The Effect Of Post-exercise Meal Composition On Insulin Action

INTRODUCTION: Exercise increases insulin stimulated glucose uptake (insulin action) if expended energy (kcal) is withheld following exercise, but the effect is blunted when expended energy is replaced as carbohydrate. Restricting carbohydrate and replacing expended energy as fat maintains increased insulin action in rodents; however, this effect has not been evaluated in humans. In humans, restricting carbohydrate intake following exercise may be a useful strategy to maximize the effect of individual exercise bouts on insulin action and promote gains in metabolic health over time. Therefore, the purpose of this study was to determine if carbohydrate restriction following exercise (carbohydrate deficit) increased insulin action in sedentary, overweight adults as hypothesized. METHODS: Ten healthy, sedentary, men and women, aged 21±2 years, body fat 37.3±3.1%, and VO2peak 34.6±1.2ml×kg-1×min-1 completed three, two-day experimental conditions in random order: 1) a no-exercise baseline condition (BASE), 2) exercise followed by a high-carbohydrate meal (HIGH-CHO= 76.3±2.5% CHO), and 3) exercise followed by a low-carbohydrate meal (LOW-CHO=17.8±0.1% CHO). On DAY 1, subjects came to the laboratory (early evening) and expended 30% of total daily energy expenditure on a cycle ergometer at 70% of VO2peak. Following exercise, an isocaloric meal (HIGH-CHO or LOW-CHO) was consumed to refeed the expended energy during exercise and venous blood samples were taken to record the insulin and glucose responses to the meals. Twelve hours later (Day 2), whole-body insulin action (steady-state glucose uptake per unit insulin) was measured using a continuous infusion of glucose with stable isotope tracers. A paired t-test was used to detect differences between exercise bouts and the glucose and insulin responses to the post-exercise meals. A one-way repeated measures ANOVA was performed to evaluate the effect of experimental condition on insulin action (p\u3c0.05, for all tests). RESULTS: Intensity (VO2peak), duration (minutes) and energy expenditure (kcal) were similar between exercise bouts. After exercise, plasma glucose and insulin concentrations were significantly higher following the HIGH-CHO meal compared to the LOW-CHO meal (p\u3c0.001, respectively). The next morning, insulin action was similar between experimental conditions (p=0.30). Non-oxidative glucose disposal was increased during the glucose infusion in Low-CHO compared to BASE (27.2±3.2 vs. 16.9±3.5µM×kg-1×min-1, p\u3c0.05). Carbohydrate oxidation was reduced in Low-CHO (8.6±1.3µM×kg-1×min-1) compared to High-CHO (12.2±1.2µM×kg-1×min-1), and to BASE (17.1 ± 2.2 µM×kg-1×min-1), p\u3c0.05 respectively. Resting fat oxidation was increased in Low-CHO compared to BASE (109.8 ± 10.5 mg×min-1 vs. 80.7 ± 9.6 mg×min-1, p\u3c0.05) and remained elevated during the glucose infusion. CONCLUSION: Limiting carbohydrate, but not energy intake after exercise (carbohydrate deficit) resulted in increased non-oxidative glucose disposal, decreased carbohydrate oxidation and increased fat oxidation during the glucose infusion, compared to baseline, indicating a favorable shift in energy metabolism. Creating a carbohydrate deficit, by withholding expended carbohydrate but not energy following exercise may be a sensible strategy to promote favorable gains in insulin action that requires further evaluation

The Nuclear Receptor Corepressor (NCoR) Controls Thyroid Hormone Sensitivity and the Set Point of the Hypothalamic-Pituitary-Thyroid Axis

The role of nuclear receptor corepressor (NCoR) in thyroid hormone (TH) action has been difficult to discern because global deletion of NCoR is embryonic lethal. To circumvent this, we developed mice that globally express a modified NCoR protein (NCoRΔID) that cannot be recruited to the thyroid hormone receptor (TR). These mice present with low serum T(4) and T(3) concentrations accompanied by normal TSH levels, suggesting central hypothyroidism. However, they grow normally and have increased energy expenditure and normal or elevated TR-target gene expression across multiple tissues, which is not consistent with hypothyroidism. Although these findings imply an increased peripheral sensitivity to TH, the hypothalamic-pituitary-thyroid axis is not more sensitive to acute changes in TH concentrations but appears to be reset to recognize the reduced TH levels as normal. Furthermore, the thyroid gland itself, although normal in size, has reduced levels of nonthyroglobulin-bound T(4) and T(3) and demonstrates decreased responsiveness to TSH. Thus, the TR-NCoR interaction controls systemic TH sensitivity as well as the set point at all levels of the hypothalamic-pituitary-thyroid axis. These findings suggest that NCoR levels could alter cell-specific TH action that would not be reflected by the serum TSH