Mechanisms underlying exercise -induced muscle damage

2006 2006

Other formats: Order a copy

Abstract (summary)

The goal of this dissertation was to identify and characterize underlying mechanisms of exercise-induced muscle damage (EIMD) and muscle adaptation to damage. Study I examined contributions of central and peripheral factors to EIMD. Forty-six subjects performed voluntary and stimulated contractions before and immediately following eccentric exercise of the elbow flexors. Subjects demonstrating greater strength loss (a hallmark of EIMD) after eccentric exercise also had greater impairment of peripheral function, but similar central function compared with lower strength loss subjects, suggesting that the mechanism(s) driving variation in strength loss are localized mainly within the periphery.

Study II further focused on peripheral factors, specifically molecular changes in gene expression within muscle tissue following eccentric exercise, to determine underlying molecular mechanisms of damage development. Three subjects performed an exercise in which one leg underwent concentric contractions, and the other leg performed both eccentric and concentric actions. Dependent variables included strength loss, soreness and serum creatine kinase activity. Muscle biopsy samples were taken 4-8h post-exercise. Microarray analysis of these samples identified upregulation of genes involved in inflammation, apoptosis (programmed cell death), structure and transcriptional regulation. These results provided the first global gene expression pattern of human muscle after eccentric exercise.

EIMD is attenuated naturally via the repeated bout effect, where an initial bout of exercise confers a protective effect on muscle that results in less damage induced by a second bout of exercise. Study III aimed to identify mechanisms driving this adaptation. Seven subjects performed two bouts of eccentric exercise of the leg spaced 4wk apart. Muscle strength and soreness were evaluated and biopsies were collected at 6h post-exercise. Muscle samples were tested for expression of a subset of inflammatory genes identified in Study II. Study III showed upregulation of monocyte chemoattractant protein-1 and the transcription factors CEBPD and ZFP36 following the repeated bout. Monocyte chemoattractant protein 1 (MCP-1) was co-localized to macrophages and satellite cells, which are vital to muscle regeneration. These data suggest that specific alterations in the inflammation response may drive the repeated bout effect, possibly by enhancing communication between macrophages and satellite cells, which may strengthen muscle regeneration following EIMD.

Indexing (details)

Sports medicine;
Anatomy & physiology;
0575: Sports medicine
0382: Rehabilitation
0382: Therapy
0433: Anatomy & physiology
0433: Animals
Identifier / keyword
Health and environmental sciences; Biological sciences; Eccentric exercise; Elbow flexors; Exercise-induced; Muscle damage; Serum creatine kinase
Mechanisms underlying exercise -induced muscle damage
Hubal, Monica J.
Number of pages
Publication year
Degree date
School code
DAI-B 67/04, Dissertation Abstracts International
Place of publication
Ann Arbor
Country of publication
United States
9780542656705, 0542656701
Clarkson, Priscilla M.
University of Massachusetts Amherst
University location
United States -- Massachusetts
Source type
Dissertations & Theses
Document type
Dissertation/thesis number
ProQuest document ID
Database copyright ProQuest LLC; ProQuest does not claim copyright in the individual underlying works.
Document URL
Access the complete full text

You can get the full text of this document if it is part of your institution's ProQuest subscription.

Try one of the following:

  • Connect to ProQuest through your library network and search for the document from there.
  • Request the document from your library.
  • Go to the ProQuest login page and enter a ProQuest or My Research username / password.