{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,30]],"date-time":"2026-09-30T19:00:57Z","timestamp":1790794857288,"version":"4.1.0"},"reference-count":57,"publisher":"American Physiological Society","issue":"2","funder":[{"DOI":"10.13039\/100004396","name":"Pepsico Inc.","doi-asserted-by":"publisher","award":["PepsiCo 2010-NDA-04113"],"award-info":[{"award-number":["PepsiCo 2010-NDA-04113"]}],"id":[{"id":"10.13039\/100004396","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Heart and Circulatory Physiology"],"published-print":{"date-parts":[[2015,7,15]]},"abstract":"<jats:p> Limb tissue and systemic blood flow increases with heat stress, but the underlying mechanisms remain poorly understood. Here, we tested the hypothesis that heat stress-induced increases in limb tissue perfusion are primarily mediated by local temperature-sensitive mechanisms. Leg and systemic temperatures and hemodynamics were measured at rest and during incremental single-legged knee extensor exercise in 15 males exposed to 1 h of either systemic passive heat-stress with simultaneous cooling of a single leg ( n = 8) or isolated leg heating or cooling ( n = 7). Systemic heat stress increased core, skin and heated leg blood temperatures (T<jats:sub>b<\/jats:sub>), cardiac output, and heated leg blood flow (LBF; 0.6 \u00b1 0.1 l\/min; P &lt; 0.05). In the cooled leg, however, LBF remained unchanged throughout ( P &gt; 0.05). Increased heated leg deep tissue blood flow was closely related to T<jats:sub>b<\/jats:sub> ( R<jats:sup>2<\/jats:sup> = 0.50; P &lt; 0.01), which is partly attributed to increases in tissue V\u0307O<jats:sub>2<\/jats:sub> ( R<jats:sup>2<\/jats:sup> = 0.55; P &lt; 0.01) accompanying elevations in total leg glucose uptake ( P &lt; 0.05). During isolated limb heating and cooling, LBFs were equivalent to those found during systemic heat stress ( P &gt; 0.05), despite unchanged systemic temperatures and hemodynamics. During incremental exercise, heated LBF was consistently maintained \u223c0.6 l\/min higher than that in the cooled leg ( P &lt; 0.01), with LBF and vascular conductance in both legs showing a strong correlation with their respective local T<jats:sub>b<\/jats:sub> ( R<jats:sup>2<\/jats:sup> = 0.85 and 0.95, P &lt; 0.05). We conclude that local temperature-sensitive mechanisms are important mediators in limb tissue perfusion regulation both at rest and during small-muscle mass exercise in hyperthermic humans. <\/jats:p>","DOI":"10.1152\/ajpheart.00078.2015","type":"journal-article","created":{"date-parts":[[2015,5,1]],"date-time":"2015-05-01T21:32:57Z","timestamp":1430515977000},"page":"H369-H380","source":"Crossref","is-referenced-by-count":61,"title":["Local temperature-sensitive mechanisms are important mediators of limb tissue hyperemia in the heat-stressed human at rest and during small muscle mass exercise"],"prefix":"10.1152","volume":"309","author":[{"given":"Scott T.","family":"Chiesa","sequence":"first","affiliation":[{"name":"Centre for Sports Medicine and Human Performance, Brunel University London, Uxbridge, UK; and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Steven J.","family":"Trangmar","sequence":"additional","affiliation":[{"name":"Centre for Sports Medicine and 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