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Beta-adrenergic or parasympathetic inhibition, heart rate and cardiac output during normoxic and acute hypoxic exercise in humans.
- Source :
-
The Journal of physiology [J Physiol] 2003 Jul 15; Vol. 550 (Pt 2), pp. 605-16. Date of Electronic Publication: 2003 May 23. - Publication Year :
- 2003
-
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.
- Subjects :
- Adult
Anaerobic Threshold physiology
Catecholamines blood
Dopamine blood
Epinephrine blood
Exercise Test
Female
Glycopyrrolate pharmacology
Humans
Male
Norepinephrine blood
Oxygen Consumption physiology
Propranolol pharmacology
Respiratory Mechanics physiology
Stroke Volume drug effects
Stroke Volume physiology
Adrenergic beta-Antagonists pharmacology
Cardiac Output drug effects
Cardiac Output physiology
Exercise physiology
Heart Rate drug effects
Heart Rate physiology
Hypoxia physiopathology
Parasympatholytics pharmacology
Subjects
Details
- Language :
- English
- ISSN :
- 0022-3751
- Volume :
- 550
- Issue :
- Pt 2
- Database :
- MEDLINE
- Journal :
- The Journal of physiology
- Publication Type :
- Academic Journal
- Accession number :
- 12766243
- Full Text :
- https://doi.org/10.1113/jphysiol.2003.040568