Abstract
Background Copious intake of soft drinks sweetened with high fructose corn syrup (HFCS) is associated with a heightened risk of cardiovascular disease, which is likely contributed to by chronic HFCS mediated endothelial dysfunction occurring secondary to decreased nitric oxide (NO) bioactivity. Acute consumption of a soft drink sweetened with HFCS does not affect cutaneous vasodilation during local heating, a functional test of NO bioactivity in the cutaneous microvasculature. However, this study was undertaken in the absence of a basal reduction in NO bioactivity, such as is speculated to occur with chronic intake of HFCS. Therefore, the present study tested the hypothesis that the cutaneous vasodilatory response to local skin heating following ischemia-reperfusion injury, which acutely reduces NO bioactivity, is attenuated following acute consumption of a caffeinated soft drink sweetened with HFCS compared to water. Methods In a randomized, counter-balanced crossover design, fourteen healthy young adults (six women) consumed 500 mL of either tap water (H2O) or a caffeinated soft drink sweetened with HFCS (Mtn. Dew®, DEW). 30 min following consumption, participants underwent 20 min of forearm ischemia and 20 min of reperfusion. Local skin heating at the forearm to 39⁰C was performed for 40 min and increased to 44⁰C for 20 min. Skin blood flow (SkBF) was measured on the dorsal forearm using laser Doppler flowmetry, blood pressure was measured using the Penaz method, and heart rate was measured via 3-lead electrocardiogram. Cutaneous vascular conductance (CVC) was calculated as the quotient of SkBF and mean arterial pressure (MAP). SkBF and CVC data during local heating to 39⁰C, which is mostly a NO mediated response, were normalized as a percentage of maximal values obtained during local skin heating to 44⁰C. Data are presented as mean ± SD. Results During local skin heating at 44⁰C, there were no differences observed between H20 and DEW trials for SkBF (H2O: 252 ± 37 PU; DEW: 240 ± 35 PU, p = 0.317), CVC (H2O: 2.6 ± 0.4 PU/mmHg; DEW: 2.4 ± 0.5 PU/mmHg, p =0.215), MAP (H2O: 96 ± 6 mmHg; DEW: 101 ± 10 mmHg, p = 0 .162), and heart rate (H2O: 59 ± 7 bpm; DEW 60 ± 10 bpm, p = 0.654). During local skin heating to 39°C, no differences were observed in absolute SkBF (H2O: 154 ± 44 PU; DEW: 152 ± 44 PU, p = 0.879), percent of maximal SkBF (H20: 60.6 ± 12.2%; DEW 62.4 ± 12.7% p = 0.272), absolute CVC (H2O: 2 ± 0.5 PU/mmHg; DEW: 1.5 ± 0.5 PU/mmHg, p = 0.368), or percent of maximal CVC (H2O): 63.8 ± 13.9%; DEW 62.6 ± 13.7% p = 0.787) in the DEW and H2O trials. However, during local heating at 39°C DEW did result in a higher MAP (H2O: 92 ± 7 mmHg; DEW: 100 ± 12 mmHg, p = 0.022) and heart rate (H2O: 56 ± 7 bpm; DEW 59 ± 8 bpm, p = 0.032) compared to H2O. Conclusion Under conditions of ischemia-reperfusion injury, these data indicate that, compared to an equivalent volume of water, consumption of 500 mL of a caffeinated soft drink sweetened with HFCS does not affect the cutaneous vasodilatory response to local heating, a mostly nitric oxide mediated response.
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