Chapter Seventeen - Exercise, Autophagy, and Apoptosis

https://doi.org/10.1016/bs.pmbts.2015.07.023Get rights and content

Abstract

Exercise is a form of physiological stress which is known to induce an adaptational response.

It is proposed that both apoptosis and autophagy are processes which are necessary for adaptation to exercise. Apoptosis and autophagy are induced during exercise to limit tissue damage, restore tissue integrity, terminate inflammatory responses, or induce direct signals for adaptation. Apoptosis is induced by specific mediators like reactive oxygen species, cytokines, and hormones. Autophagic pathways are activated by altered proteins/organelles with the aim to conserve and recycle the cellular resources. In this case, the cell is flooded with damaged molecules, the repairing mechanisms are overtaxed, and apoptosis is induced. In conclusion, autophagy seems to be necessary for adaptation by providing locally the conditions for muscle plasticity and apoptosis systemically by mobilizing progenitor cells.

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

References (56)

  • C. Mammucari et al.

    FoxO3 controls autophagy in skeletal muscle in vivo

    Cell Metab

    (2007)
  • Z. Feng et al.

    Mitochondrial dynamic remodeling in strenuous exercise-induced muscle and mitochondrial dysfunction: regulatory effects of hydroxytyrosol

    Free Radic Biol Med

    (2011)
  • L. Luo et al.

    Chronic resistance training activates autophagy and reduces apoptosis of muscle cells by modulating IGF-1 and its receptors, Akt/mTOR and Akt/FOXO3a signaling in aged rats

    Exp Gerontol

    (2013)
  • A.D. Rubinstein et al.

    The autophagy protein Atg12 associates with antiapoptotic Bcl-2 family members to promote mitochondrial apoptosis

    Mol Cell

    (2011)
  • P.H. Krammer et al.

    Life and death in peripheral T cells

    Nat Rev Immunol

    (2007)
  • S.J. Korsmeyer

    Programmed cell death and the regulation of homeostasis

    Harvey Lect

    (1999–2000)
  • J.F. Kerr et al.

    Apoptosis: a basic biological phenomenon with wide-ranging implications in tissue kinetics

    Br J Cancer

    (1972)
  • J.M. Blander

    A long-awaited merger of the pathways mediating host defence and programmed cell death

    Nat Rev Immunol

    (2014)
  • Y. Ishizaki et al.

    Programmed cell death by default in embryonic cells, fibroblasts, and cancer cells

    Mol Biol Cell

    (1995)
  • H. Wajant

    Principles and mechanisms of CD95 activation

    Biol Chem

    (2014)
  • S. Cory et al.

    The Bcl2 family: regulators of the cellular life-or-death switch

    Nat Rev Cancer

    (2002)
  • K. Krüger et al.

    Exercise-induced leukocyte apoptosis

    Exerc Immunol Rev

    (2014)
  • N.V. Vorobjeva et al.

    Neutrophil extracellular traps: mechanisms of formation and role in health and disease

    Biochemistry (Mosc)

    (2014)
  • J. Atamaniuk et al.

    Effects of ultra-marathon on circulating DNA and mRNA expression of pro- and anti-apoptotic genes in mononuclear cells

    Eur J Appl Physiol

    (2008)
  • F.C. Mooren et al.

    Exercise-induced apoptosis of lymphocytes depends on training status

    Med Sci Sports Exerc

    (2004)
  • F.C. Mooren et al.

    Lymphocyte apoptosis after exhaustive and moderate exercise

    J Appl Physiol

    (2002)
  • A.C. Levada-Pires et al.

    Induction of lymphocyte death by short- and long-duration triathlon competitions

    Med Sci Sports Exerc

    (2009)
  • J.W. Navalta et al.

    Effect of exercise intensity on exercise induced lymphocyte apoptosis

    Int J Sports Med

    (2007)
  • Cited by (0)

    View full text