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-adrenergic blockade at 4,300 m
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,
Whole
body O2 uptake (
O2)
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 O2 delivery (blood flow × arterial
O2 content) and thereby maintains
O2 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 O2 delivery were significantly lower in
propranolol- than in placebo-treated subjects. Increases in
stroke volume and O2 extraction were responsible for the
maintenance of
O2. At 4,300 m,
-adrenergic blockade had no significant effect on
O2, ventilation, alveolar
PO2, and arterial blood gases during
submaximal exercise. Despite increases in stroke volume, cardiac output
and thereby O2 delivery were still reduced in
propranolol-treated subjects compared with subjects treated with
placebo. Further reductions in already low levels of mixed venous
O2 saturation were responsible for the maintenance of
O2 on arrival and after 21 days at
4,300 m in propranolol-treated subjects. Despite similar
workloads and
O2,
propranolol-treated subjects exercised at greater perceived intensity
than subjects given placebo at 4,300 m. The values for mixed venous
O2 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 O2
delivery during submaximal exercise due to incomplete compensation by
stroke volume for the reduction in exercise heart rate. Total body
O2 is maintained at a constant level
by an interaction between mixed venous O2 saturation, the
arterial O2-carrying capacity, and hemodynamics during
exercise with acute and chronic hypoxia.
high altitude; oxygen transport
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