Sprint interval exercise disrupts mitochondrial ultrastructure driving a unique mitochondrial stress response and remodelling in men

Botella, J. ; Perri, E. ; Caruana, N. J. ; López-Calcerrada, S. ; Brischigliaro, M. ; Jamnick, N. A. ; Oorschot, V. ; Saner, N. J. ; Díaz-Lara, J. ; Taylor, D. F. ; Garnham, A. ; Fernández-Vizarra, E. (Universidad de Zaragoza) ; Ugalde, C. ; Ramm, G. ; Stroud, D. A. ; Lazarou, M. ; Bishop, D. J.

Resumen: Exercise is a key lifestyle intervention for mitochondrial health, yet the molecular mechanisms by which different exercise prescriptions regulate mitochondrial remodeling remain unclear. We conducted an open-label counterbalanced randomized controlled trial (ACTRN12617001105336) and observed that sprint-interval exercise (SIE; n = 14), compared to moderate intensity continuous exercise (MICE; n = 14), induces a mitochondrial stress signature and unfolded protein response (UPRmt
). SIE triggers morphological and structural mitochondrial alterations along with activation of the integrated stress response (ISR) and mitochondrial quality control (MQC) pathways. Following eight weeks of training, moderate-intensity continuous
training (MICT) increases mitochondrial content, complex I activity, and displays an enrichment of tricarboxylic acid (TCA) cycle and oxidative phosphorylation (OXPHOS) proteins, while sprint-interval training (SIT) improves respiratory function and upregulates pathways involved in 1-carbon metabolism and protein quality control. We identify COX7A2L accumulating in III2 + IV1 supercomplexes only after SIT. These findings elucidate how exercise intensity shapes mitochondrial remodeling, informing tailored exercise prescriptions.

Idioma: Inglés

DOI: 10.1038/s41467-025-66625-8

Año: 2025

Publicado en: Nature communications 17 (2025), 71 [19 pp.]
ISSN: 2041-1723

Financiación: info:eu-repo/grantAgreement/ES/MICINN/PID2023-147288NB-I00

Tipo y forma: Artículo (PostPrint)

Área (Departamento): Área Bioquímica y Biolog.Mole. (Dpto. Bioq.Biolog.Mol. Celular)