Echocardiography has played a fundamental role in the description of cardiac adaptation to exercise. The ability to quantify ventricular size, wall thickness, systolic function, and ventricular filling properties has served to characterize remodeling attributed to athletic training. While most forms of athletic training result in an increase in left ventricular (LV) mass with preservation of systolic function and enhancement of diastolic filling, endurance training typically results in eccentric hypertrophy whereas resistance training promotes concentric hypertrophy. Though most sporting activities actually consist of a mixture of endurance and resistance exercise, these constructs have been helpful to distinguish physiologic adaptation, the “athlete’s heart,” from pathologic entities such as hypertrophic cardiomyopathy.

Deformation imaging has advanced our understanding of myocardial mechanics and consequently the cardiac adaptation to exercise. In the evaluation of the athlete’s heart, the focus has been on structure-chamber size, wall thickness, patterns of hypertrophy, and the exclusion of occult structural abnormalities. Diastolic parameters have been useful to confirm normal filling and differentiate between physiologic and pathologic hypertrophy. The assessment of systolic function has typically been with global measures such as ejection fraction or fractional shortening. Now, the capacity exists to assess myocardial function more directly by measuring longitudinal, circumferential, and radial strain as well as twist (the basal to apical difference in LV rotation) in both systole and diastole. These indices, while numerous and at times complex, promise to unlock the basic functional changes in the myocardium that occur with training and during exercise.

The study by Lee and colleagues in this issue of the Journal adds to our understanding of the cardiac adaptation to endurance training in healthy middle age males. The authors found that endurance training results in the ability to enhance systolic twist during exercise as well as the ability to augment early diastolic filling by maintaining the time to peak untwist velocity. These properties were similar to young, healthy controls but dissimilar to healthy untrained age matched controls. This is the first description of such findings in middle aged endurance athletes and adds to a growing literature describing the effects of athletic training on myocardial mechanics.

Enhancement of systolic twist has been demonstrated in athletes at rest, but the findings have not been completely consistent. A study of university rowers following a ninety day period of endurance training demonstrated significant increases in peak LV systolic twist as well as peak early diastolic untwisting rate. A study comparing young cyclists, soccer players, and basketball players to controls demonstrated an increase in apical twist only in the cyclists. LV torsion at rest was compared in soccer players to controls and the soccer players were found to have reduced twist and basal and apical radial strain. In a study of cyclist compared to controls, apical radial strain and LV torsion were lower in the cyclists! In the current study, systolic twist values at rest were not significantly different between the controls and trained middle aged males. The heterogeneity of these findings is difficult to explain. It appears that training can enhance systolic twist, but that when compared with controls in the resting state, systolic twist may not always differentiate the athlete’s heart. The specific athletic endeavor as well as the intensity and duration of training may play an important role in the magnitude of effect on systolic twist at rest.

Other systolic indices of deformation have been shown to be accentuated in the athlete’s heart at rest. In an earlier study of university rowers, following a ninety day period of endurance training, an increase in peak systolic tissue velocities, radial strain, and longitudinal strain with a base to apex gradient was noted. Circumferential strain increased in the LV free wall but decreased in the septum. A comparison of professional soccer players to controls and patients with hypertrophic cardiomyopathy demonstrated significantly higher radial and transverse strain, but lower longitudinal strain in the soccer players than controls. Compared to patients with hypertrophic cardiomyopathy, soccer players had higher values for radial, transverse, and circumferential strain. The relationship between the various deformation indices is complex. In disease states, for instance, circumferential strain and twist may compensate for diminished longitudinal strain. Given that a subset of the available deformation indices are evaluated in the studies of athletes, it is difficult to know if certain indices are up or down regulated due to an enhanced or diminished effect of other indexes.

The effect of exercise on deformation indices has typically demonstrated an augmented reserve in trained athletes. The current study demonstrates the ability of endurance training to augment systolic twist during sub maximal exercise. Donal and colleagues compared young (<35 years) and senior (>50 years) male athletes to age matched controls and found that both athletic groups had higher LV mass and LV volumes. Stroke volume and global longitudinal strain during exercise was greater in the athletic groups, with the global strain during exercise being highest in the younger athletes. Unfortunately, the absence of a young, trained group in Lee’s study did not allow comparison of the magnitude of the training effect between young and middle aged subjects, as was possible in Donal’s study. In a study comparing elite soccer players with controls, despite similar strain values at rest, mid-ventricular and apical strain were augmented and significantly higher in athletes following hand grip exercise.

