The Morganroth hypothesis revisited: endurance exercise elicits eccentric hypertrophy of the heart

The current understanding of adaptations to cardiac morphology following exercise has been relatively unchallenged for over 35 years since the development of the ‘Morganroth hypothesis’. The Morganroth hypothesis has been widely accepted in the field of exercise physiology for describing the effects of prolonged exercise training on left ventricular (LV) adaptations. This hypothesis proposes endurance-trained athletes exhibit ‘eccentric’ LV hypertrophy, while resistance-trained athletes exhibit ‘concentric’ LV hypertrophy. Eccentric LV hypertrophy is characterized by an increased LV mass, increased LV end-diastolic volume (LVEDV) and normal LV wall thickness. Concentric LV hypertrophy is characterized by increased LV mass, increased wall thickness and normal LVEDV. The underlying physiological mechanism may be related to the transient increase in preload and afterload during endurance and resistance training, respectively. Most studies challenging the Morganroth hypothesis have been cross-sectional by design and used echocardiography to assess cardiac morphology. There are few studies that have investigated changes in cardiac remodelling with a randomized longitudinal exercise training design, which would account for within subject responses to either endurance- or resistance-training stimuli. In addition, magnetic resonance imaging (MRI) has been recognized as the ‘gold standard’ for analysing cardiac morphology as a more sensitive and reproducible tool when compared with echocardiography. In a recent issue of The Journal of Physiology, Spence et al. (2011) challenged some aspects of the Morganroth hypothesis (reviewed by Naylor et al. 2008) by taking untrained male participants and prescribing them to 6 months of either endurance (END) or resistance (RES) training. MRI was used to determine changes in cardiac morphology prior to training, following 6 months of training and after 6 weeks of detraining. It was hypothesized that END-trained participants would exhibit eccentric LV hypertrophy, while RES-trained participants would show no changes in cardiac morphology. Their study findings revealed LV adaptation to exercise in the END group, including increased LV mass and interventricular septal thickness. In contrast, no adaptations in cardiac structure were observed in the RES group. The END group also demonstrated increased aerobic capacity and muscular strength following training. In contrast, the RES group demonstrated no change in aerobic capacity; however, their improvements in muscular strength were greater than the changes observed in the END group. The RES group also had a decrease in body fat, and both groups had an increased lean body mass. It has been previously established that there is a paucity of longitudinal data to challenge the Morganroth hypothesis (Naylor et al. 2008). Therefore, the findings from Spence et al. (2011) enable us to objectively compare the effects of different exercise modalities (END vs. RES) on LV cavity dimensions and wall thickness. Haykowsky et al. (2001) has previously challenged this hypothesis by demonstrating that resistance training in older adults may improve muscular strength, but not produce changes in cardiac morphology. The findings of Spence et al. (2011) further suggest that this phenomenon, whereby cardiac morphology is unchanged following resistance training relative to endurance training, occurs across the lifespan. The Law of La Place is the underlying physiological principle that may explain these findings as it implies that chronic exercise training may produce acute changes in LV wall stress, which lead to chronic adaptations in wall thickness. Haykowsky et al. (2001) has previously shown that LV end-systolic wall stress is not associated with the Valsalva manoeuver commonly performed during resistance training. Taken together, the findings of Spence et al. (2011) and others indicate that LV wall stress is not significantly increased during resistance exercise; therefore, no chronic adaptations in LV wall structure would be expected. The novel use of cardiac MRI to assess and measure LV function and remodelling was a definite strength of this study. Longitudinal strain and strain rate were reported as sensitive measures of global LV function; however, novel MRI techniques (including peak systolic LV torsion and peak early diastolic untwisting rate) were not reported in this study despite potential implications for changes in LV function and remodelling following endurance training (Weiner et al. 2010). Future studies would benefit from including novel MRI techniques to further determine LV function and remodelling associated with endurance exercise. This study implemented a structured periodized training program for both END and RES groups, which was quite appropriate given the length of the training intervention. This training structure allowed for potentially significant increases in intensity without risking subject drop-out from fatigue or burn-out. Since running was selected for the END intervention, the researchers may have selected Olympic style lifting for the RES intervention to somewhat model the whole body aspect of running. Furthermore, Olympic style weight lifting has previously shown to elicit concentric hypertrophy; however, the use of performance-enhancing substances has been found to amplify this training adaptation (Haykowsky et al. 2002). The study by Spence et al. (2011) identified practical applications that improve our understanding of LV remodelling in response to exercise training. The authors used the individual training modalities to look at specific changes produced by either END or RES training, but not a combination of both. It remains unclear if the combination of both END and RES training act synergistically to promote LV function and remodelling. Furthermore, the participants recruited were young healthy males; however, the primary question posed by Spence and colleagues could be extended to clinical cardiac populations. Current exercise training recommendations for the general public and cardiac rehabilitation programs advocate the use of both END and RES training. Four months of combined endurance and resistance training has been shown to reduce ventricular stress and improve LV function among congestive heart failure patients (CHF) (Conraads et al. 2004). Likewise, Beckers et al. (2008) reported a greater improvement in health-related quality of life among CHF patients who received combined END and RES training compared with those who received only END training (Beckers et al. 2008). The above CHF studies also incorporated clinical biomarkers of cardiac stress (i.e. NT-proBNP), which may further delineate an acceptable clinical range of values among patients undergoing non-pharmacological interventions. Cardiac stress biomarkers have also been used in healthy, well-trained cohorts and may help to further characterize or quantify the magnitude of cardiac wall stress associated with training-induced LV remodelling. These study questions may hold greater clinical relevance when applied to cardiac rehabilitation cohorts. In conclusion, Spence et al. (2011) provided new insight into the Morganroth hypothesis by identifying that LV remodelling may be unique to the endurance-trained athlete. These novel findings need to be substantiated within a longitudinal study design involving both healthy and clinical cohorts to fully determine the cardiovascular benefits of endurance- and/or resistance-based exercise training.

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