No abstract is provided for this article.
The purpose of this study was to determine the association between visceral adipose tissue (VAT) and all-cause mortality. The sample included 1089 white men and women 18-84 years of age from the Pennington Center Longitudinal Study, a prospective cohort of participants assessed between 1995 and 2008, and followed for mortality until 31 December 2009. Abdominal VAT was measured at the L4-L5 vertebral level using computed tomography. There were 27 deaths during an average of 9.1 years of follow-up. Abdominal VAT was significantly associated with mortality after adjustment for age, sex and year of examination (hazards ratio (HR) 1.46; 95% confidence interval 1.05-2.05). The association was stronger after the inclusion of abdominal subcutaneous adipose tissue (SAT), smoking status, alcohol consumption and leisure-time physical activity as additional covariates (HR 1.74; 1.17-2.59). Limiting the sample to participants who were free of stroke, heart disease and cancer at baseline reduced the strength of the relationship slightly (HR 1.62; 1.07-2.47). Abdominal SAT was not associated with mortality, either alone or in combination with VAT and other covariates. The results support the assertion that abdominal VAT is an important therapeutic target for obesity reduction efforts.
The effects of exercise-training on energy balance and body composition are discussed in this article. A training program comprising exercise sessions of moderate duration induces only small changes in body weight. On the other hand, substantial weight losses are observed when obeses persons are subjected to a program including a large amount of exercise. Accordingly, obese individuals do not seem to increase significantly their caloric intake during such a program. Numerous studies show that regular exercise can increase resting metabolic rate, although large individual variations in the response to training are noted. The effect of exercise and exercise-training on diet-induced thermogenesis is not clearly established, some studies suggesting an increase in this parameter whereas others support the contrary. Training-induced weight loss is associated with a reduction in fat cell size. In general, the proportion of fat in the weight loss induced by training is higher than that resulting from dietary restriction. Some studies suggest that exercise-training may result in a greater depletion of fat cells than a low calorie diet, thus delaying the advent of the resistance to fat loss.
The impact of two different modes of training on body fatness and skeletal muscle metabolism was investigated in young adults who were subjected to either a 20-week endurance-training (ET) program (eight men and nine women) or a 15-week high-intensity intermittent-training (HIIT) program (five men and five women). The mean estimated total energy cost of the ET program was 120.4 MJ, whereas the corresponding value for the HIIT program was 57.9 MJ. Despite its lower energy cost, the HIIT program induced a more pronounced reduction in subcutaneous adiposity compared with the ET program. When corrected for the energy cost of training, the decrease in the sum of six subcutaneous skinfolds induced by the HIIT program was ninefold greater than by the ET program. Muscle biopsies obtained in the vastus lateralis before and after training showed that both training programs increased similarly the level of the citric acid cycle enzymatic marker. On the other hand, the activity of muscle glycolytic enzymes was increased by the HIIT program, whereas a decrease was observed following the ET program. The enhancing effect of training on muscle 3-hydroxyacyl coenzyme A dehydrogenase (HADH) enzyme activity, a marker of the activity of β-oxidation, was significantly greater after the HIIT program. In conclusion, these results reinforce the notion that for a given level of energy expenditure, vigorous exercise favors negative energy and lipid balance to a greater extent than exercise of low to moderate intensity. Moreover, the metabolic adaptations taking place in the skeletal muscle in response to the HIIT program appear to favor the process of lipid oxidation.
The concept of a metabolic syndrome (MetS), a cluster of pre-clinical metabolic alterations commonly associated with obesity, is the object of much debate. Genetic studies have the potential to contribute to some of the key questions, including the true nature of the cluster of pre-clinical features and whether it is associated with human genetic variation. This review summarizes the evidence for the presence of familial aggregation for the individual components of MetS and their heritability levels. It also provides an overview of the studies that have dealt with candidate genes for MetS. Potential leads from genome-wide linkage scans are also discussed. The assumption is made that obesity, ectopic fat deposition and abnormal adipose tissue metabolism are responsible for alterations in lipid metabolism, which in turn generates the commonly observed pre-clinical shifts in glucose tolerance, lipids and lipoprotein profile, blood pressure, inflammatory markers, endothelial function, and a prothrombotic state. Progress in the understanding of the genetic basis of MetS should occur as soon as a consensus is reached on the true nature of MetS, its components and diagnostic criteria.
There are considerable individual differences in responses to various dietary manipulations, such as diets rich in cholesterol or in saturated fats. The same phenomenon has been observed in response to chronic overfeeding. For instance, in the Vermont overfeeding study, body weight gain varied among subjects and was below the expected weight gain based upon the ingested caloric surplus (1). Much has been learned from experimental overfeeding, dietary energy restriction, or exercise-induced negative energy balance studies conducted with human subjects.
