Physical Activity Offsets the Negative Effects of a High-fructose Diet

Amy J. Bidwell; Timothy J. Fairchild; Jessica Redmond; Long Wang; Stefan Keslacy; Jill A. Kanaley

Disclosures

Med Sci Sports Exerc. 2014;46(11):2091-2098. 

In This Article

Results

Subject Characteristics

Table 1 presents the subject characteristics of the study participants. Males were significantly heavier and taller and had a lower body fat percentage than the females (P < 0.05). There were no significant differences in weight (preintervention, 67.4 ± 9.1 kg; postintervention, 10.2 kg), BMI, or percent body fat after either intervention for both males and females (P < 0.05) (data not shown). There were no gender differences in any of the lipid or inflammatory markers; therefore, all subjects were combined for further analysis. No significant differences in fasting metabolic, inflammatory, and glucose markers for both pre- and post-FR+active and -FR+ inactive interventions were observed (data not shown). Moreover, there were no significant correlations between lipid and inflammatory markers (P > 0.05).

Dietary Analysis

The baseline energy intake for all subjects was 2701 kcal (Table 1). Energy intake was not significantly different between baseline and either intervention, and we observed no change in subjects' body weight (P > 0.05). Likewise, there was no difference in the macronutrient composition between the interventions (P > 0.05) (Table 2). The subjects consumed an additional 75 g of fructose per day from the drink provided (500 kcal, 0 g of fat, 135 g of CHO, and 74.9 g of fructose).

Glucose and Insulin

The test meal induced a significant postprandial response in both glucose and insulin concentrations (P < 0.05) (Fig. 1A–B). Glucose tAUC and postprandial Δpeak concentrations were not different after either intervention, but a significant intervention–time interaction occurred in insulin concentrations (Fig. 1B). Specifically, insulin tAUC for FR+active intervention decreased from pre- to postintervention, whereas there was no change in insulin tAUC after the inactive intervention (P = 0.04) (Fig. 1B). These differences in AUC can be accounted for by a 19% lower Δpeak insulin response after the FR+active intervention, whereas the Δpeak insulin in the FR+inactive condition was 21% higher postintervention (P < 0.01) (Fig. 1C).

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–time interaction. †P < 0.05 for main effect of meal.

TG

TG concentrations significantly increased in response to the test meal under both interventions (P < 0.01) (Fig. 2A). After log transformation, TG tAUC concentrations significantly increased from pre- to post-FR+inactive intervention (P = 0.04), whereas there was no change from pre- to post-FR+active intervention (Fig. 2B). Similarly, Δpeak TG increased by 88% as a result of the FR+inactive intervention but decreased by 5% (P < 0.01) with the FR+active intervention (Fig. 2C).

Figure 2.

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

VLDL

Figure 3A represents the 6-h postprandial response of VLDL concentrations after a test meal. Both pre- and post-FR+active and -FR+inactive interventions demonstrated a significant main effect across time for VLDL concentrations, at which point, concentrations peaked at 3 h (P = 0.03). The Δpeak VLDL induced a significant intervention–time interaction, such that the difference from pre- to post-FR+inactive intervention was significantly larger than the difference from pre- to post-FR+active intervention. The inactivity induced an 84% increase in Δpeak VLDL, whereas only a 33% increase after the FR+active intervention was observed (P = 0.009) (Fig. 3B).

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–time interaction. †P < 0.05 for main effect of meal.

Cholesterol

There was a significant main effect across time after the meal for total cholesterol (P = 0.03), but tAUC and Δpeak cholesterol were not significantly different between interventions (data not shown).

Inflammatory Markers

In response to the fructose test meal, a significant meal effect was observed for TNF-α concentrations, such that the test meal resulted in an increase in TNF-α concentrations over the course of 6 h (P = 0.02); however, there were no changes in CRP concentrations over time (P > 0.05) (data not shown). The FR+active and FR+inactive interventions did not result in any significant differences in TNF-α or CRP tAUC, iAUC, or Δpeak concentrations (P > 0.05).

In response to the test meal, IL-6 concentration showed a significant main effect of time (P = 0.02) (Fig. 4A). Furthermore, Δpeak IL-6 demonstrated a significant intervention–time interaction, such that Δpeak IL-6 concentrations decreased by 30% after the FR+active intervention, whereas they increased by 116% after the FR+inactive intervention from pre- to postintervention (P = 0.048) (Fig. 4B).

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–time interaction. †P < 0.05 for main effect of meal.

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