Prolonged strenuous exercise alters the cardiovascular response to dobutamine stimulation in male athletes.

Prolonged strenuous exercise has been associated with transient impairment in left ventricular (LV) systolic and diastolic function that has been termed 'cardiac fatigue'. It has been postulated that cardiac beta-adrenoreceptor desensitization may play a central role; however, data are limited. Accordingly, we assessed the cardiovascular response to progressive dobutamine stimulation after prolonged strenuous exercise (2 km swim, 90 km bike, 21 km run). Nine experienced male athletes were studied: PRE (2-3 days before), POST (after) and REC (1-2 days later). The cardiovascular response to progressive continuous dobutamine stimulation (0, 5, 20, and 40 microg kg(-1) min(-1)) was assessed, including heart rate (HR), systolic blood pressure (SBP), LV cavity areas (two-dimensional echocardiography) and contractility (end-systolic elastance, SBP/end-systolic cavity area (ESCA)). POST there was limited evidence of myocardial necrosis (measured by troponin I), while catecholamines were elevated. HR was higher POST (mean +/-s.d.; PRE, 58 +/- 9; POST, 79 +/- 9; REC, 57 +/- 7 beats min(-1); P < 0.05), while SBP was lower (PRE, 127 +/- 15; POST, 116 +/- 9; REC, 121 +/- 12 mmHg; P < 0.05). A blunted HR, SBP and LV contractility (SBP/ESCA; PRE 29 +/- 6 versus POST 20 +/- 6 mmHg cm(-2); P < 0.05) response to dobutamine was demonstrated POST, with values returning towards baseline in REC. Following prolonged strenuous exercise, the chronotropic and inotropic response to dobutamine stimulation is blunted. This study supports the hypothesis that beta-receptor downregulation and/or desensitization may play a major role in prolonged-strenuous-exercise-mediated cardiac fatigue.

Blood volume expansion and cardiorespiratory function: effects of training modality.

PURPOSE: To evaluate the effects of different modalities of aerobic (i.e., interval (INT) and continuous (CONT)) training on cardiorespiratory function and the importance of training-induced blood volume (BV) expansion on aerobic power and LV function. We hypothesized that if modality-mediated differences in cardiorespiratory function exist after INT and CONT, they would be related directly to differences in training-induced hypervolemia. METHODS: We examined the effects of 12 wk of CONT and INT on BV, volume-regulatory hormones (angiotensin II, aldosterone, atrial natriuretic peptide), and cardiorespiratory function in 20 untrained males (mean age 30 +/- 4 (SD)). Participants were stratified (mass and VO2max) and randomly assigned to control, CONT, or INT. RESULTS: There were no significant changes in cardiorespiratory function or BV in the control group. Twelve weeks of continuous and interval training, respectively, resulted in significant changes in VO2max (23 +/- 18 vs 21 +/- 10%), peak stroke volume (20 +/- 18 vs 11 +/- 18%), and BV (12 +/- 9 vs 10 +/- 6%). Changes in VO2max were directly related to changes in BV (r = 0.47). Angiotensin II significantly increased after 1 wk of CONT and INT and thereafter returned to baseline values. There was no significant difference between the CONT and INT groups with regard to changes in vascular volumes, volume-regulatory hormones, and/or cardiorespiratory function. CONCLUSIONS: These data indicate that: 1) 12 wk of CONT and INT result in similar improvements in VO2max, and LV function and 2) training-induced hypervolemia accounts for approximately 47% of the changes in VO2max after CONT and INT.

Arteriovenous fistula-associated high-output cardiac failure: a review of mechanisms.

High-output cardiac failure can be a rare complication of high-output arteriovenous fistula. The authors present a case in which a hemodialysis patient with a high-flow arteriovenous fistula has cardiac failure that improves with fistula closure. The hemodynamic effects of a fistula are reviewed, and the hemodialysis literature regarding high-output cardiac failure is summarized. To gain insight into the problem of high-output cardiac failure, research efforts should focus on the prospective monitoring of high-access flows.

Myocardial response to incremental exercise in endurance-trained athletes: influence of heart rate, contractility and the Frank-Starling effect.

Recent evidence indicates that endurance-trained athletes are able to increase their stroke volume (SV) throughout incremental upright exercise, probably due to a progressively greater effect of the Frank-Starling mechanism. This is contrary to the widely held belief that SV reaches a plateau at a submaximal heart rate (irrespective of fitness level), owing to a limitation in the time for diastolic filling. The purpose of this investigation was to evaluate whether endurance-trained athletes rely on a progressively greater effect of the Frank-Starling mechanism throughout incremental exercise. A secondary purpose was to evaluate the effects of postural position on the cardiovascular responses to incremental exercise. Ten male cyclists participated in this investigation. Left ventricular function was assessed throughout incremental exercise in the supine and upright positions (counterbalanced) using radionuclide ventriculography. Stroke volume increased in a linear fashion during incremental exercise in both the upright and supine positions. The increases in cardiac output (Q) throughout incremental to maximal exercise (in both the supine and upright positions) were significantly related to changes in heart rate, myocardial contractility and the Frank-Starling mechanism. Percentage changes in end-diastolic volume and SV were significantly greater in the upright position versus the supine position, reflecting an increased reliance on the Frank-Starling effect to increase Q. We conclude from this investigation that highly trained endurance athletes are able to make progressively increasing usage of the Frank-Starling effect throughout incremental exercise. Postural position has a significant effect on the relative contribution of heart rate, myocardial contractility and the Frank-Starling mechanism to the increase in Q during exercise conditions.