Short- and long-termathletic training have been shown to be associated with left ventricular (LV) morphologic adaptations including increases in posterior wall thickness (PWT), ventricular septal wall thickness (VST), diastolic cavity size (LVIDd), and estimated LV mass (LVM) (12). The magnitude of the alteration in LV morphology has been shown to be related to the length of training exposure as master athletes had larger LV dimensions and mass compared with “sport-matched” junior athletes (13,14). However, a limitation of the studies assessing the “athletes heart” in junior and master athletes has been the primary focus on athletes performing endurance disciplines.
Previous studies have found that short-term resistance training (RT) was associated with increases in LV wall thickness, relative wall thickness, and estimated LVM in younger individuals (2,3). Moreover, increased age has also been shown to induce LV morphologic changes similar to that found secondary to RT (9). Therefore, it is possible that the combination of aging and RT may be a potent stimulus to induce LV hypertrophy. However, the effects of short- versus long-term RT on LV morphology have not been well studied. Accordingly, the purpose of this cross-sectional echocardiographic study was to assess the effects of short-term (<5 yr) versus long-term RT (≥18 yr) as performed by junior and master athletes on LV dimensions, mass, and systolic function.
The subjects for this study were 39 males (20 RT athletes and 19 control subjects). The RT athletes had qualified and competed at the 1995 Canadian Powerlifting Union national championships and were classified, in accordance with the International Powerlifting Federation guidelines, as junior athletes (N = 8; mean age: 21.1 ± 1.2 yr) or master athletes (N = 12; mean age: 46.0 ± 5.5 yr). The control subjects were recruited from the St. Paul’s Hospital Cardiac Echocardiography Laboratory and were of similar age as the RT athletes (8 young controls: mean age: 21.8 ± 2.8 yr and 11 middle-aged controls: mean age: 46.8 ± 4.4 yr).
Assessment of LV morphology was performed at the championship meet site at a time when all athletes could be expected to be in peak physical condition (Table 1). Ethics approval was obtained from the University of British Columbia Medical Ethics Committee, and written informed consent was obtained before study participation.
Assessment of LV dimensions, estimated mass and systolic function.
Left ventricular imaging was performed with a commercially available ultrasound instrument (Hewlett-Packard, Sonos 2500, Avondale, PA) with a 3.5-MHz transducer. Two-dimensionally guided M-mode echocardiogram examinations were performed using the parasternal long axis view just apical to the mitral valve leaflets. The echocardiographic measurements were performed in accordance with the American Society of Echocardiography guidelines (16) and included the following: PWT, VST, LVIDd, and LV systolic cavity dimension (LVIDs). Relative wall thickness (h/R) was calculated as 2 × PWT/LVIDd (6). Absolute LV mean wall thickness was measured as 1/2 × (VST + PWT). Calculated LVM was determined by the corrected American Society of Echocardiographic formula as: LVM (g) = 0.83 × [(LVIDd + VST + PWT)3 − (LVIDd)3] + 0.6. (4). Left ventricular systolic function was determined by fractional shortening (FS) and calculated as: FS = (LVIDd − LVIDs)/LVIDd.
Comparison of the echocardiographic variables between the groups was performed with a one-way analysis of variance using Statistica software. The alpha level was set a priori at P < 0.05.
By study design, the master athletes and middle-aged controls were significantly older than the junior athletes or young controls (Table 2). However, no significant difference was found between any of the groups for body surface area (Table 2). The master athletes had significantly higher resting heart rates than the middle-aged controls or young controls; however, no significant difference was found between the master athletes or junior athletes for this variable (Table 2).
Training experience and maximal muscular strength.
The master athletes had a significantly greater training exposure (18.3 ± 6.6 yr) than the junior athletes (4.4 ± 3.4 yr). No significant difference was found between the two athletic groups for the squat, bench press or deadlift one-repetition maximums (Table 1).
LV dimensions, estimated mass, and systolic function.
No significant difference was found between any of the groups for absolute or relative PWT, VST, LVIDd, LVIDs, LVM, h/R ratio, and FS (Table 3).
