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1 The Copenhagen Muscle Research Center, Department of Anaesthesia, Rigshospitalet, Blegdamsvej 9, DK-2100, Copenhagen Ø, Denmark 2 Department of Sport Sciences, Brunel University, Uxbridge, Middlesex UB8 3PH, UK 3 British Olympic Medical Institute, Northwick Park Hospital, Harrow, Middlesex HA1 3UJ, UK 4 School of Medical Sciences, College of Life Sciences and Medicine, University of Aberdeen, Aberdeen AB25 2ZD, UK 5 Research Institute for Sport and Exercise Science, Liverpool John Moores University, Liverpool L3 2ET, UK
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Abstract |
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) and an index of contractility (dP/dtmax). A venous catheter assessed that central venous pressure (CVP) was maintained throughout rest, exercise and 10 min into recovery. Both systolic blood pressure and heart rate (HR) increased with the onset of exercise (from 132 ± 5 to 185 ± 19 mmHg and from 66 ± 9 to 135 ± 23 beats min–1; increases from rest to the end of the first 5 min of exercise in SBP and HR, respectively) but systolic blood pressure did not change from 30 to 180 min of exercise (
150 mmHg), while heart rate only increased by 8 ± 9 beats min–1 (means ±
S.D.; P > 0.05). The attenuated increase in HR compared with other studies suggests that the maintained CVP (5 mmHg) helped to prevent cardiovascular drift in this protocol. Stroke volume, 
and dP/dtmax were all increased with the onset of exercise (from 85 ± 8 to 120 ± 18 ml, from 5.4 ± 1.3 to 16.5 ± 3.3 l min–1 and from 14.4 ± 4 to 28 ± 8 mmHg s–1; values from rest to the end of the first 5 min of exercise for SV, 
and dP/dtmax, respectively) and were maintained during exercise. There was no difference in the SBP/ESV ratio from pre- to postexercise. Conversely, E:A was reduced from 2.0 ± 0.4 to 1.6 ± 0.5 postexercise (P < 0.05), returning to normal values at 24 h postexercise. This change in diastolic filling could not be fully explained (r2
= 0.39) by an increased heart rate and, with CVP unchanged, it is likely to represent some depression of intrinsic relaxation properties of left ventricular myocytes. Three hours of semi-supine cycling resulted in no evidence of a depression in left ventricular systolic function, while left ventricular diastolic function declined postexercise.
(Received 4 August 2006;
accepted after revision 4 December 2006; first published online 5 December 2006)
Corresponding author E. A. Dawson: University of North Texas Health Science Center, Department of Integrative Physiology, 3500 Camp Bowie Boulevard, Fort Worth, TX 76107, USA. Email: ellendawson{at}hotmail.com
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Introduction |
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Studies examining left ventricular (LV) function following prolonged exercise, however, do have some inherent limitations. Field-based studies provide a setting for competitive ultra-endurance exercise, but are limited to pre- and postrace assessments, so the impact of the prolonged exercise on cardiac performance during the event is only assessed indirectly. Furthermore, field studies may be difficult to interpret because preload and afterload, the primary determinants of LV function, are often affected (Dawson et al. 2003). Exercise-induced reductions in blood volume and venous return may be further exacerbated by heat, humidity and altitude (Douglas et al. 1986; Davila-Roman et al. 1997)
Cardiac function has been investigated during prolonged exercise in a controlled laboratory environment. Saltin & Stenberg (1964) observed a decline in stroke volume towards the end of 3 h of exercise even when central blood volume was maintained, suggestive of depressed myocardial contractility. Conversely, no evidence of a decline in ejection fraction or in the end-systolic pressure to volume ratio was reported by Upton et al. (1980), Palatini et al. (1994) or Goodman et al. (2001). These discrepancies may relate to the use of diverse cardiovascular assessment techniques (dye dilution, Saltin & Stenberg, 1964; echocardiography, Palatini et al. 1994; and radionuclide angiography, Upton et al. 1980 and Goodman et al. 2001) as well as different exercise intensities and durations. Saltin & Stenberg (1964) employed the longest exercise protocol (3 h) with the highest exercise intensity (75% maximal oxygen uptake; 
) but only reported data for one trained subject, and they changed the exercise mode from bicycling to running. Only Goodman et al. (2001) made an attempt to maintain preload to the heart primarily via regular, non-individualized fluid intake (250 ml every 20 min), but there remained a drop in both end-diastolic volume and stroke volume (SV) towards the end of 150 min of exercise at 60%
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In an effort to clarify the consequences of prolonged exercise upon the heart, we examined LV function during prolonged exercise, whilst maintaining preload by individualized regulation of central venous pressure (CVP) by intravenous saline infusion. We assessed LV systolic and diastolic function pre- and postexercise by echocardiography in order to compare in-event and pre- to postexercise data. We hypothesized that the LV function would not decline with exercise duration when CVP was maintained.
