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J Am Coll Cardiol, 2004; 44:892-896, doi:10.1016/j.jacc.2004.04.051
© 2004 by the American College of Cardiology Foundation
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TRAINING AND LEFT VENTRICULAR MASS

Association of fat-free mass and training status with left ventricular size and mass in endurance-trained athletes

Gillian A. Whalley, MHSc, DMU*,*, Robert N. Doughty, MD, FRACP*, Greg D. Gamble, MSc*, Helen C. Oxenham, MBChB, MRCP*, Helen J. Walsh, RN, BSc*, Ian R. Reid, FRACP, MD* and James C. Baldi, PhD{dagger}

* Departments of Medicine
{dagger} Sport and Exercise Science, University of Auckland, Auckland, New Zealand

Manuscript received December 18, 2003; revised manuscript received April 21, 2004, accepted April 27, 2004.

* Reprint requests and correspondence: Ms. Gillian A. Whalley, Department of Medicine, University of Auckland, Private Bag 92 019, Auckland, New Zealand (Email: g.whalley{at}auckland.ac.nz).


   Abstract
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 Abstract
Methods
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 Discussion
 References
 
OBJECTIVES: We sought to study the relationship between left ventricular (LV) size and body composition in male endurance athletes and age-matched control subjects.

BACKGROUND: Endurance training is associated with increases in both left ventricular mass (LVM) and left ventricular end-diastolic dimension (LVEDD) in athletes. In other populations, LVM is independently predicted by fat-free mass (FFM). We hypothesized that the increase in LV size and mass observed with training may be a normal response to increased FFM.

METHODS: Twelve young and 18 older male endurance athletes and 10 young and 18 older untrained men underwent exercise testing, echocardiography, and dual-photon x-ray absorptiometry body composition analysis. Univariate correlates (Spearman) and multivariate determinants of LVM and LVEDD were sought from: height, height1.4, height2.7, height3.0, body surface area (BSA), FFM, weight, and body mass index. Un-indexed and indexed LVM and LVEDD were then compared.

RESULTS: Athletes were of a similar age, weight, and height, but had higher FFM and maximum oxygen uptake than untrained men. Both LVM and LVEDD were correlated with body size, including FFM, BSA, weight, and height (all p < 0.05). On multivariate analysis, FFM was the only independent predictor of both LVM (R2 = 0.36, p < 0.001) and LVEDD (R2 = 0.35, p < 0.001). Furthermore, LVM and LVEDD (un-indexed and indexed to BSA and height) were different between athletes and non-athletes, but not when indexed to height2.7 or FFM.

CONCLUSIONS: Both LVM and LVEDD are predicted by FFM in endurance athletes, and when indexed to FFM, no training-related differences were observed. Thus, the extent of LV remodeling (athletic heart) in trained individuals may reflect a normal physiologic response to increased FFM induced by training.

Abbreviations and Acronyms
  BMI = body mass index
  BP = blood pressure
  BSA = body surface area
  DEXA = dual-photon X-ray absorptiometry
  FFM = fat-free mass
  LV = left ventricle
  LVEDD = left ventricular end-diastolic dimension
  LVH = left ventricular hypertrophy
  LVM = left ventricular mass
  VO2max = maximum oxygen uptake

For many years, the "athletic heart," characterized by hypertrophy and dilation of the left ventricle (LV), has been discussed and evaluated. Generally, endurance-type sports are associated with LV dilation, whereas resistance exercise is associated with left ventricular hypertrophy (LVH) (1). Two meta-analyses were unable to conclusively demonstrate differences in cardiac adaptation between resistance and endurance training (2,3). It is possible that these cardiac adaptations represent a normal physiologic variation of cardiac growth.

Both LV size and left ventricular mass (LVM) are related to body size (4–7) and are often divided by body surface area (BSA) to determine normal ranges and to detect the presence of pathologic LVH (8,9). However, this overestimates LVH in lean subjects, while underestimating LVH in obese individuals. Height and height raised to various powers are now widely recommended in place of BSA (10,11) because they do not underestimate the degree of LVH in obesity. However, recent studies have demonstrated that in non-athletic populations, LVM has a closer relationship with fat-free mass (FFM) than BSA and that it is not related to fat mass (5,7). Further, as BSA is affected by fat mass, it may be an inappropriate indexing variable, especially in populations where changes in body composition occur. Although ideal, FFM is rarely used because accurate measurements are not widely available.

