Myocardial Dimensions and Hemodynamics during 24-h Ultraendurance Ergometry

Purpose: This study aimed to evaluate cardiorespiratory and hemodynamic responses during 24 h of continuous cycle ergometry in ultraendurance athletes. Methods: Eight males (mean +/- SD; age = 39 +/- 8 yr, height = 179 +/- 7 cm, body weight [Wt] = 77.1 +/- 6.0 kg) were monitored during 24 h at a constant workload,similar to 25% below the first lactate turn point at 162 perpendicular to 23 W. Measurements included Wt, HR, oxygen consumption ((V) over dotO(2)), cardiac output (Q), and stroke volume (SV) determined by a noninvasive rebreathing technique (Innocor (TM); Innovision, Odense, Denmark). Myocardial dimensions were evaluated using a two-dimensional echocardiogram. [M-mode measurement]-left atrial (LAD), ventricular end-diastolic (LVEDD), and end-systolic diameters (LVESD) were obtained over the left parasternal area. Venous blood samples were analyzed for hematocrit (Hct%), albumin (g.L-1), aldosterone (pg.mL(-1)), CK, CK-MB (U.L-1), and N-terminal pro-brain natriuretic peptide (NT-proBNP) (pg.mL(-1)). Results: HR (bpm) significantly increased (P < 0.01) from 1 h (132 +/- 11) to 6 h (143 +/- 10) and significantly decreased (P < 0.001) from 6 to 24 h (116 +/- 10). (V) over dotO(2) and (Q were unchanged during the 24 h. Wt (76.6 +/- 5.6 vs 78.7 +/- 5.4), SV (117 +/- 13 vs 148 +/- 19), LVEDD (4.9 +/- 0.3 vs 5.6 +/- 0.2), and LAD (3.6 +/- 0.5 vs 4.3 +/- 0.7) significantly increased between 6 and 24 h (P < 0.001). No significant changes were observed for LVESD. Hct (45.1 +/- 1.3 vs 41.3 +/- 1.2) significantly decreased (P < 0.05) and CK (181 +/- 60/877 +/- 515), aldosterone (48 +/- 17 vs 661 +/- 172), and NT-proBNP (23 +/- 13 vs 583 +/- 449) significantly increased (P G 0.05). The increase in SV (Delta SV) was significantly related to changes in Wt (Delta Wt), and HR (Delta HR) and Delta Wt were significantly related to Delta LAD and Delta LVEDD. Conclusion: Our findings suggest that the decrease in HR during 24 h of ultraendurance exercise was due to hypervolemia and the associated ventricular loading, increasing left ventricular diastolic dimensions because of increased SV and LVEDD, resulting in an increase in NT-proBNP.