Prolonged exercise alters beta-adrenergic responsiveness in healthy sedentary humans

Eysmann, Susan B.; Gervino, Ernest V.; Vatner, Dorothy E.; Katz, Sidney; Decker, Lisa; Douglas, Pamela S.

doi:10.1152/jappl.1996.80.2.616

Cited by 50 publications

(48 citation statements)

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“…The relatively close correlation between these variables supports data from previous literature that has demonstrated positive correlations between TDI and Doppler diastolic data at rest (Farias et al 1999;Firstenberg et al 2001). Likewise the current data reinforce the finding of a reduced E/A following a marathon race (Manier et al 1991;Lucia et al 1999;George et al 2004;Whyte et al 2005) as well as prolonged activity of shorter (Eysmann et al 1996) and longer duration (Douglas et al 1987).…”

Section: Discussionsupporting

confidence: 89%

Mitral annular myocardial velocity assessment of segmental left ventricular diastolic function after prolonged exercise in humans

George

Oxborough

Forster

et al. 2005

The Journal of Physiology

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We assessed segmental and global left ventricular (LV) diastolic function via tissue-Doppler imaging (TDI) as well as Doppler flow variables before and after a marathon race to extend our knowledge of exercise-induced changes in cardiac function. Twenty-nine subjects (age 18-62 year) volunteered to participate and were assessed pre-and post-race. Measurements of longitudinal plane TDI myocardial diastolic velocities at five sites on the mitral annulus included peak early myocardial tissue velocity (E ), peak late (or atrial) myocardial tissue velocity (A ) and the ratio E /A . Standard pulsed-wave Doppler transmitral and pulmonary vein flow indices were also recorded along with measurements of body mass, heart rate, blood pressures and cardiac troponin T (cTnT), a biomarker of myocyte damage. Pre-to post-race changes in LV diastolic function were analysed by repeated measures ANOVA. Delta scores for LV diastolic function were correlated with each other and alterations in indices of LV loading. Diastolic longitudinal segmental and mean TDI data were altered post-race such that the mean E /A ratio was significantly depressed (1.51 ± 0.34 to 1.16 ± 0.35, P < 0.05). Changes in segmental and global TDI data were not related to an elevated post-race HR, a decreased post-race pre-load or an elevated cTnT. The pulsed wave Doppler ratio of peak early transmitral flow velocity (E)/peak late (or atrial) flow velocity (A) was also significantly reduced post-race (1.75 ± 0.46 to 1.05 ± 0.30, P < 0.05); however, it was significantly correlated with post-race changes in heart rate. The lack of change in E/E from pre-to post-race (3.4 ± 0.8 and 3.3 ± 0.7, respectively) suggests that the depression in diastolic function is likely to be due to altered relaxation of the left ventricle; however, the exact aetiology of this change remains to be determined.

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Section: Discussionsupporting

confidence: 89%

Mitral annular myocardial velocity assessment of segmental left ventricular diastolic function after prolonged exercise in humans

George

Oxborough

Forster

et al. 2005

The Journal of Physiology

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“…A reduction in ␤-adrenergic sensitivity following PE has been reported by others (12,19,36,37,42); however, this is the first study to examine the contribution of exercise intensity and NA to this phenomenon. Data from animal chronic pacing studies (i.e., duration: 3 h to 20 days) have demonstrated significant reductions in ventricular function (1, 25, 44), secondary to reductions in ␤-adrenergic sensitivity and density (31, 35, 44).…”

Section: Discussionmentioning

confidence: 58%

Impaired left and right ventricular function following prolonged exercise in young athletes: influence of exercise intensity and responses to dobutamine stress

