Skeletal muscle apoptotic response to physical activity

Potential mechanisms for protection

Joe Quadrilatero, Stephen Alway, Esther Dupont-Versteegden

Research output: Contribution to journalReview article

31 Citations (Scopus)

Abstract

Apoptosis is a highly conserved type of cell death that plays a critical role in tissue homeostasis and disease-associated processes. Skeletal muscle is unique with respect to apoptotic processes, given its multinucleated morphology and its apoptosis-associated differences related to muscle and (or) fiber type as well as mitochondrial content and (or) subtype. Elevated apoptotic signaling has been reported in skeletal muscle during aging, stress-induced states, and disease; a phenomenon that plays a role in muscle dysfunction, degradation, and atrophy. Exercise is a strong physiological stimulus that can influence a number of extracellular and intracellular signaling pathways, which may directly or indirectly influence apoptotic processes in skeletal muscle. In general, acute strenuous and eccentric exercise are associated with a proapoptotic phenotype and increased DNA fragmentation (a hallmark of apoptosis), whereas regular exercise training or activity is associated with an antiapoptotic environment and reduced DNA fragmentation in skeletal muscle. Interestingly, the protective effect of regular activity on skeletal muscle apoptotic processes has been observed in healthy, aged, stress-induced, and diseased rodent models. Several mechanisms for this protective response have been proposed, including altered anti- and proapoptotic protein expression, increased mitochondrial biogenesis and improved mitochondrial function, and reduced reactive oxygen species generation and (or) enhanced antioxidant status. Given the current literature, we propose that regular physical activity may represent an effective strategy to decrease apoptotic signaling, and possibly muscle wasting and dysfunction, during aging and disease.

Original languageEnglish (US)
Pages (from-to)608-617
Number of pages10
JournalApplied Physiology, Nutrition and Metabolism
Volume36
Issue number5
DOIs
StatePublished - Oct 1 2011
Externally publishedYes

Fingerprint

Skeletal Muscle
DNA Fragmentation
Apoptosis
Muscles
Rodent Diseases
Organelle Biogenesis
Atrophy
Reactive Oxygen Species
Teaching
Homeostasis
Cell Death
Antioxidants
Exercise
Phenotype
Proteins

All Science Journal Classification (ASJC) codes

  • Endocrinology, Diabetes and Metabolism
  • Physiology
  • Nutrition and Dietetics
  • Physiology (medical)

Cite this

Skeletal muscle apoptotic response to physical activity : Potential mechanisms for protection. / Quadrilatero, Joe; Alway, Stephen; Dupont-Versteegden, Esther.

In: Applied Physiology, Nutrition and Metabolism, Vol. 36, No. 5, 01.10.2011, p. 608-617.

Research output: Contribution to journalReview article

@article{d66c6e6659c24bcb92bc8aa8fe8ab195,
title = "Skeletal muscle apoptotic response to physical activity: Potential mechanisms for protection",
abstract = "Apoptosis is a highly conserved type of cell death that plays a critical role in tissue homeostasis and disease-associated processes. Skeletal muscle is unique with respect to apoptotic processes, given its multinucleated morphology and its apoptosis-associated differences related to muscle and (or) fiber type as well as mitochondrial content and (or) subtype. Elevated apoptotic signaling has been reported in skeletal muscle during aging, stress-induced states, and disease; a phenomenon that plays a role in muscle dysfunction, degradation, and atrophy. Exercise is a strong physiological stimulus that can influence a number of extracellular and intracellular signaling pathways, which may directly or indirectly influence apoptotic processes in skeletal muscle. In general, acute strenuous and eccentric exercise are associated with a proapoptotic phenotype and increased DNA fragmentation (a hallmark of apoptosis), whereas regular exercise training or activity is associated with an antiapoptotic environment and reduced DNA fragmentation in skeletal muscle. Interestingly, the protective effect of regular activity on skeletal muscle apoptotic processes has been observed in healthy, aged, stress-induced, and diseased rodent models. Several mechanisms for this protective response have been proposed, including altered anti- and proapoptotic protein expression, increased mitochondrial biogenesis and improved mitochondrial function, and reduced reactive oxygen species generation and (or) enhanced antioxidant status. Given the current literature, we propose that regular physical activity may represent an effective strategy to decrease apoptotic signaling, and possibly muscle wasting and dysfunction, during aging and disease.",
author = "Joe Quadrilatero and Stephen Alway and Esther Dupont-Versteegden",
year = "2011",
month = "10",
day = "1",
doi = "10.1139/h11-064",
language = "English (US)",
volume = "36",
pages = "608--617",
journal = "Applied Physiology, Nutrition and Metabolism",
issn = "1715-5312",
publisher = "National Research Council of Canada",
number = "5",

