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The hypothesis was that SIT upregulates genes involved in mitochondrial function and fat metabolism. A total of 15 subjects performed three 30\u2010s all\u2010out sprints (SIT). Samples were collected from AT, skeletal muscle (SM) and blood (brachial artery and a subcutaneous AT vein) up to 15\u2009min after the last sprint. Results showed that markers of oxidative stress, such as the purines hypoxanthine, xanthine and uric acid, increased markedly by SIT in both the artery and the AT vein. Purines also increased in AT and SM tissue. Differential gene expression analysis indicated a decrease in signaling for mitochondrial\u2010related pathways, including oxidative phosphorylation, electron transport, ATP synthesis, and heat production by uncoupling proteins, as well as mitochondrial fatty acid beta oxidation. This downregulation of genes related to oxidative metabolism suggests an early\u2010stage inhibition of the mitochondria, potentially as a protective mechanism against SIT\u2010induced oxidative stress.<\/jats:p>","DOI":"10.14814\/phy2.70088","type":"journal-article","created":{"date-parts":[[2024,10,21]],"date-time":"2024-10-21T07:15:27Z","timestamp":1729494927000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":4,"title":["Decreased mitochondrial\u2010related gene expression in adipose tissue after acute sprint exercise in humans: A pilot study"],"prefix":"10.14814","volume":"12","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-9432-9725","authenticated-orcid":false,"given":"Mona","family":"Esbj\u00f6rnsson","sequence":"first","affiliation":[{"name":"Division of Clinical Physiology, Department of Laboratory Medicine Karolinska Institutet  Stockholm Sweden"},{"name":"Unit of Clinical Physiology Karolinska University 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