Prolonged exercise induces left ventricular dysfunction in healthy subjects

Abstract

To determine the effects of a moderately prolonged exercise on left ventricular systolic performance, 23 healthy male subjects, aged 18 to 51 yr (mean 37 yr) were studied. The subjects exercised first on a treadmill (brief exercise) and completed, on a separate day, a 20-km run. M-mode, two-dimensional, and Doppler echocardiography, as well as calibrated carotid pulse tracings, were obtained at rest and immediately on completion of both brief and prolonged exercise. Left ventricular systolic function was assessed by end-systolic stress-shortening relationships. Heart rate increased similarly after brief and prolonged exercise (+30%). Mean arterial pressure decreased from 99 +/- 7 to 92 +/- 8 mmHg (P less than 0.001) after prolonged exercise, but it remained unchanged after brief exercise. Left ventricular end-diastolic volume was decreased after prolonged exercise (130 +/- 23 vs. 147 +/- 18 ml at rest, P less than 0.01). Both ejection fraction and rate-adjusted mean velocity of fiber shortening decreased after prolonged exercise [from 67 +/- 5 to 60 +/- 6% (P less than 0.001) and from 1.12 +/- 0.2 to 0.91 +/- 0.2 cm/s (P less than 0.001), respectively] despite a lower circumferential end-systolic wall stress (133 +/- 23 vs. 152 +/- 20 g/cm2). The relationship between ejection fraction (or mean velocity of fiber shortening adjusted for heart rate) and end-systolic wall stress was displaced downward on race finish (P less than 0.05). These changes were independent of the changes in left ventricular end-diastolic volume and hence those in preload. The data suggest that moderately prolonged exercise may result in depressed left ventricular performance in healthy normal subjects.

Acute changes in endocrine and fluid balance markers during high-intensity, steady-state, and prolonged endurance running: unexpected increases in oxytocin and brain natriuretic peptide during exercise

“…The significant increase in [NT-proBNP] P that is seen in our subjects following prolonged endurance exercise, but not highintensity or steady-state exercise, has been noted previously (33). Because [NT-proBNP] P was not significantly elevated after the VO 2 max test (where blood pressure, heart rate, and cardiac output would be the highest (34)) but is increased fourfold after the ultramarathon (where mean arterial pressure and left ventricular diameter are significantly reduced (35)), it appears that stimuli apart from the cardiovascular system may be responsible for the increase in BNP seen after prolonged endurance exercise. Whether BNP secretion is alternatively stimulated by inflammation (36), decreased renal blood flow (37), lipolysis (38), or from a yet to be determined factor under these conditions remains to be evaluated.…”

Left ventricular performance during prolonged exercise: absence of systolic dysfunction

“…It remains unclear if LV dysfunction during such activity contributes to the decrease in stroke volume. Some investigations have described an impairment of LV function following exercise of a prolonged nature [8][9][10][11][12][13][14][15]. It is possible that a decline in ventricular output involves a depression in the contractile state ; however, despite reports of a transient decline in systolic function [8][9][10][11][12][13][14]16,17] and diastolic filling characteristics [9,13,16], several studies have failed to report a decline in LV performance [18][19][20][21].…”

Cardiac drift during prolonged exercise with echocardiographic evidence of reduced diastolic function of the heart

“…Furthermore, both a depressed LV systolic function and diastolic filling are observed after an ''Ironman'' triathlon (Whyte et al 2000) which involves a 3.8 km swim, 180 km of cycling and a 42 km run (mean duration of 10 h 40 min). On the other hand, evidence of EICF is not apparent after 10-30 min of exercise (Upton et al 1980;Douglas et al 1987;Seals et al 1988;Vanoverschelde et al 1991;Shave et al 2002b;McGavock et al 2003) indicating that EICF is time dependent.…”

“…The EICF is found in both well trained (Douglas et al 1987;Whyte et al 2000) and untrained subjects (Seals et al 1988;Vanoverschelde et al 1991;Ketelhut et al 1992Ketelhut et al , 1994Palatini et al 1994), but subjects of disparate training background within the same experimental design have not been compared. This study evaluated whether the continued increase in HR during prolonged exercise becomes manifested in response to altered preload to the heart or to EICF and/or myocardial damage as indicated by serum cTnT in healthy young males encompassing a range of maximal oxygen uptake ( _ V O 2maz ).…”