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Short-term Training Effects on Diastolic Function in Obese Persons With the Metabolic Syndrome Tracy Baynard1, Robert L. Carhart Jr2, Lori L. Ploutz-Snyder1, Ruth S. Weinstock2,3 and Jill A. Kanaley1 The aim of this study was to determine the effects of a short-term high-intensity exercise program on diastolic function and glucose tolerance in obese individuals with and without metabolic syndrome (MetSyn). Obese men and women (BMI > 30 kg/m2; 39–60 years) with and without the MetSyn (MetSyn 13; non-MetSyn 18) underwent exercise training consisting of 10 consecutive days of treadmill walking for 1 h/day at 70–75% of peak aerobic capacity. Subjects performed pre- and post-training testing for aerobic capacity, glucose tolerance (2-h meal test), and standard echocardiography. Aerobic capacity improved for both groups (non-MetSyn 24.0 ± 1.6 ml/kg/min vs. 25.1 ± 1.5 ml/kg/min; MetSyn 25.2 ± 1.8 ml/kg/min vs. 26.2 ± 1.7 ml/kg/min, P < 0.05). Glucose area under the curve (AUC) improved in the MetSyn group (1,017 ± 58 pmol/l/min vs. 883 ± 75 pmol/l/min, P < 0.05) with no change for the non-MetSyn group (685 ± 54 pmol/l/min vs. 695 ± 70 pmol/l/min). Isovolumic relaxation time (IVRT) improved in the MetSyn group (97 ± 6 ms vs. 80 ± 5 ms, P < 0.05), and remained normal in the non-MetSyn group (82 ± 6 ms vs. 86 ± 5 ms). No changes in other diastolic parameters were observed. The overall reduction in IVRT was correlated with a decrease in diastolic blood pressure (DBP) (r = 0.45, P < 0.05), but not with changes in glucose tolerance. Body weight did not change with training in either group. A 10-day high-intensity exercise program improved diastolic function and glucose tolerance in the group with MetSyn. The reduction in IVRT in MetSyn was associated with a fall in blood pressure. These data suggest that it may be possible to reverse early parameters of diastolic dysfunction in MetSyn with a high-intensity exercise program. Obesity (2008) 16, 1277–1283. doi:10.1038/oby.2008.212

Introduction

Diastolic impairment can frequently be observed before systolic dysfunction is evident (1–3). Obesity is a condition associated with the development of diastolic dysfunction in the absence of evidence of systolic dysfunction (4). Metabolic syndrome (MetSyn), common in obesity, is defined by a clustering of cardiovascular risk factors (e.g., central obesity, dyslipidemia, hypertension, and impaired glucose tolerance) associated with greater morbidity and mortality when compared to their nonMetSyn counterparts (5). Those with MetSyn are projected to be at five times greater risk for developing type 2 diabetes and at three times greater risk for having a myocardial infarction than individuals without MetSyn (5). It has been estimated that ~27% of the US population has MetSyn (6,7). There are few studies specifically examining diastolic function and MetSyn, and no reports of the effects of an intense exercise program on diastolic function in this high-risk group. Obesity is associated with low exercise tolerance, and in the presence of diastolic dysfunction exercise tolerance is further

decreased (8). This suggests that exercise training may be a useful nonpharmacologic method to improve diastolic function. One recent study (9) reported improvements in diastolic function in a group of hypertensive individuals following a 6-month training period. These authors report that diastolic improvements were related to reductions in abdominal fat, insulin resistance, and blood pressure (9), suggesting improvements in diastolic function are related to enhanced glucose metabolism. It is also possible that changes in cardiac wall tension related to lower blood pressure contributed to improved diastolic function. Several studies have demonstrated improved glucose tolerance after a short-term (7–10 days) training period (10–12). This exercise training model is important in that the beneficial effects of the exercise on glucose tolerance are observed in the absence of weight loss. Although cardiac structure would not be expected to change during a short-term training program, it is possible that positive changes in cardiac function could be measured.

