Exercise-induced cardiac remodelling: the need for assessment of regional myocardial function
Article first published online: 14 JUN 2012
© 2012 The Authors. The Journal of Physiology © 2012 The Physiological Society
The Journal of Physiology
Volume 590, Issue 12, pages 2829–2830, June 2012
How to Cite
Weiner, R. B. and Baggish, A. L. (2012), Exercise-induced cardiac remodelling: the need for assessment of regional myocardial function. The Journal of Physiology, 590: 2829–2830. doi: 10.1113/jphysiol.2012.233585
- Issue published online: 14 JUN 2012
- Article first published online: 14 JUN 2012
Exercise-induced cardiac remodelling (EICR) refers to changes in cardiac structure that occur in response to exercise training. Initial reports of cardiac enlargement in athletes date back to 1899 and subsequently numerous aspects of EICR, including ventricular chamber enlargement, myocardial hypertrophy, and atrial dilatation have been documented. Functional correlates of EICR are not as well characterized. Although global measures of left ventricular (LV) function, such as LV ejection fraction, are typically normal in athletes, recently developed advanced imaging techniques have begun to identify alterations in regional myocardial function that occur in response to exercise.
Strain imaging, also known as deformational imaging, represents a technological advancement that has been developed to objectively quantify regional myocardial function. The term strain refers to the fractional change in length compared to the end-diastolic length, and three normal strains (longitudinal, circumferential and radial) can be assessed with speckle-tracking echocardiography. Additionally, due to the helical orientation of myofibres (left-handed helix in the subepicardium and right-handed helix in the subendocardium), myocardial contraction also produces transmural (i.e. shear) strains. The circumferential–longitudinal shear strain represents LV torsion, or the wringing motion of the heart, and results from counter-directional rotation of the LV base and apex. When viewed from an apical reference point, systolic rotation at the apex is counterclockwise and the base rotates in an overall clockwise direction.
Regional myocardial function has only recently been investigated in the context of exercise training. In a longitudinal study of endurance trained athletes, we observed increases in normal strains following a 90 day period of endurance exercise training in young competitive rowers (Baggish et al. 2008). Interestingly, changes in circumferential strain showed regional heterogeneity characterized by relative dysfunction in the interventricular septum, likely resulting from concomitant right ventricular dilation. Cross-sectional reports have identified differences in LV torsion when comparing cyclists and sedentary controls (Nottin et al. 2008) and more recently a longitudinal study demonstrated changes in LV apical rotation and LV torsion after a period of endurance exercise training (Weiner et al. 2010). In a recent issue of The Journal of Physiology, Stöhr et al. (2012) add to the literature by demonstrating differences in LV apical rotation and torsion (twist) in a group of individuals with high peak oxygen consumption () versus a group with moderate . Specifically, they show that for the same augmentation index (AIx), a non-invasive estimate of aortic stiffness and perhaps aorto-ventricular coupling, the high individuals had significantly lower apical rotation and torsion, both at rest and during submaximal exercise. Importantly, these changes in regional LV function were observed in the absence of differences in LV wall thickness and cavity size between the two groups.
Two features of the results observed in the current study by Stöhr et al. (2012) warrant emphasis. First, the finding that LV apical rotation was altered, and not LV basal rotation, is consistent with other myocardial deformation studies in athletes (Nottin et al. 2008; Weiner et al. 2010) and with the notion that the magnitude of apical counterclockwise rotation is the primary determinant of overall peak systolic LV torsion (Gibbons Kroeker et al. 1993). Although measurement of LV apical rotation requires careful standardization of the echocardiographic imaging plane (Weiner et al. 2010), its assessment is less time consuming than measuring LV torsion and can be made without significant software-based post-image acquisition processing. It is therefore possible that once normative values for LV apical rotation in human health and disease are established, it may become a surrogate marker of LV torsion and will be a useful marker of LV regional function. Second, the authors note dissociation between shear strain and normal strain as high aerobic fitness was associated with decreased apical rotation/torsion but circumferential and radial strain was not influenced by aerobic fitness level. Similar dissociation between LV torsion and normal strains has been observed in previous studies of heart stress (Stöhr et al. 2011) and progressive submaximal exercise testing (Doucende et al. 2010). This highlights the complex nature of studying regional myocardial function and suggests a unique potential role for LV apical rotation as a marker of response to exercise training.
To completely determine the physiological importance of EICR, investigators need to move beyond the study of LV function at rest. Specifically, evaluation of the myocardial response to acute haemodynamic perturbation or exercise challenge represents a required step to fully define the scope and relevance of EICR. Stöhr et al. (2012) recognize this important concept as subjects in their study underwent submaximal exercise testing. Evaluation of the myocardial response to hemodynamic/exercise challenge, what we term functional myocardial profiling, may ultimately represent a method for characterizing exercise performance and also aid in the differentiation of physiological and pathological hypertrophy. For example, some forms of EICR (i.e. concentric hypertrophy in strength-trained athletes) may be difficult to distinguish from mild forms of pathological hypertrophy (i.e. hypertrophic cardiomyopathy). It is possible that defining the myocardial response to exercise challenge may produce unique myocardial profiles for these two entities, possibly obviating the need for more prolonged and intensive diagnostic manoeuvres such as prescribed detraining.
Evaluation of regional myocardial function, including LV strain, rotation and torsion, holds promise to fully characterize the functional changes that accompany the well-defined structural features of EICR. Coupled with novel techniques that can investigate the molecular and cellular changes associated with EICR, the complete functional phenotype of EICR has the potential to be unlocked. Broad knowledge of the functional characteristics of EICR will assist clinical assessments of exercise performance and may ultimately help distinguish the athlete's heart from pathological forms of LV hypertrophy.
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