{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,23]],"date-time":"2026-10-23T00:55:18Z","timestamp":1792716918290,"version":"4.5.0"},"reference-count":31,"publisher":"Wiley","issue":"2","license":[{"start":{"date-parts":[[2003,7,1]],"date-time":"2003-07-01T00:00:00Z","timestamp":1057017600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["The Journal of Physiology"],"published-print":{"date-parts":[[2003,7]]},"abstract":"<jats:p>\n                    Acute hypoxia increases heart rate (HR) and cardiac output (\n                    <jats:italic>Q<\/jats:italic>\n                    <jats:sub>t<\/jats:sub>\n                    ) at a given oxygen consumption (V\u0307\n                    <jats:sub>O2<\/jats:sub>\n                    ) during submaximal exercise. It is widely believed that the underlying mechanism involves increased sympathetic activation and circulating catecholamines acting on cardiac \u03b2 receptors. Recent evidence indicating a continued role for parasympathetic modulation of HR during moderate exercise suggests that increased parasympathetic withdrawal plays a part in the increase in HR and\n                    <jats:italic>Q<\/jats:italic>\n                    <jats:sub>t<\/jats:sub>\n                    during hypoxic exercise. To test this, we separately blocked the \u03b2\u2010sympathetic and parasympathetic arms of the autonomic nervous system (ANS) in six healthy subjects (five male, one female; mean \u00b1\n                    <jats:sc>s.e.m<\/jats:sc>\n                    . age = 31.7 \u00b1 1.6 years, normoxic maximal V\u0307\n                    <jats:sub>O2<\/jats:sub>\n                    (V\u0307\n                    <jats:sub>O2<\/jats:sub>\n                    <jats:sub>,max<\/jats:sub>\n                    ) = 3.1 \u00b1 0.3 l min\n                    <jats:sup>\u22121<\/jats:sup>\n                    ) during exercise in conditions of normoxia and acute hypoxia (inspired oxygen fraction = 0.125) to V\u0307\n                    <jats:sub>O2<\/jats:sub>\n                    <jats:sub>,max<\/jats:sub>\n                    . Data were collected on different days under the following conditions: (1)control, (2) after 8.0 mg propranolol I.V. and (3) after 0.8 mg glycopyrrolate I.V.\n                    <jats:italic>Q<\/jats:italic>\n                    <jats:sub>t<\/jats:sub>\n                    was measured using open\u2010circuit acetylene uptake. Hypoxia increased venous [adrenaline] and [noradrenaline] but not [dopamine] at a given V\u0307\n                    <jats:sub>O2<\/jats:sub>\n                    (\n                    <jats:italic>P<\/jats:italic>\n                    &lt; 0.05,\n                    <jats:italic>P<\/jats:italic>\n                    &lt; 0.01 and\n                    <jats:italic>P<\/jats:italic>\n                    = 0.2, respectively). HR\/V\u0307\n                    <jats:sub>O2<\/jats:sub>\n                    and\n                    <jats:italic>Q<\/jats:italic>\n                    <jats:sub>t<\/jats:sub>\n                    \/V\u0307\n                    <jats:sub>O2<\/jats:sub>\n                    increased during hypoxia in all three conditions (\n                    <jats:styled-content>\n                      <jats:italic>P<\/jats:italic>\n                      &lt; 0.05\n                    <\/jats:styled-content>\n                    ). Unexpectedly, the effects of hypoxia on HR and\n                    <jats:italic>Q<\/jats:italic>\n                    <jats:sub>t<\/jats:sub>\n                    were not significantly different from control with either \u03b2\u2010sympathetic or parasympathetic inhibition. These data suggest that although acute exposure to hypoxia increases circulating [catecholamines], the effects of hypoxia on HR and\n                    <jats:italic>Q<\/jats:italic>\n                    <jats:sub>t<\/jats:sub>\n                    do not necessarily require intact cardiac muscarinic and \u03b2 receptors. It may be that cardiac \u03b1 receptors play a primary role in elevating HR and\n                    <jats:italic>Q<\/jats:italic>\n                    <jats:sub>t<\/jats:sub>\n                    during hypoxic exercise, or perhaps offer an alternative mechanism when other ANS pathways are blocked.\n                  <\/jats:p>","DOI":"10.1113\/jphysiol.2003.040568","type":"journal-article","created":{"date-parts":[[2003,5,26]],"date-time":"2003-05-26T20:16:22Z","timestamp":1053980182000},"page":"605-616","source":"Crossref","is-referenced-by-count":50,"title":["\u03b2\u2010Adrenergic or parasympathetic inhibition, heart rate and cardiac output during normoxic and acute hypoxic exercise in humans"],"prefix":"10.1113","volume":"550","author":[{"given":"Susan R.","family":"Hopkins","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Harm 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