Arterial stiffness is not acutely modified by consumption of a caffeinated soft drink sweetened with high fructose corn syrup in young healthy adults

Abstract

Purpose Excessive intake of fructose is associated with an increased risk of developing cardiovascular disease. A major source of dietary fructose is the ingestion of high fructose corn syrup (HFCS) in sugar sweetened beverages (e.g., soft drinks). High arterial stiffness is an independent risk factor for cardiovascular morbidity and mortality. Thus, it is possible that regular consumption of beverages containing HFCS acutely and/or chronically increase arterial stiffness. However, this has never been explored. This study tested the hypothesis that ingestion of a caffeinated soft drink containing HFCS acutely increases arterial stiffness. Methods Fourteen healthy adults (25 ± 3 y, 6 women) reported to the laboratory for two experimental visits and consumed either 500 mL of tap water (H2O) or 500 mL of Mountain Dew® (an HFCS containing caffeinated beverage, DEW) in their first visit and consumed the other beverage in their next experimental visit, employing a counterbalanced, crossover, randomized design. Data were collected pre-consumption, 30 min post-consumption and 120 min post-consumption. Arterial stiffness was measured as carotid-to-femoral pulse wave velocity (cfPWV) using applanation tonometry. Peripheral (brachial) blood pressure was measured via electrosphygmomanometry. Central (aortic) blood pressure was estimated from transfer function analysis of the radial artery pressure waveform. Indices of pulse wave reflection were calculated from the synthesized central pressure waveforms. Data are presented as mean ± SD. Results cfPWV did not differ pre-consumption (DEW: 5.5 ± 0.6 m/s, H2O: 5.3 ± 0.7 m/s, P=0.69). At 30 min post-consumption, cfPWV was higher in the DEW trial (5.7 ± 0.6 m/s) compared to the H2O trial (5.3 ± 0.6 m/s, P=0.01), but cfPWV was not different between DEW and H2O at 120 min post-consumption (DEW: 5.7 ± 0.6 m/s, H2O: 5.5 ±0.6 m/s, P=0.13). Notably however, changes in cfPWV from pre-consumption did not differ between DEW and H2O at 30 min post- (DEW: 0.2 ± 0.3 m/s, H2O 0.0 ± 0.3 m/s, P=0.34) or 120 min post-consumption (DEW: 0.3 ± 0.4 m/s, H2O: 0.2 ± 0.3 m/s, P=0.77). Peripheral and central systolic (P≥0.50) and diastolic (P≥0.25) pressures did not differ between the DEW and H2O trials at any time point. Thus, peripheral (at 120 min post-consumption – DEW: 94 ± 6 mmHg, H2O: 92 ± 6 mmHg, P=0.31) and central (at 120 min post-consumption – DEW: 89 ± 7 mmHg, H2O: 85 ± 7 mmHg, P=0.13) mean arterial pressure also did not differ between trials. Moreover, aortic augmentation pressure, augmentation index, augmentation index corrected to a heart rate of 75 bpm, and reflection magnitude did not differ between the DEW and H2O trials at pre- (P≥0.22), 30 min post- (P≥0.55) or 120 min post-consumption (P>0.18). Conclusion Compared to drinking an equivalent volume of water, consumption of 500 mL of a commercially available caffeinated soft drink containing HFCS has little acute effect on indices of arterial stiffness or central blood pressure. The effect of chronic consumption of soft drinks containing HFCS on arterial stiffness and blood pressure regulation remain largely unknown.