The effects of large doses of anabolic steroids on 24-hour blood pressure, cardiac structure and function, and lipid profiles were studied in 10 body builders using anabolic steroids and 14 body builders who did not use steroids (control subjects). All subjects underwent noninvasive 24-hour blood pressure monitoring, echocardiography, Doppler analysis of transmitral flow, and analysis for lipoprotein and gonadotropin levels. Anabolic steroid users were studied at the end of a steroid cycle and after a period of withdrawal. Average 24-hour blood pressure was similar in the two groups, but anabolic steroid users exhibited a smaller pressure reduction during sleep than did nonusers. This finding was present both at the end of treatment and after the period of withdrawal. Echocardiographic dimensional and functional indexes did not differ substantially between anabolic steroid users and the nonusers, and were similar in anabolic steroid users during use and after withdrawal. Anabolic steroid users also had higher LDL and lower HDL cholesterol levels than nonusers; Lp(a) was higher in nonusers, although this difference did not attain the level of statistical significance. These differences were more striking at the end of the treatment period. The results of this study show that chronic anabolic steroid intake causes an abnormal 24-hour blood pressure pattern, characterized by a flattening of the diurnal curve, and minor changes of the dimensional echocardiographic parameters.

The effect of semi-supine long lasting exercise to exhaustion [61 (SD 10) min] on left ventricular systolic performance was studied by echocardiography in 16 young healthy volunteers. During the incremental phase of exercise, the ejection fraction increased from 65.2 (SD 4.1)% to 80.1 (SD 4.8)% (P < 0.0001), then it levelled off up to the end of exercise [81.7 (SD 4.4)%, P < 0.0001 vs rest]. During recovery, the ejection fraction rapidly and steadily decreased to a value similar to that at rest [66.1 (SD 5.0)%, n.s.). A similar pattern was shown by the systolic blood pressure/end-systolic volume coefficient, which rose from 3.2 (SD 0.8) mmHg.ml-1 to 7.5 (SD 2.7) mmHg.ml-1 (P < 0.0001) in the initial phase and subsequently did not change until the end of exercise [7.0 (SD 2.2) mmHg.ml-1, P < 0.0001 vs rest], to fall sharply after the cessation of exercise [2.9 (SD 1.1) mmHg.ml-1 at the 10th min, n.s. vs rest]. Exercise and recovery indices of left ventricular performance were not correlated with exercise duration, maximal heart rate and increase in free fatty acids. The present results indicated that, after the initial increase, left ventricular performance remained elevated during prolonged high intensity exercise and that conclusions on exercise cardiac performance drawn from postexercise data can be misleading.

1. Central and peripheral post-exercise haemodynamics were studied in 18 physically trained male subjects (10 hypertensive and eight normotensive) engaging in sports activities for 3-5 h/week. After a preliminary multistage bicycle ergometric test to evaluate their maximal oxygen consumption and anaerobic threshold, they underwent prolonged exercise at anaerobic threshold in the semi-supine position at 30% grade until exhaustion (mean duration 60.0 +/- 16.7 min in the normotensive subjects and 61.0 +/- 5.7 min in the hypertensive subjects, not significant). During the recovery time, intra-arterial blood pressure, echocardiographic cardiac output and indium-gallium strain-gauge plethysmographic peripheral flow were measured, and total, forearm and leg peripheral resistances were calculated respectively from mean blood pressure/cardiac output and mean blood pressure/peripheral resistance. 2. Systolic blood pressure was decreased during the entire recovery period in comparison with the baseline values (-8.4 mmHg, -43.8 mmHg and -39.7 mmHg at the 1st, 5th and 10th min in the hypertensive subjects, P = 0.001, P = 0.0001 and P = 0.0001 respectively; -18.8, -25.5 and -24.1 mmHg in the normotensive subjects, not significant, P = 0.01 and P = 0.01, respectively) without any significant difference between the two groups, whereas the reduction in diastolic blood pressure was not statistically significant. Peripheral flow increased and peripheral resistance decreased in parallel in the forearm and the leg and showed similar trends in the hypertensive subjects and the normotensive subjects. The increase in cardiac output and left ventricular ejection fraction and the decrease in total resistance were also similar in the two groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Debate continues on whether left ventricular (LV) systolic function during exercise is abnormal in young subjects with mild hypertension and on whether the abnormal blood pressure (BP) trend observed in hypertensives during prolonged exercise is due to impaired LV function. LV function was measured by means of M-mode echocardiography during prolonged exercise in 13 physically trained, young, mild hypertensives and 12 age-matched, trained normotensives with similar working capacity. Systolic BP/end-systolic volume (SBP/ESV) and end-systolic stress/ESV at rest were greater in the hypertensives (P < 0.0001 and P = 0.034), while LV filling was impaired (P = 0.05). BP changes during the first 20 min of exercise were similar in the two groups, but thereafter the between-group BP difference tended to decline progressively. LV diastolic dimension was similar at rest. During exercise it slightly increased in the normotensives and slightly decreased in the hypertensives (P = 0.032). Exercise ejection fraction (P = 0.018), SBP/ESV (P < 0.0001) and stress/ESV (P = 0.027) were greater in the hypertensives throughout the test. SBP/ESV normalized for LV wall thickness (P < 0.0001) and the changes in SBP/ESV from rest to exercise were also greater in the hypertensives (P = 0.002). Stroke volume increased to a lower extent in the hypertensives, but the between-group difference was not statistically significant. The increase in SBP/ESV from rest to exercise was related to the concentric remodelling of the ventricle in the hypertensives (P < 0.0001) and the subjects grouped together (P < 0.0001), but not in the normotensives. In conclusion, increased LV systolic performance is present early in hypertension not only at rest but also during vigorous exercise. It is partly due to concentric remodelling of the left ventricle and partly to enhanced inotropic state.

The aim of the study was to examine the effect of chronic angiotensin converting enzyme inhibition on haemodynamics and left ventricular performance during long-lasting exercise at the anaerobic threshold. For this purpose exercise haemodynamics and left ventricular performance were assessed in 14 physically trained hypertensives (aged 26 y) before and after 3 months on quinapril 20 mg once daily. During exercise intraarterial blood pressure was monitored using the Oxford method and left ventricular dimensions were measured by M-mode echocardiography. Quinapril significantly decreased mean blood pressure during the initial incremental phase of the exercise protocol and caused a slight, nonsignificant decline during the steady-state phase. The drug-induced fall in blood pressure was accounted for mainly by change in cardiac output. Exercise duration and left ventricular performance were not affected by treatment. In conclusion, quinapril 20 mg once daily smoothed the blood pressure increase which occurs during the initial phase of vigorous endurance exercise. This result was achieved without affecting physical performance or left ventricular contractility.