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J Physiol Volume 569, Number 1, 325-330, November 15, 2005 DOI: 10.1113/jphysiol.2005.096412
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Prolonged strenuous exercise alters the cardiovascular response to dobutamine stimulation in male athletes

Robert C. Welsh1, Darren E. R. Warburton1,2, Dennis P. Humen1, Dylan A. Taylor1, Jonathon McGavock2 and Mark J. Haykowsky1,3

1 Division of Cardiology, Faculty of Medicine
2 Faculty of Physical Education and Recreation
3 Faculty of Rehabilitation Medicine, University of Alberta, Edmonton, Alberta, Canada


   Abstract
Top
 Abstract
Introduction
 Methods
 Results
 Discussion
 References
 
Prolonged strenuous exercise has been associated with transient impairment in left ventricular (LV) systolic and diastolic function that has been termed ‘cardiac fatigue’. It has been postulated that cardiac ß-adrenoreceptor desensitization may play a central role; however, data are limited. Accordingly, we assessed the cardiovascular response to progressive dobutamine stimulation after prolonged strenuous exercise (2 km swim, 90 km bike, 21 km run). Nine experienced male athletes were studied: PRE (2–3 days before), POST (after) and REC (1–2 days later). The cardiovascular response to progressive continuous dobutamine stimulation (0, 5, 20, and 40 µg kg–1 min–1) was assessed, including heart rate (HR), systolic blood pressure (SBP), LV cavity areas (two-dimensional echocardiography) and contractility (end-systolic elastance, SBP/end-systolic cavity area (ESCA)). POST there was limited evidence of myocardial necrosis (measured by troponin I), while catecholamines were elevated. HR was higher POST (mean ±S.D.; PRE, 58 ± 9; POST, 79 ± 9; REC, 57 ± 7 beats min–1; P < 0.05), while SBP was lower (PRE, 127 ± 15; POST, 116 ± 9; REC, 121 ± 12 mmHg; P < 0.05). A blunted HR, SBP and LV contractility (SBP/ESCA; PRE 29 ± 6 versus POST 20 ± 6 mmHg cm–2; P < 0.05) response to dobutamine was demonstrated POST, with values returning towards baseline in REC. Following prolonged strenuous exercise, the chronotropic and inotropic response to dobutamine stimulation is blunted. This study supports the hypothesis that beta-receptor downregulation and/or desensitization may play a major role in prolonged-strenuous-exercise-mediated cardiac fatigue.

(Received 10 August 2005; accepted after revision 1 September 2005; first published online 8 September 2005)
Corresponding author R. C. Welsh: 2C2 Walter Mackenzie Health Sciences Centre, University of Alberta Hospital, Edmonton, Alberta, Canada T6G 2B7. Email: rwelsh{at}cha.ab.ca


   Introduction
Top
 Abstract
 Introduction
Methods
 Results
 Discussion
 References
 
Regular aerobic exercise is associated with well-established cardiac benefits; however, prolonged strenuous exercise of longer than 4 h has been associated with a transient impairment in left ventricular (LV) function (McGavock et al. 2002). This impairment is not entirely explained by changes in LV pre-load or after-load, and a significant reduction in LV contractility has been observed which has been termed cardiac fatigue (Niemela et al. 1984, 1987; Douglas et al. 1987, 1990; Seals et al. 1988; Manier et al. 1991; Rowe, 1992; Whyte et al. 2000; Haykowsky et al. 2001; Dawson et al. 2003).

Several investigators have suggested that sustained elevated endogenous circulating catecholamine levels associated with prolonged strenuous exercise may lead to decreased cardiac ß-receptor function or desensitization through downregulation or uncoupling, with subsequent diminished chronotropic response and inferentially LV contractility (Friedman et al. 1987; Hammond et al. 1987; Eysmann et al. 1996). Animal models, as well as clinical states including chronic heart failure and transient cardiac dysfunction associated with withdrawal of prolonged pharmacological inotropic stimulation, support this hypothesis (Colucci et al. 1989; Prichard et al. 1991; Eysmann et al. 1996). Furthermore, it has been shown in healthy sedentary subjects that the dose of isoproterenol required to elevate heart rate by 25 beats min–1 is significantly increased following prolonged exercise, demonstrating decreased chronotropic responsiveness (Eysmann et al. 1996; Douglas et al. 1998). Although this theory offers an attractive physiological mechanism to explain the cardiac fatigue syndrome, the current evidence remains limited and inconclusive. Dobutamine is an attractive alternative to isoproterenol administration due to its routine clinical use for pharmacological stress testing, ability to be infused continuously, and predominant inotropic stimulation compared with chronotropic stimulation with isoproterenol. Dobutamine administration therefore represents an important pharmacological intervention to examine the importance of ß-receptor desensitization/downregulation in the phenomenon of cardiac fatigue.