If FFM is the main determinant of LVM in athletes, as it is in non-athletes, then the increase in FFM associated with training may lead to increased LV size. Furthermore, by indexing LV measurements to other body measures that do not adequately reflect changes in FFM, the degree of LVH may be exaggerated in athletes.

This study investigated the relationship between LV size and body composition in male endurance athletes and age-matched untrained control subjects, in order to confirm the hypothesis that LV size is closely related to FFM in athletes.


   Methods
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After preliminary screening, 18 untrained and 18 endurancetrained older men (age 60 to 80 years) and 10 untrained and 12 endurance-trained younger men (20 to 30 years) were enrolled. We excluded smokers and subjects with musculoskeletal, metabolic or cardiovascular disease, hypertension (seated blood pressure [BP] >160/90 mm Hg), recent illness, or those taking any prescription medication (12). A total of 17 people (26%) had a systolic BP between 140 and 160 mm Hg: 15 control subjects (2 young, 13 older) and two athletes (1 young, 1 older).

Control subjects had not participated in regular endurance training in the previous two years. Athletes competed regionally, nationally, or internationally in endurance sports and had trained regularly for at least two years. The University of Auckland Human Subjects Ethics Committee approved the study protocol, and all subjects provided informed, written consent.

All subjects completed a medical history questionnaire and reviewed their medical history with a study investigator. Older subjects received a physical examination, 12-lead electrocardiogram, and Bruce protocol exercise test to rule out coronary artery disease. Maximal oxygen uptake (VO2max) was determined by incremental treadmill testing.

Body composition was measured by dual-photon X-ray absorptiometry (DEXA) (Lunar DPX-IQ, Madison, Wisconsin). Extended analysis of total body images using the manufacturer's standard software packages was done to estimate total mass, FFM (bone mineral content plus nonfat soft tissue), and fat mass (total mass – FFM).

Echocardiograms were obtained using a standardized protocol by a trained research sonographer (ATL HDI 5000, Bothell, Washington) and digitally acquired and analyzed off-line (NovaMicrosonics, Allendale, New Jersey). Parasternal long-axis M-mode recordings (100 mm/s) were made with the cursor at the mitral valve leaflet tips, perpendicular to the chamber cavity. Leading-edge LV measurements were made and LVM was calculated (American Society of Echocardiography formula [13]) in triplicate. The coefficient of variation for test-retest measurement of LVM in our laboratory is 14.8% and that for intra-observer measurement is 7.8%. All data were collected and analyzed by technicians who were unaware of the subjects' training status.

Univariate correlation (Spearman) was examined between LVM and body size measurements, and stepwise logistic regression was used to determine the independent predictors of LVM; the LVM model includedBSA, body mass index (BMI), height, weight, height2.7, height1.4, height3.0, FFM, fat mass, and VO2max. For all analyses, young and old athletes were combined into one group, as were the young and old control subjects, and the Student t test was used for comparison.


   Results
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Discussion
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Height, weight, and BSA were similar between athletes and controls, but the athletes had a lower BMI, less body fat, higher FFM, lower resting heart rate and BP, and higher VO2max compared with non-athletes (Table 1). Athletes had a larger left ventricular end-diastolic diameter (LVEDD) and end-systolic diameter and higher LVM than controls, but wall thickness was similar. A total of 9 people (14%) had wall thickness ≥11 mm: 4 athletes (2 older, 2 young) and 5 controls.


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  		Table 1. Subject Characteristics and Echocardiographic Measurements
 
Both LVM and LVEDD correlated with several measures of body size (Table 2). The most important of these were FFM, height2.7, and BSA, but neither correlated with fat mass (Fig. 1). No significant differences were observed between the groups.


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  		Table 2. Univariate Correlates of Left Ventricular End-Diastolic Dimension and Left Ventricular Mass in Trained Male Endurance Athletes and Untrained Men
 


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  		Figure 1 Spearman correlation of left ventricular (LV) mass and left ventricular end-diastolic diameter (LVEDD) with body surface area (BSA), height2.7, fat free mass (FFM), and fat mass (open circles = untrained men; solid circles = trained endurance athletes).

