Effects of Acute Hypoxia at Moderate Altitude on Stroke Volume and Cardiac Output During Exercise

Abstract

SummaryIt has been unclear how acute hypoxia at moderate altitude affects stroke volume (SV), an index of cardiac function, during exercise. The present study was conducted to reveal whether acute normobaric hypoxia might alter SV during exercise.Nine healthy male subjects performed maximal exercise testing under normobaric normoxic, and normobaric hypoxic conditions (O 2 : 14.4%) in a randomized order. A novel thoracic impedance method was used to continuously measure SV and cardiac output (CO) during exercise.Acute hypoxia decreased maximal work rate (hypoxia; 247 ± 6 [SE] versus normoxia; 267 ± 8 W, P < 0.005) and VO 2 max (hypoxia; 2761 ± 99 versus normoxia; 3039 ± 133 mL/min, P < 0.005). Under hypoxic conditions, SV and CO at maximal exercise decreased (SV: hypoxia; 145 ± 11 versus normoxia; 163 ± 11 mL, P < 0.05, CO: hypoxia; 26.7 ± 2.1 versus normoxia; 30.2 ± 1.8 L/min, P < 0.05). In acute hypoxia, SV during submaximal exercise at identical work rate decreased. Furthermore, in hypoxia, 4 of 9 subjects attained their highest SV at maximal exercise, while in normoxia, 8 of 9 subjects did.Acute normobaric hypoxia attenuated the increment of SV and CO during exercise, and SV reached a plateau earlier under hypoxia than in normoxia. Cardiac function during exercise at this level of acute normobaric hypoxia might be attenuated. (Int Heart J 2010; 51: 170-175) Key words: Normobaric hypoxia, Cardiac output, Oxygen uptake, Exercise testing D uring ascent to a moderate to high altitude, individuals are exposed to progressive decreases in atmospheric pressure that lead to a reduction in inspired, alveolar, and arterial oxygen pressures. Training at moderate altitude (corresponding to 2000 -3000 m) is associated with relatively severe hypoxemia during submaximal and maximal exercise, 1) and acute hypoxia of this level decreases VO 2 max as well as exercise capacity.2-4) Thus, hypoxia at moderate altitude limits training intensity, which leads to relative deconditioning in elite athletes, although endurance athletes often use hypoxic training to improve sea-level performance. 5) Because VO 2 is the product of cardiac output (CO) and the arterio-venous oxygen content difference (C(a-v)O 2 ), a decrease in VO 2 max at maximal exercise may be due to a decrease of either factor, or both.Acute hypoxia may induce abnormalities in cardiac function and redistribution of CO not only at rest but also during exercise. In an animal study, CO at rest increased during acute severe hypoxia (FiO 2 10% and 5%), and blood flow to all organs increased except for the skin and muscle.6) In humans under acute hypoxia, heart rate (HR) and CO increase while systemic vascular resistance decreases. 7)Echocardiography also reveals altered mitral flow patterns, suggestive of mild LV diastolic dysfunction.8) Subacute hypoxia (FiO 2 12%, simulating an altitude of approximately 4000 m) induced mild diastolic dysfunction in young healthy individuals. 9)Stroke volume (SV) increases as the work rate increases at low to moderate intensity exercise, ...

Cardiac Output Response to Exercise in Chronic Cardiac Failure Patients

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