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

Discussion

The purpose of the current study was to determine whether manipulation of PA levels would alter individual susceptibility for metabolic risk factors associated with consumption of a moderate dose of excess fructose (approximately 75 g·d−1) over a 2-wk period, independent of energy intake. This study demonstrated in young healthy individuals that consumption of an additional 75 g of fructose per day in conjunction with physical inactivity (approximately 4200 steps per day) resulted in increased postprandial lipidemia and is a precursor to low-grade inflammation. These results were not observed when fructose was consumed during the 2-wk high PA intervention (approximately 13,000 steps per day), suggesting that the higher level of PA conferred protection against the metabolic stress of the additional fructose.

Previous research has identified that a diet high in fructose induces hepatic DNL, causing an increase in plasma TG and VLDL concentrations.[1,28,32] In addition, although not studied in this particular study, physical inactivity may reduce LPL activity, resulting in reduced rates of fatty acid use and oxidation in peripheral tissues (34). Therefore, we speculated that the increased rates of DNL associated with high fructose consumption seen previously,[32] coupled with the reduction in LPL activity with sedentary behavior (34) and, thus, reduced clearance rates of blood lipids, likely explain the increases observed in TG and VLDL concentrations. In agreement with previous research,[15,34] postprandial TG and VLDL concentrations in this study were elevated by 88% and 84% from baseline, respectively, in the FR+inactive intervention; however, no changes were observed in the active intervention.

Although glucose concentration was unaffected by the additional fructose intake during either 2-wk intervention, insulin concentration was 19% lower during the FR+active intervention when compared with that during the FR+inactive intervention. This is consistent with previous research showing decreased plasma insulin concentrations with PA.[21] Regular PA has beneficial effects on insulin sensitivity by enhancing insulin signaling, glucose transport, and substrate metabolism in muscles.[21] Therefore, although a high-fructose diet increases postprandial plasma lipids, which may alter the insulin-signaling cascade, increased PA seems to offset these deleterious consequences, most likely by altering intracellular substrate use.

Our data show a 116% increase in postprandial-induced peak IL-6 concentration in response to the FR+inactive intervention (Fig. 4), which was not observed in response to the FR+active intervention. Although the current study did not find changes in CRP and TNF-α (Table 2), the changes in IL-6 are in line with those in the study of Højbjerre et al.[16] who demonstrated an association between physical inactivity (without dietary modification) and elevated IL-6 concentrations. In the present study, the low PA (approximately 50% reduction in steps per day) during 2 wk seemed sufficient to increase postprandial IL-6 systemic concentration. In contrast, we found a 30% decrease in IL-6 levels after PA (increasing steps per day by approximately 50%). PA is a known protector against increases in inflammatory markers.[17] The acute increases in IL-6 levels that occur after exercise stimulate the release of many anti-inflammatory cytokines, particularly from the skeletal muscle, which may cause a long-term effect of attenuating low-grade inflammation and chronic IL-6 release.[17,27] As stated in previous research, physical inactivity increases IL-6 concentrations, which is known to reduce the expression of insulin substrate receptor 1 and glucose transporter type 4 receptors in adipocytes and decrease insulin-stimulated glucose transport, resulting in insulin resistance and glucose intolerance.[17] On the basis of previous studies and results from the current study, it is possible to speculate that a longer duration of physical inactivity, in conjunction with a diet high in fructose, could lead to deleterious effects of insulin signaling as a consequence of chronically elevated IL-6 concentrations.[3]

Although proinflammatory markers are often up-regulated with physical inactivity,[31] the addition of PA did not cause any change in TNF-α concentrations. These results were not unexpected because research has suggested that TNF-α concentrations are not affected by exercise.[16] Moreover, 2 wk of a moderately high-fructose diet may not be long enough to induce up-regulation of TNF-α.

In conclusion, in a population of young, healthy individuals, being physically inactive (approximately 4200 steps per day) while consuming an additional 75 g of fructose resulted in increased postprandial lipidemia and signs of potential low-grade inflammation, independent of energy intake, in as few as 2 wk. However, increased PA levels (approximately 13,000 steps per day) seem to protect against these adverse changes. Thus, low PA may increase susceptibility to both metabolic and cardiovascular risk factors within just 2 wk in a nonclinical population. While future research in clinical populations and additional dietary modifications should be explored in combination with other lifestyle factors, it becomes evident that basic advice concerning increased exercise needs to continue in the clinical setting.

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