000168235 001__ 168235
000168235 005__ 20260128162438.0
000168235 0247_ $$2doi$$a10.1038/s41467-025-66625-8
000168235 0248_ $$2sideral$$a146948
000168235 037__ $$aART-2025-146948
000168235 041__ $$aeng
000168235 100__ $$aBotella, J.
000168235 245__ $$aSprint interval exercise disrupts mitochondrial ultrastructure driving a unique mitochondrial stress response and remodelling in men
000168235 260__ $$c2025
000168235 5060_ $$aAccess copy available to the general public$$fUnrestricted
000168235 5203_ $$aExercise 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.
000168235 536__ $$9info:eu-repo/grantAgreement/ES/MICINN/PID2023-147288NB-I00
000168235 540__ $$9info:eu-repo/semantics/openAccess$$aby-nc-nd$$uhttps://creativecommons.org/licenses/by-nc-nd/4.0/deed.es
000168235 655_4 $$ainfo:eu-repo/semantics/article$$vinfo:eu-repo/semantics/acceptedVersion
000168235 700__ $$aPerri, E.
000168235 700__ $$aCaruana, N. J.
000168235 700__ $$aLópez-Calcerrada, S.
000168235 700__ $$aBrischigliaro, M.
000168235 700__ $$aJamnick, N. A.
000168235 700__ $$aOorschot, V.
000168235 700__ $$aSaner, N. J.
000168235 700__ $$aDíaz-Lara, J.
000168235 700__ $$aTaylor, D. F.
000168235 700__ $$aGarnham, A.
000168235 700__ $$0(orcid)0000-0002-2469-142X$$aFernández-Vizarra, E.$$uUniversidad de Zaragoza
000168235 700__ $$aUgalde, C.
000168235 700__ $$aRamm, G.
000168235 700__ $$aStroud, D. A.
000168235 700__ $$aLazarou, M.
000168235 700__ $$aBishop, D. J.
000168235 7102_ $$11002$$2060$$aUniversidad de Zaragoza$$bDpto. Bioq.Biolog.Mol. Celular$$cÁrea Bioquímica y Biolog.Mole.
000168235 773__ $$g17 (2025), 71 [19 pp.]$$tNature communications$$x2041-1723
000168235 8564_ $$s16568725$$uhttps://zaguan.unizar.es/record/168235/files/texto_completo.pdf$$yPostprint
000168235 8564_ $$s1475727$$uhttps://zaguan.unizar.es/record/168235/files/texto_completo.jpg?subformat=icon$$xicon$$yPostprint
000168235 909CO $$ooai:zaguan.unizar.es:168235$$particulos$$pdriver
000168235 951__ $$a2026-01-28-15:38:26
000168235 980__ $$aARTICLE