Microvascular Vasodilatory Consequences of Acute Consumption of a High Fructose Caffeinated Soft Drink
Authors: Greenshields Joel , Freemas Jessica A. , Baker Tyler B. , Johnson Blair D. , Carter Stephen J. , Schlader Zachary 
Published: April 2020

Purpose

Excessive intake of high fructose sugar sweetened beverages is associated with a greater risk of cardiovascular disease. This increased risk may be attributed, in part, to fructose‐mediated elevations in vasoconstrictor tone. Compared to water, consumption of a high fructose caffeinated soft drink elicits vasoconstriction in the kidneys and augments the renal vasoconstrictor response during sympathetic stimulation. It is unknown if these observed effects are specific to the kidneys or are indicative of a systemic vascular response. Endothelial dysfunction, which is characterized by a pro‐vasoconstrictor shift mostly due to reductions in nitric oxide bioavailability, is one of the earliest pathogenic vascular changes leading to cardiovascular disease. Experimental investigation of microvascular endothelial function may offer insight into the mechanisms contributing to the elevated cardiovascular disease risk associated with intake of high fructose sugar sweetened beverages. Therefore, the purpose of this study was to test the hypothesis that acute consumption of a high fructose caffeinated soft drink attenuates the cutaneous microvascular vasodilatory response to local heating, a primarily nitric oxide mediated response.

Methods

In a randomized cross‐over design, 8 healthy adults (26 ± 2 y, 4 women) consumed either 500 mL of a high‐fructose caffeinated beverage (Mountain Dew®, Soda) or 500 mL of water (H2O) while resting supine. Red blood cell flux, an index of skin blood flow, was measured at two sites on the dorsal aspect of the forearm using laser‐Doppler flowmetry probes seated in a local heater. Skin blood flow, blood pressure (finger photoplethysmography) and heart rate (ECG) were continuously measured. Data were analyzed at baseline, 30 min post‐consumption, and the last 5 min following 40 min of local heating at 39°C and 20 min of local heating at 44°C. Heating at 39°C was chosen because at this skin temperature and duration of heating the skin blood flow response is primarily nitric oxide dependent. Skin blood flow measures were averaged between sites and expressed as cutaneous vascular conductance (CVC), calculated as skin blood flow divided by mean arterial pressure. Data are presented as a percentage of the CVC response to local heating at 44°C (CVCmax).

Results

Mean arterial pressure did not differ between Soda and H2O at any time‐point (P=0.82). Heart rate was higher in Soda during local heating to 44°C (56 ± 7 vs. 52 ± 8 bpm, P=0.04), but did not differ at any other time‐point (P≥0.35). CVCmax did not differ between the Soda (3.5 ± 1.2 PU/mmHg) and H2O (3.4 ± 0.5 PU/mmHg) trials (P=0.82). CVC 30 min post‐consumption (Soda: 9 ± 7, H2O: 13 ± 18% CVCmax, P=0.53) or during local heating at 39°C (Soda: 58 ± 17, H2O: 58 ± 18% CVCmax, P=0.91) were not different between Soda and H2O.

Conclusions

These preliminary findings suggest the cutaneous microvascular vasodilator response to local heating is not affected by acute consumption of high fructose caffeinated beverage. It is possible that the vasoconstrictor response following acute high fructose caffeinated soft drink consumption may be specific to the kidneys and that systemic changes may not occur.