O2 extraction maintains O2 uptake during submaximal exercise with beta -adrenergic blockade at 4,300 m

• Published in: Journal of applied physiology (1985) 1998-09, Vol.85 (3), p.1092-1102
• Main Authors: Wolfel, Eugene E, Selland, Mark A, Cymerman, A, Brooks, George A, Butterfield, Gail E, Mazzeo, Robert S, Grover, Robert F, Reeves, John T
• Format: Article
• Language: English
• Subjects: Adrenergic beta-Agonists - pharmacology; Adrenergic beta-Antagonists - pharmacology; Adult; Altitude; Applied physiology; Biological and medical sciences; Blood Gas Analysis; Diet; Exercise - physiology; Hemodynamics - physiology; Human physiology applied to population studies and life conditions. Human ecophysiology; Humans; Hypoxia - metabolism; Hypoxia - physiopathology; Isoproterenol - pharmacology; Male; Medical sciences; Oxygen Consumption - physiology; Propranolol - pharmacology; Regional Blood Flow - drug effects; Space life sciences; Transports. Aerospace. Diving. Altitude
• ISSN: 8750-7587; 1522-1601
• DOI: 10.1152/jappl.1998.85.3.1092

1  Cardiovascular Pulmonary Research Laboratory, Division of Cardiology, University of Colorado Health Sciences Center, Denver, Colorado 80262; 2  US Army Research Institute of Environmental Medicine, Natick, Massachusetts 01760; 3  University of California, Berkeley 94720; 4  Veterans Affairs Health Care System, Palo Alto, California 94304; and 5  University of Colorado, Boulder, Colorado 80309 Whole body O 2 uptake ( O 2 ) during maximal and submaximal exercise has been shown to be preserved in the setting of -adrenergic blockade at high altitude, despite marked reductions in heart rate during exercise. An increase in stroke volume at high altitude has been suggested as the mechanism that preserves systemic O 2 delivery (blood flow × arterial O 2 content) and thereby maintains O 2 at sea-level values. To test this hypothesis, we studied the effects of nonselective -adrenergic blockade on submaximal exercise performance in 11 normal men (26 ± 1 yr) at sea level and on arrival and after 21 days at 4,300 m. Six subjects received propranolol (240 mg/day), and five subjects received placebo. At sea level, during submaximal exercise, cardiac output and O 2 delivery were significantly lower in propranolol- than in placebo-treated subjects. Increases in stroke volume and O 2 extraction were responsible for the maintenance of O 2 . At 4,300 m, -adrenergic blockade had no significant effect on O 2 , ventilation, alveolar P O 2 , and arterial blood gases during submaximal exercise. Despite increases in stroke volume, cardiac output and thereby O 2 delivery were still reduced in propranolol-treated subjects compared with subjects treated with placebo. Further reductions in already low levels of mixed venous O 2 saturation were responsible for the maintenance of O 2 on arrival and after 21 days at 4,300 m in propranolol-treated subjects. Despite similar workloads and O 2 , propranolol-treated subjects exercised at greater perceived intensity than subjects given placebo at 4,300 m. The values for mixed venous O 2 saturation during submaximal exercise in propranolol-treated subjects at 4,300 m approached those reported at simulated altitudes >8,000 m. Thus -adrenergic blockade at 4,300 m results in significant reduction in O 2 delivery during submaximal exercise due to incomplete compensation by stroke volume for the reduction in exercise heart rate. Total body O 2 is maintained at a constant level by an interaction between mixed venous O 2 saturation, the arterial O 2