The prevalence of obesity has reached epidemic proportions in western societies, and rates of obesity have rapidly increased in young people (9). A possible consequence of obesity, in both adults and children, is impaired cardiac diastolic function (19,30). Although it has been suggested that exercise training is associated with improvements in diastolic function (17), no previous studies have assessed the impact of an exercise intervention on these measures in obese adolescents.
Many echocardiographic studies have reported impaired indices of left ventricular (LV) diastolic function in obese adults (6,14,21,23), including recent studies using tissue Doppler approaches that are somewhat less sensitive to loading conditions than previously used transmitral flow measures. Peterson et al. (25) reported decreased global early diastolic peak myocardial velocity (E′) in healthy obese women, whereas Wong et al. (38) reported reduced E′ and myocardial strain in severely obese and, to a lesser degree, mildly obese subjects. These studies endorse previous evidence that impairment in diastolic function is correlated with body mass index (BMI) in obesity (23,27). Such observations may be of clinical relevance, given that impaired diastolic function predicts prognosis in subjects with other cardiovascular risk factors (3,29,35).
Exercise has been documented to produce improvements in cardiac function in adults with previously impaired diastolic function (10,16,32). Further support for the use of exercise interventions in such subjects comes from recent evidence that shows a direct relationship between early diastolic tissue velocity (E′) and exercise capacity (39). Despite this, to our knowledge, the impact of exercise training on diastolic function in obese populations has not been studied. In the present study, we decided to compare the impact on early diastolic function of resistance exercise, involving large muscle group repetitive dynamic exercise performed against an external load. Our rationale was based on the putative benefits of this form of exercise, which is accepted as the optimal modality for enhancing skeletal muscle hypertrophy, lean body mass, and possibly insulin sensitivity (13). Indeed, a recent study performed in rats indicated that high-intensity training reduced ventricular stiffness via an intrinsic effect, which was independent of neurohormones, HR, or pericardial restraint (18). However, no previous studies have examined the impact of resistance training (RT) on diastolic function in humans. The aim of the present study, therefore, was to examine whether resistance-based exercise training induces improvement in indices of early diastolic tissue velocity in obese children.
Thirteen obese subjects were recruited to participate in a supervised 8-wk exercise training program. Our decision to use an 8-wk intervention period was based on our previous experience, which has indicated that this duration of training is sufficient to induce various physiological adaptations (2,36,37). Obesity was defined as BMI greater than an age and gender equivalent of 30 kg·m−2 (7). To account for any differences associated with growth and maturation over the 8-wk period, a further 10 obese subjects were recruited into a control group. This group underwent echocardiographic assessments, 8 wk apart, with no exercise intervention. Subject characteristics of the obese groups are displayed in Table 1.
All subjects attended a dedicated study room, and all echocardiographic measures were collected by two experienced echocardiographers. Post hoc analysis of the studies was carried out by an operator who was blinded to the identity of each subject. All participants and their parent or guardian gave written informed consent, and the study was approved by the Princess Margaret Hospital Ethics Committee.
The exercising subjects entered a group RT program (n=13) for an 8-wk training period, consisting of three 1-hsessions per week. The individually prescribed exercise training programs were designed and supervised by an experienced exercise physiologist; the RT program was designed to increase lean muscle mass and strength.
Exercise Training Programs
The RT program concentrated on the large muscle groups. Exercise was performed on weight-stack machines (Pulsestar, Cheshire, UK). After a 10-min warm-up period of stretching and low-intensity cycle or treadmill exercise, each RT session would begin with 1 min of exercise consisting of eight repetitions performed on a given machine. This exercise was initially set at an intensity of ∼75% maximum voluntary contractile strength, which was progressively increased to ∼90%. After this initial minute of exercise, subjects rested and performed stretching exercises for 1 min before turning to the next weights machine where another eight repetitions of exercise were performed. This circuit continued until all 10 machine stations were completed. Subjects completed two sets of the weights circuit at each visit. Inclusive of the final 10-min cooldown period, the RT exercise sessions therefore lasted approximately 60 min.
All group exercise sessions were supervised, with a maximum subject-to-staff ratio of 6:1. Exercise intensity (HR and weights lifted) was maintained within the target zones by intermittent checking undertaken in all subjects throughout each session.
Assessment of exercise capacity.