Banks

Sasson

Busato

et al. 2010

Journal of Applied Physiology

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Banks L, Sasson Z, Busato M, Goodman JM. Impaired left and right ventricular function following prolonged exercise in young athletes: influence of exercise intensity and responses to dobutamine stress. J Appl Physiol 108: 112-119, 2010. First published November 5, 2009 doi:10.1152/japplphysiol.00898.2009We examined the effect of intensity during prolonged exercise (PE) on left (LV) and right ventricular (RV) function. Subjects included 18 individuals (mean Ϯ SE: age ϭ 28.1 Ϯ 1.1 yr, maximal aerobic power ϭ 55.1 Ϯ 1.6 ml · kg Ϫ1 · min Ϫ1 ), who performed 150 min of exercise at 60 and 80% maximal aerobic power on two separate occasions. Transthoracic echocardiography assessed systolic and diastolic performance, and blood sampling assessed hydration status and noradrenaline levels before (pre), during (15 and 150 min), and 60 min following (post) PE. ␤-Adrenergic sensitivity pre-and post-PE was assessed by dobutamine stress. High-intensity PE (15 vs. 150 min) induced reductions in LV ejection fraction (69.3 Ϯ 1.3 vs. 63.5 Ϯ 1.3%, P ϭ 0.000), LV strain (Ϫ23.5 Ϯ 0.6 vs. Ϫ22.3 Ϯ 0.6%, P ϭ 0.034), and RV strain (Ϫ26.3 Ϯ 0.6 vs. Ϫ23.0 Ϯ 0.6%, P Ͻ 0.01). Both exercise intensities induced diastolic reductions (pre vs. post) in the ratio of septal early wave of annular tissue velocities to late/atrial wave of annular tissue velocities (2.15 Ϯ 0.15 vs. 1.62 Ϯ 0.09; 2.21 Ϯ 0.15 vs. 1.48 Ϯ 0.10), ratio of lateral early wave of annular tissue velocities to late/atrial wave of annular tissue velocities (3.84 Ϯ 0.42 vs. 2.49 Ϯ 0.20; 3.56 Ϯ 0.32 vs. 2.08 Ϯ 0.18), ratio of early to late LV strain rate (2.42, Ϯ 0.16 vs. 1.97 Ϯ 0.13; 2.30 Ϯ 0.15 vs. 1.81 Ϯ 0.11), and ratio of early to late RV strain rate (2.03 Ϯ 0.17 vs. 1.51 Ϯ 0.09; 2.16 Ϯ 0.16 vs. 1.44 Ϯ 0.11) (P Ͻ 0.001). Evidence of ␤-adrenergic sensitivity was supported by a decreased strain, strain rate, ejection fraction, and systolic pressure-volume ratio response to dobutamine (P Ͻ 0.05) with elevated noradrenaline (P Ͻ 0.01). PE-induced reductions in LV and RV systolic function were related to exercise intensity and ␤-adrenergic desensitization. The clinical significance of exercise-induced cardiac fatigue warrants further research. ␤-adrenergic receptor; cardiac fatigue; echocardiography PROLONGED EXERCISE (PE) MAY produce transient impairments in cardiac function, a phenomenon termed exercise-induced cardiac fatigue (EICF) (6). Our group (17) and others (7,14,21,32,34) have shown a decline in left ventricular (LV) diastolic function following exercise of varying durations. Less consistent findings for LV systolic function have been reported, with many showing a decline in systolic performance following exercise (8 -10, 38, 39, 41), and some reporting no change (17,18,21,23). Recently, our laboratory has demonstrated a decline in diastolic performance and systolic performance after 150 min of intensive exercise (17), with no change observed during exercise, suggesting that alterations in LV contractility may be unique to the recovery period and possibly the rapidly chang...

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“…The same is basically true in heart failure, with the highest levels of the catecholamines (3-6 times above normal) found in those patients with severe cardiac dysfunction and cachexia (Anker et al 1997). Also, in both situations the heart responds by downregulating its b-ARs (Eysmann et al 1996;Smiley et al 1998). The fact that these changes in the sympathoadrenal-b-ARs axis are similar begs the question of why regular moderate exercise does not cause much, if any, damage to the heart or skeletal muscles while the failing heart appears to experience ongoing progressive damage in both muscle types (Del Carlos & O'Connor, 1999;Missov & Mair, 1999;Murdoch & McMurray, 1999).…”

Section: Figurementioning

confidence: 78%

Cardiomyocyte Death and the Ageing and Failing Heart

Goldspink

Burniston

Tan

2003

Experimental Physiology

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Mammalian cardiomyocytes have limited regenerative capacity, such that cell death can result in a net loss of viable contractile elements and a decrease in cardiac functional reserve, both during normal ageing and after insults to the myocardium leading to heart failure. At least four types of cell death have been described, with apoptosis and necrosis being the most extreme phenotypes and most extensively studied. Many of the classical morphological and biochemical features associated with these forms of cell death have been derived from studies conducted in vitro and these may not always faithfully reflect events occurring in vivo. Before therapeutic interventions can be realistically developed, more studies need to be undertaken in vivo to simultaneously investigate these different death pathways, their control mechanisms and their relative contributions in depleting the pool of viable cardiomyocytes. We recently demonstrated immunohistochemically that a single injection of either a natural or synthetic catecholamine induces both cardiomyocyte apoptosis (identified by an anti‐caspase 3 antibody) and necrosis (identified by an anti‐myosin antibody) in the rat heart in vivo. After optimising the experimental conditions for hormone dose and temporal and spatial peaks of damage, the incidence of necrosis was 4‐10 times greater than the incidence of apoptosis. Myocytes in the soleus muscle were also severely (7‐10%) damaged, involving both apoptosis and necrosis. In both striated muscles high levels of myocyte co‐localisation for apoptosis and necrosis were observed, suggesting that secondary necrosis had occurred in most of the apoptotic myocytes in vivo. The ability of the catecholamines to cause myocyte death suggests that they might play an aetiological role in the progression of heart failure where over‐activation of the sympathetic system results in sustained pathophysiological levels of these catecholamines.

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Prolonged exercise alters beta-adrenergic responsiveness in healthy sedentary humans

Cited by 50 publications

References 0 publications

Mitral annular myocardial velocity assessment of segmental left ventricular diastolic function after prolonged exercise in humans

Mitral annular myocardial velocity assessment of segmental left ventricular diastolic function after prolonged exercise in humans

Impaired left and right ventricular function following prolonged exercise in young athletes: influence of exercise intensity and responses to dobutamine stress

Cardiomyocyte Death and the Ageing and Failing Heart

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