Assessment of fat-mass loss during weight reduction in obese women.

Urho Kaleva Kekkonen Institute for Health Promotion Research, Tampere, Finland.Methods for assessing body fat mass (FM) loss were compared in 32 obese (body mass index [BMI], 29 to 41 kg/m2) premenopausal women before and after a weight loss of 13.0 +/- 3.4 kg (mean +/- SD). A four-component (4C) model was used as the criterion. The other methods were as follows: three-component models (body density with total body water [3W] or bone minerals [3M]), underwater weighing, dual-energy x-ray absorptiometry ([DXA] XR-26, software 2.5.2; Norland, Ft Atkinson, WI), bioelectric impedance analysis (BIA) with an obese-specific equation [Segal et al), skinfolds (Durnin and Womersley), and an equation with BMI (Deurenberg et al). The 3W model (bias +/- SD, 0.5 +/- 0.4 kg), XR-26 (0.6 +/- 2.1 kg), and BMI equation (-0.3 +/- 2.1 kg) gave practically unbiased mean estimations of fat loss. All other methods underestimated fat loss by at least 1.6 kg (range of bias, -2.7 to -1.6 kg). The small bias (0.7 +/- 1.0 kg) between underwater weighing and model 4C before weight reduction indicates that the two-component assumptions were valid in premenopausal, weight-stable obese women. However, particularly the water fraction of the fat-free body component (4C model) was increased after weight reduction (before, 72.9% +/- 1.4%; after, 75.7% +/- 2.2%), making both underwater weighing and the 3M model uncertain for assessment of body composition changes. A general tendency for overestimating FM was seen before and more clearly after weight reduction. However, most methods underestimated fat loss, apparently because of unexpected changes in hydration of the fat-free body component

Modulation of thermogenesis and metabolic health:a built environment perspective

\u3cp\u3eLifestyle interventions, obviating the increasing prevalence of the metabolic syndrome, generally focus on nutrition and physical activity. Environmental factors are hardly covered. Because we spend on average more that 90% of our time indoors, it is, however, relevant to address these factors. In the built environment, the attention has been limited to the (assessment and optimization of) building performance and occupant thermal comfort for a long time. Only recently well-being and health of building occupants are also considered to some extent, but actual metabolic health aspects are not generally covered. In this review, we draw attention to the potential of the commonly neglected lifestyle factor ‘indoor environment’. More specifically, we review current knowledge and the developments of new insights into the effects of ambient temperature, light and the interaction of the two on metabolic health. The literature shows that the effects of indoor environmental factors are important additional factors for a healthy lifestyle and have an impact on metabolic health.\u3c/p\u3

Hypoxia induces no change in cutaneous thresholds for warmth and cold sensation

Hypoxia can affect perception of temperature stimuli by impeding thermoregulation at a neural level. Whether this impact on the thermoregulatory response is solely due to affected thermoregulation is not clear, since reaction time may also be affected by hypoxia. Therefore, we studied the effect of hypoxia on thermal perception thresholds for warmth and cold. Thermal perception thresholds were determined in 11 healthy overweight adult males using two methods for small nerve fibre functioning: a reaction-time inclusive method of limits (MLI) and a reaction time exclusive method of levels (MLE). The subjects were measured under normoxic and hypoxic conditions using a cross-over design. Before the thermal threshold tests under hypoxic conditions were conducted, the subjects were acclimatized by staying 14 days overnight (8 h) in a hypoxic tent system (Colorado Altitude Training: 4,000 m). For normoxic measurements the same subjects were not acclimatized, but were used to sleep in the same tent system. Measurements were performed in the early morning in the tent. Normoxic MLI cold sensation threshold decreased significantly from 30.3 ± 0.4 (mean ± SD) to 29.9 ± 0.7°C when exposed to hypoxia (P < 0.05). Similarly, mean normoxic MLI warm sensation threshold increased from 34.0 ± 0.9 to 34.5 ± 1.1°C (P < 0.05). MLE measured threshold for cutaneous cold sensation was 31.4 ± 0.4 and 31.2 ± 0.9°C under respectively normoxic and hypoxic conditions (P > 0.05). Neither was there a significant change in MLE warm threshold comparing normoxic (32.8 ± 0.9°C) with hypoxic condition (32.9 ± 1.0°C) (P > 0.05). Exposure to normobaric hypoxia induces slowing of neural activity in the sensor-to-effector pathway and does not affect cutaneous sensation threshold for either warmth or cold detection