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Methods |
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55.4 ± 5.4 ml min–1 kg–1 (means ±
S.D.). Prior to commencing the study, subjects provided written informed consent. The studies conformed to the code of Ethics of the World Medical Association (Declaration of Helsinki), and all procedures conducted during the study were approved by the Ethics Comittee of Copenhagen and Frederiksberg communities.
Subjects were required to attend the laboratory (with conditions set to 20°C and 50% humidity) on two occasions separated by a minimum of 3 days. On the first occasion, after familiarization, subjects completed incremental semi-recumbent cycling on a Krogh cycle ergometer to volitional exhaustion in order to assess 
. Pulmonary gas exchange was measured using an Oxyscreen metabolic cart (CPX/D; Medical Graphics Corporation, St Paul, MN, USA). On the second visit to the laboratory, the subjects completed a 3 h bout of semi-recumbent cycling at 70% of their 
(±5%). This exercise duration and intensity were chosen to match as closely as possible the work intensity applied by Saltin & Stenberg (1964).
Cardiovascular assessment
During the 3 h exercise bout, cardiovascular function was monitored using an indwelling catheter (1.1 mm i.d.; 20 gauge) placed in the brachial artery of the non-dominant arm. From the arterial line, systolic (SBP) and diastolic blood pressure (DBP) and heart rate (HR) were recorded. Beat-to-beat SV and cardiac output (
) were calculated from the arterial pulse wave by the pulse contour [method Modelflow (Finometer TPD Biomedical Instrumentation, Amsterdam, the Netherlands); Wesseling et al. 1993; Sugawara et al. 2003]. Stroke volume is calculated by the Modlelfow system from the area under the arterial pressure wave. The arterial system is simulated as a non-linear, time varying, three-element model of aortic input impedance (aortic characteristic impedance, arterial compliance and total peripheral resistance) which takes into account the non-linear aortic pressure–area relationship, and includes a correction for age and sex. Cardiac output is then calculated as the product of stroke volume and heart rate (Wesseling et al. 1993).
The Modelflow method has several potential limitations; it is possible that the assumptions of the model could be influenced by an enhanced sympathetic activity during intense exercise or that the propagation of a pressure pulse might be increased with ageing (Sugawara et al. 2003). The model assumes that the aortic dimension and elastic properties remain constant (Gratz et al. 1992).
It has been demonstrated that unless it is calibrated against a ‘gold’ standard (all of which are open to limitations) then the absolute values that are produced by the Modelflow can be suspect (Remmen et al. 2002). However, the technique has been shown to accurately track relative changes in cardiac output when compared with thermodilution and Doppler ultrasound (Remmen et al. 2002) during rest, exercise (Sugawara et al. 2003) and head-up tilt (van Lieshout et al. 2003), during withdrawal of blood volume (Leonetti et al. 2004) and in patients with cardiovascular disease (Wesseling et al. 1993; Schreuder et al. 1995; Jellema et al. 1999).
