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Myocardial Dimensions and Hemodynamics during 24-h Ultraendurance Ergometry


Medicine & Science in Sports & Exercise: February 2014 - Volume 46 - Issue 2 - p 268–275
doi: 10.1249/MSS.0b013e3182a64639
Basic Sciences

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:

Submitted for publication March 2013.

Accepted for publication July 2013.

Because ultraendurance exercise constitutes an extreme physiological challenge, concerns have been raised regarding possible adverse biochemical, acute cardiac, and long-term effects (8,9,15,16,23,26,27,31–35,43,45).

The primary concerns in ultraendurance performance events are dehydration and the associated decline in total blood volume, which further augments cardiovascular drift (15,37). Bircher et al. (3) reported an increase in body weight (Wt) after 3 d of an ultraendurance cycling race and a reduction in Wt after 6 d. Other studies report a reduced cardiovascular drift in HR but an increase in oxygen uptake (V˙O2) at fixed workloads during 24 h ultraendurance exercise (25,26) and increases in plasma volume (25) and total body water (21). Another concern is the reported decline in HR during ultra endurance exercise, oftentimes attributed to cardiac fatigue as the underlying mechanism (11,13,17,29,31,32,44,45). At present, few data are available regarding the physiological responses during ultraendurance performance.

In a single male subject pilot case report (36), we observed that during 46 h of continuous cycling at a power output range of 145–155 W measured with the SRM-system (Schoberer Rad Messtechnik, Jülich, Germany), the HR response markedly decreased toward the end of the exercise bout. This isolated observation suggested that the decrease in HR during sustained exercise at a constant workload was associated with increases in body Wt and NT-proBNP, presumably due to hypervolemia.

The present study was undertaken to evaluate myocardial dimensions and hemodynamic responses during an acute and continuous 24 h cycle ergometer exercise bout in the laboratory, with specific reference to the HR response, SV, left atrial and ventricular dimensions, selected myocardial biomarkers, blood markers, and associated changes in body Wt.

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Subjects and pretest.

Eight male ultraendurance cycling athletes (mean ± SD; age = 39 ± 8 yr, height = 179 ± 7 cm, Wt = 77.1 ± 6.0 kg) volunteered to participate in the study. All subjects were healthy, asymptomatic, and nonsmokers, having previously completed 5–10 ultraendurance cycling races. One week before the continuous 24-h ultraendurance performance, subjects completed a single incremental cycle ergometer exercise test to volitional fatigue. Blood lactate concentration was used to assess the first and second lactate turn point (LTP1 and LTP2) (18) and the corresponding power output for each subject to subsequently determine the appropriate submaximal workload that the athlete could sustain and complete during the ultraendurance test (Table 1).



All subjects were informed about the procedures, possible risks, and their right to withdraw from the study at any time, and written informed consent was obtained. The study protocol was approved by the ethics committee of the Medical University of Vienna in Austria.

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Exercise tests.

The incremental pretest and continuous 24 h workload ultraendurance tests were performed on an electronically braked cycle ergometer (Lode Excalibur Sport, Groningen, the Netherlands). All tests started between 1100 and 1300 h. The power output for the 24-h ultraendurance performance was set below the LTP1 (23,24,27) because even our highly trained athletes would have been unable to sustain 24 h workload at LTP1 as determined during the initial incremental maximal power output test. Tests were performed in a standard laboratory environment at room temperature of 21°C and 60% relative humidity.

The continuous 24 h cycle ergometer test workload was individually assessed in consultation with each athlete, approximating 75% of the power output determined at LTP1. This resulted in a constant mean power output of 162 ± 3 W for the entire 24 h ultraendurance test.

