Cardiac response to head-out water immersion in man.
- Author:
Jang Kyu CHOI
1
;
Won Kun PARK
Author Information
1. Department of Physiology, Kosin Medical College, Pusan, Korea.
- Publication Type:Original Article
- MeSH:
Acceleration;
Arterial Pressure;
Blood Flow Velocity;
Cardiac Output;
Cardiography, Impedance;
Heart Rate;
Humans;
Immersion*;
Male;
Stroke Volume;
Systole;
Water*
- From:The Korean Journal of Physiology and Pharmacology
2000;4(3):253-261
- CountryRepublic of Korea
- Language:English
-
Abstract:
Head-out water immersion induces marked increase in the cardiac stroke volume. The present study was undertaken to characterize the stroke volume change by analyzing the aortic blood flow and left ventricular systolic time intervals. Ten men rested on a siting position in the air and in the water at 34.5degreeC for 30 min each. Their stroke volume, heart rate, ventricular systolic time intervals, and aortic blood flow indices were assessed by impedance cardiography. During immersion, the stroke volume increased 56%, with a slight (4%) decrease in heart rate, thus cardiac output increased ~50%. The slight increase in R-R interval was due to an equivalent increase in the systolic and diastolic time intervals. The ventricular ejection time was 20% increased, and this was mainly due to a decrease in pre-ejection period (28%). The mean arterial pressure increased 5 mmHg, indicating that the cardiac afterload was slightly elevated by immersion. The left ventricular end-diastolic volume index increased 24%, indicating that the cardiac preload was markedly elevated during immersion. The mean velocity and the indices of peak velocity and peak acceleration of aortic blood flow were all increased by ~30%, indicating that the left ventricular contractile force was enhanced by immersion. These results suggest that the increase in stroke volume during immersion is characterized by an increase in ventricular ejection time and aortic blood flow velocity, which may be primarily attributed to the increased cardiac preload and the muscle length-dependent increase in myocardial contractile force.