}

TY - JOUR

T1 - Skeletal muscle apoptotic response to physical activity

T2 - Potential mechanisms for protection

AU - Quadrilatero, Joe

AU - Alway, Stephen

AU - Dupont-Versteegden, Esther

PY - 2011/10/1

Y1 - 2011/10/1

N2 - Apoptosis is a highly conserved type of cell death that plays a critical role in tissue homeostasis and disease-associated processes. Skeletal muscle is unique with respect to apoptotic processes, given its multinucleated morphology and its apoptosis-associated differences related to muscle and (or) fiber type as well as mitochondrial content and (or) subtype. Elevated apoptotic signaling has been reported in skeletal muscle during aging, stress-induced states, and disease; a phenomenon that plays a role in muscle dysfunction, degradation, and atrophy. Exercise is a strong physiological stimulus that can influence a number of extracellular and intracellular signaling pathways, which may directly or indirectly influence apoptotic processes in skeletal muscle. In general, acute strenuous and eccentric exercise are associated with a proapoptotic phenotype and increased DNA fragmentation (a hallmark of apoptosis), whereas regular exercise training or activity is associated with an antiapoptotic environment and reduced DNA fragmentation in skeletal muscle. Interestingly, the protective effect of regular activity on skeletal muscle apoptotic processes has been observed in healthy, aged, stress-induced, and diseased rodent models. Several mechanisms for this protective response have been proposed, including altered anti- and proapoptotic protein expression, increased mitochondrial biogenesis and improved mitochondrial function, and reduced reactive oxygen species generation and (or) enhanced antioxidant status. Given the current literature, we propose that regular physical activity may represent an effective strategy to decrease apoptotic signaling, and possibly muscle wasting and dysfunction, during aging and disease.

AB - Apoptosis is a highly conserved type of cell death that plays a critical role in tissue homeostasis and disease-associated processes. Skeletal muscle is unique with respect to apoptotic processes, given its multinucleated morphology and its apoptosis-associated differences related to muscle and (or) fiber type as well as mitochondrial content and (or) subtype. Elevated apoptotic signaling has been reported in skeletal muscle during aging, stress-induced states, and disease; a phenomenon that plays a role in muscle dysfunction, degradation, and atrophy. Exercise is a strong physiological stimulus that can influence a number of extracellular and intracellular signaling pathways, which may directly or indirectly influence apoptotic processes in skeletal muscle. In general, acute strenuous and eccentric exercise are associated with a proapoptotic phenotype and increased DNA fragmentation (a hallmark of apoptosis), whereas regular exercise training or activity is associated with an antiapoptotic environment and reduced DNA fragmentation in skeletal muscle. Interestingly, the protective effect of regular activity on skeletal muscle apoptotic processes has been observed in healthy, aged, stress-induced, and diseased rodent models. Several mechanisms for this protective response have been proposed, including altered anti- and proapoptotic protein expression, increased mitochondrial biogenesis and improved mitochondrial function, and reduced reactive oxygen species generation and (or) enhanced antioxidant status. Given the current literature, we propose that regular physical activity may represent an effective strategy to decrease apoptotic signaling, and possibly muscle wasting and dysfunction, during aging and disease.

UR - http://www.scopus.com/inward/record.url?scp=80054022526&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=80054022526&partnerID=8YFLogxK

U2 - 10.1139/h11-064

DO - 10.1139/h11-064

M3 - Review article

VL - 36

SP - 608

EP - 617

JO - Applied Physiology, Nutrition and Metabolism

JF - Applied Physiology, Nutrition and Metabolism

SN - 1715-5312

IS - 5

ER -