Plasma α-Actin as an Early Marker of Muscle Damage After Repeated Bouts of Eccentric Cycling
- Sebastian Jannas-Vela,
- Alvaro Bustamante,
- ,
- Luis Peñailillo
- Universidad Finis Terrae,
- Universidad de O'Higgins,
- ,
- ,
- ,
Publication Information
Output type
Original language
EnglishPages from-to (Number of pages)
Pages 853-860 (8 pages)Journal (Volume, Issue Number)
Research Quarterly for Exercise and Sport (Volume 94, Issue 3)Publication milestones
- Published - 01/01/2023
Publication status
ISSN
0270-1367Publication IDs
- Scopus: 85132607927
- PubMed: 35522171
Abstract
Purpose: This study aimed to examine the changes in skeletal muscle (SM) α-actin, myoglobin (Mb) and hydroxyproline (HP) in plasma and other indirect markers of muscle damage after repeated bouts of eccentric cycling. Methods: Ten healthy men (23.3 ± 2.8 years) performed two 30-min eccentric cycling bouts at 100% of maximal concentric power output (230.7 ± 36.9 W) separated by 2 weeks (ECC1 and ECC2). Maximal voluntary isometric contraction (MVIC) peak force of the knee extensor muscles, muscle soreness (SOR), pain pressure threshold (PPT) and plasma levels of SM α-actin, Mb, and HP were measured before, 0.5, 3, 24–168 h after each cycling bout. Results: MVIC peak force decreased on average 10.7 ± 13.1% more after ECC1 than ECC2. SOR was 80% greater and PPT was 12–14% lower after ECC1 than ECC2. Plasma SM α-actin levels increased at 0.5, 3, and 24–72 h after ECC1 (26.1–47.9%), and SM α-actin levels at 24 h after ECC1 were associated with muscle strength loss (r = −0.56, P =.04) and SOR (r = 0.88, P =.001). Mb levels increased at 0.5, 3, and 24 h after ECC1 (200–502%). However, Mb levels at 24 h after ECC1were not associated with muscle strength loss and SOR. HP levels remained unchanged after ECC1. ECC2 did not increase SM α-actin, Mb and HP levels. Conclusion: Our results indicate that α-actin could be used as a potential marker for the early identification of SM damage due to its early appearance in plasma and its association with other indirect markers of muscle damage.
