EXERCISE-INDUCED CARDIAC-HYPERTROPHY - FACT OR FALLACY

After a century of research reports, the notion of exercise-induced ca rdiac hypertrophy is still an expected adaptation to regular exercise training. Experimental evidence reported both in animals and in humans over the past 3 decades suggests, however, that this conclusion may n ot be totally warranted. Data from 20 years of echocardiographic inves tigations of athletes and nonathletes indicate that differences in car diac dimensions are not very large. Cross-sectional comparisons of ove r 1000 athletes and roughly 800 control individuals indicate an averag e difference of 1.6 mm in left ventricular (LV) wall thickness and of 5.3mm in end-diastolic diameter. Differences reported after training p rogrammes lasting 4 to 52 weeks are even smaller, with average increas es of 0.3 mm in LV wall thickness and only 2.1 mm in end-diastolic dia meter. This article reviews data from animal and human studies concern ing cardiac morphology and exercise training to show that the traditio nal interpretation of the literature has failed to take into account s everal methodological considerations or factors that may act as confou nders in the interpretation of data. Results from animal studies indic ate that the observation of cardiac hypertrophy is equivocal at best. In many reports the reported changes in heart size are not significant , and in instances where significant changes are reported these may be seen to be confounded by a number of factors. For-example, in rats th e reported training-induced hypertrophy may be related to gender diffe rence in the responsiveness of cardiac dimension or body and/or organ growth rather than to true heart hypertrophy. Furthermore, the interpr etation or results from training studies in rats has often been based on the assumption that the metabolic, haemodynamic and thermoregulator y requirements of swimming and running exercise in rats are similar, w hich may in fact not be the case. In addition, the use of the heart we ight/body weight ratio as an index of cardiac hypertrophy. although wi despread in animal studies, is open to criticism owing to failure to c ontrol for concurrent changes in bodyweight. Several methodological co nsiderations and factors confounding the outcome of exercise training in humans have also been omitted when interpreting echocardiographic c ross-sectional and longitudinal findings. For example. in adult echoca rdiography the practical resolution of the echocardiographic technique amounts to roughly 2.2mm. It follows, therefore, that unless differen ces of changes in cardiac dimensions exceed the limit of resolution th ey are meaningless although statistically significant. Results from a meta-analysis of echocardiographic investigations published over the l ast 20 years indicate that the average change reported for left ventri cular (LV) wall thickness remains well under the limit of resolution. The mean increase in LV internal diameter reported equals or slightly exceeds the technical resolution. Its significance, however, may be qu estioned since neither training brachycardia nor training-induced plas ma volume expansion have been taken into account. It is likely, theref ore, that 'increased diastolic filling rather than true eccentric hype rtrophy explains the differences reported. Another factor that has not been acknowledged in the investigation of the 'athlete's heart' is th e fact that 'athletes' generally exhibit anthropometric characteristic s which typically differentiate them from sedentary individuals. Despi te the well known relationship between cardiac dimensions and body siz e, this was often not considered in the interpretation of cross-sectio nal data. Re-analysis of cardiac dimensions reported in athletes and t heir sedentary counterparts indicate that differences in LV wall thick ness between groups are in fact eliminated when a correction for body surface are is introduced. Illegal drug supplementations may also cont ribute to the cross-sectional differences reported. Finally, re-evalua tion of the evidence in light of potential confounders indicates that athletes present cardiac dimensions that are proportional to their bod y size but do not exceed the normal limits. Endurance training induces a modest increase in LV internal diameter which may be explained by i ncreased diastolic filling resulting from resting bradycardia and hype rvolaemia.