title: Beta-adrenergic or parasympathetic inhibition, heart rate and cardiac output during normoxic and acute hypoxic exercise in humans.
abstract: Acute hypoxia increases heart rate (HR) and cardiac output (Qt) at a given oxygen consumption (VO2) during submaximal exercise. It is widely believed that the underlying mechanism involves increased sympathetic activation and circulating catecholamines acting on cardiac beta 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 Qt during hypoxic exercise. To test this, we separately blocked the beta-sympathetic and parasympathetic arms of the autonomic nervous system (ANS) in six healthy subjects (five male, one female; mean +/- S.E.M. age = 31.7+/-1.6 years, normoxic maximal VO2 (VO2,max)=3.1+/-0.3 l min(-1)) during exercise in conditions of normoxia and acute hypoxia (inspired oxygen fraction=0.125) to VO2,max. 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. Qt was measured using open-circuit acetylene uptake. Hypoxia increased venous [adrenaline] and [noradrenaline] but not [dopamine] at a given VO2 (P<0.05, P<0.01 and P=0.2, respectively). HR/VO2 and Qt/VO2 increased during hypoxia in all three conditions (P<0.05). Unexpectedly, the effects of hypoxia on HR and Qt were not significantly different from control with either beta-sympathetic or parasympathetic inhibition. These data suggest that although acute exposure to hypoxia increases circulating [catecholamines], the effects of hypoxia on HR and Qt do not necessarily require intact cardiac muscarinic and beta receptors. It may be that cardiac alpha receptors play a primary role in elevating HR and Qt during hypoxic exercise, or perhaps offer an alternative mechanism when other ANS pathways are blocked.
authors.affiliation: Department of Medicine, University of California, San Diego, La Jolla, CA 92093, USA. shopkins@ucsd.edu
authors.forename: Susan R
authors.initials: SR
authors.lastname: Hopkins
authors.forename: Harm J
authors.initials: HJ
authors.lastname: Bogaard
authors.forename: Kyuichi
authors.initials: K
authors.lastname: Niizeki
authors.forename: Yoshiki
authors.initials: Y
authors.lastname: Yamaya
authors.forename: Michael G
authors.initials: MG
authors.lastname: Ziegler
authors.forename: Peter D
authors.initials: PD
authors.lastname: Wagner
mesh_terms: D000319:Adrenergic beta-Antagonists / Q000494:pharmacology*; D000328:Adult; D015308:Anaerobic Threshold / Q000502:physiology; D002302:Cardiac Output / Q000187:drug effects* / Q000502:physiology*; D002395:Catecholamines / Q000097:blood; D004298:Dopamine / Q000097:blood; D004837:Epinephrine / Q000097:blood; D015444:Exercise / Q000502:physiology*; D005080:Exercise Test; D005260:Female; D006024:Glycopyrrolate / Q000494:pharmacology; D006339:Heart Rate / Q000187:drug effects* / Q000502:physiology*; D006801:Humans; D000860:Hypoxia / Q000503:physiopathology*; D008297:Male; D009638:Norepinephrine / Q000097:blood; D010101:Oxygen Consumption / Q000502:physiology; D010276:Parasympatholytics / Q000494:pharmacology*; D011433:Propranolol / Q000494:pharmacology; D015656:Respiratory Mechanics / Q000502:physiology; D013318:Stroke Volume / Q000187:drug effects / Q000502:physiology
chemical_list: D000319:Adrenergic beta-Antagonists; D002395:Catecholamines; D010276:Parasympatholytics; D011433:Propranolol; D006024:Glycopyrrolate; D004298:Dopamine; D009638:Norepinephrine; D004837:Epinephrine