This study evaluated the effects of body weight and lean mass abnormalities on health-related quality of life (HRQL) in obstructive airways disease.Body weight, lean mass (using dual-energy X-ray absorptiometry), and HRQL (using the St George's Respiratory Questionnaire (SGRQ)) were measured in 50 patients. Low lean mass was defined as a lean mass index (lean mass/height 2 ) below the fifth percentile of a control population. Dyspnoea was measured by the baseline dyspnoea index.The mean (SD) age was 69±9 yrs; the forced expiratory volume in one second (FEV1) was 39±19% of predicted. Patients had 2.4±4.1 kg less lean mass than predicted. Increased dyspnoea was the most influential predictor of poor HRQL. Compared to normal-weight patients, those who were underweight had significantly greater impairment in activity, impact, and total SGRQ scores, while those who were overweight had greater impairment in impact and total SGRQ scores. Low lean mass was associated with greater impairment in symptoms, activity and impact subscores and the total SGRQ score. When dyspnoea was added to the model as a covariate, neither weight nor lean mass remained significantly related to HRQL.Thus, although body weight and lean mass abnormalities influence health-related quality of life, their effects appear to be mediated through increased levels of dyspnoea. Eur Respir J 1997; 10: 1576-1580 A significantly reduced body weight, which is common in individuals with advanced chronic obstructive pulmonary disease (COPD) [1,2], is related to decreased exercise performance [3,4] and increased mortality [5,6]. In addition, analyses using bioimpedance techniques have demonstrated reductions in fat-free mass in normal-weight and underweight patients [7]. Decreased fat-free mass may be a predictor of poor exercise performance independently of body weight [3].Although the effect of nutritional status on exercise performance is established, little attention has been given to its effect on health-related quality of life (HRQL). To evaluate this, we measured two nutritional parameters, body weight and total body lean mass determined by dual-energy X-ray absorptiometry, in 50 patients with symptomatic obstructive lung disease. These two variables were then compared with HRQL measured by the St George's Respiratory Questionnaire (SGRQ). MethodsThe study was approved by the Medical Center's Institutional Review Board and informed consent was obtained from all subjects before participation in the study. All testing was performed in the Osteoporosis Center, which is in close proximity to the University of Connecticut Health Center.Adults with obstructive lung disease who were symptomatic with dyspnoea despite medical therapy, were recruited for the study. All had moderate-to-severe airways obstruction following bronchodilator inhalation and were clinically stable at the time of the study. Most had previously completed an out-patient pulmonary rehabilitation programme and many were in a postrehabilitation exercise maintenance programme. Patient...

Rector RS, Warner SO, Liu Y, Hinton PS, Sun GY, Cox RH, Stump CS, Laughlin MH, Dellsperger KC, Thomas TR. Exercise and diet induced weight loss improves measures of oxidative stress and insulin sensitivity in adults with characteristics of the metabolic syndrome. Am J Physiol Endocrinol Metab 293: E500-E506, 2007. First published May 1, 2007; doi:10.1152/ajpendo.00116.2007.-Obesity and insulin resistance (IR) increase the risk for coronary heart disease; however, much of this risk is not attributable to traditional risk factors. We sought to determine whether weight loss associated with supervised aerobic exercise beneficially alters biomarkers of oxidative stress and whether these alterations are associated with improvements in measures of insulin resistance. Twenty-five sedentary and overweight to obese [body mass index (BMI) ϭ 33.0 Ϯ 0.8 kg/m 2 ] individuals, with characteristics of the metabolic syndrome, participated in a 4-to 7-mo weight loss program that consisted of energy restriction (reduced by ϳ500 kcal/day) and supervised aerobic exercise (5 days/wk, 45 min/day at 60% V O2 max; ϳ375 kcal/day). IR and insulin sensitivity were assessed by the calculation of the homeostasis model assessment (HOMA) and quantitative insulin sensitivity check index (QUICKI), respectively. Oxidative stress was assessed by oxidized LDL (oxLDL), myeloperoxidase (MPO), and low-and high-density lipoprotein (LDL and HDL) lipid hydroperoxide concentrations in serum. Indexes for antioxidative status included apolipoprotein A1 (apoA1) concentrations and paraoxonase-1 (PON1) activity and protein concentrations. Exercise-and diet-induced weight loss (ϳ10%) significantly (P Ͻ 0.05) increased insulin sensitivity and reduced IR, oxLDL, and LDL lipid hydroperoxides but did not alter HDL lipid hydroperoxides or MPO concentrations. Lifestyle modification impacted systemic antioxidative status by increasing apoA1 concentrations and reducing serum PON1 protein and activity. Changes in oxidative stress were not associated with alterations in HOMA or QUICKI. Diet-and exercise-induced weight loss (ϳ10%) improves measures of insulin sensitivity and beneficially alters biomarkers of oxidative status. insulin resistance; oxidized low-density lipoprotein; paraoxonase-1; energy restriction AMERICANS ARE EXPERIENCING a weight gain epidemic, and recent epidemiological studies suggest an increased risk of coronary heart disease (CHD) and type 2 diabetes in overweight and obese individuals. In addition, patients with type 2 diabetes, impaired glucose tolerance, and insulin resistance (IR) are at elevated risk for CHD (24). Despite elevated levels of hypertension, obesity, and dyslipidemia in these individuals, epidemiological studies suggest that traditional risk factors do not explain all of the elevated risk of CHD (24,29). This suggests that other underlying abnormalities are present and contributing to the etiology of the disease.One possible link between IR and CHD is reduced levels of high-density lipoproteins (HDL) and increased oxidative stress....