Our finding of no significant alteration in PWT, VST, LVIDd, or LVM between the junior and master athletes was similar to that previously reported by others (5,8). However, our results differ from two earlier studies that found that master athletes had larger LV dimensions and mass compared to sport-matched younger athletes (13,14). The disparity between studies may be related to the underlying duration of sport participation. For example, Nishimura and associates (14) found that the absolute increase in LV dimensions and LVM secondary to sport participation was related to the duration of the training stimulus. In their study, 60 elite cyclists were divided into three groups based on their age and training exposure (group 1: age range: 20–29 years, mean training experience: 5 yr; group 2: age range: 30–39 yr: mean training experience: 14 yr; group 3, age range: 40–49 yr: mean training experience: 26.5 yr). Echocardiographic analysis revealed that the older athletes with three decades of training experience had significantly larger LV wall thickness and estimated LVM compared with either group of younger cyclists. However, not unlike our findings, no significant difference was found for LV wall thickness and estimated LVM between the two younger groups with 5–14 yr of training experience. The findings of Nishimura and coworkers (14) suggest that an extremely long duration of training (i.e., ≥3 decades or more) may be required for master athletes to attain a larger LV wall thickness and estimated LVM compared with sport-matched junior athletes. Currently, the effects of three decades of RT on LV morphology have not been well examined. However, one of our athletes (a master national and world champion) with 32 years of training experience was found to have a measured absolute PWT, VST, LVIDd, LVIDs, and LVM within normal limits (Table 4). Therefore, in some individuals, four decades of RT may be an insufficient stimulus to alter LV morphology.
Previous studies assessing the master “athlete’s heart” have found that elite middle-aged or older athletes had larger LV dimensions and LVM compared with age-matched sedentary individuals (7,8). In the current study, no significant difference was found between the master athletes and age-matched sedentary controls. The disparity between our results and those of others may be related to the types of athletes studied. Spirito and associates (17) reported that the magnitude of the alteration in LV morphology secondary to athletic conditioning was independently related to the mode of sport participation. For example, endurance training had the greatest impact on increasing LV wall thickness and cavity size, whereas RT was found to be an insufficient stimulus to result in more than a mild increase in LV wall thickness. Therefore, it may be possible that increases in LV dimensions and LVM secondary to long-term exercise training may be limited to master athletes participating in endurance disciplines.
The measured echocardiographic variables, in the junior athletes, were similar to that previously reported for younger RT athletes (1,10,11,15). However, the upper limit of LV wall thickening secondary to long-term (>18 yr) RT has not been well studied. Figure 1 demonstrates that no junior or master athlete was found to have an absolute LV mean wall thickness above normal clinical limits (i.e., ≤12 mm). These findings confirm and extend the results of Pelliccia and associates (15), who found that the upper limit of LV wall thickening in younger RT athletes was ≤12 mm. Together these findings suggest that if a junior or master RT athlete is found to have an absolute LV mean wall thickness >12 mm then further investigations may be required (to rule out other forms of pressure overload hypertrophy) as this adaptation appears to be an unlikely consequence of short or long-term RT.
A limitation of our study was that a majority of the athletes were only willing to participate in the study during the time period between the official “weigh in” and the actual competition. Therefore, the elevated resting heart rates, in the powerlifters, may be the result of the heightened anticipation (increased central command) associated with competing at a national powerlifting contest. Despite the elevated heart rates there were no differences in LV cavity dimensions, wall thickness or systolic function between the athletes and their respective controls.
In summary, short- or long-term RT as performed by junior or master RT athletes was not associated with changes in PWT, VST, LVIDd, LVIDs, h/R, estimated LVM, or LV systolic function. Moreover, the upper limit of left ventricular mean wall thickening secondary to short or long-term RT does not exceed normal clinical limits. Therefore, short-term or long-term RT as performed by elite junior or master powerlifters appears to be an insufficient stimulus to alter LV morphology.
The authors would like to thank Dave Buchaski and the Hewlett Packard Canada for providing the ultrasound machine at the National Powerlifting Championships. M. J. Haykowsky was the recipient of a Heart and Stroke Foundation of Canada/National Health Research and Development Ph.D. studentship in Applied Cardiovascular and Cerebrovascular Health Research.
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