Magnetic Resonance Imaging–Derived Right Ventricular Adaptations to Endurance versus Resistance Training

Angela L. Spence; Howard H. Carter; Conor P. Murray; David Oxborough; Louise H. Naylor; Keith P. George; Daniel J. Green

Disclosures

Med Sci Sports Exerc. 2013;45(3):534-541. 

In This Article

Discussion

We demonstrate for the first time using MRI that RV mass was increased after 6 months of progressive and intense E or R training in young, healthy, and previously untrained male subjects. The change in RV mass in absolute terms was small and not significantly different between groups, although the relative response was greater after E (9%) than R training (3%). A similar pattern emerged in relation to changes in RVEDV after training. The ratios of LV-to-RV morphology and function were unchanged after training, indicative of a modest but balanced adaptation to the exercise stimulus. These cardiac structural adaptations occurred in the absence of any significant change in global myocardial function.

These data are in partial agreement with the hypothesis that exposure to chronic endurance exercise training induces an eccentric-type hypertrophy of the right ventricle. The current data provide support for previous cross-sectional echocardiographic studies in athletes that reported increased end-diastolic diameter of the RV outflow tract[6,13,16,21,29,30] and MRI studies that have reported increased RV mass and RVEDV[26,27] in athletes compared with controls subjects. Similarly, a longitudinal study of endurance-trained athletes demonstrated further increases in RV parameters after 3 months of unsupervised training.[2] It is possible that the hemodynamic overload due to the repetitive episodic increases in preload, which occur during endurance activity,[20] may play a role in the mechanistic cascade for RV adaptation to E exercise.

Scharhag et al.[27] reported increased LV and RV mass of 36% and 37%, respectively, in elite endurance athletes compared with matched controls using MRI. Likewise previous echocardiography studies have described greater differences in RV morphology between athletes and controls than those seen after training in the current study. Although the between group difference in LV and RV mass demonstrated by Scharhag et al.[27] exceeds the 9% increase in RV mass we observed with E exercise, a longer history of training in the athletic cohort could largely account for this difference. Longer training studies to approach athletic training loads would be valuable but are logistically difficult.

The current data support a balanced response of the left and right ventricles to training that has been observed in some cross-sectional athlete–control comparisons.[26,27] In contrast to our findings, some descriptive studies have reported asymmetrical hypertrophy of the right ventricle of athletes.[18,23] A recent multimodal imaging study found disproportionate RV structural adaptation in middle-age endurance athletes (mean age = ~36 yr) versus controls.[17] The authors suggest this asymmetry was due to a disproportionate end-systolic wall stress imposed on the right ventricle compared with the left ventricle during an acute bout of exercise. We did not assess wall stress in response to acute exercise (either E or R training) in the present study, but this may be worth assessing in future training studies. Arguably, the assessment of end-diastolic wall stress (an indicator of preload) may be a more viable method of assessing the stimulus for adaptation to ventricular volume overload. In addition, the mean age of the subjects in our study is ~10 yr younger than those of La Gerche et al.,[17] which may partially account for the differences we observed.

Cross-sectional athlete–control studies (either MRI or echocardiography) are equivocal in their description of a concentric hypertrophy in resistance-trained subjects.[5,9,23,32] The current study supports the contention that R training has a somewhat smaller effect on RV morphology when compared with E training. To our knowledge, Baggish et al.[2] conducted the only other longitudinal evaluation of RV structure comparing endurance and resistance exercise training. Although this 3-month echocardiographic study was observational in nature, with no supervised, structured, or controlled interventions, "endurance" collegiate rowers significantly enhanced RV dimension by 6% from baseline, whereas "strength" collegiate American footballers had no alteration in RV diameter. These findings are largely supported by the current MRI data. The smaller RV adaptation we and others observed in response to R training may be explained by the limited magnitude and time duration of exposure to increased RV loading within R training that is characterized by intermittent activity that does not place a constant, steady-state hemodynamic overload on the heart.[20] Interestingly, in the hemodynamic stimulus thought to promote cardiac adaptation to R training,[10] an increased LV end-systolic wall stress may not even occur during R exercise,[12] which raises the question whether the hemodynamic stimulus is sufficient to induce cardiac morphological adaptation.

Using traditional global functional indices (RV ejection fraction and stroke volume) or the novel application of myocardial speckle tracking echocardiography, we have demonstrated no significant change in RV myocardial function in a young, healthy men undergoing 6 months of intense and progressive E or R training. Further, the lack of functional adaptation occurred despite modest changes in RV morphology after exercise training. As global strain derived from myocardial speckle tracking is free from angle dependence, some of the geometric limitations of ultrasound are overcome,[22] and it can be successfully applied to multimodal assessment of the right ventricle.

Limitations

Magnetic resonance imaging is considered the gold standard for structural assessment of the right ventricle[18] yet is subject to some limitations. First, it is difficult to distinguish the RV inflow area with the tricuspid valve from the outflow tract and pulmonary valve in the most basal RV slice.[11,14] Although long-axis and biplane methods may be an alternative for assessing RV volume,[1] these methods rely heavily on geometric assumption of ventricular shape. By adopting a standardized method of tracing the epi- and endocardial borders, we have attempted to minimize the error associated with movement of the atrial–ventricular plane during diastole. Furthermore, delineation of the endocardial border can be difficult because of the thin RV lateral wall and increased trabeculations, particularly during systole.[11] The combination of a descriptive analysis protocol[24] and the steady-state precision technique (TrueFISP) used in our imaging procedure allowed for improved contrast between myocardium and blood pool to reduce this limitation. We recruited only male subjects for this study. Previous research suggests that the cardiac morphology of female athletes may adapt differently compared with their male athletic counterparts.[2] Lastly, we acknowledge that exposure to a longer training stimulus may evoke greater adaptive responses and thus cannot rule out some adaptation because of R exercise under such circumstances. Our findings should be judiciously compared with previous cross-sectional studies of lifelong endurance or resistance athletes. However, we maximized the training responses observed by recruiting previously untrained subjects and closely supervising the intensive training sessions. In summary, additional longitudinal approaches, particularly in women, will be required to determine the long-term health implications and gender differences of exercise training on RV adaptation and to ascertain any dose-response relationship.

In conclusion, a 24-wk intensive, supervised, and controlled E exercise-training program resulted in a modest but increase in RV mass and RVEDV, suggestive of eccentric remodeling. This was similar to the pattern of change observed in the left ventricle. Changes in RV morphology were small after R training but not significantly different from those observed with E training. No significant changes in global or regional RV function at rest were observed because of either E or R training.

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