Subjects were fitted with a facemask (Hans Rudolf, Shawnee, KS), using an antibacterial filter (PALL Pro 1087, Pall, East Hills, NY). Respiratory gas exchange measures were collected at rest (5 min) and during the last 5 min of each hour of the 24-h ultraendurance test. For cardiac output (Q) measurements, three trials of habituation were used to familiarize each subject with ambient air rebreathing technique while sitting on the cycle ergometer, as previously described (40). Immediately at the end of the third familiarization trial, Q, hemodynamic variables and respiratory gas exchange measures were obtained in the seated position at rest and during the last 5 min of every hour throughout the 24-h ultraendurance performance. After resting, measurements were obtained, and the subjects started pedaling at a rate of ≥70 revolutions per minute (rpm) that was maintained throughout the 24-h performance test. HR was recorded continuously in 5-s intervals using Polar Vantage NV telemetry (Polar Electro, Kempele, Finland). Cardiac output, V˙O2, carbon dioxide production (V˙CO2), minute ventilation ( E), blood pressure (measured by the auscultation method), and two-dimensional (2-D) echocardiograms were obtained at the end of each hour during the 24-h ultraendurance performance test. Every 3 h during the 24-h test, we incorporated a 5-min break to allow for the voiding of bodily fluids and body Wt measurements.

After minimal venous occlusion, whole-blood samples were collected at rest and every 6 h from an antecubital vein directly into plastic tubes to determine blood Hct (EDTA), or serum, for the quantification of albumin, total protein, sodium, aldosterone, creatine kinase (CK), creatine kinase isoform MB (CK-MB), and N-terminal pro-brain natriuretic peptide (NT-proBNP).

Fluids and food intake during the 24-h test were consumed ad libitum. Fluid consumption and voiding were measured; however, we did not assess sweat rate or fluid loss via respiration.

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Determination of cardiac output.

Cardiac output (Q) was measured by an inert gas rebreathing unit in breath-by-breath mode (InnocorTM, Innovision, Odense, Denmark) (14). The closed rebreathing system consisted of a three-way respiratory valve connected to a facemask, an antistatic rubber bag, and an infrared photoacoustic gas analyzer (5). Before each rebreathing, the anesthesia bag was filled with a volume of 3–6 L, depending on the individual subject’s predicted vital capacity (37). For rebreathing gases, we used nitrous oxide and sulfur hexafluoride diluted with oxygen and atmospheric air. The rebreathing variables for assessing Q at rest were set to a total gas mixture volume of 40% of the predicted vital capacity (37), to 20% of bolus volume, and to a rebreathing frequency of 20 min−1. For Q measures during exercise, the system calculated the rebreathing variables for each subject. Generally, we allowed a maximal bolus volume of 40% with a minimal oxygen content of 13%, and a maximal carbon dioxide content of 15%. Subjects performed rebreathing over five to eight breaths, of which the first two to three breaths were excluded from calculation due to incomplete gas mixing. The InnocorTM software calculated pulmonary blood flow and Q from the rate of uptake of nitrous oxide, accounting for estimated shunt flow (37). The calculation was based on the slope of a regression line through the logarithmically transformed alveolar nitrous oxide concentrations plotted against time, whereas the system’s gas volume was corrected using the end-tidal sulfur hexafluoride concentration (12).

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Echocardiographic measurement.

Two-dimensional echocardiograms were obtained using a commercially available instrument (GE Vingmed Ultrasound AS Vivid 7 and 3.5-MHz transducer, Horten, Norway). The 2-D images in the parasternal long-axis were measured in a sitting position at rest and after each Q determination during the exercise test. We used Vingmed’s Anatomical M-Mode equipped with a special feature that allows for extraction of M-Mode sweeps from stored 2-D Loops and obtained the M-Mode measurements just distal to the tips of the mitral and aortic valve leaflets. For the evaluation of exercise-dependent myocardial dimensions, left atrial (LAD), left ventricular end-diastolic (LVEDD), and end-systolic (LVESD) diameters were obtained and shortening fraction (SF%) was calculated.

To assess individual changes, the difference (Δ) between the maximal and minimal values for HR, SV, body Wt, LAD, and LVEDD were calculated. Linear regression analysis was used to determine the relationship between ΔSV and Δbody Wt as well as between ΔHR and Δbody Wt, ΔLAD, and ΔLVEDD.

