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An open-label counterbalanced randomized controlled trial compared sprint-interval exercise (SIE) and moderate-intensity continuous exercise (MICE). SIE induced a mitochondrial stress signature with UPRmt, triggering mitochondrial morphological and structural changes plus ISR and MQC activation. After eight weeks, MICT increased mitochondrial content, complex I activity, and enriched TCA cycle/OXPHOS proteins, while sprint training improved respiration and upregulated 1-carbon metabolism and protein quality control pathways. COX7A2L accumulated in III2+IV1 supercomplexes only after SIT.",{"@graph":69,"@context":123},[70,84,106],{"@type":71,"itemListElement":72},"BreadcrumbList",[73,77,79,82],{"item":74,"name":75,"@type":76,"position":8},"https://docshare.wps.com","Home","ListItem",{"item":78,"name":9,"@type":76,"position":14},"https://docshare.wps.com/document/",{"item":80,"name":35,"@type":76,"position":81},"https://docshare.wps.com/document/healthcare/",3,{"item":83,"name":65,"@type":76,"position":19},"https://docshare.wps.com/document/sprint-interval-exercise-disrupts-mitochondrial-ultrastructure-driving-a-unique-mitochondrial-stress-response-and-remodelling-in-men/441003/",{"url":83,"name":65,"@type":85,"image":86,"author":91,"headline":65,"publisher":94,"fileFormat":97,"inLanguage":63,"description":67,"dateModified":98,"datePublished":99,"encodingFormat":97,"isAccessibleForFree":100,"interactionStatistic":101},"DigitalDocument",{"url":87,"@type":88,"width":89,"height":90},"https://docshare.wps.com/thumbnails/sprint-interval-exercise-disrupts-mitochondrial-ultrastructure-driving-a-unique-mitochondrial-stress-response-and-remodelling-in-men/441003.png","ImageObject",300,407,{"name":92,"@type":93},"Noah","Person",{"url":74,"name":95,"@type":96},"DocShare","Organization","application/pdf","2026-10-29","2026-09-29",true,{"@type":102,"interactionType":103,"userInteractionCount":105},"InteractionCounter",{"@type":104},"ViewAction",14,{"@type":107,"mainEntity":108},"FAQPage",[109,115,119],{"name":110,"@type":111,"acceptedAnswer":112},"What was the main research question of the study?","Question",{"text":113,"@type":114},"How different exercise prescriptions regulate mitochondrial remodeling through molecular mechanisms.","Answer",{"name":116,"@type":111,"acceptedAnswer":117},"How did sprint-interval exercise (SIE) compare with moderate-intensity continuous exercise (MICE) in effects on mitochondria?",{"text":118,"@type":114},"SIE induced a mitochondrial stress signature and activated UPRmt, ISR, and MQC pathways, along with mitochondrial structural changes; MICE increased mitochondrial content, complex I activity, and enriched TCA/OXPHOS proteins.",{"name":120,"@type":111,"acceptedAnswer":121},"What key finding was unique to sprint-interval training (SIT) regarding protein accumulation?",{"text":122,"@type":114},"COX7A2L accumulated in III2+IV1 supercomplexes only after SIT.","https://schema.org",{"og:url":83,"og:type":125,"og:title":65,"og:site_name":95,"og:description":67},"article",{"robots":127,"canonical":83},"index,follow",{"doc_id":129,"site_id":62},441003,1790716547,{"code":4,"msg":5,"data":132},{"doc_id":129,"user_id":133,"nickname":92,"user_avatar":134,"doc_module":4,"category_id":34,"category_name":35,"doc_title":65,"doc_description":67,"doc_content":135,"file_id":136,"file_url":137,"file_type":138,"file_size":139,"view_count":105,"is_deleted":4,"is_public":8,"is_downloadable":8,"audit_status":8,"page_count":56,"language":140,"language_code":63,"site_id":62,"html_lang":63,"table_of_contents":141,"faqs":142,"seo_title":143,"seo_description":67,"update_tm":144,"read_time":145,"preview_page_count":4},8796095462418,"https://ap-avatar.wpscdn.com/avatar/80000253c1241d02b47?x-image-process=image/resize,m_fixed,w_180,h_180&k=1778826106357471780","Article [https://doi.org/10.1038/s41467-025-66625-8](https://doi.org/10.1038/s41467-025-66625-8)  \nSprint interval exercise disrupts mitochondrial ultrastructure driving a unique mitochondrial stress response andremodelling in men  \nReceived: 25 January 2025  \n\n| Accepted: 11 November 2025 |\n| --- |\n| |\n| Check for updates |\n\nJ. Botella 1,2 , E. Perri1,3, N. J. Caruana 1,4, S. López-Calcerrada 5, M. Brischigliaro 6,7,8, N. A. Jamnick1,2, V. Oorschot 9,10, N. J. Saner1, J. Díaz-Lara 1,11, D. F. Taylor1, A. Garnham1, E. Fernández-Vizarra 6,7,12, C. Ugalde5,13,14, G. Ramm 9,15, D. A. Stroud 4,16,17, M. Lazarou 15,18,19 &  \nD. J. Bishop 1   \nExercise 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 moderateintensity 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.  \nMitochondria are critical organelles involved in many biological functions, including metabolism, inflammation, and cell death1. Owing to this, suboptimal mitochondrial characteristics (e.g., decreased respiratory function) have been implicated in various medical conditions2,3. These same mitochondrial characteristics are often enhanced in the skeletal muscle of athletes4–7. Given the large energetic demands of contracting skeletal muscle8, it is not surprising that exercise provides a powerful stimulus that can trigger enduring  \nchanges to mitochondrial content, enzyme activity, and respiratory chain function.  \nExercise is a well-known intervention that stimulates the synthesis of new mitochondrial components—a process termed mitochondrial biogenesis9,10. While many of the underlying mechanisms are poorly understood11,12, exercise also remains one of the most effective lifestyle interventions for the prevention of non-communicable diseases13,14. The benefits of exercise are thought to stem from the contraction-induced  \nA full list of affiliations appears at the end of the paper. [e-mail:](e-mail: javier.botella.ruiz@gmail.com)[ javier.botella.ruiz@gmail.com](e-mail: javier.botella.ruiz@gmail.com); [david.bishop@vu.edu.au](david.bishop@vu.edu.au)  \nTable 1 | Baseline characteristics of the participants in the two exercise training groups  \n\n|  | MICE/\u003Cbr>MICT (n =14) | SIE/SIT (n = 14) | ANOVA\u003Cbr>p value |\n| --- | --- | --- | --- |\n| Biological |  |  |  |\n| Age (years) | 26.1± 5.7 | 26.9± 4.9 | 0.685 |\n| Body mass (kg) | 77.0± 10.7 | 76.5± 9.7 | 0.909 |\n| BMI (kg m−2) | 24.1± 2.6 | 23.7± 2.8 | 0.748 |\n| Physiological |  |  |  |\n| ̇VO2max (mL min−1 kg−1) | 52.2± 6.4 | 51.9± 6.5 | 0.789 |\n| ̇Wmax (W kg−1) | 4.2± 0.6 | 4.2± 0.8 | 0.998 |\n| 20 km-TT (W kg−1) | 2.7± 0.5 | 2.7± 0.5 | 0.955 |\n| 4km-TT (W kg−1) | 3.2± 0.5 (n = 13) | 3.1± 0.5 | 0.741 |\n| Molecular |  |  |  |\n| Mitochondrial volume density (%) | 5.2± 0.7 (n =10) | 5.4± 1.6 (n =12) | 0.728 |\n| Citrate Synthase Activity (mol h−1 kg protein−1) | 2.4± 0.5 (n = 12) | 2.6± 0.7 (n =12) | 0.459 |\n| Mitoch","cbCaibJsyqr4WX3o","https://ap.wps.com/l/cbCaibJsyqr4WX3o","pdf",2631479,"English","# Background\n## Exercise and mitochondrial remodeling\n## Mitochondria in health and disease\n# Methods\n## Trial design and groups\n# Results\n## Mitochondrial stress response (UPRmt)\n## Structural and pathway changes after training\n## COX7A2L supercomplex accumulation\n# Implications\n## Tailored exercise prescriptions for mitochondrial health","[{\"question\":\"What was the main research question of the study?\",\"answer\":\"How different exercise prescriptions regulate mitochondrial remodeling through molecular mechanisms.\"},{\"question\":\"How did sprint-interval exercise (SIE) compare with moderate-intensity continuous exercise (MICE) in effects on mitochondria?\",\"answer\":\"SIE induced a mitochondrial stress signature and activated UPRmt, ISR, and MQC pathways, along with mitochondrial structural changes; MICE increased mitochondrial content, complex I activity, and enriched TCA/OXPHOS proteins.\"},{\"question\":\"What key finding was unique to sprint-interval training (SIT) regarding protein accumulation?\",\"answer\":\"COX7A2L accumulated in III2+IV1 supercomplexes only after SIT.\"}]","Sprint Interval Exercise Disrupts Mitochondrial Ultrastructure - Driving a Unique Mitochondrial Stress Response and Remodelling in Men | PDF",1790694245,48]