{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,9]],"date-time":"2026-10-09T05:23:01Z","timestamp":1791523381833,"version":"4.3.4"},"reference-count":41,"publisher":"American Physiological Society","issue":"4","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Journal of Applied Physiology"],"published-print":{"date-parts":[[2014,8,15]]},"abstract":"<jats:p> The primary objective of this study was to determine whether cardiovascular compensatory response phenotypes exist in the face of a reduced perfusion pressure challenge to exercising muscle oxygen delivery (O<jats:sub>2<\/jats:sub>D), and whether these responses might be exercise intensity (EI) dependent. Ten healthy men (19.5 \u00b1 0.4 yr) completed two trials of progressive forearm isometric handgrip exercise to exhaustion (24.5 N increments every 3.5 min) in each of forearm above and below heart level [forearm arterial perfusion pressure (FAPP) difference of 29.5 \u00b1 0.97 mmHg]. At the end of each EI, measurements of forearm blood flow (FBF; ml\/min) via brachial artery Doppler and echo ultrasound, mean arterial blood pressure (MAP; mmHg) via finger photoplethysmography, and exercising forearm venous effluent via antecubital vein catheter revealed distinct cardiovascular response groups: n = 6 with compensatory vasodilation vs. n = 4 without compensatory vasodilation. Compensatory vasodilators were able to blunt the perfusion pressure-evoked reduction in submaximal O<jats:sub>2<\/jats:sub>D in the arm-above-heart condition, whereas nonvasodilators did not (\u221222.5 \u00b1 13.6 vs. \u221265.4 \u00b1 14.1 ml O<jats:sub>2<\/jats:sub>\/min; P &lt; 0.05), and in combination with being able to increase O<jats:sub>2<\/jats:sub> extraction, nonvasodilators defended submaximal V\u0307o<jats:sub>2<\/jats:sub> and experienced less of an accumulated submaximal O<jats:sub>2<\/jats:sub>D deficit (\u221280.7 \u00b1 24.7 vs. \u2212219.1 \u00b1 36.0 ml O<jats:sub>2<\/jats:sub>\/min; P &lt; 0.05). As a result, the compensatory vasodilators experienced less of a compromise to peak EI than nonvasodilators (\u221224.5 \u00b1 3.5 N vs. \u221252.1 \u00b1 8.9 N; P &lt; 0.05). In conclusion, in the forearm exercise model studied, vasodilatory response phenotypes exist that determine individual susceptibility to hypoperfusion and the degree to which aerobic metabolism and exercise performance are compromised. <\/jats:p>","DOI":"10.1152\/japplphysiol.01155.2013","type":"journal-article","created":{"date-parts":[[2014,6,27]],"date-time":"2014-06-27T03:53:33Z","timestamp":1403841213000},"page":"392-405","source":"Crossref","is-referenced-by-count":16,"title":["Individual susceptibility to hypoperfusion and reductions in exercise performance when perfusion pressure is reduced: evidence for vasodilator phenotypes"],"prefix":"10.1152","volume":"117","author":[{"given":"Robert F.","family":"Bentley","sequence":"first","affiliation":[{"name":"School of Kinesiology and Health Studies, Queen's University, Kingston, Ontario, Canada"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"J. 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