A submaximal exercise test was performed in each obese subject. This test involved three consecutive 4-min incremental epochs of exercise on a braked bicycle ergometer (Monark, Vansbro, Sweden) with subjects continuously cycling at 60 rpm. HR was continuously measured by telemetric method (Polar Electro, Kempele, Finland). Identical exercise intensities were used before and after exercise training in each subject, and changes in fitness were assessed by comparing HR responses at these matched workloads.
Body composition and muscle strength assessments.
Eleven of the 13 subjects in the RT group underwent repeated maximal strength assessments for dual leg press and bench press exercises using the one repetition maximum (1RM) technique. All repeat testing was done within a week of the final exercise session. One subject was unavailable due to illness and the other due to family commitments. These strength measures were summed to determine maximal voluntary contractile strength. Body weight (Model 770; Seca, Hamburg, Germany), height, and BMI were obtained in each subject before the exercise intervention. Subjects in the RT group also underwent repeat DEXA scans (XR36 pencil beam; Norland Corporation, Fort Atkinson, WI) to assess the impact of their training intervention on whole body and regional fat and lean tissue mass. DEXA allows for precise measurement of fat mass and fat-free mass, the latter being comprised of fat-free soft tissue and bone mineral content. Although DEXA involves low-dose x-ray exposure (effective dose, ∼0.4-2.0 μSv), it was not considered appropriate for control subjects to be exposed to repeated scanning. The scanner was calibrated daily in a two-part process. The first used a calibration standard to test system diagnostics. The second part involved a scan of the quality control phantom to ascertain the precision and accuracy of the scanner. Reliability of the repeat DEXA measures was enhanced by ensuring that bone mineral content values for each body segment (head, upper limbs, lower limbs, thorax, abdomen), which would not be expected to markedly change across the 8-wk training period, were statistically comparable before and after training. All DEXA scans were performed and analyzed by a qualified and experienced operator.
Measures of cardiac morphology.
Two-dimensional ultrasound imaging, M-mode imaging, pulsed wave, and tissue Doppler imaging (TDI) measurements were collected by two experienced echocardiographers. LV dimensions were measured using two-dimensional-guided M-mode measurements on an ultrasound machine equipped with a 2.5-MHz multiarray transducer (Vivid 7; GE Medical, Milwaukee, WI). The mean value of at least five measurements of each dimension of the LV was determined: interventricular septal thickness (IVS), left ventricular internal dimension during diastole (LVIDd), posterior wall thickness (PWT), and left ventricular internal dimension during systole (LVIDs). Although we acknowledge the limitations inherent in calculating left ventricularmass (LVM) in children and adolescents, we nevertheless performed these calculations to allow comparisons to previous studies. LVM was calculated according to the recommendationsof the American Society of Echocardiography (ASE):
LVM was indexed to gender-specific body length exponents validated for the assessment of LV hypertrophy in children and adolescents (11).
Measures of cardiac diastolic function.
Diastolic function was assessed using conventional and pulsed wave TDI. Transmitral flow measurements were made according to the ASE guidelines (26). TDI was performed in the four-chamber view, placing the Doppler sample volume adjacent to the mitral annulus. Early LV diastolic function was determined by measuring the transmitral peak early filling velocity (peak E) and the early diastolic peak myocardial velocity (E′ wave, cm·s−1) (22). The E/E′ ratio, a measure linearly related to left atrial pressure, was calculated. Late diastolic filling peak velocity (A′ wave, cm·s−1) was also assessed.
All statistical analysis was performed using the Statistical Package for the Social Sciences for Windows (version 11.0; SPSS Inc., Chicago, IL). Unpaired t-tests were used to assess significance between the groups at baseline. For each variable of interest, two-way ANOVA was performed to determine whether differences existed between the RT and the control groups across the 8-wk intervention period, with paired t-tests subsequently performed within groups across time. All data were reported as mean ± SE, and statistical significance was assumed at P < 0.05.
Comparison of subject characteristics at entry.
Nodifferences existed between obese subject groups in terms ofage (P = 0.09), height (P = 0.4), weight (P = 0.9), BMI (P= 0.6), or systolic blood pressure (P = 0.9). Diastolic blood pressure (P < 0.05) was significantly lower in the control subjects than in the RT subjects (Table 1). No significant differences were evident for any echocardiographic measures of LV geometry (Table 2) or diastolic filling (Table 3) at study entry between the RT and the control groups.