Using the hyperphagic, obese, Otsuka Long-Evans Tokushima Fatty (OLETF) rat, we sought to determine if progression to type 2 diabetes alters visceral white adipose tissue (WAT) mitochondrial content and if these changes are modified through prevention of type 2 diabetes with daily exercise. At 4 weeks of age, OLETF rats began voluntary wheel running (OLETF-EX) while additional OLETF rats (OLETF-SED) and Long-Evans Tokushima Otsuka (LETO-SED) rats served as obese and lean sedentary controls, respectively, for 13, 20 and 40 weeks of age (n = 6-8 for each group at each age). OLETF-SED animals displayed insulin resistance at 13 and 20 weeks and type 2 diabetes by 40 weeks. OLETF-SED animals gained significantly (P < 0.001) more weight and omental fat mass compared with OLETF-EX and LETO-SED. Markers of WAT mitochondrial protein content (cytochrome c, COXIV-subunit I, and citrate synthase activity) significantly increased (P < 0.05) from 13 to 40 weeks in the LETO-SED, but were significantly attenuated in the OLETF-SED rats. Daily exercise normalized WAT cytochrome c and COXIV-subunit I protein content in the OLETF-EX to the healthy LETO-SED animals. In conclusion, increases in omental WAT mitochondrial content between 20 and 40 weeks of age in LETO control animals are attenuated in the hyperphagic, obese OLETF rat. These alterations occurred in conjunction with the progression from insulin resistance to type 2 diabetes and were prevented with daily exercise. Reduced ability to increase WAT mitochondrial content does not appear to be a primary cause of insulin resistance, but may play a key role in the worsening of the disease condition.

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.

Background/Objectives Moderate, long-term weight loss results in loss of bone mass in overweight or obese premenopausal women. However, whether these changes persist during weight maintenance or regain remains to be determined. Subjects/Methods Overweight or obese (BMI: 25.8–42.5 kg/m2) women (n=40) with at least two risk factors for the metabolic syndrome participated in this 12-mo 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 mo, 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 ANOVA tested the effects of weight loss on BMD and bone turnover, and a two-way RM ANOVA (time, exercise) was used to examine the effects of exercise during weight regain. Results 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. Conclusions 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.

Type 2 diabetes (T2D) is a metabolic disease characterized by obesity, insulin resistance, and the dysfunction of several key glucoregulatory organs. Among these organs, impaired liver function is recognized as one of the earliest contributors to impaired whole-body glucose homeostasis, with well-characterized hepatic insulin resistance resulting in elevated rates of hepatic glucose production (HGP) and fasting hyperglycemia. One portion of this review will provide an overview of how HGP is regulated during the fasted state in healthy humans and how this process becomes dysregulated in patients with T2D. Less well-appreciated is the liver's role in post-prandial glucose metabolism, where it takes up and metabolizes one-third of orally ingested glucose. An abundance of literature has shown that the process of hepatic glucose uptake is impaired in patients with T2D, thereby contributing to glucose intolerance. A second portion of this review will outline how hepatic glucose uptake is regulated during the post-prandial state, and how it becomes dysfunctional in patients with T2D. Finally, it is well-known that exercise training has an insulin-sensitizing effect on the liver, which contributes to improved whole-body glucose metabolism in patients with T2D, thereby making it a cornerstone in the management of the disease. To this end, the impact of exercise on hepatic glucose metabolism will be thoroughly discussed, referencing key findings in the literature. At the same time, sources of heterogeneity that contribute to inconsistent findings in the field will be pointed out, as will important topics for future investigation.

J Clin Hypertens (Greenwich). 2010;12:64–72. ©2009 Wiley Periodicals, Inc. 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.

No abstract