1 Department of Exercise Science, Syracuse University, Syracuse, New York, USA; 2Department of Medicine, SUNY Upstate Medical University, Syracuse, New York, USA; 3Department of Veterans Affairs Medical Center, Syracuse, New York, USA. Correspondence: Tracy Baynard ([email protected])

Received 18 July 2007; accepted 16 February 2008; published online 3 April 2008. doi:10.1038/oby.2008.212 obesity | VOLUME 16 NUMBER 6 | JUNE 2008

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articles integrative physiology The aim of this study was to determine the effects of a shortterm exercise training protocol (10 days) on measures of diastolic function in obese individuals with and without MetSyn. The secondary aim was to determine the relationship between observed changes in glucose tolerance and diastolic function. We hypothesized that short-term training would not alter cardiac structure, but that it would improve diastolic function, and that improved glucose tolerance would be positively related to changes in diastolic function. Methods and procedures Subjects Thirty-one obese men and women aged between 39 and 60 years volunteered to participate in this study. Participants were defined as having MetSyn and non-MetSyn according to the criteria of the International Diabetes Federation (13). This criteria was selected prior to subject recruitment because of its ethnic-specific values and that this criteria requires central obesity for classification. MetSyn subjects had central obesity (waist circumference ≥94 cm for men and ≥80 cm for women; ethnic-specific values exist for non-Europids). Subjects also ­exhibited two of the following four conditions: elevated triglyceride levels (≥150 mg/dl), reduced high-density lipoprotein-cholesterol (110 mm Hg were excluded. Each subject signed an informed consent. This study was approved by the Institutional Review Board in compliance with the Department of Health and Human Services Regulations for the Protection of Human Research Subjects. Design Subjects underwent pre- and post-training evaluations for glucose tolerance and myocardial function. Glucose tolerance was assessed using a 2-h meal test, with blood samples for glucose and insulin levels obtained once every 0.5 h for 2 h. Myocardial function was assessed following an overnight fast using standard echocardiography and was performed prior to training and within 12–24 h of the last exercise session. Exercise training consisted of walking on a treadmill at 70–75% of peak aerobic capacity for 1 h/day for 10 consecutive days. Body composition and anthropometric measures Total percent body fat and fat-free mass was determined by air displacement plethysmography using the BOD POD (Life Measurements Instruments, Concord, CA). This method is highly reliable and valid, as it is correlated highly with hydrostatic weighing (r = 0.96) (ref. 14). In addition, both waist and hip circumferences were measured. Maximal exercise testing Peak aerobic capacity (VO2peak ) was assessed on a motorized treadmill using a continuous walking protocol (15). Treadmill speed began at 2.5 mph and 0% grade. Every 2 min velocity increased by 0.5 mph until 3.5 mph was reached. After this point, treadmill speed was maintained at 3.5 mph and percent grade increased by 2% every 1278

Table 1 Descriptive characteristics Nonmetabolic syndrome (n = 18)

Metabolic syndrome (n = 13)

Age (years)

52 ± 1

52 ± 1

Height (cm)

169.2 ± 2.5

170.6 ± 2.5

Weight (kg)

93.3 ± 5.1

104.5 ± 5.6

BMI (kg/m )

33.0 ± 1.1

35.5 ± 1.6

Body fat (%)

39.6 ± 2.1

39.6 ± 2.3

2

HbA1c (%)

5.2 ± 0.06

Waist (cm)

5.9 ± 0.25*

104.8 ± 2.8

112.2 ± 4.4

Triglyceride (mg/dl)

96 ± 8

208 ± 34*

HDL (mg/dl)

53 ± 4

38 ± 4*

4.7 ± 0.1

5.7 ± 0.5*

Glucose (mmol/l)

HbA1c, hemoglobin A1c; HDL, high-density lipoprotein. *P < 0.05, between group difference.

Table 2  Medications by group Nonmetabolic syndrome

Metabolic syndrome

  Statins

3

5

  Ezetimibe

0

1

  Metformin

0

4

  Sulfonylurea

0

2

  HCTZ

1

1

  ACE-I

0

3

  Angiotensin   II–receptor blocker

1

1

Antidepressants

2

3

Other medications

11

10

No medications

8

2

Medication type Lipid lowering

Glucose lowering

Antihypertensive

ACE-I, angiotensin converting enzyme inhibitor; HCTZ, hydrochlorothiazide.

2 min until volitional fatigue was reached. Metabolic ­measurements were obtained using a calibrated Cosmed Quark b2 metabolic breath-by-breath system (Cosmed, Rome, Italy). Heart rate was monitored and recorded using a 12-lead electrocardiogram. Rating of perceived exertion (16) and blood pressure was collected at the end of each 2-min stage. Peak effort was defined as achieving two of the following criteria: (i) rating of perceived exertion ≥17, (ii) an increase in oxygen uptake (VO2) of 16, the speed and/or grade of the treadmill was decreased slightly to ensure completion of the full hour. obesity | VOLUME 16 NUMBER 6 | JUNE 2008