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Blood analysis.

Capillary blood samples for the analysis of blood lactate concentration (LA) during the initial incremental cycle ergometer exercise test were collected from the hyperemic ear lobe at rest, during the last 10 s of each stage and at the end of the exercise test. LA was measured by a fully enzymatic amperometric method in whole blood using the Eppendorf automatic analyzer (EBIO 6666, Eppendorf, Germany).

Eighteen milliliters of whole blood was collected every 6 h and subsequently cooled and centrifuged using Heraeus Megafuge 1.0 R (Heraeus Instruments GmbH, Bad Grund, Harz, Germany). Serum was frozen at −80°C and analyzed for variables specified in Table 1 within 1 wk.

Sodium concentration was obtained by indirect potentiometry using an ion-selective electrode (4). Aldosterone was determined by Coat-A-Count® RIA (Siemens, Vienna, Austria), and NTproBNP assays were measured with a Roche reagent pack on an Elecsys 20.10 Immunoanalyzer (Roche Diagnostics). CK and CK-MB were quantified as previously described (46).

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Variables are expressed as mean ± SD. Repeated-measures ANOVA was used to evaluate differences in body Wt, HR, Q, SV, LVEDD, LVESD, LAD, V˙O2, systolic/diastolic blood pressure (SBP, DBP), Hct, albumin, total protein, sodium, aldosterone, CK, CK-MB, and NT-proBNP. Post hoc comparisons were conducted by using the least significant differences test. Relationships between variables were detected using Pearson product moment correlation analysis. A level of significance was set at P ≤ 0.05.

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Submaximal and maximal values of power output, V˙O2 and HR at LTP1 and LTP2 are depicted in Table 1.

Results of the 24-h ultraendurance performance are shown in Table 1, including values for V˙O2, Q, SBP, DBP, Hct, albumin, total protein, sodium, aldosterone, CK, CK-MB, and NT-proBNP. No significant changes were noted for V˙O2, Q, SBP, DBP, albumin, total protein, and sodium from 1 h to the completion of the 24-h ultraendurance exercise. CK-MB changes were minimal and not clinically relevant. A significant (P ≤ 0.05) decrease in Hct occurred between 6 and 24 h, while CK, aldosterone, and NT-proBNP increased significantly (P ≤ 0.05).

During the 24-h cycling, the peak HR (144 ± 10 min−1) was observed at 6.5 ± 1.25 h, and the minimal HR (116 ± 11 min−1) occurred at 21.5 ± 2.3 h. The increase in HR from 1 h (132 ± 11 min−1) to peak HR was significant (P ≤ 0.01) and decreased by 27 ± 10 min−1 (P ≤ 0.001) when comparing the peak to the minimal values; however, the HR at the end of first hour was significantly higher (P ≤ 0.001) than the minimal HR at ∼21.5 h (Fig. 1).



Body Wt did not change significantly from rest to ∼6 h of the ultraendurance test; however, there was a significant increase (P ≤ 0.001) in body Wt from ∼6 h to ∼21 h, 2.03 ± 0.9 kg (Fig. 2). Fluid consumption throughout the 24-h ultraendurance test was ad libitum, with large variation between subjects; however, fluid voiding was inconsistent due to some subjects voiding more than others. Voiding increased between 15 and 24 h, but the increase was not significant (Table 1).



Stroke volume remained unchanged from 1 to 6 h but increased significantly (31 ± 15 mL) from 6 to 21 h (P < 0.01) (Fig. 3). A similar response was observed for LVEDD (P ≤ 0.01), but not for LVESD (Fig. 4). Consequently, SF% also increased significantly, exhibiting a similar pattern (Table 1).





Left atrial dimension responded similarly to SV and LVEDD, with no change from 1 to 6 h and subsequent increases from 6 to 21 h (P < 0.001) (Fig. 5).



