Chapter Seventeen - Exercise, Autophagy, and Apoptosis
Section snippets
Apoptosis
The term apoptosis describes a special process of cell death that allows cells to die and be lysed in a well-controlled fashion. In general, apoptotic processes play an important role during development and in maintaining tissue homeostasis by guaranteeing a balance between the generation of new cells and the removal of damaged or aged cells. In case of apoptosis induction, the cell is eliminated without necrotic processes which are known to result in local inflammatory conditions.1 Therefore,
Exercise and Apoptosis
Exercise is a type of physiological stress which affects concentration of several cytokines, hormones, growth factors, and the oxidative status. Additionally, exercise affects energy balance by mobilizing and metabolizing high amounts of substrates like carbohydrates and free fatty acids. All these factors are known to potentially mediate either accelerated death or prolonged cellular survival. Thereby, exercise-induced apoptosis signaling depends on exercise intensity and duration, which
Autophagy
Under physiological conditions, autophagy is an intracellular recycling system, which is involved in the clearance of damaged cell components. For proper function, proteins need to be folded into a correct three-dimensional structure, which is challenged by internal processing errors like transcriptional and translational errors as well as external stressors such as high temperature, osmotic stress, and hypoxia. Cells employ several systems to guarantee protein quality control. Heat-shock
Effects of Exercise on Autophagy
Exercise is a newly defined stimulus that induces autophagy in vivo. Although a first description of exercise-induced autophagy dates back to 1984, this topic has attracted more attention just recently. In 2011, Grumati and coworkers showed that physical exercise activated autophagy in skeletal muscle as indicated by an enhanced conversion of LC3-I to LC3-II and the presence of autophagosomes. In collagen VI null mice, which show an impaired autophagic flux, the acute exercise stimulus
Autophagy and Apoptosis: Concluding Remarks
The “self-destroying” ability of cells displayed during apoptosis shows some similarities with the cellular “self-eating” mechanisms during autophagy. Therefore, the relationships or interactions between both degrading mechanisms are of considerable interest. Both autophagy and apoptosis can be activated by similar stress signals. Both processes show similar regulation by BCL-2 which exhibits both antiautophagic and antiapoptotic characteristics. However, the antiautophagic effects of BCL-2 are
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