RESUMO
PURPOSE: Obesity and type 2 diabetes are associated with an increased risk of cardiovascular disease (CVD) and the combination of weight loss and increased physical exercise are commonly recommended to reduce CVD. This study examined whether people with obesity and type 2 diabetes with an abnormal graded exercise tolerance test (GXT) or a history of CVD would have less success in achieving weight loss and improved fitness, compared to adults without these conditions. METHODS: The Look AHEAD Study examined whether an intensive lifestyle intervention (ILI) compared with diabetes support and education (DSE) reduced cardiovascular events in adults with overweight/obesity and type 2 diabetes. Participants underwent a baseline maximal GXT and provided medical history data. Weight loss and fitness change were examined in 5011 participants over four years in those with or without an abnormal baseline GXT and/or history of CVD. RESULTS: After four years, weight loss in both ILI and DSE were significantly greater in those without a prior history of CVD than in those with a CVD history (6.69% vs 5.98%, p=0.02, in ILI and 0.73 vs -.07% (weight gain), p=0.01, in DSE). Likewise, those without a prior history of CVD experienced greater improvements in fitness in both ILI and DSE relative to those with a history of CVD. Having an abnormal GXT at baseline did not affect weight loss or fitness. CONCLUSIONS: A history of CVD at baseline modestly lessened weight loss and fitness changes at 4 years, whereas having any abnormality on the baseline GXT did not affect these outcomes. Thus, weight loss and improved fitness are achievable in adults with a history of CVD or ECG abnormalities.
RESUMO
STUDY OBJECTIVES: To examine the effect of changes in cardiorespiratory fitness on obstructive sleep apnea (OSA) severity prior to and following adjustment for changes in weight over the course of a 4-y weight loss intervention. METHODS: As secondary analyses of a randomized controlled trial, 263 overweight/obese adults with type 2 diabetes and OSA participated in an intensive lifestyle intervention or education control condition. Measures of OSA severity, cardiorespiratory fitness, and body weight were obtained at baseline, year 1, and year 4. Change in the apnea-hypopnea index (AHI) served as the primary outcome. The percentage change in fitness (submaximal metabolic equivalents [METs]) and change in weight (kg) were the primary independent variables. Primary analyses collapsed intervention conditions with statistical adjustment for treatment group and baseline METs, weight, and AHI among other relevant covariates. RESULTS: At baseline, greater METs were associated with lower AHI (B [SE] = -1.48 [0.71], P = 0.038), but this relationship no longer existed (B [SE] = -0.24 [0.73], P = 0.75) after adjustment for weight (B [SE] = 0.31 [0.07], P < 0.0001). Fitness significantly increased at year 1 (+16.53 ± 28.71% relative to baseline), but returned to near-baseline levels by year 4 (+1.81 ± 24.48%). In mixed-model analyses of AHI change over time without consideration of weight change, increased fitness at year 1 (B [SE] = -0.15 [0.04], P < 0.0001), but not at year 4 (B [SE] = 0.04 [0.05], P = 0.48), was associated with AHI reduction. However, with weight change in the model, greater weight loss was associated with AHI reduction at years 1 and 4 (B [SE] = 0.81 [0.16] and 0.60 [0.16], both P < 0.0001), rendering the association between fitness and AHI change at year 1 nonsignificant (B [SE] = -0.04 [0.04], P = 0.31). CONCLUSIONS: Among overweight/obese adults with type 2 diabetes, fitness change did not influence OSA severity change when weight change was taken into account. CLINICAL TRIAL REGISTRATION: ClinicalTrials.gov identification number NCT00194259.
Assuntos
Fenômenos Fisiológicos Cardiovasculares , Diabetes Mellitus Tipo 2/complicações , Sobrepeso/complicações , Aptidão Física/fisiologia , Apneia Obstrutiva do Sono/complicações , Apneia Obstrutiva do Sono/fisiopatologia , Redução de Peso , Idoso , Índice de Massa Corporal , Diabetes Mellitus Tipo 2/fisiopatologia , Feminino , Nível de Saúde , Humanos , Estilo de Vida , Masculino , Pessoa de Meia-Idade , Obesidade/complicações , Obesidade/fisiopatologia , Sobrepeso/fisiopatologia , Educação de Pacientes como Assunto , Fenômenos Fisiológicos Respiratórios , Apneia Obstrutiva do Sono/diagnóstico , Resultado do TratamentoAssuntos
Humanos , Animais , Dieta Redutora , Exercício Físico , Comportamento Alimentar , Hiperlipidemias/etiologia , Necessidades Nutricionais , Obesidade/dietoterapia , Obesidade/tratamento farmacológico , Obesidade/genética , Obesidade/metabolismo , Redução de Peso , Metabolismo Energético , Camundongos ObesosRESUMO
Obesity has a major effect on the prevalence and severity of diabetes mellitus. The prevalence of reported diabetes is 2.9 times higher in overweight than in non-overweight persons in the National Health Examination Survey (NHANES) data. There is a strong correlation between the relative weight and the prevalence of diabetes in population groups. There have been prospective studies in a number of countries, including the United States, Norway, Sweden and Israel, which have shown that overweight increases the risk of diabetes mellitus. Cross-sectional studies have also shown that obese patients have an increased relative risk for diabetes. Obesity is rare in insulin-dependent type I diabetes mellitus (NIDDM). About 85 percent of diabetics can be classified as type 2 and, of these, 90 percent are obese. The distribution of body fat is important in increasing the risks of developing diabetes. Recently, in prospective study of Mexican Americans, a higher "Centrality Index" (that is, body fat in a central or upper body pattern) has been found to be predictive of the development of diabetes mellitus. In Sweden, a similar independent effect of waist-to-hip ratio as apredictor of diabetes has been found. The relationship of obesity to diabetes mellitus is not totally clear, but some facts are incontrovertible. The accretion of excess body fat is associated with increasing insulin resistance. This is manifested in the liver by increased hepatic glucose output and in the periphery by a decreased glucose uptake by peripheral tissues, primarily muscle and adipose tissue. This is caused by both receptor and post-receptor defects in insulin action. There is a decrease in the number of insulin receptors on the cells of target tissues, but there does not seem to be a significant alteration in the affinity to the receptors for insulin. Insulin receptor binding is decreased. Skeletal muscle is equally and severely resistant to insulin in obese patients with or without NIDDM, while adipose tissue is less insulin-resistant in obesity than it is once diabetes has supervened (AU)