Significant correlations were found between ΔWt and ΔSV (r = 0.5417, P ≤ 0.05) as well as between ΔWt and ΔHR (r = 0.6527, P ≤ 0.05), ΔHR and ΔLVEDD (r = 0.5088, P ≤ 0.05), and ΔHR and ΔLAD (r = 0.7592, P ≤ 0.05).

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The present study may be the first to apply a constant load cycle ergometer 24-h ultraendurance exercise bout in the laboratory setting, detailing the associated changes in myocardial dimensions and hemodynamic responses. Our findings confirm the well-described decline in exercise HR that was previously reported in varied experimental settings during ultraendurance events (11,13,17,44,45), presumably representing cardiac fatigue. However, hemodynamic and blood chemistry data obtained in our study suggests overload of the heart by distinct blood volume shifts after 6–8 h of constant exercise, increasing SV due to increased central venous pressure (7) without changes in venous capacitance, the Frank–Starling mechanism and decreasing HR, with unchanged cardiac output and oxygen uptake (Table 1). Similar results have been reported for the use of a volume expander (20); however, in this study, Q also increased modestly. Grant et al. (16) described comparable responses, suggesting that an increase in blood volume (hypervolemia) was responsible for the reduction in HR toward the end of a prolonged exercise bout.

The decline in HR over time is a typical response observed in ultraendurance races (2,8,29,31,32,36). However, extensive laboratory experiments over 24 h of prolonged ultraendurance performance had not yet been performed. Mattson et al. (26) used a controlled laboratory setting and assessed only the HR response and no other hemodynamic variables during 24 h ultraendurance exercise. These authors suggested that the occurrence of cardiac fatigue due to the desensitization of heart’s adrenergic receptors was caused by high concentrations of catecholamines. Moreover, they reported a similar response in blood Hct, suggesting a volume shift that is in agreement with the results of our study.

To avoid potentially confounding variables typical for ultraendurance races such as changes in speed, race tactics, unexpected weather, ambient temperature and humidity, road conditions, and inclines and declines, we conducted a constant load exercise bout that could be performed continuously in a controlled laboratory setting for 24 h.

In agreement with other investigations, our results demonstrated a previously reported exercise-induced increase in HR from 1 to 6 h (1,10,26,38), presumably due to an increase in body temperature, enhanced fat oxidation, fluid loss via sweating and respiration, sympathetic activation, blood volume shifts to the periphery for temperature regulation, or combinations thereof.

However, after 6 to 8 h, a steady decline in exercise HR occurred (26,29,31,32,45), the cause of which remains unclear. Several hypotheses have been put forth, such as a cardiac fatigue (26,29,31,32,45) and volume overload (36), suggesting that short-term physiological adaptations compensate for volume shifts within the body during ultraendurance exercise. Whyte et al. (45) found evidence for acute myocardial injury and transient cardiac dysfunction after an Ironman triathlon as substantiated by ultrasound measurements and selected blood chemistry parameters; however, no rationale was given to explain the phenomenon. This study investigated a 5–10 h endurance event, much shorter than the 24-h challenge in our study and included higher intensities during the event to explain some of the differences observed. Similar to our study, body Wt decreased during the first 6 h, suggesting that dehydration occurs during the first 6 h of the 24-h challenge, resulting in a nonsignificant decrease in SV and LVEDD. Neumayr et al. (28,30) described cardiac fatigue by elevated postexercise Troponin T values, a highly specific marker of myocardial injury, which was shown to be reversible shortly after the end of the race. Contrary to these authors (28,30), our subjects increased body Wt—obviously as a mismatch between hyperhydration and fluid retention that caused hypervolemia and the concomitant changes in ventricular dimensions.

