The aim of this study was to evaluate the acute cardio- and cerebrovascular changes in response to a popular commercially available energy drink, RB. To the best of our knowledge, this is the first study that has evaluated the influence of an energy drink using beat-to-beat hemodynamics and cerebrovascular measurements. We show that ingestion of one can of RB resulted in an augmented workload to the heart as evidenced by elevated BP, HR, CO and DP values. Based on our findings that ingestion of RB does not lead to diminished microvascular endothelial function in response to acetylcholine, our study suggests that impaired endothelial function, at least in the microvasculature, is unlikely to account for the increased BP-elevating effect of RB. Furthermore, consumption of RB substantially decreased cerebral blood flow velocity and increased cerebrovascular resistance, which stands in agreement with the observed reduction in etCO2. The observed overall negative hemodynamic profile in response to one can of an energy drink could aggravate pre-existing health problems and warrants further studies using appropriate patient groups.
Energy drinks are one of the most rapidly increasing beverages promoted aggressively for their claimed beneficial effects on body and mental strength, but the data presented here suggest that consumption of energy drinks is potentially harmful because of the extra cardiac work load and the decreased cerebral blood flow velocity observed during resting conditions. While our data here showing BP-elevating effects of RB in young adults appear to be in conflict with several past studies in which RB ingestion was not found to increase BP, two main explanations can be put forward to account for these apparent discrepancies.
First, analysis of the time course of the changes in BP and heart rate in our study indicates that differences in response to the RB drink versus water control only became statistically significant as from 1 h post-drink, with peak values being reached between 80 and 90 min. Our study thus underscores the potential importance of assessing the cardiovascular effects of RB for periods lasting at least 1 h. This contention is consistent with the results of Alford et al.  and those of Baum and Weiss  where no BP-elevating effect of 250 or 500 mL of RB, respectively, was observed at 30 or 40 min post-drink. It is also in agreement with the data of Bichler et al.  where a change in BP or heart rate could not be demonstrated within 45 min after ingesting capsules containing 100 mg of caffeine and 1,000 mg of taurine, i.e., in amounts equivalent to those found in a 250 mL RB drink. Conversely, our data showing that BP-elevating effects of RB became significant between 1 and 2 h post-drink was in line with the findings of Worthley et al.  where an increase in BP was found 1 h after ingesting 250 mL of a sugar-free RB-like drink compared to a lack of change after water ingestion. Our data are also consistent with the report of Steinke et al.  that consumption of 500 mL of an energy drink that is similar in its composition to RB resulted in significant increases in heart rate (+5–7 beats per min) as well as in systolic and diastolic BP (+4–8 mmHg) between 1 and 4 h post-drink. Thus, unless the assessment of cardiovascular responses to RB and other energy drinks are conducted over periods of 1 h or more, there is a high risk for false-negative results.
Second, differences in the acute cardiovascular responses to RB between our study showing increased BP compared to those showing no effect can also be related to the use of different methodological approaches for measuring BP. Unlike our approach that measured BP by continuous beat-by-beat hemodynamics monitoring, the measurement of BP in previously reported studies by sphygmomanometry only occasionally throughout the experiment is likely to lack the degree of sensitivity required to detect statistically significant modest changes in BP. For example, Ragsdale et al. , in a double-blind experiment in 68 participants where 250 mL of RB was compared to control drinks, reported no changes in BP over a 2 h post-drink period with BP assessed by sphygmomanometry only at 0, 60 and 120 min in response to RB. A more detailed analysis of their data, however, reveals that at the 60 min measurement time-point, BP had increased by 3 mmHg (but non-significantly) in response to the RB drink but not with the control drink. In light of our findings that both systolic and diastolic BP peaks at 80–90 min post-drink, one therefore cannot disregard the possibility that this tendency of an increase in BP, with the RB at 60 min post-drink in Ragsdale’s study , may have been detected as a significant increase by continuous measurement of BP over the 2-h test period.
