Earlier experiments and investigations observed an increased oxygen uptake caused by aldosterone in vitro and in vivo during the submaximal and maximal exercise. This phenomenon seems to be due to an augmented aerobic metabolic rate of the muscles. Some recent investigations showed a direct positive inotropic effect of the aldosterone on the heart. The aim of this present study was to reveal cardiac effects of the aldosterone in trained swimmers during and after maximal exercise. Methods 10 experienced male swimmers were required to perform an 800 m crawl under competitive conditions. In the aldosterone experiments (AE) Aldocorten - 0.5 mg - was injected subcutaneously 5 and 3 hours before starting exercise. Half of the subjects performed control experiments (CE) seven days before AE. In the CE a placebo - isotonic solution of NaCl - was similarly injected. The swimming times for each 100 m and also the mean values of the heart rate (HR) before (0 m), during (25 to 800 m) and after (10 s to 10 min) swimming exercise were measured. Results After aldosterone application the subjects swam significantly faster over the last 600 m. This resulted in a decrease of the total time of 6.52.1 s (P<0.01). They also displayed diminished elevation in HR up to the 500 m distance (Fig. 1). The HR in AE reached lower values compared to those obtained in control conditions until the final stage of swimming (Fig. 2). The acid -base values of the blood, taken from the ear lobe before and after exercise did not differ between AE and CE. In the recovery period it can be noticed a more evident decrement of HR after aldosterone injection compared to the CE. Discussion/Conclusion The results of the present study show that the behavior of the HR and the swimming times during exhaustive swimming exercise are influenced by the treatment with aldosterone, while the acid-base balance is not. The aldosterone effects consist in an improving of the cardiac performance, by swimming faster and diminishing elevations in HR, meaning a delay of fatigue during the exercise. This could be explained by the increasing left ventricular inotropism due to aldosterone and by an increase of aerobic metabolism; meanwhile the anaerobic part of energy supply remains unchanged. The slightly delayed increase of the HR during exercise might express a delayed production of lactate under aldosterone conditions, lactate having a dominant influence on regulation of HR. The faster decreased of the HR after the end of the swimming exercise expresses an accelerated regeneration in AE.
© Copyright 2004 Book of Abstracts - 9th Annual Congress European College of Sport Science, July 3-6, 2004, Clermont-Ferrand, France. Alle Rechte vorbehalten.