Statistical analyses Descriptive characteristics were calculated and independent t-tests were used to determine whether any group differences existed at baseline. All cardiac measures, glucose tolerance, and peak cardiopulmonary data were compared pre- and post-training with a mixed-model two-way ANOVA with repeated measures (group (2) × time (2)). Post hoc analyses were performed if significant interactions were observed. Pearson correlations were calculated to determine whether a relationship exists between changes in cardiac function and changes in aerobic capacity and/or glucose tolerance. Data are presented as the mean ± s.e. Statistical significance was set at P < 0.05. SPSS (v.14) was used for statistical analyses (SPSS, Chicago, IL). Results

The groups were similar for age, height, weight, percent body fat, and waist circumference (Table 1). Group differences were observed for other baseline descriptive characteristics, with the MetSyn group having higher hemoglobin A1c, triglyceride, and fasting glucose concentrations, and lower high-density lipoprotein-cholesterol levels (P < 0.05) (Table 1). Body weight did not change with training (Table 3). Exercise training effects were observed for VO2peak, VEpeak, and maximal treadmill test time (P < 0.05), while maximal heart rate was not altered with training (Table 3). Glucose tolerance

Glucose area under the curve (AUC) was greater in the MetSyn group (P < 0.01) and exercise training elicited a group– by-training interaction (P < 0.05) (Figure 1a). The MetSyn group improved their glucose AUC with short-term ­training, whereas the non-MetSyn group did not change. Figure 1b depicts the glucose results from the 2-h meal test. The MetSyn group had higher glucose values at each time point of the meal test vs. the non-MetSyn group (P < 0.05). The non-MetSyn group had a normal glucose response to the challenge with glucose levels returning to baseline by 120 min. Short-term training yielded improvements in the glucose response to the meal test at the 90- and 120-min test points in those with MetSyn (P < 0.05). Insulin concentrations during the meal test are shown in Figure 2. Fasting insulin levels were greater in the  MetSyn Table 3 Peak cardiopulmonary data and weight pre- and post-training Nonmetabolic syndrome VO2peak (ml/kg/min)* VO2 (ml/min)*

Metabolic syndrome

Pre

Post

Pre

Post

24.0 ± 1.6

25.1 ± 1.5

25.2 ± 1.8

26.2 ± 1.7

2,289 ± 196 2,380 ± 187 2,529 ± 221 2,670 ± 211

HRpeak (bpm)

170 ± 3

VEpeak (l/min)*

83.8 ± 6.0

Test time (min)*

14.1 ± 0.6

Weight (kg)

93.3 ± 5.1

169 ± 3

167 ± 3

165 ± 4

92.3 ± 6.1

93.5 ± 6.8

98.5 ± 6.9

14.8 ± 0.6

14.0 ± 0.7

14.7 ± 0.7

92.9 ± 5.1 104.5 ± 5.6

104.7 ± 5.6

No group differences observed for any variable. HRpeak, peak heart rate (beats per min); test time, peak treadmill test time; VEpeak, peak minute ventilation; VO2peak, peak aerobic capacity. *Significant exercise effect; P < 0.05. 1279

articles integrative physiology a

Table 4 Cardiac structure measurements

Glucose AUC (mmol/l × min)

1,200

Nonmetabolic syndrome

1,000

MetSyn Non-MetSyn

800 600

b

Pre

Post

12

*

Glucose (mmol/l)

10

MetSyn pre

6

1.00 ± 0.03

1.13 ± 0.05*

1.18 ± 0.04*

1.02 ± 0.05

1.08 ± 0.05

1.15 ± 0.06

1.14 ± 0.06

LVIDs (cm)

2.98 ± 0.15

2.91 ± 0.14

2.89 ± 0.19

2.99 ± 0.18

0

30

60

90

120

700

*

600 500

MetSyn-pre

400

MetSyn-post

300

Non-MetSyn pre Non-MetSyn post

*

100 0

30

60 Time (min)

90

34 ± 3

30 ± 3

36 ± 4

38 ± 4

Table 5 Diastolic function measurements Nonmetabolic syndrome E (ms)

Figure 1  (a) Glucose area under the curve (AUC) was greater in the metabolic syndrome (MetSyn) group (P < 0.01) and exercise training elicited a group-by-training interaction (*P < 0.05). (b) The MetSyn group had higher glucose values at each time point of the meal test vs. the non-MetSyn group (P < 0.05) and training yielded improvements in the glucose response to the meal test at the 90- and 120-min test points in those with MetSyn (*P < 0.05).