In addition, the arterial pulse wave was recorded to data acquisition hardware (MacLab/8S with Chart 4.0 software; AD Instruments, Castle Hill, Australia; connected to a Power Macintosh 6100/66 computer) and used to measure the first derivative of the arterial wave (dP/dt) throughout the cardiac cycle for the assessment of the maximal value for dP/dt (dP/dtmax), an index of the initial velocity of myocardial contraction (Germano et al. 1998). Left ventricular dP/dtmax has been used in many animal studies to assess left ventricular function in numerous different conditions, including exercise and disease states (Demirel et al. 2001; Miyashita et al. 2001). As with other measurements of contractility, though, it can be influenced by changes in loading conditions. Measurements were recorded every 5 min for the first 15 min and then at 15 min intervals throughout exercise and 10 min following exercise cessation.
A venous catheter (Baxter Healthcare Corp.) was employed to record CVP. The catheter was inserted into the brachial vein and advanced to the superior caval vein. Assessment of CVP served two purposes. Firstly, it provided an index of preload to the heart and secondly, it provided information to enable individual adjustment of saline infusions to maintain CVP. Constant measurements of haematocrit (Hct) were taken, and if either CVP or Hct decreased from the values recorded after the first 5 min of exercise, then saline was infused and the Hct and CVP were measured again. This was continued until values returned to the 5 min value. Thus, during exercise saline was infused based on changes in CVP and Hct, with an average of 728 ± 414 ml of saline being infused during exercise. Throughout the trial, subjects were allowed to consume water ad libitum, and the volume of fluid consumed by each subject was recorded. The arterial line was kept patent throughout the trial by continuous infusion of isotonic saline (3 ml h–1).
Prior to, within 15 min postexercise and 24 h after the exercise trial, echocardiographic assessment of LV systolic and diastolic function was completed. Echocardiographic evaluation was conducted by a single experienced sonographer, employing a 2.5 MHz transducer connected to a Logic 500 MD (General Electric, KPI, CA, USA) with simultaneous ECG recording.
For all evaluations, subjects were positioned in the left lateral decubitus position. Two-dimensional, M-mode and Doppler echocardiographic scans were performed according to the American Society of Echocardiography guidelines (Schiller et al. 1989), with system settings adjusted to obtain the best signal to noise ratio. The measurements obtained were LV internal diameters during diastole and systole (LVIDd and LVIDs, respectively) and the LV posterior free wall during systole (LVPWs). In order to evaluate systolic function, SV, ejection fraction (EF) and the end-systolic pressure to volume ratio (SBP/ESV) were calculated, employing the equations
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In order to assess diastolic function, a two-dimensional apical four-chamber view was imaged, taking care to maximize the diameter of the mitral valve annulus. Pulsed-wave Doppler interrogation of mitral valve inflow velocities was performed, with alignment of the sample volume cursor parallel to flow at the level of the mitral annulus, while transducer adjustments were made to obtain the highest velocity with least spectral dispersion display. Peak early transmitral velocity flow (E wave, in cm s–1) and peak atrial transmitral velocity flow (A wave, in cm s–1) were measured, and the ratio of the two (E:A) was calculated as a measure of the global diastolic function. For all echocardiographic measurements, three to five consecutive cardiac cycles were digitized and the measurements averaged.
Data analysis
Data are presented as the means ±
S.D. at rest, after 5, 30 and every subsequent 30 min of exercise and after 10 min of supine recovery. The data were analysed by repeated measures one-way ANOVA, and the Bonferroni post hoc analysis for the effect of exercise duration on measures and indices of the haemodynamic load (CVP, SBP, DBP and HR) placed upon the left ventricle as well as variables of left ventricular function (SV, 
and dP/dtmax). Echocardiographic data for left ventricular function (SV, EF and SBP/ESV) as well as LVMWS (a further estimate of afterload) were analysed. Systolic functional data obtained during exercise and pre- to postmeasurements were compared by a correlation analysis. To examine the influence of altered HR postexercise upon any change in diastolic filling changes (pre- to postexercise), HR changes were correlated with changes in E:A. All statistical analyses were completed using Statistica (Statsoft Ltd, Tulsa, OK, USA) computer software. A critical 
value of 0.05 was selected.
