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Individuals show high variability in body weight responses to exercise training. Expectations and motivation towards effects of exercise on body weight might influence eating behaviour and could conceal regulatory mechanisms. We conducted 2 single-blind exercise trials (4 weeks (study 1) and 8 weeks (study 2)) with concealed objectives and exclusion of individuals with weight loss intention. Circuit exercise training programs (3 times a week (45-90 min), intensity 50%-90% peak oxygen uptake for 4 and 8 weeks) were conducted. Thirty-four females finished the 4-week intervention and 36 females the 8-week intervention. Overweight/obese (OV/OB) and lean female participants' weight/body composition responses were assessed and fasting and postprandial appetite hormone levels (PYY, insulin, amylin, leptin, ghrelin) were measured before and after the intervention for understanding potential contribution to individuals' body weight response to exercise training (study 2). Exercise training in both studies did not lead to a significant reduction of weight/body mass index (BMI) in the participants' groups; however, lean participants gained muscle mass. Appetite hormones levels were significantly ( p < 0.05) altered in the OV/OB group, affecting fasting (−24%) and postprandial amylin (−14%) levels. Investigation of individuals' BMI responses using multiple regression analysis revealed that levels of fasting leptin, postprandial amylin increase, and BMI were significant predictors of BMI change, explaining about 43% of the variance. In conclusion, tested exercise training did not lead to weight loss in female participants, while a considerable proportion of variance in body weight response to training could be explained by individuals' appetite hormone levels and BMI. [ABSTRACT FROM AUTHOR]

Stimulation of the energy sensor AMP-activated kinase (AMPK) has been viewed as a targeted approach to increase glucose uptake by skeletal muscle and control blood glucose homeostasis. Rosemary extract (RE) has been reported to activate AMPK in hepatocytes and reduce blood glucose levels in vivo but its effects on skeletal muscle are not known. In the present study, we examined the effects of RE and the mechanism of regulation of glucose uptake in muscle cells. RE stimulated glucose uptake in L6 myotubes in a dose- and time-dependent manner. Maximum stimulation was seen with 5 μg/mL of RE for 4 h (184% ± 5.07% of control, p < 0.001), a response comparable to maximum insulin (207% ± 5.26%, p < 0.001) and metformin (216% ± 8.77%, p < 0.001) stimulation. RE did not affect insulin receptor substrate 1 and Akt phosphorylation but significantly increased AMPK and acetyl-CoA carboxylase phosphorylation. Furthermore, the RE-stimulated glucose uptake was significantly reduced by the AMPK inhibitor compound C, but remained unchanged by the PI3K inhibitor, wortmannin. RE did not affect GLUT4 or GLUT1 glucose transporter translocation in contrast with a significant translocation of both transporters seen with insulin or metformin treatment. Our study is the first to show a direct effect of RE on muscle cell glucose uptake by a mechanism that involves AMPK activation. [ABSTRACT FROM AUTHOR]

This study compared accelerometer-measured physical activity by body placement to daily total energy expenditure (TEE) and activity energy expenditure (AEE) measured using doubly labeled water (DLW). Forty-nine adult participants wore accelerometers placed on the nondominant wrist, dominant wrist, and chest while also undergoing DLW assessments. In adjusted models, wrist-measured physical activity ( p  < 0.05), but not chest-measured physical activity ( p  > 0.05), was associated with TEE and AEE and explained a significant amount of variance that was not explained by age, sex, height, or body composition ( R 2 change = 0.04-0.08; all p  < 0.05). Accelerometer placement location is an important consideration when using accelerometry to provide information about energy expenditure.

This study examined acute physiologic responses to a thermogenic nutritional supplement at rest, during exercise, and during recovery from exercise in women. Twelve women (mean ± SD age, 22.9 ± 3.1 years) were recruited for this randomized, double-blinded, placebo-controlled, crossover study. Each testing session consisted of 4 phases: 30 min of presupplementation resting, followed by the ingestion of the placebo or thermogenic nutritional supplement; 50 min of postsupplementation resting; 60 min of walking (at 3.2-4.8 km·h−1); and 50 min of postexercise resting. Energy expenditure (EE), oxygen consumption, respiratory exchange ratio (RER), oxygen (O2) pulse, and heart rate (HR) values were recorded during all 4 phases. Systolic (SBP) and diastolic (DBP) blood pressure were recorded during the rest, postsupplementation, and postexercise recovery phases; ratings of perceived exertion (RPE) were recorded only during exercise. There were no significant differences for EE, oxygen consumption, O2 pulse, HR, SBP, or DBP between the supplement and placebo during the presupplementation resting or postsupplementation phases. The RER, however, was higher with the supplement at 30 min postsupplementation. During exercise, EE and O2 pulse were 3%-6% greater with the supplement than placebo; there were no significant differences in RPE. Postexercise, EE, oxygen consumption, and DBP were 3%-7% greater with the supplement than placebo. These findings suggest that a thermogenic nutritional supplement, when combined with exercise, increases metabolic rate but has no effect on the perception of effort and results in only minimal changes in cardiovascular function. [ABSTRACT FROM AUTHOR]