The effect of warmth acclimation on behaviour, thermophysiology and perception

Public and commercial buildings tend to overheat and considerable energy is consumed by air-conditioning and ventilation. However, many occupants remain unsatisfied and consequently exhibit thermoregulatory behaviour (TRB), e.g. opening windows or controlling the air-conditioning. This, in turn, might negatively influence the building energy use. This paper hypothesizes that warmth acclimation influences thermophysiology, perception and TRB in a warm environment. Therefore, the effect of warmth acclimation on TRB, physiology and perception is investigated. Twelve participants underwent a so-called SWITCH protocol before and after warmth acclimation (7 days, 6h/day, about 33 degrees C, about 22% RH). During SWITCH, the participants chose between a warm (37 degrees C) and a cold (17 degrees C) condition. TRB was determined by the number of switches and the time spent in a specific condition. Mean skin temperature was recorded to assess behavioural thresholds. Thermal comfort and sensation were indicated on visual analogue scales (VAS). After acclimation, the upper critical behavioural threshold significantly increased from 35.2 +/- 0.6 to 35.5 +/- 0.5 degrees C (p0.05) and the range of mean skin temperatures at which no behaviour occurred significantly widened (3.6 +/- 0.7 to 4.2 +/- 0.6;

Brown adipose tissue activity after a high-calorie meal in humans.

BACKGROUND: Studies in rodents have shown that brown adipose tissue (BAT) is activated on food intake, thereby reducing metabolic efficiency. OBJECTIVE: The current study investigated whether a single high-calorie, carbohydrate-rich meal activates BAT in lean human adults. DESIGN: BAT activity was studied in 11 lean adult men [age: 23.6 +/- 2.1 y; body mass index (BMI; in kg/m2): 22.4 +/- 2.1] after consumption of a high-calorie, carbohydrate-rich meal (1622 +/- 222 kcal; 78% carbohydrate, 12% P, 10% F). BAT activity during 2 h of mild cold exposure served as a positive control experiment. BAT activity was assessed by [18F]fluorodeoxyglucose (FDG)-positron emission tomography-computed tomography. Energy expenditure was measured by indirect calorimetry. RESULTS: Postprandial [18F]FDG uptake was significantly higher in BAT [1.65 +/- 0.99 mean standard uptake value (SUVmean)] than in subcutaneous (0.35 +/- 0.15 SUVmean; P < 0.05) and visceral (0.49 +/- 0.24 SUVmean; P < 0.05) white adipose tissue and liver (0.95 +/- 0.28 SUVmean; P < 0.05). Postprandial BAT activity was lower than cold-induced BAT activity (7.19 +/- 2.09 SUVmean). However, postprandial BAT activity may have been underestimated because of high postprandial [18F]FDG uptake in skeletal muscle compared with cold (1.36 +/- 0.31 compared with 0.59 +/- 0.07 SUVmean, P < 0.05), which reduces [18F]FDG bioavailability for BAT and other tissues. No direct relation was found between BAT and diet-induced thermogenesis (DIT). CONCLUSIONS: Glucose uptake in BAT increases after a meal in humans, which indicates a role for BAT in reducing metabolic efficiency. However, the quantitative contribution of BAT to DIT relative to other tissues, such as skeletal muscle, remains to be investigated. This trial was registered at www.controlled-trials.com as ISRCTN21413505