{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,2]],"date-time":"2026-10-02T19:21:20Z","timestamp":1790968880271,"version":"4.1.0"},"reference-count":48,"publisher":"American Physiological Society","issue":"8","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Regulatory, Integrative and Comparative Physiology"],"published-print":{"date-parts":[[2015,4,15]]},"abstract":"<jats:p> Hyperthermia during prolonged exercise leads to hyperventilation, which can reduce arterial CO<jats:sub>2<\/jats:sub> pressure (Pa<jats:sub>CO<jats:sub>2<\/jats:sub><\/jats:sub>) and, in turn, cerebral blood flow (CBF) and thermoregulatory response. We investigated 1) whether humans can voluntarily suppress hyperthermic hyperventilation during prolonged exercise and 2) the effects of voluntary breathing control on Pa<jats:sub>CO<jats:sub>2<\/jats:sub><\/jats:sub>, CBF, sweating, and skin blood flow. Twelve male subjects performed two exercise trials at 50% of peak oxygen uptake in the heat (37\u00b0C, 50% relative humidity) for up to 60 min. Throughout the exercise, subjects breathed normally (normal-breathing trial) or they tried to control their minute ventilation (respiratory frequency was timed with a metronome, and target tidal volumes were displayed on a monitor) to the level reached after 5 min of exercise (controlled-breathing trial). Plotting ventilatory and cerebrovascular responses against esophageal temperature (T<jats:sub>es<\/jats:sub>) showed that minute ventilation increased linearly with rising T<jats:sub>es<\/jats:sub> during normal breathing, whereas controlled breathing attenuated the increased ventilation (increase in minute ventilation from the onset of controlled breathing: 7.4 vs. 1.6 l\/min at +1.1\u00b0C T<jats:sub>es<\/jats:sub>; P &lt; 0.001). Normal breathing led to decreases in estimated Pa<jats:sub>CO<jats:sub>2<\/jats:sub><\/jats:sub> and middle cerebral artery blood flow velocity (MCAV) with rising T<jats:sub>es<\/jats:sub>, but controlled breathing attenuated those reductions (estimated Pa<jats:sub>CO<jats:sub>2<\/jats:sub><\/jats:sub> \u22123.4 vs. \u22120.8 mmHg; MCAV \u221210.4 vs. \u22123.9 cm\/s at +1.1\u00b0C T<jats:sub>es<\/jats:sub>; P = 0.002 and 0.011, respectively). Controlled breathing had no significant effect on chest sweating or forearm vascular conductance ( P = 0.67 and 0.91, respectively). Our results indicate that humans can voluntarily suppress hyperthermic hyperventilation during prolonged exercise, and this suppression mitigates changes in Pa<jats:sub>CO<jats:sub>2<\/jats:sub><\/jats:sub> and CBF. <\/jats:p>","DOI":"10.1152\/ajpregu.00419.2014","type":"journal-article","created":{"date-parts":[[2015,1,29]],"date-time":"2015-01-29T01:53:30Z","timestamp":1422496410000},"page":"R669-R679","source":"Crossref","is-referenced-by-count":23,"title":["Voluntary suppression of hyperthermia-induced hyperventilation mitigates the reduction in cerebral blood flow velocity during exercise in the heat"],"prefix":"10.1152","volume":"308","author":[{"given":"Bun","family":"Tsuji","sequence":"first","affiliation":[{"name":"Institute of Health and Sport Sciences, University of Tsukuba, Tsukuba City, Ibaraki, Japan; and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yasushi","family":"Honda","sequence":"additional","affiliation":[{"name":"Institute of Health and Sport 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