We conducted microvascular endothelial function testing to investigate whether hemodynamic changes following ingestion of energy drinks are linked to endothelial dysfunction. Using peripheral arterial tonometry to investigate a potential role of energy drinks in endothelial dysfunction, Worthley et al.  presented detrimental effects on endothelial function in their study. In addition, a case report revealed abnormal endothelial function, worse at 90 min following ingestion of a 24 oz (710 mL) Monster energy beverage using the brachial flow-mediated dilation method . These appear to be in contrast to our findings where acetylcholine-mediated endothelial function showed an augmented vasodilation after consumption of RB. Explanations for these differential findings may be related to differences in the method utilized to investigate endothelial function (i.e., microvascular endothelial function testing, which uses iontophoresis with acetylcholine and sodium-nitroprusside vs. flow-mediated dilation, which assesses the diameter of the brachial artery in response to reactive hyperemia using an ultrasound technique), differences in sugar content, the total volume of drink consumed and to differences in the content of caffeine and taurine in the drinks utilized. Our subjects ingested 355 mL RB containing 39.1 g of sugar while Worthley et al.  used a sugar-free energy drink with 250 mL drink volume containing also less caffeine and taurine compared to the RB drink in our study. Furthermore, a recent publication focusing on the impact of acute administration of caffeine on vascular function found that caffeine augments endothelium-dependent vasodilation in a healthy young subpopulation . However, caffeine may reduce myocardial blood flow during exercise, and therefore, given that many consume energy drinks and then exercise, this is an area that needs further study . Furthermore, as somnolence due to sleep deprivation is often an underlying reason for young people to consume energy drinks, studies investigating the interaction between caffeinated beverages and sleep deprivation on vascular functions are also warranted. On the other hand, it was observed that a daily taurine supplementation of 1.5 g in healthy humans had a beneficial impact on microvascular endothelial function in smokers as well as in control non-smokers . Because our study’s focus was on the cardiovascular responses to the energy drink per se rather to its specific ingredients, we can only conclude that microvascular endothelial dysfunction is not responsible for our observed increase in BP in response to RB. This conclusion is further supported through our hemodynamic beat-to-beat derived data where no change in the total peripheral resistance could be observed.
To our knowledge, this is the first documentation where cerebral blood flow velocity in response to ingestion of an energy drink has been evaluated. In our study, cerebral blood flow velocity started to decline immediately after the drink, reaching a minimum at 80 min and remained below baseline levels for at least 120 min post-drink. This was accompanied by an increased cerebrovascular resistance which could in part account for the observed decrease in velocity. As CO2 is known as one of the strongest metabolites affecting cerebral blood flow [30, 31], our findings that etCO2 levels are significantly decreased in response to the RB drink suggest that the observed drop in cerebral blood flow velocity and the accompanied rise in cerebrovascular resistance could be due, at least partly, to the change in etCO2 levels. Indeed, when taken together with the results of a previous study  which in evaluating the role of oral administered caffeine on cerebral circulation could not find a relation between CO2 and decreasing cerebral blood flow, the possibility arises that our observed changes in respiration parameters are not solely responsible for the observed changes in cerebral blood flow velocity. We cannot be sure whether other vasoactive substances in RB are also responsible for this novel observation, but caffeine is a likely candidate. Similarly, it is tempting to attribute the BP-elevating effects of RB to its caffeine content, but a recent pilot study  reported that repeated consumption of RB drinks between 8:00 and 19:00 led to an increase in mean 24 h and daytime ambulatory BP when compared to caffeine consumption alone. This raises the possibility that other ingredients in RB—in their own rights or in interaction with caffeine—may underline the BP-elevating effect of RB.
Our main findings here are that the RB drink results in an elevation in BP and diminished cerebral blood flow velocity, which contrast with the lack of effect of a similar volume of water (a control vehicle drink) on these hemodynamic parameters. There are of course numerous factors that could—via sensorial and/or metabolic effects—explain the observed differences between the RB drink and water vehicle. Further experiments are warranted to tease out the distinct component(s) of the RB drink (including sweet taste, calorie content, sugars, caffeine, taurine and glucuronolactone) that either in their own rights or through interactions with each other could be contributing to these differential hemodynamic effects.
In conclusion, our results show a negative hemodynamic profile in response to ingestion of RB in young and healthy humans and which could not be explained by impairments in endothelial function. Moreover, ingestion of an energy drink was associated with a substantial drop in cerebral blood flow, hence critically questioning the manufactures promotion about a better mental profile.