Dataset Information

Mitochondrial stress drives skeletal muscle remodelling following sprint-interval exercise.

ABSTRACT: Mitochondria play a central role in cellular metabolism and are crucial for maintaining cellular health. Exercise is a proven intervention to enhance mitochondrial function and prevent non-communicable diseases, yet the molecular mechanisms driving exercise-induced mitochondrial remodelling remain unclear. This study compares the effects of moderate-intensity continuous exercise (MICE) and sprint-interval exercise (SIE) on mitochondrial adaptations. We demonstrate that SIE induces mitochondrial stress and activates the mitochondrial unfolded protein response (UPRmt), alongside disturbances in mitochondrial structure while MICE promotes mitochondrial adaptations characterized by increased mitochondrial content. Over an 8-week training period, moderate-intensity continuous training (MICT) and sprint-interval training (SIT) show divergent mitochondrial remodelling. Findings provide novel insights into the mechanisms by which different exercise prescriptions modulate mitochondrial signalling and remodelling in human skeletal muscle, offering a basis for personalized exercise strategies to optimize mitochondrial health.

INSTRUMENT(S):

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Skeletal Muscle

SUBMITTER: David Stroud

LAB HEAD: David Stroud

PROVIDER: PXD059070 | Pride | 2026-01-12

REPOSITORIES: Pride

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			Action	DRS
	20210923_111933_Javi_2021-09-14_Report.xls	Xls
	210811_Nikeisha_NC-2843_DDA_F1.raw	Raw
	210811_Nikeisha_NC-2843_DDA_F10.raw	Raw
	210811_Nikeisha_NC-2843_DDA_F11.raw	Raw
	210811_Nikeisha_NC-2843_DDA_F12.raw	Raw

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Publications

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

Botella J J Perri E E Caruana N J NJ López-Calcerrada S S Brischigliaro M M Jamnick N A NA Oorschot V V Saner N J NJ Díaz-Lara J J Taylor D F DF Garnham A A Fernández-Vizarra E E Ugalde C C Ramm G G Stroud D A DA Lazarou M M Bishop D J DJ

Nature communications 20251201 1

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 (UPR<sup>mt</sup>). SIE ...[more]

PMID: 41326383

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