Insulin (pmol/l)

0.93 ± 0.04

LVPW (cm)

Non-MetSyn post

Time (min)

120

Figure 2  A group-by-training effect was observed for fasting insulin and the response to the meal test. Group differences were observed for fasting insulin concentrations and insulin levels the 90-min time point (*P < 0.05). MetSyn, metabolic syndrome.

group than the non-MetSyn group (P < 0.05), and a ­group-by-training effect was also observed at this time point (P < 0.05). In the MetSyn group, training elicited a decrease in fasting insulin (56 ± 12 pmol/l vs. 30 ± 4 pmol/l; P < 0.01), whereas no change in fasting insulin was observed in the nonMetSyn group after the training period (18 ± 11 pmol/l vs. 22 ± 4 pmol/l). In response to the meal test, insulin levels increased and did not return to baseline by 120 min for either group, and only significantly differed by group at 90 min (P < 0.05). The MetSyn had lower insulin concentrations at 90 min (P < 0.01) with no change in the non-MetSyn group. While the 120-min time point appears to demonstrate a similar pattern, the group by training interaction was not significant (P = 0.064). Changes in insulin AUC pre- and post-exercise were not significant (MetSyn 48,097 ± 8,095 pmol/l vs. 34,423 ± 4,113 pmol/l × min; non-MetSyn 30,605 ± 7,820 vs. 31,546 ± 3,974 pmol/l × min; 1280

IVSD (cm)

Non-MetSyn pre

2

0

Post

MetSyn post

4

200

Pre

No group differences or interactions for LVPW, LVIDs, or FS. FS, fractional shortening; IVSD, intraventricular septal diameter; LVIDs, left ­ventricular internal diameters (systole); LVPW, left ventricular posterior wall thickness. *P < 0.001, between group differences.

*

8

0

Post

FS (%)

400

Metabolic syndrome

Pre

*

Metabolic syndrome

Pre

Post

Pre

82.6 ± 4.0

77.2 ± 3.6

79.3 ± 5.4

77.4 ± 4.9

Post

A (ms)

67.8 ± 3.7

64.8 ± 3.9

71.8 ± 5.0

72.4 ± 5.4

E/A

1.27 ± 0.07

1.23 ± 0.06

1.14 ± 0.10

1.10 ± 0.08

82 ± 6

86 ± 5

97 ± 6*

80 ± 5**

IVRT (ms)

A, late transmitral velocity; E, early transmitral velocity; E/A, ratio of E to A velocities; IVRT, isovolumic relaxation time. *Group with metabolic syndrome had a longer IVRT pre-training compared to the obese nonmetabolic syndrome group (P < 0.05). **Significant group by exercise interaction (P = 0.01), with the group with metabolic syndrome having a decrease in IVRT with short-term training. No group differences or interactions observed for E, A, or E/A.

P = 0.074). Group differences were observed for insulin resistance (MetSyn 0.372 ± 0.013, P < 0.01 vs. non-MetSyn 0.434 ± 0.012), but there were no significant changes after training. Cardiac structure

The MetSyn group had a greater overall intraventricular septal diameter vs. the non-MetSyn group (P < 0.001), however intraventricular septal diameter did not change with training (Table 4). Neither group differences nor exercise training effects were observed for any other measure of cardiac structure or fractional shortening, which is used a global indicator of systolic function (Table 4). Diastolic function

No group differences or interactions were observed for E, A, or E/A. A group by exercise interaction was observed for IVRT (P = 0.01) (Table 5). IVRT was longer for the MetSyn group prior to exercise training, and training shortened IVRT in this group. Group differences were observed for both resting SBP and diastolic blood pressure (DBP) prior to training (SBP and DBP) (MetSyn 124/77 ± 2/1 mm Hg vs. non-MetSyn 116/73 ± 2/1 mm Hg, P < 0.05). An exercise training effect was found for overall DBP (pre-training 77 ± 1 mm Hg vs. post-training 74 ± 1 mm Hg, P < 0.01). The change in DBP was correlated with the change in IVRT (r = 0.45, P < 0.05). No group  × training interactions were observed for either SBP or DBP ­(post-training: MetSyn 124/74 ± 2/1 mm Hg vs. non-MetSyn 114/67 ± 2/1 mm Hg). VOLUME 16 NUMBER 6 | JUNE 2008 | www.obesityjournal.org

articles integrative physiology Correlation between glucose tolerance and diastolic function