Accordingly, the aim of this investigation was to examine the comprehensive cardiovascular response to continuous progressive dobutamine stimulation before, immediately after, and during recovery in experienced athletes completing a half-ironman triathlon. We hypothesized that prolonged strenuous exercise would be associated with an abnormal response consistent with ß-receptor downregulation and/or desensitization.


   Methods
Top
 Abstract
 Introduction
 Methods
Results
 Discussion
 References
 
Nine experienced male triathletes (mean ±S.D., age 32 ± 5 years, with 9 ± 5 years of competitive experience) entered in a half-ironman triathlon (2 km swim, 90 km cycle, and 21 km run) participated in this investigation. Average total training volume was 12 ± 3 h week–1 (swimming 3 ± 1.2 h, cycling 6 ± 1.6 h, and running 4 ± 1.6 h). Prior to participation, all subjects underwent a complete cardiac evaluation with detailed medical history and physical examination to exclude any significant comorbid conditions and/or symptoms suspicious for cardiovascular disease. The participants completed the event at their own pace, and had access to water, rehydrating fluid and food during the event.

All participants were assessed 2–3 days prior to the event (PRE), immediately after (POST), and after 1–2 days of recovery (REC). Pre-event evaluations were conducted in a rested state, with subjects encouraged to complete no training in the preceding 24 h period. Post-event evaluations were completed as soon as possible, after athletes had a brief opportunity to cool down and consume food and drink. Pre-race and recovery assessments were performed in a tertiary care medical centre, while the immediate post-event assessments were undertaken at the race site in a dedicated testing area. A physician and a registered nurse supervised all testing. The human ethics and research board at the institution approved the study, and all participants provided written informed consent.

Haematological and biochemical measures

Blood was withdrawn from an intravenous cannula inserted in the antecubital vein for haematological and biochemical analyses including: (1) markers of myocardial damage (total serum creatine kinase, creatine kinase MB fractionation, creatine kinase MB mass, and cardiac-specific troponin I (via standard fluorogenic ELISA)) and (2) a complete haematological and biochemical profile, as reported elsewhere (Warburton et al. 2002). Immediately post-event, myoglobin (via ELISA) and catecholamines (norepinephrine, epinephrine and dopamine; via standard HPLC procedures) were measured.

Cardiovascular assessment

A single experienced sonographer obtained echocardiographic images of the LV in the left lateral decubitus position via two-dimensional echocardiography (3.5 MHz transducer, SONOS 5500; Hewlett Packard, Andover, MA, USA). LV two-dimensional images were obtained from the transthoracic short-axis view at the level of the mid-papillary muscles, according to the American Society of Echocardiography guidelines (Sahn et al. 1978; Schiller et al. 1989). The measurements included end-diastolic (EDCA) and end-systolic cavity areas (ESCA), while fractional area change and LV end-systolic meridional wall stress were calculated using standard formulas (Haykowsky et al. 2001). LV contractility was assessed by changes in: (1) fractional area change in relation to end-systolic meridional wall stress (stress-shortening relationship; Douglas et al. 1987) and (2) end-systolic elastance (systolic blood pressure (SBP)/ESCA; Schulman et al. 1996; Haykowsky et al. 2001).

Dobutamine is a synthetic analogue of dopamine that stimulates ß1- and ß2-adrenergic receptors with mild {alpha}1 effects. Physiologically, it is a cardiac inotropic agent with peripheral vasodilatation and modest chronotropic effects. It was administered by continuous infusion in incremental doses (0, 5, 20 and 40 µg kg–1 min–1) increased at 3 min time intervals, as per local clinical stress echocardiographic protocol. Thirty seconds prior to each dosage increment: heart rate (ECG) and blood pressure measurements were obtained in conjunction with the echocardiographic images. A single physician blinded to the participant and testing period interpreted all echocardiographic images, and the mean of four images was used for analysis.

Statistical analysis

All values in the tables are reported as the means ± standard deviation, and the figures contain means ± standard error of the mean. All measures were evaluated using repeated measures analysis of variance (ANOVA). Post hoc comparisons (Tukey) were conducted if a main effect for time period and/or dobutamine dosage was found. The level of significance was set a priori at P < 0.05.


   Results
Top
 Abstract
 Introduction
 Methods
 Results
Discussion
 References
 
The racing event was conducted during an overcast and cool day with slight rain and wind (temperature: 18°C, precipitation 0.8 cm, and wind speed 7 km h–1 (gusts 34 km h–1)). All subjects completed the event with an average finishing time of 5 h (5 h 01 min ± 25 min).