Effects of exercise training
Compliance with the prescribed exercise sessions was excellent, averaging 85 ± 4% in the RT group. No subject attended less than two-thirds of the prescribed sessions. Subjects were carefully monitored throughout each session for adherence to their individually determined resistance exercise intensity prescription.
RT was associated with a modest, although significant, decrease in SBP (120 ± 2 vs 116 ± 3 mm Hg, P < 0.05), whereas no difference was evident in controls (122 ± 2 vs 122 ± 2 mm Hg). No changes were evident in either group in terms of DBP (RT: 66 ± 2 vs 68 ± 3 mm Hg; controls: 58 ± 2 vs 59 ± 2 mm Hg) or HR (RT: 79 ± 3 vs 79 ± 3 bpm; controls: 70 ± 3 vs 69 ± 3 bpm).
Body weight did not change in either of the groups (RT: 84.9 ± 6.5 vs 85.5 ± 6.6 kg, P = 0.4; controls: 82.1 ± 8.3 vs 82.5 ± 8.3 kg, P = 0.7), and no change in BMI was evident (RT: 32.5 ± 1.9 vs 31.9 ± 2.0 kg·m−2, P = 0.9; controls: 30.2 ± 2.6 vs 30.0 ± 2.6 kg·m−2, P = 0.8). DEXA-derived measures of body composition revealed an increase in lean body mass in the RT group (41.2 ± 3.7 vs 42.1 ± 3.0 kg, P < 0.05), which in turn was predominantly due to an increase in lower limb lean mass (14.6 ± 1.1 vs 15.0 ± 1.1 kg, P < 0.05). A nonsignificant decline in fat mass (43.1 ± 3.5 vs 42.8 ± 3.6 kg) was also evident. This slight decrease, along with the increase in lean body mass, rendered the percent fat mass significantly lower after RT (49.6 ± 1.4% vs 48.5 ± 1.5%, P < 0.01).
In the RT group, the sum of bench press and dual leg press maximal strengths (1RM) significantly increased (77 ± 4 to 117 ± 9 kg, P < 0.0001) due principally to a large increase in leg strength (55 ± 3 to 92 ± 8 kg, P < 0.001). Neither the RT nor the control subjects exhibited significant changes in exercise HR at any level of cycle ergometer intensity.
Effects of exercise training on cardiac morphology and function.
No training effect was evident in LVM or indices of LVM in either group (Table 2). Similarly, no changes were observed in wall thickness, diastolic, or systolic internal diameter measures. Changes in stroke volume in the RT (81 ± 6 vs 85 ± 6 mL) and the control group (79 ± 5 vs 78 ± 6 mL) did not achieve significance. Similarly, changes in fractional shortening (RT: 40 ± 1% vs 42 ± 1%; controls: 39 ± 1% vs 40 ± 1%) were not significant.
In terms of tissue Doppler measures, a significant main effect for time (i.e., training) was evident for E′ (P < 0.01), with a significant increase present in the RT group (P < 0.005; Table 3) but no change in the controls. ANOVA also revealed significant time and interaction effects for A′, with post hoc analysis revealing a significant increase in the RT cohort (P < 0.0001) with no change in the controls. Finally, E/E′ also differed significantly with training between the groups (P < 0.05); a significant decrease evident as a result of RT (P < 0.01) but no change in controls. No significant time or training effects were evident for E wave velocity (Table 3), although A wave velocity decreased in the RT group (P < 0.05). No differences in transmitral measures were evident over time in the control subjects.
This is the first study, to our knowledge, to assess the impact of exercise training on measures of diastolic tissue velocities in obese young subjects. The principal finding is that an 8-wk period of resistance-based exercise training improved E′, whereas no such improvement was evident in the control group. This improvement in early diastolic tissue velocity in the RT group occurred independently of change in LV geometry, HR, transmitral flow (E), and in the presence of a decrease in E/E′, an indirect measure of left atrial pressure. Taken together, these findings suggest that the enhanced diastolic tissue velocity observed after resistance exercise training may be due to a change in intrinsic properties of the myocardial wall rather than simply changes in loading conditions.
