Physical activity offsets the negative effects of a high-fructose diet

Abstract

Objective: This study aimed to determine the interaction between a high-fructose diet and PA levels on postprandial lipidemia and inflammation in normal-weight, recreationally active individuals.

Methods: Twenty-two men and women (age, 21.2 ± 0.6 yr; body mass index, 22.5 ± 0.6 kg · m(-2)) consumed an additional 75 g of fructose for 14 d on two separate occasions: high physical activity (PA) (approximately 12,500 steps per day) (FR+active) and low PA (approximately 4500 steps per day) (FR+inactive). A fructose-rich test meal was given before and at the end of each intervention. Blood was sampled at baseline and for 6 h after the meal for triglycerides (TG), VLDL, total cholesterol, glucose, insulin, tumor necrosis factor-α, interleukin 6, and C-reactive protein.

Results: Log-transformed TG area under the curve (AUC) significantly increased from before (10.1 ± 0.1 mg · dL(-1) × min for 6 h) to after (10.3 ± 0.08 mg · dL(-1) × min for 6 h, P = 0.04) the FR+inactive intervention, with an 88% increase in Δ peak TG (P = 0.009) and an 84% increase in Δ peak VLDL (P = 0.002). Δ Peak interleukin 6 also increased by 116% after the FR+inactive intervention (P = 0.009). Insulin total AUC significantly decreased after FR+active intervention (P = 0.04), with no change in AUC after the FR+inactive intervention. No changes were observed in glucose, tumor necrosis factor-α, and C-reactive protein concentrations (P > 0.05).

Conclusions: Low PA during a period of high fructose intake augments fructose-induced postprandial lipidemia and inflammation, whereas high PA minimizes these fructose-induced metabolic disturbances. Even within a young healthy population, maintenance of high PA (>12,500 steps per day) decreases susceptibility to cardiovascular risk factors associated with elevated fructose consumption.

Figure 1

(A) Postprandial response to the test meal on glucose concentrations. (B) Postprandial response to the test meal on insulin concentrations (C) insulin tAUC. (D) Δpeak insulin concentrations. Data are expressed as mean ± SEM. *P<0.05 significant intervention x time interaction. † P<.05 for main effect of meal.

Figure 2

(A) Postprandial effects of the test meal on triglyceride concentrations. (B) Triglyceride tAUC during the 6-hour test visits. (C) Change in triglyceride concentrations from baseline to peak levels. Data are expressed as mean ± SEM. *P< 0.05 intervention x time interaction. †P< 0.05 for main effect of meal.

Figure 3

(A) Postprandial effects of the test meal on VLDL concentrations. (B) Change in VLDL concentrations from baseline to peak levels. Data are expressed as mean ± SEM. *P<0.05 intervention x time interaction. †P< 0.05 main effect of meal.

Figure 4

(A) Postprandial effects of the test meal on IL-6 concentrations. (B) Change in IL-6 concentrations from baseline to peak levels. Data are expressed as mean ± SEM. *P<0.05 intervention x time interaction. †P< 0.05 meal main effect