OBJECTIVE: To assess acute and chronic effects of exercise performed before versus after nutrient ingestion on whole-body and intramuscular lipid utilization and postprandial glucose metabolism.
DESIGN: (1) Acute, randomized, crossover design (Acute Study); (2) 6-week, randomized, controlled design (Training Study).
SETTING: General community.
PARTICIPANTS: Men with overweight/obesity (mean ± standard deviation, body mass index: 30.2 ± 3.5 kg⋅m-2 for Acute Study, 30.9 ± 4.5 kg⋅m-2 for Training Study).
INTERVENTIONS: Moderate-intensity cycling performed before versus after mixed-macronutrient breakfast (Acute Study) or carbohydrate (Training Study) ingestion.
RESULTS: Acute Study-exercise before versus after breakfast consumption increased net intramuscular lipid utilization in type I (net change: -3.44 ± 2.63% versus 1.44 ± 4.18% area lipid staining, P < 0.01) and type II fibers (-1.89 ± 2.48% versus 1.83 ± 1.92% area lipid staining, P < 0.05). Training Study-postprandial glycemia was not differentially affected by 6 weeks of exercise training performed before versus after carbohydrate intake (P > 0.05). However, postprandial insulinemia was reduced with exercise training performed before but not after carbohydrate ingestion (P = 0.03). This resulted in increased oral glucose insulin sensitivity (25 ± 38 vs -21 ± 32 mL⋅min-1⋅m-2; P = 0.01), associated with increased lipid utilization during exercise (r = 0.50, P = 0.02). Regular exercise before nutrient provision also augmented remodeling of skeletal muscle phospholipids and protein content of the glucose transport protein GLUT4 (P < 0.05).
CONCLUSIONS: Experiments investigating exercise training and metabolic health should consider nutrient-exercise timing, and exercise performed before versus after nutrient intake (ie, in the fasted state) may exert beneficial effects on lipid utilization and reduce postprandial insulinemia.
METHODS: Fifty-two females (21.43 ± 4.8 years) were divided into "normal" (BMI = 18-24.9 kg/m2) and "high" (BMI ≥ 25 kg/m2) BMI groups. Participants wore pedometers throughout the day for nine weeks. Pre-post intervention tests performed on anthropometric, biochemical, and nutrient intake variables were tested at p ≤ 0.05.
RESULTS: Participants walked 7056 ± 1570 footsteps/day without a significant difference between normal (7488.49 ± 1098) and high (6739.18 ± 1793) BMI groups. After week 9, the normal BMI group improved significantly in BMI, body fat mass (BFM), and waist-hip ratio (WHR). Additionally, percent body fat, waist circumference (WC), and visceral fat area also reduced significantly in the high BMI group. A significant decrease in triglycerides (TG) (71.62 ± 29.22 vs. 62.50 ± 29.16 mg/dl, p=0.003) and insulin (21.7 ± 8.33 µU/l vs. 18.64 ± 8.25 µU/l, p=0.046) and increase in HMW-Adip (3.77 ± 0.46 vs. 3.80 ± 0.44 μg/ml, p=0.034) were recorded in the high BMI group. All participants exhibited significant inverse correlations between daily footsteps and BMI (r=-0.33, p=0.017), BFM (r=-0.29, p=0.037), WHR (r=-0.401, p=0.003), and MetS score (r=-0.49, p < 0.001) and positive correlation with HMW-Adip (r=0.331, p=0.017). A positive correlation with systolic (r=0.46, p=0.011) and diastolic (r=0.39, p=0.031) blood pressures and inverse correlation with the MetS score (r=-0.5, p=0.005) were evident in the high BMI group.
CONCLUSION: Counting footsteps using a pedometer is effective in improving MetS components (obesity, TG) and increasing HMW-Adip levels.
METHODS: Twenty-four male, 8-week old Sprague Dawley rats with an initial weight of 160 to 200 g were randomised into three groups (n = 6 for each group): groups A (standard rat chow), B (high-fat, high-sucrose diet), and C (high-fat, high-sucrose diet + 100 mg/kg/d of glycyrrhizic acid via oral administration). The rats were treated accordingly for 4 wk. Glycaemic parameters, lipid profile, stress hormones, and adiponectin levels were measured after the treatment. Relative gene expressions of peroxisome proliferator-activated receptor α and γ, lipoprotein lipase as well as gluconeogenic enzymatic activities in different tissues were also determined.
RESULTS: Consumption of high-fat, high-sucrose diet triggered hyperglycaemia, insulin resistance, and dyslipidemia, which were effectively attenuated by supplementation with glycyrrhizic acid. Glycyrrhizic acid supplementation also effectively reduced circulating adrenaline, alleviated gluconeogenic enzymes overactivity, and promoted the upregulation of lipoprotein lipase expression in the cardiomyocytes and skeletal muscles. A high calorie diet also triggered hypoadiponectinaemia and suppression of peroxisome proliferator-activated receptor γ expression, which did not improve with glycyrrhizic acid treatment.
CONCLUSION: Supplementation with glycyrrhizic acid could alleviate high calorie diet-induced glucose and lipid metabolic dysregulations by reducing circulatory stress hormones, normalizing gluconeogenic enzyme activities, and elevating muscular lipid uptake. The beneficial effects of these bioactivities outweighed the adverse effects caused by diet-induced repression of peroxisome proliferator-activated receptor γ expression, resulting in the maintenance of lipid and glucose homeostasis.