Convertino (6) reported that there is little further decrease in plasma volume with prolonged exercise, suggesting a protective mechanism against the profound reduction of circulating blood volume. In addition, these mechanisms include increasing plasma protein oncotic pressure, differences in peripheral vasoconstriction in active muscles and inactive tissue, and associated increase in lymph flow (6). Although our subjects consumed, on average, approximately 0.87 L of fluid per hour, this is not excessive and within the normal range for prolonged and ultraendurance performance (41,42). Sweat loss may have also diminished over time, contributing to the observed hypervolemia because the sweat rate was not controlled. Because our subjects drank ad libitum and did not appear to be dehydrated, the hypervolemia that occurred may be due to the increase in plasma protein oncotic pressure as the primary contributor to the increase in plasma shift and greater fluid retention in interstitial space (Table 1). In addition, our subjects exhibited diminished initial urinary fluid loss and an increase in absolute plasma protein (albumin) that added to the increase in plasma volume and the subsequent changes in hemodynamic variables. Collectively, these factors likely resulted in hypervolemia in our subjects and an increase in body Wt at the end of 24 h of ultraendurance challenge. Nevertheless, the specific modulators for these volume shifts warrant further investigation.

Regarding the chronic effects of higher doses of distance running, extreme exercise (33) may be associated with diminished health benefits as compared with more moderate exercise regimens. These authors (33) suggested that after decades of high-volume, high-intensity exercise and repetitive injury, this pattern may lead to patchy myocardial fibrosis, particularly in the pliable walls of the heart such as the atria and right ventricle, creating a substrate for atrial and potentially malignant ventricular arrhythmias. In addition, they suggested that long-term excessive exercise may accelerate the aging of the heart, as substantiated by increased coronary artery calcification, diastolic ventricular dysfunction, and large-artery wall stiffening (34). We are not able to corroborate these findings (33) as these were not the focus of our study of acute effects of ultraendurance exercise.

Mattson et al. (26) studied 24 h HR response in kayak, cycling, and running athletes in a laboratory setting in an ambient environment with controlled constant workload cycling of 20 min using the last 10 min of each 20 min as a reference value. This 20 min constant workload cycling was repeated every 6 h during the 24-h test. The investigators reported an increase in HR of ∼15 bpm at 6 h and a gradual but consistent decrease of ∼12–13 bpm at 18 to 24 h. We observed similar responses in our athletes who also increased their HR significantly at 6 h, presumably due to a reduction in central blood volume, and demonstrated a gradual and significant decrease in HR after 6 h that persisted to the end of the prolonged exercise bout. Because our subjects drank fluids ad libitum throughout the 24-h test, they may have been hyperhydrated with reduced sweat loss. Fluid voiding gradually decreased between 3 and 12 h, increasing over time thereafter (to 24 h). We postulate that the associated hypervolemia as indicated by the increase in body Wt, led to a cascade of physiologic responses that may have been responsible for the gradual decrease in HR after 6 h of cycling. It is noteworthy that the HR response at ∼21 h was actually below the HR determined during the initial stages of our study protocol (Fig. 1). In contrast to Mattson et al. (26), we found no significant differences in submaximal V˙O2 during the 24-h test (Table 1).

In light of a fivefold increase in CK (43), which represents a marker of muscle cell damage, we hypothesize that numerous proteins may have also leaked into the bloodstream, thereby increasing blood oncotic pressure during the 24-h bout of continuous cycle ergometry. Presumably, due to changes in oncotic and osmotic pressures, there was a significant decrease in Hct from 6 to 24 h (Table 1). Although fluid intake was ad libitum, body Wt of our subjects increased significantly from 6 to 21 h. We postulate that voiding, sweating, and respiratory fluid loss (not measured) could not compensate for the fluid intake alone, although there was a 13-fold increase in aldosterone with no significant changes in sodium concentration. In addition, renal function may have been temporarily reduced due to the prolonged vigorous exercise, an adaptation that has been previously described (29). Thus, the observed hypervolemia may have resulted from a combination of an adequate fluid intake, possibly lower sweating rate, reduced urinary fluid loss, increased total protein content, and thus oncotic pressure, and increased central venous pressure and extracellular fluid retention, leading to the observed increase in body Wt and associated hemodynamic changes.