Biochemical measures

Creatine kinase and myoglobin (861 ± 612 U l–1; normal range, 19–92 U l–1) were elevated post-event, with cardiac fractionation of creatine kinase, suggesting skeletal myonecrosis without evidence of cardiac myonecrosis (Table 1). Troponin I was elevated in a single subject (9 µg l–1), but returned to normal (<0.5 µg l–1) after 24 h of recovery. This subject was 23 years old and the highest ranked finisher in the study (seventh place overall, 4 h 17 min 31 s) with borderline CK-MB activity and CK-MB mass (total CK 430, CK-MB activity 22, 0.05% fraction, and CK-MB mass 30, 0.07 mass index). There were no obvious associated cardiovascular issues with this subject, who continued to race, achieving a second place finish (4 h 11 min) in a subsequent half-ironman event 4 weeks later.


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  		Table 1. Markers of myocardial damage
 
The post-event catecholamine levels were: epinephrine 522.7 ± 280.8 pmol l–1 (normal, 0–360 pmol l–1), norepinephrine 4.17 ± 1.30 nmol l–1 (normal, 0.38–1.89 nmol l–1) and dopamine 337.3 ± 145.8 pmol l–1 (normal, 0–650 pmol l–1). As reported elsewhere, there were no significant electrolyte disturbances documented in these subjects in association with completing this event (Warburton et al. 2002).

Cardiovascular assessment

Heart rate (HR) was elevated post-event in comparison to pre-event and recovery (PRE, 58 ± 9; POST, 79 ± 9; REC, 57 ± 7 beats min–1; P < 0.05). The SBP was lower post-event in comparison to pre-event and recovery (PRE, 127 ± 15 mmHg; POST, 116 ± 9 mmHg; REC, 121 ± 12 mmHg; P < 0.05). The HR and SBP responses to incremental dobutamine were blunted post-event in comparison to pre-event and recovery (Figs 1 and 2).



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  		Figure 1.  The heart rate response to an incremental dobutamine stress test
The response was measured before (PRE), immediately after (POST), and 24–48 h after (REC) prolonged strenuous exercise. Values are means ±S.E.M.*Significantly attenuated response during POST in comparison to PRE and REC.

 


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  		Figure 2.  The systolic blood pressure response to incremental dobutamine infusion
The response was measured PRE, POST and REC prolonged strenuous exercise. Values are means ±S.E.M.*Significantly attenuated response during POST in comparison to PRE and REC.

 
Echocardiographic measures in response to dobutamine and the three study periods are summarized in Table 2. The LV preload (EDCA) was significantly reduced post-event. The LV end-systolic meridionial wall stress remained unchanged during incremental dobutamine infusion pre-event and recovery; however, wall stress progressively decreased with increasing dobutamine during post-event (P < 0.05).


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  		Table 2. Cardiovascular responses to dobutamine infusion before and after prolonged strenuous exercise
 
The interaction of fractional area change and wall stress was significantly displaced downwards post-event, demonstrating impaired LV contractility (Fig. 3). Additionally, there was a differential response in end-systolic elastance (i.e. LV contractility) to incremental dobutamine infusion immediately post-event (Fig. 4). In particular, the response to dobutamine infusion was attenuated at the highest dosage post-event (P < 0.05). Although EDCA was reduced post-event, no significant relationship was observed between the change in LV contractility and EDCA. Finally, both the stress shortening relationship and end-systolic elastance returned towards normal after recovery.



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  		Figure 3.  Fractional area change and wall stress relationship
The relationship was measured PRE, POST and REC prolonged strenuous exercise. *Significantly attenuated response during POST in comparison to PRE and REC.

 


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  		Figure 4.  The contractile response to incremental dobutamine infusion
The response was measured PRE, POST and REC prolonged strenuous exercise. Values are means ±S.E.M.*Significantly attenuated response during POST in comparison to PRE and REC.

 

   Discussion
Top
 Abstract
 Introduction
 Methods
 Results
 Discussion
References
 
To the best of our knowledge, this is the first investigation to comprehensively examine the cardiovascular response to incremental and continuous intravenous infusion of dobutamine before, immediately after, and during recovery following prolonged strenuous exercise in athletes. The major findings of this investigation are as follows: (1) there was limited evidence of myocardial necrosis, as determined by creatine kinase and troponin I levels; and (2) the cardiovascular response to incremental dobutamine infusion was abnormal with an attenuated HR, SBP and LV contractility response.

