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Increased Gastrointestinal Permeability During Prolonged Physical Stress Is Associated with Lower Energy Intakes but Not Dietary Macronutrient Composition

Increased gastrointestinal permeability (GP) induced by prolonged physical stress may contribute to systemic inflammation by facilitating translocation of microbial compounds from the gut. Though undernutrition and macronutrient intake independently modulate GP, relationships between diet and GP during prolonged physical stress are not well characterized. To examine the effects of energy and macronutrient intakes on GP during prolonged physical stress, 73 soldiers (71M/2F, 20 ± 1 yr, BMI 23 ± 2 kg/m2 [M ± SD]) were provided 3 combat rations/d, or 3 rations/d supplemented with 1000 kcal/d from protein‐ or carbohydrate‐based snacks during a 4‐d, 51 km cross‐country ski march (SKI). Energy intake was measured using ration‐specific checklists, and daily energy expenditure was measured in a subset (n = 41) by doubly‐labeled water. GP was measured in a subset (n = 48) over 24 hr before and again during SKI by dual sugar (sucralose and mannitol) absorption test. Plasma lipopolysaccharide (LPS) and serum IL‐6 were measured immediately before and after SKI as markers of microbial translocation and inflammation, respectively. Energy expenditure during SKI averaged 6179 ± 670 kcal/d. Energy deficit during SKI averaged 55 ± 12% in the combined cohort and was associated with a 2.8 ± 1.2 kg weight loss. GP increased 48 ± 7% (P < 0.001) during SKI independent of diet group (P = 0.96), and was positively associated with changes in LPS (r = 0.31, P = 0.04). Individuals with increased LPS experienced greater increases in IL‐6 relative to individuals with decreased LPS (P‐interaction = 0.07). Energy (r = −0.29), fat (r = −0.34), and carbohydrate (r = −0.31) intakes were associated with changes in GP (P ≤ 0.05), whereas the magnitude of energy deficit (r = 0.05, P = 0.79) and protein intake (r = −0.06, P = 0.67) were not. Associations between macronutrient intake and changes in GP were not significant when adjusted for total energy intake. Although correlative, these findings are consistent with microbial translocation concurrent to increased GP contributing to the inflammation induced by prolonged physical stress. Low energy intake, independent of the magnitude of energy deficit or dietary macronutrient composition, may potentiate increases in GP during periods of high energetic demand.