The change in IVRT was not significantly correlated with any change in aerobic fitness or glucose tolerance (data not shown). The reduction in the glucose concentrations pre- to post-training at the 2-h time point correlated with improved aerobic capacity (relative) (r = 0.60, P = 0.004). To note, separate analyses with removal of the four subjects with type 2 diabetes did not alter the initial significant findings for aerobic capacity, glucose tolerance, and IVRT. Discussion

To our knowledge, this is the first study investigating diastolic function in response to short-term intense exercise in obese individuals with MetSyn. Our 10-day training program resulted in a 17.5% decrease in IVRT in the MetSyn group which was related to a small (4%) reduction in DBP. These observations were not directly related to changes in glucose tolerance or insulin resistance. Previous studies have demonstrated that short (2 week) exercise training improves blood pressure (20). Our results further demonstrate, by measuring IVRT, that the ability of the heart to begin the diastolic filling phase rapidly can be enhanced by 10 days of exercise in MetSyn in the absence of weight loss, which demonstrates an independent effect of exercise. Previous studies have examined the effects of longer training periods on cardiac function (9,21–23). A recent report (9) showed that individuals who experienced the greatest improvements in physical fitness, reductions in abdominal fatness, and insulin resistance after a 6-month exercise training program also experienced improved LV diastolic function. These authors did not correlate physical fitness, abdominal fat, or insulin resistance with IVRT (9). They suggested that abdominal obesity may not directly cause diastolic dysfunction, but rather the decrease in abdominal obesity accompanied increased fitness and decreased blood pressure, both of which improve diastolic function. This study supports this concept because no changes in body weight were found, yet diastolic function did improve in the MetSyn group. Although aerobic capacity was improved overall in both groups, it was not associated with the improvement in IVRT. This implies that larger improvements in aerobic capacity may be necessary to demonstrate improvement in IVRT (and/or other measures of diastolic function such as E, A, and E/A), especially given that the fitness improvements observed in this study were ~5% and not 10–15% often found in traditional training studies. An overall training effect was found for both SBP and DBP, and the change in DBP was correlated with the change in IVRT (r = 0.45, P = 0.042). Individuals with the larger changes in diastolic pressure also had larger changes in IVRT (correlation between change in IVRT and DBP for MetSyn group: r = 0.79, P = 0.017). Despite the small sample size in this study, our results suggest that changes in cardiac function occur early in a training program in individuals with MetSyn. This rapid change in diastolic function may be attributed, in part, to poorer baseline cardiac health status in those with MetSyn compared with the non-MetSyn group. obesity | VOLUME 16 NUMBER 6 | JUNE 2008

The improvements in blood pressure may mediate the  change observed in diastolic function. Müller-Brunotte et  al.  (24) found that blood pressure could explain 20% of the variance associated with IVRT. We also observed that the change in DBP explained ~20% of the variance in IVRT (r = 0.45, r2 = 0.20). This relationship may be related to changes in wall ­tension (25,26). Elevated BP is associated with increased wall tension which makes it more difficult for the heart to relax (27). Our findings are consistent with this concept in that the change in BP was related to the change in IVRT. One recent study has examined the effect of short-term training (5 days of high-intensity cycling) on LV diastolic function in young and old men (28). Harris et al. (28) found that although aerobic capacity did not change for either group, early filling (E) was improved in the elderly group after the training period, yet they did not measure IVRT. Their results support the concept that improvements can occur in selected (but not all) measures of LV diastolic function with high-intensity training in individual groups. Improved glucose tolerance (i.e., reduced glucose AUC, fasting insulin level) was not associated with the change in IVRT as we hypothesized. Several studies indicate that chronic hyperglycemia and metabolic abnormalities associated with insulin resistance can cause altered myocardial function (29–32). It is possible the improvements for glucose tolerance observed in this study were not large enough or that the meal test was not sensitive enough to detect large changes that might be observed using the more sensitive clamp techniques. Furthermore, shortterm training may not have a large impact myocardial function and only long-term changes in glucose tolerance are capable of eliciting change. It is also possible that more time is necessary for metabolic changes to alter myocardial function. There are very few studies on diastolic function in individuals with impaired glucose tolerance or in individuals with MetSyn, while there are numerous studies showing patients with type 2 diabetes exhibiting diastolic dysfunction (1–3,33,34). The literature is also somewhat mixed regarding improvements in glycemic control and cardiac function. Two studies found that improved glycemic control was associated with improved cardiac function (35–37), via dietary intervention or insulin treatment, however it is unknown whether these findings are related to decreased body weight, as the authors do report changes in weight. Conversely, two studies have demonstrated that improvements in glycemic control in newly diagnosed individuals with type 2 diabetes are not associated with increased diastolic function (34,38). Beljic and Miric (34) administered 6 months of drug therapy and found that diastolic function did not improve after 1 year of good glycemic control. Gough et al. (38) reported that 6 months of dietary therapy did not result in improvements in diastolic function despite improvement in hemoglobin A1c (~3%). These disparate findings indicate that more work is needed. Our study adds to the literature, as no other study to date has investigated the effect of exercise training in participants with MetSyn and it effects on concomitant changes in glucose control and diastolic function. Additionally, this study is important because the independent 1281

