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Autophagic Cell Death

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Updated: Mar 31, 2026

Activating Autophagy by Aerobic Exercise in Mice

Activating Autophagy by Aerobic Exercise in Mice

Published on: February 3, 2017

Exercise, Autophagy, and Apoptosis.

Frank C Mooren¹, Karsten Krüger¹

¹Department of Sports Medicine, University of Giessen, Giessen, Germany.

Progress in Molecular Biology and Translational Science

|October 20, 2015

Summary

This summary is machine-generated.

Exercise triggers cellular adaptation through apoptosis and autophagy. These processes manage tissue damage and aid muscle plasticity, crucial for adapting to physical stress.

Keywords:

Adaptation process Cell death Cell stress Inflammation Protein degradation Signaling Tissue damage

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Published on: July 21, 2017

Area of Science:

Cellular Biology
Exercise Physiology

Background:

Exercise acts as a physiological stressor, initiating adaptational responses.
Cellular mechanisms like apoptosis and autophagy are implicated in exercise adaptation.

Purpose of the Study:

To explore the roles of apoptosis and autophagy in the body's adaptation to exercise.
To understand how these cellular processes contribute to tissue repair and plasticity post-exercise.

Main Methods:

The study proposes the involvement of apoptosis and autophagy in exercise adaptation.
It discusses mediators like reactive oxygen species, cytokines, and hormones in apoptosis induction.
It highlights the activation of autophagic pathways by damaged proteins and organelles.

Main Results:

Apoptosis and autophagy are induced during exercise to mitigate tissue damage and inflammation.
Autophagy recycles cellular resources, while apoptosis is triggered when repair mechanisms are overwhelmed.
Exercise adaptation involves both local muscle plasticity (autophagy) and systemic progenitor cell mobilization (apoptosis).

Conclusions:

Autophagy is essential for creating conditions for muscle plasticity during exercise adaptation.
Apoptosis plays a systemic role by mobilizing progenitor cells, contributing to overall adaptation.
Both processes are vital for managing cellular stress and promoting tissue integrity in response to exercise.