Because we observed changes in the HR response during the 24-h constant ultraendurance exercise, an influence of circadian rhythms on selected variables, especially during the night, should also be considered. Our subjects began cycling between 1100 and 1300 h, a time that should correspond to the beginning of the normal circadian cycle (39). The HR remained relatively unaltered from 21 h (116 ± 11 bpm) to the end of the 24 h (121 ± 11 bpm) but was significantly lower (P ≤ 0.01) compared with the first hour of the 24-h test (132 ± 11 bpm). The decrease in HR during the evening and night hours may not depend exclusively on circadian variation and may only partially account for the reduction in HR during the nighttime hours. Although, resting HR is significantly influenced by circadian variation, with an amplitude of ∼8.6%, reaching a peak during the middle of a given biological day (∼1600 h) and continuing into the biological night (∼0400 h), there appears to be little influence of circadian rhythm on the HR response to prolonged exercise (39).

Oxygen uptake and Q increased nonsignificantly during the first 6 h and were largely unchanged during the remainder of the prolonged exercise bout (>Table 3). Increased SV (Fig. 3) was a result of enhanced LVEDV without concomitant changes in LVESD as determined from echocardiographic measurements (Fig. 4). In contrast to these data, La Gerche et al. (22) studied a cohort of 40 highly endurance trained athletes competing in endurance events including marathon (mean time to completion, 3 h), half-ironman triathlon (5.5 h), full-ironman triathlon (11 h), and alpine bicycle race (8 h). Right ventricular volumes increased in the postrace setting, whereas left ventricular volumes decreased, resulting in a decrease in right but not left ventricular ejection fraction. Moreover, these intense endurance exercise efforts evoked elevations in biomarkers of myocardial injury (myocardial troponins and B-type natriuretic peptide), which were correlated with reductions in RVEF, but not LVEF, in the immediate (mean, 45 min) postrace setting. The observed increase in LVEDD is most likely responsible for the increase in NT-proBNP (19).

Furthermore, we postulate that the body Wt gains observed at the end of the ultraendurance exercise bout were related to the associated hypervolemia, thus explaining the significant relationship between body Wt and SV as well as the negative correlation between body Wt and HR, secondary to an increase in central blood volume. Moreover, the reduced HR and enlarged LVEDD and LAD were significantly related to left ventricular and atrial dilatation.

Although our results are largely in agreement with previous reports (11,13,17,44), the present findings refute the hypothesis that an increase in catecholamines may be responsible for the so-called cardiac fatigue and subsequent reduction in HR due to reduced sensitivity of myocardial receptors (26).

A question that needs to be addressed is the recovery of the changes in hemodynamic responses and blood variables after ultraendurance exercise. Unfortunately, we did not obtain these measures postexercise, which represents a limitation of this study. According to a recent review, these changes are generally restored within 1 wk and suggest that repeated ultraendurance exercise may be harmful over the long term (34). In our study, no clear pathophysiological signs were detected, although all subjects had a history of ultraendurance sports participation. Additional limitations of the study were that we did not measure blood osmolality, our subjects consumed self-prepared drinks, and the exact composition of each drink was not analyzed. Only the ingested volumes were recorded.

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In summary, our findings indicate that the decrease in HR during a 24-h constant workload did not suggest cardiac fatigue as indicated by changes in ventricular workload validated by echocardiographic measurements. Subjects increased their body Wt due to hypervolemia, which appears to be the result of a mismatch of a lower sweat loss, reduced voiding, and increase in total protein content with recommended fluid intake. These factors contributed to an increase in SV caused by an increase in end-diastolic volume and unchanged end-systolic volume, as reflected by a 25-fold increase in NT-proBNP and consequently a reduced HR.

The authors declare no conflict of interest, and no funding was obtained for this study.

Results of the present study do not constitute endorsement by the American College of Sports Medicine.

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