BackgroundSeveral studies have correlated elevations in cardiac biomarkers of injury post marathon with transient and reversible right ventricular (RV) systolic dysfunction as assessed by both transthoracic echocardiography (TTE) and cardiovascular magnetic resonance (CMR). Whether or not permanent myocardial injury occurs due to repeated marathon running in the aging population remains controversial.ObjectivesTo assess the extent and severity of cardiac dysfunction after the completion of full marathon running in individuals greater than 50 years of age using cardiac biomarkers, TTE, cardiac computed tomography (CCT), and CMR.MethodsA total of 25 healthy volunteers (21 males, 55 ± 4 years old) from the 2010 and 2011 Manitoba Full Marathons (26.2 miles) were included in the study. Cardiac biomarkers and TTE were performed one week prior to the marathon, immediately after completing the race and at one-week follow-up. CMR was performed at baseline and within 24 hours of completion of the marathon, followed by CCT within 3 months of the marathon.ResultsAll participants demonstrated an elevated cTnT post marathon. Right atrial and ventricular volumes increased, while RV systolic function decreased significantly immediately post marathon, returning to baseline values one week later. Of the entire study population, only two individuals demonstrated late gadolinium enhancement of the subendocardium in the anterior wall of the left ventricle, with evidence of stenosis of the left anterior descending artery on CCT.ConclusionsMarathon running in individuals over the age of 50 is associated with a transient, yet reversible increase in cardiac biomarkers and RV systolic dysfunction. The presence of myocardial fibrosis in older marathon athletes is infrequent, but when present, may be due to underlying occult coronary artery disease.

We studied the contribution of phasic left atrial (LA) function to left ventricular (LV) filling during exercise. We hypothesized that reduced LV filling time at moderate-intensity exercise limits LA passive emptying and increases LA active emptying. Twenty endurance-trained males (55 ± 6 yr) were studied at rest and during light- (∼100 beats/min) and moderate-intensity (∼130 beats/min) exercise. Two-dimensional and Doppler echocardiography were used to assess phasic volumes and diastolic function. LV end-diastolic volume increased from rest to light exercise (54 ± 6 to 58 ± 5 ml/m(2), P < 0.01) and from light to moderate exercise (58 ± 5 to 62 ± 6 ml/m(2), P < 0.01). LA maximal volume increased from rest to light exercise (26 ± 4 to 30 ± 5 ml/m(2), P < 0.01) related to atrioventricular plane displacement (r = 0.55, P < 0.005), without further change at moderate exercise. LA passive emptying increased at light exercise (9 ± 2 to 13 ± 3 ml/m(2), P < 0.01) and then returned to baseline at moderate exercise, whereas LA active emptying increased appreciably only at moderate exercise (6 ± 2 to 14 ± 3 ml/m(2), P < 0.01). Thus, the total atrial emptying volume did not increase beyond light exercise, and the increase in LV filling at moderate exercise could be attributed primarily to an increase in the conduit flow volume (19 ± 3 to 25 ± 5 ml/m(2), P < 0.01). LA filling increases during exercise in relation to augmented LV longitudinal contraction. Conduit flow increases progressively with exercise in athletes, although this is driven by LV properties rather than intrinsic LA function. The pump function of the LA augments only at moderate exercise due to a reduced diastolic filling time and the Frank-Starling mechanism.

The range of PAWP responses to submaximal exercise is broad in health, but also time-variant. PAWP may routinely exceed 20 mm Hg early in exercise. Initial increases in PAWP and mean pulmonary artery pressures do not necessarily reflect abnormal cardiopulmonary physiology, as pressures may normalise within a period of minutes.