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

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Plotkin, Daniel L. ; Mattingly, Madison L. ; Anglin, Derick A. ; Michel, J. Max ; Godwin, Joshua S. ; Mcintosh, Mason C. ; Kontos, Nicholas J. ; Bergamasco, Joao G. A. ; Scarpelli, Maira C. ; Angleri, Vitor ; Taylor, Lemuel W. ; Willoughby, Darryn S. ; Mobley, C. Brooks ; Kavazis, Andreas N. ; Ugrinowitsch, Carlos ; Libardi, Cleiton A. ; Roberts, Michael D.

• Tipo de documento: Artigo Científico
• Fonte: Experimental Physiology; v. 109, n. 10, p. 16-pg., 2024-08-24.

Resumo

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/na & iuml;ve 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 (MyHCTotal) increased 3 h post-RE (similar to 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/na & iuml;ve 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 MyHCTotal fragmentation, similar to 8% VL atrophy with 2 weeks of leg immobilization increased MyHC(Total) fragmentation (similar to 108%, P < 0.001). Mechanistic C2C12 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. (AU)

• Processo FAPESP: 23/04739-2 - Progressão do treinamento de força: efeitos no remodelamento da matriz extracelular de humanos
• Beneficiário: Cleiton Augusto Libardi
• Modalidade de apoio: Auxílio à Pesquisa - Regular