 14.85% higher than the original WS 2 ) and lower total polarization (about 21% lower than original WS 2 ). This work provides a beginning for further study of sulfur vacancies defect materials as the cathode of thermal batteries.