Submitted to: Nutrition and Metabolism
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 4/28/2011
Publication Date: 4/28/2011
Citation: Smith, T.J., Schwartz, J., Montain, S.J., Rood, J., Pikosky, M.A., Castaneda-Sceppa, C., Glickman, E., Young, A.J. 2011. High protein diet maintains glucose production during exercise-induced energy deficit: a controlled trial. Nutrition and Metabolism. 8(1):26. Interpretive Summary: Glucose (a carbohydrate) is the body’s primary fuel source during strenuous exercise. The body is able to maintain glucose production when energy intake matches energy output, but glucose production is reduced in response to prolonged fasting. It is unclear if this same response occurs when energy deficit (that is, energy intake < energy expenditure) is caused by an increase in exercise (instead of a decrease in energy intake) and whether additional dietary protein can prevent a decrease in glucose production. Nineteen men increased their exercise by 1000 calories per day for 5 days (one group received enough calories to support the increase in exercise and two groups did not). Isotope tracer methodology was use to determine how glucose is utilized by the body (i.e. glucose and glycerol- a type of fat- are injected in the arm followed by blood draws to measure their presence in the blood). The group that did not get enough calories to support the increase in exercise had a decline in glucose production. However, the group that received extra protein in their diet was able to maintain glucose production even though they also did not get enough calories to support the increase in exercise. Therefore, additional protein blunted the effects of an energy deficit caused by an increase in exercise on GP. This knowledge can be applied to persons who are not able to eat enough to meet the demands of an increase in exercise (such as soldiers) or in individuals trying to lose weight via an increase in exercise.
Technical Abstract: 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. Nineteen men ([mean +/- SD] 23 +/- 2 y, VO2peak 59 +/- 5 ml x kg-1 x 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. 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 x kg-1 x min-1), due to reduced GB from D4 (1.40 +/- 0.28 mg x kg-1 x min-1) to D12 (1.16 +/- 0.17 mg x kg-1 x 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 x kg-1 x min-1, respectively) by maintaining GB. Exercise-induced energy deficit decreased GP and additional dietary protein mitigated that effect.