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High Protein Diet Maintains Glucose Production During Exercise-Induced Energy Deficit: A Controlled Trial

机译:高蛋白饮食在运动诱导的能量缺乏期间维持葡萄糖生成:对照试验

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Inadequate energy intake induces changes in endogenous glucose production (GP) to preserve muscle mass. Whether addition provision of dietary protein modulates GP response to energy deficit is unclear. The objective was to determine whether exercise-induced energy deficit effects on glucose metabolism are mitigated by increased dietary protein. Methods:Nineteen men (( mean +/- SD) 23 +/- 2 y, VO(sub2 peak) 59 +/- 5 ml-kg(exp-1)min(exp-1)) were divided into three groups, two consuming moderate (MP; 0.9 g protein-kg(exp-1)- d(exp-1)), and one high (HP; 1.8 g protein-kg(exp-1)-d(exp -1)) protein diets (55% energy from carbohydrate) for 11 days. Following 4 days of energy balance (D1-4), energy expenditure was increased for 7 days (D5-12) in all groups. Energy intake was unchanged in two, creating a 1000 kcal-d(exp-1) deficit (DEF- MP, DEF-HP; n = 6,both groups), whereas energy balance was maintained in the third (BAL-MP, n=7). Biochemical markers of substrate metabolism were measured during fasting rest on D4 and D12,as were GP and contribution of gluconeogenesis to endogenous glucose production (fgng) using 4-h primed, continuous infusions of 6,6-2H2 glucose (dilution-method) and 2-13C glycerol (MIDA technique). Glycogen breakdown (GB) was derived from GP and f(sub gng). Results: Plasma beta-hydroxybutyrate levels increased, and plasma glucose and insulin declined from D4 to D12,regardless of group. DEF-MP experienced decreased plasma GP from D4 to D12 ((mean change +/- SD) 0.24 +/- 0.24 mg- kg(exp-1)min(exp-1)), due to reduced GB from D4 (1.40 +/- 0.28 mg-kg(exp- 1)min(exp-1)) to D12 (1.16 +/- 0.17 mg-kg(exp-1)-min(exp-1)), P.

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