articles integrative physiology effects of exercise on diastolic function were evaluated without the confounder of weight loss. As expected, IVRT did not change with training in the nonMetSyn group because their values were well within the normal range for their age (39), indicating that these obese individuals did not exhibit any diastolic impairment as measured by echocardiography. Pascual et al. (40) reported IVRT did not differ among varying levels of obesity (mild to severe) and a non-obese control group, although MetSyn was not specifically analyzed. In contrast, earlier data suggest even uncomplicated obesity, particularly higher degrees of obesity, is associated with diastolic dysfunction (4,40–43), however some of these studies employed different technology (e.g., tissue Doppler, ultrasonic integrated backscatter) to assess cardiac function, which may be more sensitive to small differences in this population. No changes in cardiac structure were observed with training in our study. This was not unexpected considering longer training studies have not consistently demonstrated changes in cardiac structure. Stewart et al. (9) reported no change in cardiac structure with a 6-month training program in a group of hypertensives, however they noted a slight increase in LV mass index in those individuals who exhibited the largest reductions in fat mass. Likewise, Park et al. (44) found no change in cardiac structure or function with a 6-month training protocol in elderly women. Furthermore, alterations in cardiac structure are commonly found in elite athletes who train for many years at high intensities (45). Therefore, our findings in conjunction with earlier reports imply that long-term training, most likely >1 year, is necessary for cardiac changes, particularly in obese, hypertensives, or older individuals. Strengths/limitations

One of the strengths of this study was that 98% compliance was achieved with the training sessions. Additionally, the full hour of exercise was able to be completed 98% of the time, and no subject had any exercise-related musculoskeletal discomfort or injuries during the training period. Finally, a meal test was employed to assess glucose tolerance to mimic true physiological conditions. Limitations include a relatively small sample size. Further, our participants were prescreened for heart disease so our subjects had relatively normal echocardiography measurements, restricting the opportunity to observe significant change. It is also possible that the medications the subjects were on may have influenced the results. However, we attempted to “minimize” these effects by having the subjects take the same medication and dose at the same time of day both pre- and post-testing. While medications may be viewed as a limitation, we feel it is a strength because of the ability to examine these effects under our subjects’ “normal” circumstances. Finally, it is important to note that diastolic function is generally best measured using multiple parameters. IVRT alone is not a complete or ideal marker of diastolic function and we did not find any significant change in additional diastolic measures. Furthermore, all of our diastolic measures were load-dependent and load was not controlled. Thus, our results need to be interpreted with 1282

caution. Other techniques such as tissue Doppler, which is load-independent, in conjunction with traditional echocardiography will be necessary to further our findings. In conclusion, a 10-day high-intensity training program results in improvements in diastolic function (IVRT), DBP, aerobic capacity, and glucose tolerance in obese individuals with MetSyn. These data indicate it may be possible to reverse early diastolic dysfunction with exercise in this group with high risk for significant cardiovascular disease. Acknowledgments We extend our gratitude to Mrs Marty Lange for her technical expertise. This work was supported by the following grants: Sigma Delta Epsilon—Graduate Women in Science, Mid-Atlantic Regional Chapter of the American College of Sports Medicine, Syracuse University, National Institutes of Health—R21 DK063179 (to J.A.K.).

disclosure The authors declared no conflict of interest. © 2008 The Obesity Society

