LV hypertrophy in resistance or endurance trained athletes: the Morganroth hypothesis is obsolete, most of the time

摘要

A widely accepted principle in sport cardiology is that the pattern of LV hypertrophy that occurs with athletic training is related to the type of exercise performed. This principle is based largely on the nearly four-decade-old seminal echocardiographic study by Morganroth et al who reported that the increased LV mass in highly trained (collegiate or world class) male long distance runners or swimmers compared with age-matched and sex-matched non-athlete controls was primarily due to increased LV end-diastolic volume with little or no increase in LV wall thickness (eccentric LV hypertrophy pattern). In contrast, the increased LV mass in highly trained wrestlers and shot-putters was solely due to an increased LV wall thickness as LV end-diastolic volume was normal (concentric LV hypertrophy pattern). Based on the divergent LV remodelling patterns observed, Morganroth et al hypothesised that the haemodynamic burden (volume overload) associated with endurance exercise training (ET) may be similar to that which occurs in patients with mitral or aortic regurgitation. Conversely, the increased haemodynamic burden (pressure overload) associated with performing a Valsalva manoeuvre (VM) during resistance training (RT) may mimic the stress imposed on the heart by systemic hypertension or aortic stenosis. Despite the widespread acceptance of the Morganroth hypothesis, several research groups have questioned whether a divergent 'athletes heart' phenotype exists.