Athlete’s Heart: Is the Morganroth Hypothesis Obsolete?

doi:10.1016/j.hlc.2018.04.289

Heart, Lung and Circulation

Volume 27, Issue 9, September 2018, Pages 1037-1041

https://doi.org/10.1016/j.hlc.2018.04.289 Get rights and content

In 1975, Morganroth and colleagues reported that the increased left ventricular (LV) mass in highly trained endurance athletes versus nonathletes was primarily due to increased end-diastolic volume while the increased LV mass in resistance trained athletes was solely due to an increased LV wall thickness. Based on the divergent remodelling patterns observed, Morganroth and colleagues hypothesised that the increased “volume” load during endurance exercise may be similar to that which occurs in patients with mitral or aortic regurgitation while the “pressure” load associated with performing a Valsalva manoeuvre (VM) during resistance exercise may mimic the stress imposed on the heart by systemic hypertension or aortic stenosis. Despite widespread acceptance of the four-decade old Morganroth hypothesis in sports cardiology, some investigators have questioned whether such a divergent “athlete’s heart” phenotype exists. Given this uncertainty, the purpose of this brief review is to re-evaluate the Morganroth hypothesis regarding: i) the acute effects of resistance exercise performed with a brief VM on LV wall stress, and the patterns of LV remodelling in resistance-trained athletes; ii) the acute effects of endurance exercise on biventricular wall stress, and the time course and pattern of LV and right ventricular (RV) remodelling with endurance training; and iii) the value of comparing “loading” conditions between athletes and patients with cardiac pathology.

Introduction

The seminal ‘athletes heart’ study published over four decades ago by Morganroth et al. demonstrated that, compared to age and sex-matched nonathletic controls, endurance trained athletes had increased left ventricular (LV) mass that was primarily due to an increased LV end-diastolic volume [1], [2]. In contrast, the increased LV mass in resistance trained athletes versus age-matched nonathletic controls was solely due to increased LV septal and posterior wall thickness [1], [2]. Based on the dichotomous LV remodelling patterns, Morganroth and colleagues hypothesised that the endurance training-mediated haemodynamic (volume) load is similar to that found in patients with aortic or mitral regurgitation [1], [2]. Moreover, the resistance training-mediated haemodynamic (pressure) load associated with performing a strenuous Valsalva manoeuvre (VM) was proposed to be similar to that found in systemic hypertension or in patients with aortic stenosis [1], [2].

Despite widespread acceptance of the Morganroth hypothesis [3], some investigators have questioned whether resistance exercise performed with a brief VM is exclusively a “pressure overload” stress [4], [5], [6], [7], [8], or that endurance exercise is primarily a “volume overload” stimulus [9]. Given this uncertainty, the purpose of this brief review is to re-evaluate the Morganroth hypothesis regarding: i) the acute effects of resistance exercise performed with a brief VM on LV wall stress, and the patterns of LV remodelling in resistance-trained athletes; ii) the acute effects of endurance exercise on biventricular wall stress, and the time course and pattern of LV and right ventricular (RV) remodelling with endurance training; and iii) the value of comparing “loading” conditions between athletes and patients with cardiac pathology.

Section snippets

Acute Effects of Resistance Exercise on Ventricular Wall Stress

In accordance with Laplace’s law, LV meridional wall stress is often simplified as a function of systolic arterial blood pressure and LV geometry. More correctly, LV wall stress should consider the forces on both sides of the LV wall. Specifically, LV wall stress is a function of the difference between intracavity pressure and intrathoracic pressure (e.g. transmural pressure [10], [11]) and LV geometry. The Morganroth hypothesis failed to consider changes in intra-thoracic pressure during

Patterns of Ventricular Remodelling With Resistance Training

Several cross-sectional or longitudinal echocardiographic studies have demonstrated that resistance training is not associated with a change in LV wall thickness, cavity size, or mass in healthy young, middle-aged or older men or women [14], [15], [16], [17], [18]. In contrast, a meta-analysis by Utomi et al. found that the increased LV mass in male endurance trained (n = 64 studies, 1099 participants) or resistance trained (n = 25 studies, 510 participants) athletes compared with sedentary

Acute Effect of Endurance Exercise on Ventricular Wall Stress

Morganroth et al. suggested that endurance exercise is primarily a “volume” load stress, however Stickland et al, using invasive haemodynamic monitoring at rest and during upright cycle exercise in younger LO (n = 3, VO_2max: 43 ml/kg/min) and HI fit (n = 5, VO_2max: 60 ml/kg/min) male subjects, found that mean pulmonary artery pressure increased by 61% and 129% from rest to submaximal and peak exercise, respectively while end-systolic pressure increased by 32% and 42% [22]. A consequence of the

Time Course and Pattern of Ventricular Remodelling With Endurance Training

Several recent studies have examined the time course and pattern of ventricular remodelling associated with endurance training [9], [24]. Arbab-Zadeh et al. assessed RV and LV adaptations in response to a 12-month progressive endurance exercise training in 12 (mean age: 29 years, seven men and five women) previously sedentary subjects [9]. The main finding was that during the first 6 months, when lower intensity exercise was performed, the increased LV mass was solely the result of an increase

Ventricular Wall Stress in Athletes Versus Patients With Cardiac Pathology: Intermittent Versus Permanent Load

A key factor unique to athletic remodelling but not considered in the Morganroth hypothesis is that the haemodynamic load imposed by exercise is a transient phenomenon. Specifically, given that the haemodynamic stimulus for ventricular remodelling is only present during exercise, the extent of remodelling is probably influenced by the percentage of time spent exercising. This may well explain why those athletes who spend the greatest amount of time training and racing (e.g. cyclists,

Conclusion

Despite being widely accepted in the sport cardiology field [3], we contend that the four-decade-old Morganroth hypothesis that resistance exercise performed with a brief VM is primarily a ‘pressure’ load stress (similar to aortic stenosis or long standing hypertension) that results in concentric LV hypertrophy is obsolete (Table 1) [5], [6], [7], [8]. Further, contrary to the Morganroth hypothesis, endurance exercise is associated with both an acute “volume” and “pressure” load [4], [22], [23]

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ReviewAthlete’s Heart: Is the Morganroth Hypothesis Obsolete?

Introduction

Section snippets

Acute Effects of Resistance Exercise on Ventricular Wall Stress

Patterns of Ventricular Remodelling With Resistance Training

Acute Effect of Endurance Exercise on Ventricular Wall Stress

Time Course and Pattern of Ventricular Remodelling With Endurance Training

Ventricular Wall Stress in Athletes Versus Patients With Cardiac Pathology: Intermittent Versus Permanent Load

Conclusion

Cardiol Clin

Chest

Am J Cardiol

Am J Cardiol

Comparative left ventricular dimensions in trained athletes

Ann Intern Med

The athletes heart syndrome: a new perspective

Ann N Y Acad Sci

The multi-modality cardiac imaging approach to the Athlete’s heart: an expert consensus of the European Association of Cardiovascular Imaging

Eur Heart J Cardiovasc Imaging

Resistance training and cardiac hypertrophy: unravelling the training effect

Sports Med

LV hypertrophy in resistance or endurance trained athletes: the Morganroth hypothesis is obsolete, most of the time

Heart

Left ventricular remodelling and the athlete’s heart: time to revisit the Morganroth hypothesis

J Physiol

Cardiac remodeling in response to 1 year of intensive endurance training

Circulation

Arterial, cerebrospinal and venous pressures in man during cough and strain

Am J Physiol

Review
Athlete’s Heart: Is the Morganroth Hypothesis Obsolete?