This study aimed to evaluate cardiorespiratory and hemodynamic responses during 24 h of continuous cycle ergometry in ultraendurance athletes.
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,∼25% below the first lactate turn point at 162 ± 23 W. Measurements included Wt, HR, oxygen consumption (V˙O2), cardiac output (Q), and stroke volume (SV) determined by a noninvasive rebreathing technique (InnocorTM; 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).
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˙O2 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 < 0.05). The increase in SV (ΔSV) was significantly related to changes in Wt (ΔWt), and HR (ΔHR) and ΔWt were significantly related to ΔLAD and ΔLVEDD.
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.
1Department of Sport Sciences, University of Vienna, Vienna, AUSTRIA; 2Center for Life Style Medicine, Linz, AUSTRIA; 3Department of Internal Medicine II, Medical University of Vienna, Vienna, AUSTRIA; 4Human Performance Laboratory, Department of Kinesiology, St. Cloud State University, St. Cloud, MN; 5Preventive Cardiology, William Beaumont Hospital, Royal Oak, MI; 6Department of Sport Sciences, University of Salzburg, Salzburg, AUSTRIA; 7Center for Physiology and Pharmacology, Institute of Physiology, Medical University of Vienna, Vienna, AUSTRIA; and 8Exercise Physiology and Training Research Group, Institute of Sports Science, University of Graz, AUSTRIA
Address for correspondence: Serge P. von Duvillard, Ph.D., FACSM, FECSS., Department of Kinesiology, Human Performance Laboratory, St. Cloud State University, 327 Halenbeck Hall, St. Cloud, MN 56301; E-mail: firstname.lastname@example.org.
Submitted for publication March 2013.
Accepted for publication July 2013.