Skeletal muscle myosin heavy chain fragmentation as a potential marker of protein degradation in response to resistance training and disuse atrophy.

Autor: Plotkin DL; School of Kinesiology, Auburn University, Auburn, Alabama, USA., Mattingly ML; School of Kinesiology, Auburn University, Auburn, Alabama, USA., Anglin DA; School of Kinesiology, Auburn University, Auburn, Alabama, USA., Michel JM; School of Kinesiology, Auburn University, Auburn, Alabama, USA., Godwin JS; School of Kinesiology, Auburn University, Auburn, Alabama, USA., McIntosh MC; School of Kinesiology, Auburn University, Auburn, Alabama, USA., Kontos NJ; School of Kinesiology, Auburn University, Auburn, Alabama, USA., Bergamasco JGA; MUSCULAB - Laboratory of Neuromuscular Adaptations to Resistance Training, Department of Physical Education, Federal University of São Carlos - UFSCar, São Carlos, SP, Brazil., Scarpelli MC; MUSCULAB - Laboratory of Neuromuscular Adaptations to Resistance Training, Department of Physical Education, Federal University of São Carlos - UFSCar, São Carlos, SP, Brazil., Angleri V; MUSCULAB - Laboratory of Neuromuscular Adaptations to Resistance Training, Department of Physical Education, Federal University of São Carlos - UFSCar, São Carlos, SP, Brazil., Taylor LW; School of Health Professions, University of Mary Hardin-Baylor, Belton, Texas, USA., Willoughby DS; School of Health Professions, University of Mary Hardin-Baylor, Belton, Texas, USA., Mobley CB; School of Kinesiology, Auburn University, Auburn, Alabama, USA., Kavazis AN; School of Kinesiology, Auburn University, Auburn, Alabama, USA., Ugrinowitsch C; School of Physical Education and Sport, University of São Paulo - USP, São Paulo, SP, Brazil.; Department of Health Sciences and Human Performance, The University of Tampa, Tampa, Florida, USA., Libardi CA; MUSCULAB - Laboratory of Neuromuscular Adaptations to Resistance Training, Department of Physical Education, Federal University of São Carlos - UFSCar, São Carlos, SP, Brazil., Roberts MD; School of Kinesiology, Auburn University, Auburn, Alabama, USA.
Jazyk: angličtina
Zdroj: Experimental physiology [Exp Physiol] 2024 Oct; Vol. 109 (10), pp. 1739-1754. Date of Electronic Publication: 2024 Aug 24.
DOI: 10.1113/EP092093
Abstrakt: We examined how resistance exercise (RE), cycling exercise and disuse atrophy affect myosin heavy chain (MyHC) protein fragmentation. The 1boutRE study involved younger men (n = 8; 5 ± 2 years of RE experience) performing a lower body RE bout with vastus lateralis (VL) biopsies being obtained prior to and acutely following exercise. With the 10weekRT study, VL biopsies were obtained in 36 younger adults before and 24 h after their first/naïve RE bout. Participants also engaged in 10 weeks of resistance training and donated VL biopsies before and 24 h after their last RE bout. VL biopsies were also examined in an acute cycling study (n = 7) and a study involving 2 weeks of leg immobilization (n = 20). In the 1boutRE study, fragmentation of all MyHC isoforms (MyHC Total ) increased 3 h post-RE (∼200%, P = 0.018) and returned to pre-exercise levels by 6 h post-RE. Interestingly, a greater magnitude increase in MyHC type IIa versus I isoform fragmentation occurred 3 h post-RE (8.6 ± 6.3-fold vs. 2.1 ± 0.7-fold, P = 0.018). In 10weekRT participants, the first/naïve and last RE bouts increased MyHC Total fragmentation 24 h post-RE (+65% and +36%, P < 0.001); however, the last RE bout response was attenuated compared to the first bout (P = 0.045). Although cycling exercise did not alter MyHC Total fragmentation, ∼8% VL atrophy with 2 weeks of leg immobilization increased MyHC Total fragmentation (∼108%, P < 0.001). Mechanistic C 2 C 12 myotube experiments indicated that MyHC Total fragmentation is likely due to calpain proteases. In summary, RE and disuse atrophy increase MyHC protein fragmentation. Research into how ageing and disease-associated muscle atrophy affect these outcomes is needed. HIGHLIGHTS: What is the central question of this study? How different exercise stressors and disuse affect skeletal muscle myosin heavy chain fragmentation. What is the main finding and its importance? This investigation is the first to demonstrate that resistance exercise and disuse atrophy lead to skeletal muscle myosin heavy chain protein fragmentation in humans. Mechanistic in vitro experiments provide additional evidence that MyHC fragmentation occurs through calpain proteases.
(© 2024 The Author(s). Experimental Physiology published by John Wiley & Sons Ltd on behalf of The Physiological Society.)
Databáze: MEDLINE