Abstract
The α7β1 integrin is increased in skeletal muscle in response to injury-producing exercise, and transgenic overexpression of this integrin in mice protects against exercise-induced muscle damage. The present study investigates whether the increase in the α7β1 integrin observed in wild-type mice in response to exercise is due to transcriptional regulation and examines whether mobilization of the integrin at the myotendinous junction (MTJ) is a key determinant in its protection against damage. A single bout of downhill running exercise selectively increased transcription of the α7 integrin gene in 5-wk-old wild-type mice 3 h postexercise, and an increased α7 chain was detected in muscle sarcolemma adjacent to tendinous tissue immediately following exercise. The α7B, but not α7A isoform, was found concentrated and colocalized with tenascin-C in muscle fibers lining the MTJ. To further validate the importance of the integrin in the protection against muscle damage following exercise, muscle injury was quantified in α7-/- mice. Muscle damage was extensive in α7 -/- mice in response to both a single and repeated bouts of exercise and was largely restricted to areas of high MTJ concentration and high mechanical force near the Achilles tendon. These results suggest that exercise-induced muscle injury selectively increases transcription of the α7 integrin gene and promotes a rapid change in the α7β integrin at the MTJ. These combined molecular and cellular alterations are likely responsible for integrin-mediated attenuation of exercise-induced muscle damage.
Original language | English (US) |
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Pages (from-to) | R1623-R1630 |
Journal | American Journal of Physiology - Regulatory Integrative and Comparative Physiology |
Volume | 295 |
Issue number | 5 |
DOIs | |
State | Published - Nov 2008 |
Keywords
- Exercise
- Injury
- Repeated bout effect
- Tenascin-C
ASJC Scopus subject areas
- General Medicine