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Results |
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in the final hour of exercise and, subsequently, dropped their power to a level equivalent to 50%
for the third hour. Data for these subjects were therefore removed from the statistical analysis in order not to skew measures of left ventricular function in relation to exercise intensity. These subjects did not demonstrate any systolic or diastolic dysfunction. Cardiovascular assessment
In an attempt to maintain preload to the heart, 720 ml of saline was infused (range, 250–1300 ml) and the subjects drank 1858 ml of water (range, 150–3500 ml). The limited change in CVP (Fig. 1), and no significant change in LVIDd, suggests that ad libitum drinking and saline infusions maintained preload to the heart throughout the study.
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At the onset of exercise, SV and 
rose, in line with the differences in absolute exercise intensity among the subjects (Fig. 2). Beyond 30 min of exercise, however, SV and 
did not change until the recovery period, when both dropped without reaching resting values. Values of dP/dtmax followed a similar response to SV and 
, rising with the onset of exercise and remaining elevated throughout the exercise bout. Following exercise, dP/dtmax fell but had not returned to baseline values within the study period.
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Discussion |
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with maintained preload as indicated by central venous pressure. Yet there was a postexercise drop in diastolic function independent of left ventricular loading and heart rate. Maintained CVP seems to attenuate cardiovascular drift, suggesting that cardiovascular drift is related to insufficient volume loading. However, other factors, including temperature, may also play a role in cardiovascular drift (Coyle & Gonzalez-Alonso, 2001). Left ventricular loading
An important aspect of this study was the assessments of CVP; it was continually monitored in order to tailor saline infusions individually to help maintain preload to the heart throughout exercise. This is in contrast to Goodman et al. (2001), who used a predefined regimen of fluid intake. Whilst SBP rose at the onset of exercise, it remained stable throughout the remainder of the exercise bout. Cardiovascular drift, defined as a progressive rise in HR with increasing exercise duration at a given intensity, often seen during prolonged exercise (e.g. Saltin & Stenberg, 1964), was seemingly blunted in this study potentially by two mechanisms: firstly, by maintenance of CVP through infusion of saline and adequate drinking and secondly, as a result of the semi-recumbent exercise, which would support CVP compared with the upright position.
Cardiovascular assessment
Figure 2 demonstrates that SV, 
and dP/dtmax did not change with exercise duration. Thus, there is no evidence of a depression in left ventricular contractile function indicative of ‘exercise-induced cardiac fatigue’. The present data are at odds with the study of Saltin & Stenberg (1964), who found depressed systolic function despite maintained blood volume, but support the conclusions of studies examining contractile function during prolonged exercise (Upton et al. 1980; Palatini et al. 1994; Goodman et al. 2001). The present study extends these data by employing a longer duration and higher exercise intensities as well as the direct maintenance of preload. The impact of the close monitoring and intervention to maintain CVP and thus presumably preload to the heart may also be important, although data from Saltin & Stenberg (1964) are at odds with this because they reported depressed systolic function despite no significant depression in blood volume throughout exercise. It is possible that CVP was depressed, however, without a change in total blood volume.
The lack of any significant changes in left ventricular contractility during 3 h of exercise could reflect one of three potential circumstances. Firstly, exercise-induced cardiac fatigue is uniquely associated with pre- to postexercise measurements that do not reflect left ventricular function during prolonged exercise. Secondly, exercise-induced cardiac fatigue was prevented by the maintenance of left ventricular loading. Thirdly, irrespective of the maintenance of left ventricular loading, the duration and intensity (or both) employed in the present study were not great enough to provoke a pronounced depression in left ventricular contractility (McGavock et al. 2002; Dawson et al. 2003).
Cardiovascular assessment (pre- and postexercise)
Data for CVP and LVIDd as well as for LVMWS suggest that left ventricular loading was similar at the pre- and postexercise echocardiographic assessment. Despite some individual variability, SV, EF and ESP/ESV postexercise revealed no depression as a result of the 3 h exercise bout. This supplements in-exercise data and is similar to another laboratory-based study that have found no depression in LV function after prolonged exercise of similar duration (Goodman et al. 2001) and to field-based studies employing similar durations of exercise (Perrault et al. 1986; Lucia et al. 1999; George et al. 2004, 2005).