References 1. Celentano A, Vaccaro O, Tammaro P et al. Early abnormalities of cardiac function in non-insulin-dependent diabetes mellitus and impaired glucose tolerance. Am J Cardiol 1995;76:1173–1176. 2. Galderisi M, Anderson KM, Wilson PW, Levy D. Echocardiographic evidence for the existence of a distinct diabetic cardiomyopathy (the Framingham Heart Study). Am J Cardiol 1991;68:85–89. 3. Raev DC. Which left ventricular function is impaired earlier in the evolution of diabetic cardiomyopathy? An echocardiographic study of young type I diabetic patients. Diabetes Care 1994;17:633–639. 4. Wong CY, O’Moore-Sullivan T, Leano R et al. Alterations of left ventricular myocardial characteristics associated with obesity. Circulation 2004; 110:3081–3087. 5. Isomaa B, Almgren P, Tuomi T et al. Cardiovascular morbidity and mortality associated with the metabolic syndrome. Diabetes Care 2001;24:683–689. 6. Ford ES, Giles WH, Mokdad AH. Increasing prevalence of the metabolic syndrome among U.S. adults. Diabetes Care 2004;27:2444–2449. 7. Ford ES, Giles WH, Dietz WH. Prevalence of the metabolic syndrome among US adults: findings from the third National Health and Nutrition Examination Survey. JAMA 2002;287:356–359. 8. Poirier P, Garneau C, Bogaty P et al. Impact of left ventricular diastolic dysfunction on maximal treadmill performance in normotensive subjects with well-controlled type 2 diabetes mellitus. Am J Cardiol 2000;85:473–477. 9. Stewart KJ, Ouyang P, Bacher AC, Lima S, Shapiro EP. Exercise effects on cardiac size and left ventricular diastolic function: relationships to changes in fitness, fatness, blood pressure and insulin resistance. Heart 2006;92:893–898. 10. Brown MD, Moore GE, Korytkowski MT, McCole SD, Hagberg JM. Improvement of insulin sensitivity by short-term exercise training in hypertensive African American women. Hypertension 1997;30:1549–1553. 11. Cononie CC, Goldberg AP, Rogus E, Hagberg JM. Seven consecutive days of exercise lowers plasma insulin responses to an oral glucose challenge in sedentary elderly. J Am Geriatr Soc 1994;42:394–398. 12. Rogers MA, Yamamoto C, King DS et al. Improvement in glucose tolerance after 1 wk of exercise in patients with mild NIDDM. Diabetes Care 1988; 11:613–618. 13. Alberti KG, Zimmet P, Shaw J. Metabolic syndrome—a new world-wide definition. A Consensus Statement from the International Diabetes Federation. Diabet Med 2006;23:469–480. 14. McCrory MA, Gomez TD, Bernauer EM, Mole PA. Evaluation of a new air displacement plethysmograph for measuring human body composition. Med Sci Sports Exerc 1995;27:1686–1691. 15. Kanaley JA, Giannopoulou I, Tillapaugh-Fay G, Nappi JS, Ploutz-Snyder LL. Racial differences in subcutaneous and visceral fat distribution in postmenopausal black and white women. Metabolism 2003;52:186–191. 16. Scarpello JH, Martin TR, Ward JD. Ultrasound measurements of pulsewave velocity in the peripheral arteries of diabetic subjects. Clin Sci (Lond) 1980;58:53–57. VOLUME 16 NUMBER 6 | JUNE 2008 | www.obesityjournal.org

articles integrative physiology 17. Teicholz L, Kreulen T, Herman M, Gorlin R. Problems in echocardiographic volume determinations: echocardiographic-angiographic correlations in the presence or absence of asynergy. Am J Cardiol 1976;37:7–11. 18. Appleton CP, Jensen JL, Hatle LK, Oh JK. Doppler evaluation of left and right ventricular diastolic function: a technical guide for obtaining optimal flow velocity recordings. J Am Soc Echocardiogr 1997;10:271–292. 19. Katz A, Nambi SS, Mather K et al. Quantitative insulin sensitivity check index: a simple, accurate method for assessing insulin sensitivity in humans. J Clin Endocrinol Metab 2000;85:2402–2410. 20. Kokkinos PF, Narayan P, Papademetriou V. Exercise as hypertension therapy. Cardiol Clin 2001;19:507–516. 21. Myers J, Wagner D, Schertler T et al. Effects of exercise training on left ventricular volumes and function in patients with nonischemic cardiomyopathy: application of magnetic resonance myocardial tagging. Am Heart J 2002;144:719–725. 22. Obert P, Mandigout S, Vinet A et al. Effect of aerobic training and detraining on left ventricular dimensions and diastolic function in prepubertal boys and girls. Int J Sports Med 2001;22:90–96. 23. Rodrigues AC, de Melo Costa J, Alves GB et al. Left ventricular function after exercise training in young men. Am J Cardiol 2006;97:1089–1092. 24. Müller-Brunotte R, Kahan T, Malmqvist K, Edner M; Swedish ibesartan left ventricular hypertrophy investigation vs atenolol (SILVHIA). Blood pressure and left ventricular geometric pattern determine diastolic function in hypertensive myocardial hypertrophy. J Hum Hypertens 2003;17:841–849. 25. Galderisi M, Petrocelli A, Alfieri A, Garofalo M, de Divitiis O. Impact of ambulatory blood pressure on left ventricular diastolic dysfunction in uncom­ plicated arterial systemic hypertension. Am J Cardiol 1996;77:597–601. 26. von Spiegel T, Wietasch G, Hoeft A. Basics of myocardial pump function. Thorac Cardiovasc Surg 1998;46(Suppl 2):237–241. 27. Ludbrook PA, Byrne JD, Kurnik PB, McKnight RC. Influence of reduction of preload and afterload by nitroglycerin on left ventricular diastolic pressurevolume relations and relaxation in man. Circulation 1977;56:937–943. 28. Harris SK, Petrella RJ, Overend TJ, Paterson DH, Cunningham DA. Shortterm training effects on left ventricular diastolic function and oxygen uptake in older and younger men. Clin J Sport Med 2003;13:245–251. 29. Rodrigues B, Cam MC, McNeill JH. Metabolic disturbances in diabetic cardiomyopathy. Mol Cell Biochem 1998;180:53–57. 30. Taegtmeyer H, McNulty P, Young ME. Adaptation and maladaptation of the heart in diabetes: Part I: general concepts. Circulation 2002;105:1727–1733. 31. Jain A, Avendano G, Dharamsey S et al. Left ventricular diastolic function in hypertension and role of plasma glucose and insulin. Comparison with diabetic heart. Circulation 1996;93:1396–1402.