Several authors have postulated that myocardial damage may occur as the result of prolonged strenuous exercise (Rowe, 1992; Dawson et al. 2003). In the present investigation, we demonstrated a significant elevation of myoglobin and total creatinine kinase. However, in the majority of our subjects there was no evidence of myocardial necrosis with a normal CK/CK-MB fraction, CK/CK-MB mass index, and no significant elevation in cardiac-specific troponin I. The single subject with elevated markers of myocardial necrosis had no obvious untoward effects, but further analysis of these issues in the most competitive endurance athletes is required. It is also important to note, that the athletes in the present investigation had no electrolyte or haematological changes that would explain the observed altered cardiovascular response to inotropic stimulation (Warburton et al. 2002). Therefore the altered LV contractility response to inotropic stimulation after the half-ironman triathlon does not appear to have haematological or biochemical aetiologies.

LV systolic function is related to LV pre-load, after-load and contractility. In the present investigations, the LV pre-load (EDCA) and after-load responses to incremental dobutamine infusion were altered immediately post-event. A decrease in pre-load following prolonged strenuous exercise is not uncommon; however, the lack of correlation between the change in EDCA and the change in LV contractility suggests that other factors were responsible for the reduced LV systolic function, consistent with past research (Niemela et al. 1984, 1987; Douglas et al. 1987; Dawson et al. 2003). We found that LV end-systolic wall stress (after-load) response, post-event, was attenuated in response to incremental dobutamine infusions, and thus does not explain the observed reduction in LV contractility. In fact, the progressive reduction in LV wall stress with incremental dobutamine dose post-event would be expected to actually enhance ejection fraction. Our finding that the end-systolic elastance response to increasing dosages of dobutamine was attenuated immediately after the race compared with pre-event and recovery suggests a true decline in LV contractility. Also, there was a significantly greater reduction in fractional area change for a given increase in after-load when all data were combined, a finding that further supports the hypothesis of reduced LV contractility following prolonged strenuous exercise.

It is known that the endogenous concentration of many biologically active substances, including the adrenergic system, is associated with end-organ desensitization (downregulation and/or uncoupling) by negative-feedback mechanisms. Several clinical models of LV dysfunction that involve prolonged exposure to elevated catecholamine levels are associated with ß-receptor desensitization, including congestive heart failure, pheochromocytoma, subarachnoid haemorrhage, sepsis, and withdrawal of inotropic support (Colucci et al. 1989; Jones & Romano, 1990; Prichard et al. 1991). The assessment of myocardial ß-receptor density and function in human subjects remains problematic, since direct assessment is not possible without invasive myocardial biopsy. Accordingly, the effect of chronic exercise on ß-receptor density and adrenergic response in humans has not been well studied. Friedman et al. (1987), using a canine model, revealed decreased chronotropic responsiveness to isoproterenol after 1 h of continuous exercise. Similar results have been found in sedentary individuals engaging in prolonged strenuous exercise, and athletes participating in an ironman triathlon (Eysmann et al. 1996; Douglas et al. 1998). Although these authors recognized the limitations of this indirect assessment of ß-receptor function, this research revealed that cardiac fatigue might be due, in part, to ß-receptor desensitization.

Although previous research has attempted to evaluate ß-receptor function using chronotropic response to isoproterenol, the present investigation is the first to determine comprehensive cardiovascular response, including HR, SBP and LV contractility, during a continuous inotropic infusion with dobutamine after prolonged strenuous exercise. Our findings that the endogenous circulating catecholamines (epinephrine and norepinephrine) are elevated immediately post-event are consistent with past research (Meyer et al. 1988). The potential association of ß-receptor downregulation/desensitization as a physiological explanation of prolonged-strenuous-exercise-mediated cardiac fatigue remains attractive.

The limitations of echocardiographic assessment of LV function are well known. Similar to previous studies, we used a single-point load-independent estimate of LV contractility (i.e. end-systolic elastance). In addition, although fractional area change is known to be load dependent, it is an acceptable index of LV systolic performance, and, in this study, it was corrected for LV end-systolic meridional wall stress. A final limitation of this investigation was that we did not examine LV diastolic function, thus future studies are required to examine the effect of prolonged strenuous exercise on diastolic function during dobutamine stress.

Conclusion

Transient altered cardiovascular response to continuous progressive dobutamine infusion occurs in male triathletes after a half-ironman triathlon. The blunted chronotropic and inotropic response demonstrated in this study was unrelated to changes in LV pre-load, after-load, electrolyte abnormalities and myocardial necrosis. Although the underlying mechanism responsible for prolonged-strenuous-exercise-mediated cardiac fatigue was not fully elucidated, our results suggest that it may be due, in part, to altered ß-receptor function.


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   Acknowledgements
 
Agilent (Hewlett Packard) of Canada supplied the echocardiographic machine for race-site investigations.




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