Aging causes degenerative changes such as epigenetic changes and mitochondrial dysfunction in skeletal muscle. Exercise can upregulate muscle mitochondrial homeostasis and enhance antioxidant capacity and represents an effective treatment to prevent muscle aging. Epigenetic changes such as DNA methylation, histone posttranslational modifications, and microRNA expression are involved in the regulation of exercise-induced adaptive changes in muscle mitochondria. Reactive oxygen species (ROS) play an important role in signaling molecules in exercise-induced muscle mitochondrial health benefits, and strong evidence emphasizes that exercise-induced ROS can regulate gene expression via epigenetic mechanisms. The majority of mitochondrial proteins are imported into mitochondria from the cytosol, so mitochondrial homeostasis is regulated by nuclear epigenetic mechanisms. Exercise can reverse aging-induced changes in myokine expression by modulating epigenetic mechanisms. In this review, we provide an overview of the role of exercise-generated ROS in the regulation of mitochondrial homeostasis mediated by epigenetic mechanisms. In addition, the potential epigenetic mechanisms involved in exercise-induced myokine expression are reviewed.

The mitochondrial unfolded protein response (UPRmt) can repair and remove misfolded or unfolded proteins in mitochondria and enhance mitochondrial protein homeostasis. Reactive oxygen species (ROS) produced by regular exercise is a crucial signal for promoting health, and skeletal muscle mitochondria are the primary source of ROS during exercise. To verify whether UPRmt is related to ROS produced by mitochondria in skeletal muscle during regular exercise, we adapted MitoTEMPO, mitochondrially targeted antioxidants, and ROS production by mitochondria. Our results showed that mitochondrial ROS is the key factor for activating UPRmt in different pathways.

In real world, the ecological systems are usually perturbed by human exploitation activities such as planting and harvesting and so on. In order to obtain a more accurate description for such phenomenon, the impulsive differential equations play an important role. This paper is concerned with a kind of almost periodic Schoener’s competition model with pure-delays and impulsive effects. By using the comparison theorem and the Lyapunov functional method of the impulsive differential equations, some sufficient conditions are obtained for the persistence and existence of a unique uniformly asymptotically stable positive almost periodic solution in a class of impulsive Schoener’s competition model with pure-delays. The main results in this paper improve some results in recent years. And the method used in this paper provides a possible and effective method to study the permanence and existence of a unique uniformly asymptotically stable positive almost periodic solution of the models with impulsive perturbations in biological populations. Finally, an example and numerical simulations are given to illustrate the feasibility and effectiveness of our main results.