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,∼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).
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˙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.
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.
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.