Although no previous longitudinal studies have investigated the impact of exercise training on tissue Doppler measures of diastolic function in obese humans, Libonati (17) summarized evidence relating to the impact of exercise on diastolic function from the era preceding TDI and concluded that training improved diastolic function in healthy adults exhibiting physiological hypertrophy and reversed diastolic dysfunction in animal models of pathological hypertrophy. Indeed, diastolic function at rest may be enhanced in athletes (8,24), and two studies that used rapid infusion of saline and lower body negative pressure to modulate ventricular filling pressure whilst measuring SV in resting subjects (1,15), reported that both young and old endurance-trained athletes exhibited Frank-Starling curves, which were shifted upward and to the left relative to controls. The authors concluded that endurance training improves ventricular compliance. A more recent study, which observed lower LV filling pressures in subjects with higher V(dot)dot;O2max values during exercise at matched submaximal stroke volumes, also concluded that trained subjects possess superior diastolic function and compliance duringsubmaximal and maximal exercise (31). Although Vinereanu et al. (34) recently observed enhanced diastolic tissue Doppler velocities in adult endurance athletes, relative to a strength-trained group, this is the first study to our knowledge to use a longitudinal design to directly assess the impact of resistance exercise training on diastolic function in humans.
The mechanisms responsible for improvements in diastolic filling with RT are unknown, but previous animal studies suggest that exercise training reduces ventricular stiffness (40), an effect that may be related to changes in cardiac collagen content (5) or myocyte metabolism (28,33). Indeed, a recent study performed in rats indicated that high-intensity training reduced ventricular stiffness via an intrinsic effect, which was independent of neurohormones, HR, or pericardial restraint (18).
Another possible mechanistic explanation relates to the impact of RT on insulin resistance (13), a condition that is common in obese subjects. Holzmann et al. (12) reported that there is a continuous relationship between concentrations of fasting glucose, glycated hemoglobin, and LV diastolic function assessed by TDI (E′). The authors concluded that cardiac function is affected by, and related to, the concentrations of glucose and glycated hemoglobin, even below the threshold of diabetes. In a recent publication involving obese young subjects who undertook a circuit exercise training program of similar duration to that used in the present study, we reported insulin resistance in a population similar to the one in this study (2). We observed a significant improvement in insulin sensitivity using the euglycemic-hyperinsulinemic clamp technique (Mlbm = 8.20± 3.44 to 10.03 ± 4.33 mg·kg−1·min−1, P < 0.05). A possible beneficial effect of the RT exercise program used in the present study is further supported by the significant increase in skeletal muscle mass, a major disposal site of circulating blood glucose. Increasing muscle mass may therefore improve insulin sensitivity (13) and active myocardial relaxation, although this speculative mechanism requires further verification.
RT was associated with a significant increase in late diastolic filling peak velocity at the mitral septal annulus (A′). The explanation for this finding is unclear, but the enhanced intrinsic myocardial relaxation suggested by an increased E′, in the absence of changes in E and decrease in E/E′, may have contributed to an increased ventricular myocardial velocity after atrial systole. Further studies will be required to confirm and to further investigate this finding.
There are several important limitations of the present study. Due to the nature of the exercise training interventions used, the number of subjects in each group was relatively small and we cannot rule out the possibility of a chance statistical finding. However, we took care to blind the analysis of the echocardiographic studies; previously published studies of the impact of exercise training have used similar sample sizes, and we included a control group in whom no significant changes were evident. Finally, we did not collect repeated strength measures in the control group; however, given the finding that leg strength almost doubled in the trained subjects, we do not suspect this to have resulted purely from maturational change across the relatively short intervention period. There are, in fact, very few studies that have collected repeated measure of strength in inactive control groups over time, but one recent example (4) observed around two- to fivefold larger increases in upper and lower body strength in resistance-trained subjects relative to controls.
In summary, we observed significant improvements in diastolic tissue velocity as a result of resistance-type exercise training in young obese subjects. No such changes were observed in the control group. Overweight and obesity in childhood and adolescence are associated with insulin resistance (2) and, ultimately, the risk of cardiovascular mortality and morbidity in adulthood, regardless of the adult weight (20). Diastolic dysfunction is an important consequence of obesity and insulin resistance in adulthood, and resistance exercise training may potentially play an important role in preventing or slowing the progression of this phenomenon.
This research was supported by a grant from the National Heart Foundation of Australia.
The results of the present study do not constitute endorsement by ACSM.
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Keywords:©2008The American College of Sports Medicine
ECHOCARDIOGRAPHY; DIASTOLIC FUNCTION; TISSUE DOPPLER; EXERCISE