The response of resistance training on myocardial mechanics has not been as extensively evaluated but appears, at rest, to be similar to endurance athletes. D’ Andrea and colleagues described peak and regional systolic strain and global longitudinal strain in 370 endurance and 280 power athletes and demonstrated comparable deformation indices between the groups despite morphologic differences trending toward eccentric hypertrophy in the endurance athletes and concentric hypertrophy in the power athletes.

The response of deformation indices following exercise has been variable, in part due to the type, intensity, and duration of exercise studied. Rowers examined before and after a 2,000 meter sprint were found to have increased septal and lateral strain and increased LV torsion. Reduced radial and circumferential strain was demonstrated in a study following ultra-endurance exercise.

It is interesting that ejection fraction was no different at rest or after exercise between groups in the current study, while systolic twist increased in the young healthy and trained middle aged subjects. Ejection fraction has not been shown to distinguish between athletes and normal controls at rest. Additionally, the exercise ejection fraction response in athletes has not been shown to distinguish between trained and untrained healthy controls. In fact, in many of the studies referenced above, the ejection fraction was not different between controls and athletes at rest or during exercise despite clear alterations in the deformation indices. This suggests that ejection fraction is an inadequately sensitive index to detect the subtle systolic changes induced by athletic training. The more direct measures of myocardial strain and twist are able to detect these changes, and will likely become useful measures to characterize systolic function in the athlete’s heart.

Lee et al suggests that endurance training prevents at least some of the age related changes of early diastolic filling during exercise. Myocardial twist and recoil are major factors in the critical transition from systole to diastole. Potential energy is stored as the ventricle achieves maximal twist at end systole to then be released as recoil in early diastole, creating the suction and force necessary for rapid early diastolic filling. While enhanced diastolic filling has long been recognized as a characteristic of endurance athletes, identifying a property of myocardial recoil , the time to peak untwisting velocity, that helps explain how early filling is facilitated is novel and perhaps creates another measure by which to assess diastolic function more directly and precisely during exercise. The authors describe at length the advantages a compliant ventricle and enhanced filling has for the ability to increase cardiac output, particularly at the high heart rates demanded of endurance athletes. That chronic endurance training can prevent some of the deleterious diastolic consequences of aging may have significant relevance as a public health strategy given the increasing rates of heart failure with preserved ventricular function in the aging population. The diastolic enhancements induced by training may also explain the beneficial effects of exercise programs in patients with heart failure or those recovering from myocardial infarction.

The current study raises many questions. In this, and many of the other studies of myocardial mechanics in athletes, only men are studied. The chamber enlargement and wall hypertrophy adaptations to exercise displayed among female athletes are not typically of the same magnitude as males. Are the myocardial mechanics in female athletes similar? Are the responses of the middle aged trained men recruitable from the chronically untrained, and if so what level and duration of training is necessary? What are the underling genetic signals that allow these changes with endurance training, and are there ways induce them other than training? Will deformation indices be robust enough to become parameters that distinguish physiologic from pathologic remodeling?

There remains much work to do in this area. As with the current study by Lee and colleagues, most of the reports of myocardial mechanics in athletes have relatively few subjects. Most studies focus on a subset of the available deformation indices. There is heterogeneity in how subjects are studied—at rest before or after a period of training; during exercise—sub maximal or maximal; or following varying levels of exercise. There is also difficulty in neatly classifying athletes as endurance-trained or strength-trained, so comparison of results across groups of athletes is problematic. Deformation imaging, while powerful in its ability to assess myocardial mechanics, is highly dependent on good image quality. Some studies report inadequate data on large percentages of subjects. Variability exists between vendor platforms for the specific measures, so cross-vendor comparison is difficult. Although these techniques have made a large impact in the research laboratory, routine clinical application has been lagging.

Despite these hurdles, great optimism is warranted. The current study by Lee et al adds to the growing literature describing the effects of endurance training on myocardial mechanics at rest and during exercise. It highlights myocardial twist and recoil as important functions that are enhanced by endurance training and facilitate augmentation of cardiac output. As newer imaging modalities allow a greater understanding of myocardial mechanics, we realize that our older constructs regarding the athlete’s heart are perhaps a bit simplistic. While addressing structure, they do not adequately address the underlying mechanisms of function. The tools now exist to define those mechanisms and describe the athlete’s heart in much greater detail. As with any new season, hope springs eternal!