Exercise and the metabolic syndrome with weight regain

Department of Nutrition and Exercise Physiology, University of Missouri, Columbia, MO 65211, USA.
Journal of Applied Physiology (Impact Factor: 3.43). 02/2010; 109(1):3-10. DOI: 10.1152/japplphysiol.01361.2009
Source: PubMed

ABSTRACT Weight loss improves metabolic syndrome (MetS) factors, but risk may return with weight regain. This study was designed to determine if exercise training can maintain improvements in MetS risk factors during weight regain. In a randomized control trial,102 overweight or obese (body mass index 25.0-39.9 kg/m(2)) men and women (age 21-52 yr), with characteristics of the MetS, lost 10% of body weight with supervised walking/jogging at 60% of maximal oxygen consumption (Vo(2 max)) (-400 kcal/session), 5 days/wk, and caloric restriction (-600 kcal/day) over a 4- to 6-mo period. After weight loss, 77 remaining subjects underwent programmed weight regain (+50% of lost weight) for 4-6 mo with random assignment to two groups: no exercise (NoEX) or continued supervised exercise (EX). Blood pressure, regional fat, glucose homeostasis, lipids, and inflammatory markers were assessed at baseline, post-weight loss, and post-weight regain. Groups were compared by two-way repeated-measures ANOVA on the 67 subjects. After weight loss (9.7 +/- 0.2% of body weight), significant (P < 0.05) improvements were observed in almost all parameters assessed. Following weight regain (54.4 +/- 1.6% of lost weight), the NoEX group exhibited deterioration in most metabolic markers, while the EX group maintained improvements in Vo(2 max), blood pressures, glucose homeostasis, high- and low-density lipoprotein cholesterol (HDL-C and LDL-C), oxidized LDL, and other markers of inflammation, but did not maintain improvements in triglyceride and cholesterol concentrations or abdominal fat. Results of this design of controlled human weight regain suggest that aerobic exercise can counter the detrimental effects of partial weight regain on many markers of disease risk.

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    • "Weight gain and obesity can have many negative health implications. Not only does it result in increased visceral or WAT but is associated with impaired glucose regulation (Thomas et al. 2010) and increased systemic inflammation . Visceral adiposity has been associated both with impaired peripheral insulin sensitivity (Kelley et al. 2000; Miyazaki et al. 2002) and adipose and hepatic insulin resistance (IR; Miyazaki et al. 2002). "
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    ABSTRACT: As white adipose tissue (WAT) expands under obesogenic conditions, local WAT hypoxia may contribute to the chronic low-grade inflammation observed in obesity. Aerobic exercise training is beneficial in treating WAT inflammation after obesity is established, but it remains unknown whether exercise training, while on a concomitant high-fat (HF) diet, influences WAT inflammation during the development of obesity. We sought to determine the effects of 4, 8, and 12 weeks of HF feeding and/or moderate intensity treadmill exercise training (EX) on the relationship between inflammatory and hypoxic gene expression within mouse WAT. Male C57Bl6/J mice (n = 113) were randomized into low-fat (LF)/sedentary (SED), LF/EX, HF/SED, or HF/EX groups. The low-fat and high-fat diets contained 10% and 60% energy from fat, respectively. Exercise training consisted of treadmill running 5 days/week at 12 m/min, 8% incline, 40 min/day. Quantitative real-time PCR was used to assess gene expression. HF diet impaired glucose regulation, and upregulated WAT gene expression of inflammation (IL-1β, IL-1ra, TNFα), macrophage recruitment and infiltration (F4/80 and monocyte chemoattractant protein), and M1 (CD11c) and M2 (CD206 and Arginase-1) macrophage polarization markers. Treadmill training resulted in a modest reduction of WAT macrophage and inflammatory gene expression. HF diet had little effect on hypoxia-inducible factor-1α and vascular endothelial growth factor, suggesting that WAT inflammatory gene expression may not be driven by hypoxia within the adipocytes. Treadmill training may provide protection by preventing WAT expansion and macrophage recruitment.
    07/2014; 2(7). DOI:10.14814/phy2.12071
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    • "This study, which is the first to examine changes in bone mass and turnover during carefully controlled weight regain, found that weight-loss-induced perturbations in bone mass and turnover persisted after partial weight regain, regardless of whether regular, weight-bearing aerobic exercise was continued. However, it is important to note that continuation of aerobic exercise countered the detrimental effects of partial weight regain on many markers of the metabolic syndrome, as previously reported (Thomas et al. 2010). "
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    ABSTRACT: Moderate, long-term weight loss results in the loss of bone mass in overweight or obese premenopausal women. However, whether these changes persist during weight maintenance or regain remains to be determined. Overweight or obese (body mass index: 25.8-42.5 kg/m(2)) women (n=40) with at least two risk factors for the metabolic syndrome participated in this 12-month study that examined the effects of prescribed weight loss and regain, with or without exercise, on bone turnover and on bone mineral density (BMD) in a subset of participants (n=24). During the first 6 month, participants lost ≈ 10% of their initial body weight via energy restriction and supervised aerobic exercise. Following weight loss, participants were randomly assigned to either an exercise or a no exercise treatment for the regain (+50% of weight lost) phase. A one-way (time) repeated measures one-factor analysis of variance (RMANOVA) tested the effects of weight loss on BMD and bone turnover, and a two-way RMANOVA (time, exercise) was used to examine the effects of exercise during weight regain. Hip (P=0.007) and lumbar spine (P=0.05) BMD decreased with weight loss, and remained reduced after weight regain with or without exercise. Likewise, the weight-loss-associated increases in osteocalcin (P<0.001) and C-terminal peptide of type I collagen (P<0.001) persisted following weight regain, independent of exercise. The results of the present study, which is the first to examine changes in bone mass and turnover during carefully controlled weight regain, suggest that weight-loss-induced perturbations in bone mass and turnover persist after partial weight regain, regardless of whether regular weight-bearing aerobic exercise was continued.
    European journal of clinical nutrition 12/2011; 66(5):606-12. DOI:10.1038/ejcn.2011.212 · 2.95 Impact Factor
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    ABSTRACT: To determine whether resistance training effectively maintains improvements in cardiometabolic syndrome risk factors during weight regain, 9 individuals lost 4% to 6% of their body weight during an 8- to 12-week diet- and aerobic exercise-induced weight loss phase followed by a controlled weight regain phase (8-12 weeks), during which they regained approximately 50% of the lost weight while participating in a supervised resistance training program. Following weight loss (6.0%+/-0.3%), body mass index, body fat percentage, waist circumference, all abdominal adipose tissue depots, total cholesterol, low-density lipoprotein cholesterol, insulin, and homeostasis model assessment (HOMA) were significantly reduced, while quantitative insulin-sensitivity check index (QUICKI) and cardiorespiratory fitness (maximal oxygen consumption) significantly increased. During weight regain (48.3%+/-3.3% of lost weight), body fat percentage, waist circumference, and maximal oxygen consumption were maintained and muscular strength and lean body mass significantly increased. Abdominal adipose tissue depots, insulin, HOMA, and QUICKI did not significantly change after weight regain. Resistance training was effective in maintaining improvements in metabolic health during weight regain.
    Journal of Clinical Hypertension 01/2010; 12(1):64-72. DOI:10.1111/j.1751-7176.2009.00209.x · 2.96 Impact Factor
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