 
On multivariate analysis, the only independent predictor of LVM was FFM (R2 = 0.365, p < 0.001) and that of LVEDD was FFM (R2 = 0.35, p < 0.001). In a simplified model, including age, height2.7, FFM, fat mass, and VO2max, FFM remained the only independent predictor of LVM. When the groups were analyzed separately (young athletes, young untrained, older athletes, older untrained men), FFM remained the only independent predictor of LVM and LVEDD.

Athletes had a significantly larger LVEDD, and this persisted when LVEDD was indexed to height or BSA. However, indexing to either height2.7 or FFM eliminated this difference (Table 3). The LVM, LVM/BSA, and LVM/height were significantly higher in the athletes than in non-athletes, but when LVM was indexed to height2.7 or FFM, no difference was observed between athletes and non-athletes (Table 3).


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  		Table 3. Left Ventricular Dimension and Mass Indexed to Various Measures of Body Size
 

   Discussion
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 Abstract
 Methods
 Results
 Discussion
References
 
This study supports the hypothesis that the left ventricular dilation and hypertrophy observed in endurance athletes may be physiologic. Both LVM and LVEDD were greater in athletes compared with non-athletes, either indexed to BSA or un-indexed, as shown previously (1). However, LVM and LVEDD indexed to FFM were similar between the groups, and both were predicted by FFM alone, suggesting that the greater FFM in trained athletes explains the larger LVM and dimensions. This is the first study to utilize DEXA with echocardiography to compare athletes with age-matched control subjects.

Heart size to body size index.   This study confirms the importance of scaling heart size to body size and highlights the importance of body composition. Previous studies have shown that LV size is closely related to body size and composition (4,5,10,11,14) and that FFM is the only independent predictor of LVM (5). Fat-free mass is rarely used, because accurate measurements are not widely available. Instead, BSA is often used to index echocardiographic measurements (13), but BSA is affected by fat mass, which is neither correlated with nor predicts LVM (5), and hence this method is unreliable. Height and height raised to various powers are also correlated with LV size and used widely (6,10,11), but height-derived values do not independently predict heart size, and if changes in body composition occur (e.g., in athletes), this method may be inappropriate.

The athlete's heart.   The relationship between heart size and FFM has been previously studied in male endurance athletes using skin-fold thickness measurements (15) and hydrostatic weighing (16). In both studies, athletes had higher LVM and LVM/FFM than controls. Unfortunately, these methods are not as accurate as DEXA (17), and the two-compartment model used may lack validity in athletes due to the changes in bone mineral content and total body water (18). Our findings, using very accurate assessment of FFM, disagree with these studies and suggest that the changes observed in athletes' hearts are related to FFM.

When LV measurements are indexed to BSA or height, the differences observed between athletes and non-athletes persist (19,20). Some studies have matched control subjects to athletes for body size (height, weight, BSA) and found that athletes still had higher LVM and LVM/BSA (2,20). If the current hypothesis—that LVM is determined by FFM—is correct, the matching of non-athletes and athletes on the basis of body size would further emphasize the difference in LVM, as both endurance (21) and resistance training (22) increase muscle size and hence FFM. For example, a male athlete would have a higher FFM for a given BSA, as compared with an untrained man of similar height, weight, and BSA. Thus, studies comparing athletes with untrained controls of similar body size but disparate FFM may have led to spurious conclusions. In the absence of FFM measurements, indexing measurements to height2.7 will help to identify significant abnormalities in athletes. However, to detect longitudinal changes associated with training, indexing to any measure of height will be misleading. Height is unlikely to change in adult athletes, and any changes in heart size will be amplified if changes in FFM occur.

Study limitations.   This study investigated the relationship between LVM and FFM in a small group of endurance-trained athletes, and further work is needed in athletes with different training regimes, loading conditions, and associated physiologic characteristics. Because of the small sample size, there is a possibility of selection bias, and thus larger patient populations need to be evaluated. These findings require confirmation in a longitudinal study of the effects of training, with subjects acting as their own controls.

Conclusions.   This study suggests that the LV dilation and LVH observed in endurance-trained athletes may reflect a normal physiologic response to increased FFM and highlights the importance of accurate assessment of FFM in athletes to fully evaluate the effects of training on cardiac morphology. If the findings of this study are confirmed in other groups, the proposed methodology for indexing LV measurements has the potential to better characterize physiologic LV remodeling in athletes.


   Footnotes
 
Ms. Whalley is supported by a National Heart Foundation of New Zealand post-graduate scholarship.


   References
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