Assuntos
Treino Aeróbico , Adaptação Fisiológica , Criança , Coração , Humanos , Resistência Física , PuberdadeRESUMO
Limited research has characterized the metabolic health benefits of bodyweight interval exercise (BWE) performed outside of a laboratory setting. Metabolic responses to exercise can also be influenced by meal timing around exercise, but the interactive effects of BWE and nutrition are unknown. This study investigated the effects of BWE performed in the fasted or fed state on postprandial glycemia, post-exercise fat oxidation and appetite perceptions. Twelve females (23 ± 2 years; 22 ± 2 kg/m2) underwent two virtually-monitored trials that involved completing BWE (10 × 1 min, 1 min recovery) 5 min before (FastEX) or beginning BWE 10 min after (FedEX) a standardized breakfast. Heart rate and rating of perceived exertion (RPE) were measured during exercise and capillary glucose concentrations were measured for 2 h postprandial. Following exercise, appetite perceptions were assessed and Lumen expired carbon dioxide percentage (L%CO2) was measured as an index of fat oxidation. Heart rate (85 ± 5%) and RPE (14 ± 2) did not differ between conditions (p > 0.05). Postprandial glucose mean (6.1 ± 0.6 vs. 6.8 ± 0.8 mmol/L, p = 0.03), peak (7.4 ± 1.2 vs. 8.5 ± 1.5 mmol/L, p = 0.01), and area under the curve (AUC) (758 ± 72 vs. 973 ± 82 mmol/L × 2 h, p = 0.004) were lower in FedEX versus FastEX. Appetite perceptions were lower in FedEX versus FastEX (-87.63 ± 58.51 vs. -42.06 ± 34.96 mm, p = 0.029). Post-exercise L%CO2 was transiently decreased 30 min post-exercise in both conditions (4.03 ± 0.38 vs. 4.29 ± 0.34%, p = 0.0023), reflective of increased fat oxidation following BWE. These findings demonstrate that BWE performed in the fed compared to the fasted state lowered postprandial glycemia and appetite perceptions in females.
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Background: Improved glycemic control has been reported for â¼24 h following low-volume high-intensity interval exercise (HIIE), but it is unclear if this is a direct effect of exercise or an indirect effect of the exercise-induced energy deficit. The purpose of this study was to investigate the effect of carbohydrate-energy replacement after low-volume HIIE on 24 h glycemic control in women. Methods: Seven untrained women (age: 22 ± 2 yr; BMI: 22 ± 3 kg/m2; VO2peak: 33 ± 7 ml/kg/min) completed three 2-day trials in the mid-follicular phase of the menstrual cycle. Continuous glucose monitoring was used to measure blood glucose concentrations during, and for 24 h following three conditions: (1) HIIE followed by a high-carbohydrate energy replacement drink (EX-HC); (2) HIIE followed by a non-caloric taste-matched placebo drink (EX-NC); and (3) seated control with no drink (CTL). HIIE involved an evening session (1,700 h) of 10 × 1-min cycling efforts at â¼90% maximal heart rate with 1 min recovery. Diet was standardized and identical across all three 2-day trials, apart from the post-exercise carbohydrate drink in EX-HC, which was designed to replenish the exercise-induced energy expenditure. Postprandial glycemic responses to the following days breakfast, snack, lunch, and dinner, as well as 24 h indices of glycemic control, were analyzed. Results: The day after HIIE, postprandial glycemia following breakfast and snack were reduced in EX-NC compared to EX-HC, as reflected by lower 3 h glucose mean (breakfast: 5.5 ± 0.5 vs. 6.7 ± 1, p = 0.01, Cohen's d = 1.4; snack: 4.9 ± 0.3 vs. 5.7 ± 0.8 mmol/L, p = 0.02, d = 1.4) and/or area under the curve (AUC) (breakfast: 994 ± 86 vs. 1,208 ± 190 mmol/L x 3 h, p = 0.01, d = 1.5). Postprandial glycemic responses following lunch and dinner were not different across conditions (p > 0.05). The 24 h glucose mean (EX-NC: 5.2 ± 0.3 vs. EX-HC: 5.7 ± 0.7 mmol/L; p = 0.02, d = 1.1) and AUC (EX-NC: 7,448 ± 425 vs. EX-HC: 8,246 ± 957 mmol/L × 24 h; p = 0.02, d = 1.1) were reduced in EX-NC compared to EX-HC. Conclusion: Post-exercise carbohydrate-energy replacement attenuates glycemic control the day following a single session of low-volume HIIE in women.
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Type 2 diabetes (T2D) is a rapidly growing yet largely preventable chronic disease. Exaggerated increases in blood glucose concentration following meals is a primary contributor to many long-term complications of the disease that decrease quality of life and reduce lifespan. Adverse health consequences also manifest years prior to the development of T2D due to underlying insulin resistance and exaggerated postprandial concentrations of the glucose-lowering hormone insulin. Postprandial hyperglycemic and hyperinsulinemic excursions can be improved by exercise, which contributes to the well-established benefits of physical activity for the prevention and treatment of T2D. The aim of this review is to describe the postprandial dysmetabolism that occurs in individuals at risk for and with T2D, and highlight how acute and chronic exercise can lower postprandial glucose and insulin excursions. In addition to describing the effects of traditional moderate-intensity continuous exercise on glycemic control, we highlight other forms of activity including low-intensity walking, high-intensity interval exercise, and resistance training. In an effort to improve knowledge translation and implementation of exercise for maximal glycemic benefits, we also describe how timing of exercise around meals and post-exercise nutrition can modify acute and chronic effects of exercise on glycemic control and insulin sensitivity. Novelty: Exaggerated postprandial blood glucose and insulin excursions are associated with disease risk. Both a single session and repeated sessions of exercise improve postprandial glycemic control in individuals with and without T2D. The glycemic benefits of exercise can be enhanced by considering the timing and macronutrient composition of meals around exercise.