Abstract
BackgroundInadequate 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.MethodsNineteen men ([mean ± SD] 23 ± 2 y, VO2peak 59 ± 5 ml·kg-1·min-1) were divided into three groups, two consuming moderate (MP; 0.9 g protein kg-1 d-1), and one high (HP; 1.8 g protein kg-1 d-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-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 fgng.ResultsPlasma β-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-1·min-1), due to reduced GB from D4 (1.40 ± 0.28 mg·kg-1·min-1) to D12 (1.16 ± 0.17 mg·kg-1·min-1), P < 0.05. Conversely, BAL-MP and DEF-HP sustained GP from D4 to D12 ([mean change ± SD] 0.1 ± 0.5 and 0.0 ± 0.2 mg·kg-1·min-1, respectively) by maintaining GB.ConclusionExercise-induced energy deficit decreased GP and additional dietary protein mitigated that effect.
Highlights
Inadequate energy intake induces changes in endogenous glucose production (GP) to preserve muscle mass
Protein intake in BAL-MP and DEF-MP was slightly higher than prescribed (~1.0 g·kg-1·d-1), while the DEF-HP met the prescribed level during BL and EX (~1.8 g·kg-1·d-1)
There was no difference in energy deficit between DEF-MP and DEF-HP
Summary
Inadequate energy intake induces changes in endogenous glucose production (GP) to preserve muscle mass. The objective was to determine whether exercise-induced energy deficit effects on glucose metabolism are mitigated by increased dietary protein. 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). Energy deficit induced by energy restriction or by the accumulation of additional physical activity results in negative nitrogen and protein balance [1,2]. A separate consequence of energy deficit is a reduction in hepatic glucose production [11,12]. Fluxes through intrahepatic glucoseproducing metabolic pathways are measured at rest, gluconeogenesis contributes approximately one-third and glycogenolysis contributes approximately two-thirds to the glucose released into the blood. Whether provision of gluconeogenic precursors, via provision of amino acids, affects the down regulation of hepatic glucose production has not been examined
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