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32. Sasso FC, Carbonara O, Cozzolino D et al. Effects of insulin-glucose infusion on left ventricular function at rest and during dynamic exercise in healthy subjects and noninsulin dependent diabetic patients: a radionuclide ventriculographic study. J Am Coll Cardiol 2000;36:219–226. 33. Astorri E, Fiorina P, Gavaruzzi G, Astorri A, Magnati G. Left ventricular function in insulin-dependent and in non-insulin-dependent diabetic patients: radionuclide assessment. Cardiology 1997;88:152–155. 34. Beljic T, Miric M. Improved metabolic control does not reverse left ventricular filling abnormalities in newly diagnosed non-insulin-dependent diabetes patients. Acta Diabetol 1994;31:147–150. 35. Hiramatsu K, Ohara N, Shigematsu S et al. Left ventricular filling abnormalities in non-insulin-dependent diabetes mellitus and improvement by a short-term glycemic control. Am J Cardiol 1992;70:1185–1189. 36. Uusitupa M, Mustonen J, Laakso M et al. Impairment of diastolic function in middle-aged type 1 (insulin-dependent) and type 2 (non-insulin-dependent) diabetic patients free of cardiovascular disease. Diabetologia 1988;31: 783–791. 37. Uusitupa M, Siitonen O, Aro A, Korhonen T, Pyorala K. Effect of correction of hyperglycemia on left ventricular function in non-insulin-dependent (type 2) diabetics. Acta Med Scand 1983;213:363–368. 38. Gough SC, Smyllie J, Barker M et al. Diastolic dysfunction is not related to changes in glycaemic control over 6 months in type 2 (non-insulindependent) diabetes mellitus. A cross-sectional study. Acta Diabetol 1995;32:110–115. 39. Otto CM. Textbook of Clinical Echocardiography, 3rd edn. W.B. Saunders: Philadelphia, PA, 2004. 40. Pascual M, Pascual DA, Soria F et al. Effects of isolated obesity on systolic and diastolic left ventricular function. Heart 2003;89:1152–1156. 41. Scaglione R, Dichiara MA, Indovina A et al. Left ventricular diastolic and systolic function in normotensive obese subjects: influence of degree and duration of obesity. Eur Heart J 1992;13:738–742. 42. Zarich SW, Kowalchuk GJ, McGuire MP et al. Left ventricular filling abnormalities in asymptomatic morbid obesity. Am J Cardiol 1991;68: 377–381. 43. Chakko S. Obesity and Ventricular Function in Man: Diastolic Function. Armonk: New York, 1998, pp 57–76. 44. Park SK, Park JH, Kwon YC, Yoon MS, Kim CS. The effect of long-term aerobic exercise on maximal oxygen consumption, left ventricular function and serum lipids in elderly women. J Physiol Anthropol Appl Human Sci 2003;22:11–17. 45. Fagard RH. Impact of different sports and training on cardiac structure and function. Cardiol Clin 1997;15:397–412.

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