Exercise-Induced Changes in Hemodynamics, Hormones, Electrolytes, and Inflammatory Markers in Veteran Athletes with and without Coronary Atherosclerosis.

Abstract

Aims: Middle-aged and older male athletes have more coronary atherosclerosis than less active peers. We aimed to explore mechanisms that can contribute to this accelerated coronary atherosclerosis by comparing exercise-induced changes in hemodynamic factors, circulating hormones, electrolytes, and inflammatory markers across athletes with and without coronary atherosclerosis.

Methods: Fifty-nine male athletes recruited from the MARC-2 study were stratified as controls (coronary artery calcium score [CACS] = 0, n = 20), high CACS (≥300 Agatston units or ≥75th Multi-Ethnic Study of Atherosclerosis percentile, n = 20), or significant stenosis (≥50% in any coronary artery, n = 19). At rest, during an exhaustive endurance cycling test and after 3 h of recovery, we measured blood pressure and blood concentrations of parathyroid hormone (PTH), calcium, magnesium, phosphate, C-reactive protein (CRP), IL-6, IL-1RA, IL-10, intercellular adhesion molecule 1 (ICAM-1), VCAM-1, and E-selectin.

Results: Fifty-eight participants completed the exercise test (76 ± 14 min). All biomarkers changed during exercise, except CRP, ICAM-1, and VCAM-1. Systolic blood pressure, PTH, calcium, phosphate, IL-6, IL-1RA, and E-selectin concentrations increased during exercise. By contrast, diastolic blood pressure and magnesium concentrations decreased during exercise. The magnitude of exercise-induced responses of hemodynamic factors, circulating hormones, electrolytes, cytokines, and adhesion molecule concentrations did not, however, differ across groups.

Conclusions: Blood pressure, hormone, electrolyte, and cytokine concentrations changed after an exhaustive endurance exercise test, but the magnitude of these responses did not differ between athletes with versus without coronary atherosclerosis. These findings suggest that accelerated coronary atherosclerosis in endurance athletes may not be explained by differences in responses to exercise but by differences in exercise exposure or other mechanisms not assessed in this study.