The impact of exercise upon diastolic function, assessed via Doppler echocardiography, was different from that observed for systolic function as reported by Goodman et al. (2001) and in field studies employing similar exercise of a similar duration (Lucia et al. 1999; George et al. 2004, 2005). Furthermore, changes in diastolic function are detectable before changes in systolic function owing to the primary reliance of diastolic filling upon longitudinal myocyte function which represents the smallest component of total myocyte mass.
Diastolic function postexercise is affected by HR and the loading conditions (Libonati, 1999). Given the maintenance of loading and an r2 of only 0.39 between the change in HR and the change in E:A, the changes in diastolic function postexercise were taken to reflect other factors related to either left atrial pressure development or intrinsic relaxation properties of the left ventricle. George et al. (2005), using tissue Doppler evaluation of diastolic function after a marathon race, suggested that the left atrial pressure may not be as important as alterations in left ventricular pressure decay in precipitating a ‘diastolic cardiac fatigue’. A postexercise decrease in left ventricular compliance owing to altered Ca2+ metabolism has been postulated to explain the decrease in diastolic function of the heart (Dawson et al. 2003).
We did not evaluate whether a postexercise depression in diastolic filling mirrors alteration in diastolic function during exercise. Flow propagation velocity (Middleton et al. 2006) and tissue Doppler imaging (George et al. 2005) may be useful in evaluating diastolic function in laboratory-based studies. Recent data from our group suggest that tissue Doppler imaging provides similar results to standard echocardiography (George et al. 2005; Middleton et al. 2006). Data available for strain imaging are more limited, and this is clearly an area that is worthy of future investigation. Although our data suggest that the maintained CVP helped to attenuate cardiovascular drift, we did not have a control condition where the subjects performed the same exercise protocol without volume replacement.
In the two subjects who dropped the exercise intensity in the final hour, there was no change in postexercise systolic or diastolic function. In-exercise systolic function followed a similar trend to the other subjects, with an increase at the start of exercise to 15 mmHg s–1, which was maintained throughout the exercise protocol, although there was a slight drop in the last hour, probably as a result of the decrease in exercise intensity. The subjects were unable to maintain the higher exercise intensity owing to skeletal muscle fatigue. Apparently, they did not reduce their workload owing to cardiac fatigue.
It should be stated that the changes seen in this study are not directly comparable to those observed in clinical populations and so this probably does not have any immediate implications for health. It is also unlikely that the changes in peak diastolic filling velocities affected preload (since LVIDd was unchanged) or systolic function. However, since diastolic changes may precede changes in systolic function in very prolonged exercise (George et al. 2004), the decreased diastolic function may have some impact on performance in longer bouts of exercise.
Conclusion
This study examined cardiac function during, as well as before and after, prolonged exercise. Importantly, CVP was maintained throughout the 3 h exercise bout and blood pressure remained relatively stable. There was no significant increase in HR over the exercise period, suggesting that, in this protocol, a maintained CVP attenuated cardiovascular drift. The impact of 3 h of semi-recumbent cycle ergometry upon left ventricular function was negligible. Furthermore, there was no evidence of exercise-induced cardiac fatigue in indices of left ventricular contractility assessed postexercise. A postexercise depression in diastolic filling was reported that was independent of loading and not wholly explained by an increase in HR postexercise.
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References |
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. CVP, central venous pressure; SBP, systolic blood pressure; DBP, diastolic blood pressure; and HR, heart rate. All values of heart rate and systolic blood pressure were increased from rest to exercise. Heart rate during recovery was higher than at rest, while systolic blood pressure during recovery was lower than at rest. * Significantly different from rest; 
significantly different from rest and exercise (P < 0.05).
, cardiac output; SV, stroke volume; and dP/dtmax, maximal rate of change in pressure during ejection. Values of 
, SV and dP/dtmax were increased from rest to exercise. Values of 
, SV and dP/dtmax during recovery were higher than rest. * Significantly different from rest; 
significantly different from rest (P < 0.05).