Exercise before breakfast increases 24-h fat oxidation in female subjects

BackgroundExercise performed in a postprandial state does not increase 24-h fat oxidation of male and female subjects. Conversely, it has been shown in male subjects that exercise performed in a postabsorptive state increases 24-h fat oxidation compared with that in sedentary control and that with exercise trials performed after breakfast, lunch, or dinner. There is a paucity of study evaluating the effect of exercise performed in a postabsorptive state in female subjects.MethodNine young female subjects participated in indirect calorimetry measurement over 24-h using a room-size metabolic chamber in which subjects remained sedentary or performed 60 min exercise before breakfast at 50% of . Exercise was accompanied by an increase in energy intake to ensure that subjects were in a similar state of energy balance over 24 h for the two trials.FindingsCompared with the sedentary condition, exercise performed before breakfast increased 24-h fat oxidation (519 ± 37 vs. 400 ± 41 kcal/day). Time courses of relative energy balance differed between trials with transient negative energy balance observed before breakfast. The lowest values of relative energy balance observed during the 24-h calorimetry, i.e., transient energy deficit, were greater in exercise trials than in sedentary trials. The transient deficit in carbohydrate balance was also observed before breakfast, and magnitude of the deficit was greater in exercise trial compared to that of sedentary trial.InterpretationUnder energy-balanced conditions, exercise performed in a post-absorptive state increases 24-h fat oxidation in female subjects. The effect of exercise performed before breakfast can be attributed to nutritional state: a transient deficit in energy and carbohydrate at the end of exercise

CD206+ M2-like macrophages regulate systemic glucose metabolism by inhibiting proliferation of adipocyte progenitors

Adipose tissue resident macrophages have important roles in the maintenance of tissue homeostasis and regulate insulin sensitivity for example by secreting pro-inflammatory or anti-inflammatory cytokines. Here, we show that M2-like macrophages in adipose tissue regulate systemic glucose homeostasis by inhibiting adipocyte progenitor proliferation via the CD206/TGFβ signaling pathway. We show that adipose tissue CD206+ cells are primarily M2-like macrophages, and ablation of CD206+ M2-like macrophages improves systemic insulin sensitivity, which was associated with an increased number of smaller adipocytes. Mice genetically engineered to have reduced numbers of CD206+ M2-like macrophages show a down-regulation of TGFβ signaling in adipose tissue, together with up-regulated proliferation and differentiation of adipocyte progenitors. Our findings indicate that CD206+ M2-like macrophages in adipose tissues create a microenvironment that inhibits growth and differentiation of adipocyte progenitors and, thereby, control adiposity and systemic insulin sensitivity

電場が温水処理に伴うSiO2-TiO2系ゲルコーティング膜のチタニア微結晶生成に及ぼす影響

Sol-gel derived SiO2-TiO2 coatings on indium tin oxide (ITO)-coated glass substrates were treated with hot water at 90°C under electric field aiming at the control of morphology and crystalline phase of the titania precipitates. The shape of the precipitates on 75SiO2•25TiO2 (mol%) coating at the negative electrode changed from granular to ramiform by applying an electric field to the substrates during the treatment, whereas such changes in the shape of titania nanocrystals with the electric field were not observed at the positive electrode. The granular and ramiform precipitates were identified as anatase (TiO2) and hydrated titania (n(TiO2)•mH2O), respectively. The ramiform shape of the titania precipitates became significant with increasing the applied voltage, while the coatings gradually dark-colored due to the reduction of Ti4+ to Ti3+

Exercise Increases 24-h Fat Oxidation Only When It Is Performed Before Breakfast

Background: As part of the growing lifestyle diversity in modern society, there is wide variation in the time of day individuals choose to exercise. Recent surveys in the US and Japan have reported that on weekdays, more people exercise in the evening, with fewer individuals exercising in the morning or afternoon. Exercise performed in the post-prandial state has little effect on accumulated fat oxidation over 24 h (24-h fat oxidation) when energy intake is matched to energy expenditure (energy-balanced condition). The present study explored the possibility that exercise increases 24-h fat oxidation only when performed in a post-absorptive state, i.e. before breakfast. Methods: Indirect calorimetry using a metabolic chamber was performed in 10 young, non-obese men over 24 h. Subjects remained sedentary (control) or performed 60-min exercise before breakfast (morning), after lunch (afternoon), or after dinner (evening) at 50% of VO2max. All trials were designed to be energy balanced over 24 h. Time course of energy and substrate balance relative to the start of calorimetry were estimated from the differences between input (meal consumption) and output (oxidation). Findings: Fat oxidation over 24 h was increased only when exercise was performed before breakfast (control, 456 ± 61; morning, 717 ± 64; afternoon, 446 ± 57; and evening, 432 ± 44 kcal/day). Fat oxidation over 24 h was negatively correlated with the magnitude of the transient deficit in energy and carbohydrate. Interpretation: Under energy-balanced conditions, 24-h fat oxidation was increased by exercise only when performed before breakfast. Transient carbohydrate deficits, i.e., glycogen depletion, observed after morning exercise may have contributed to increased 24-h fat oxidation

Exercise before breakfast increases 24-h fat oxidation in female subjects - Fig 1

<p>Time course of energy expenditure (a), carbohydrate oxidation (b) and fat oxidation (c) for sedentary (red) and exercise trials (blue). Mean ± SE values plotted at 1-h intervals except for 6:00–6:30 and 7:30–8:00; 6:00–6:30. Significant differences between exercise and sedentary trials: *, P < 0.05; **, P < 0.01.</p

Energy metabolism during 24 h.

<p>Energy metabolism during 24 h.</p

Energy metabolism during exercise.

<p>Energy metabolism during exercise.</p