PurposeEnergy drinks are beverages containing vasoactive metabolites, usually a combination of caffeine, taurine, glucuronolactone and sugars. There are concerns about the safety of energy drinks with some countries banning their sales. We determined the acute effects of a popular energy drink, Red Bull, on cardiovascular and hemodynamic variables, cerebrovascular parameters and microvascular endothelial function.MethodsTwenty-five young non-obese and healthy subjects attended two experimental sessions on separate days according to a randomized crossover study design. During each session, primary measurements included beat-to-beat blood pressure measurements, impedance cardiography and transcranial Doppler measurements for at least 20 min baseline and for 2 h following the ingestion of either 355 mL of the energy drink or 355 mL of tap water; the endothelial function test was performed before and two hours after either drink.ResultsUnlike the water control load, Red Bull consumption led to increases in both systolic and diastolic blood pressure (p < 0.005), associated with increased heart rate and cardiac output (p < 0.05), with no significant changes in total peripheral resistance and without diminished endothelial response to acetylcholine; consequently, double product (reflecting myocardial load) was increased (p < 0.005). Red Bull consumption also led to increases in cerebrovascular resistance and breathing frequency (p < 0.005), as well as to decreases in cerebral blood flow velocity (p < 0.005) and end-tidal carbon dioxide (p < 0.005).ConclusionOur results show an overall negative hemodynamic profile in response to ingestion of the energy drink Red Bull, in particular an elevated blood pressure and double product and a lower cerebral blood flow velocity.

a M. Girona and E. K. Grasser contributed equally to this work.Abstract Aim: Drinking water induces short-term cardiovascular and metabolic changes. These effects are considered to be triggered by gastric distension and osmotic factors, but little is known about the influence of water temperature. Methods: We determined, in a randomized crossover study, the acute cardiovascular and metabolic responses to 500 mL of tap water at 3°C (cold), 22°C (room) and 37°C (body) in 12 young humans to ascertain an effect of water temperature. We measured continuous beat-to-beat haemodynamics, skin blood flux with laser-Doppler flowmetry and resting energy expenditure by indirect calorimetry starting with a 30-min baseline followed by a 4-min drink period and a subsequent 90-min post-drink observation. Results: Ingestion of cold-and room-tempered water led to decreased heart rate (P < 0.01) and double product (P < 0.01), and increased stroke volume (P < 0.05); these effects were not observed with body-tempered water. Drinking cold-and room-, but not body-tempered water, led to increased high frequency power of heart rate variability (P < 0.05) and baroreflex sensitivity (P < 0.05). Cold-and room-tempered water increased energy expenditure over 90 min by 2.9% (P < 0.05) and 2.3% (ns), respectively, accompanied by a diminished skin blood flux (P < 0.01), thereby suggesting that both small increases in heat production together with decreased heat loss contribute to warming up the ingested water to intra-abdominal temperature levels. Conclusions: Overall, ingestion of cold-and room-, but not body-tempered water reduced the workload to the heart through a reduction in heart rate and double product which could be mediated by an augmented cardiac vagal tone.

Globally, the popularity of energy drinks is steadily increasing. Scientific interest in their effects on cardiovascular and cerebrovascular systems in humans is also expanding and with it comes a growing number of case reports of adverse events associated with energy drinks. The vast majority of studies carried out in the general population report effects on blood pressure and heart rate. However, inconsistencies in the current literature render it difficult to draw firm conclusions with regard to the effects of energy drinks on cardiovascular and cerebrovascular variables. These inconsistencies are due, in part, to differences in methodologies, volume of drink ingested, and duration of postconsumption measurements, as well as subject variables during the test. Recent well-controlled, randomized crossover studies that used continuous beat-to-beat measurements provide evidence that cardiovascular responses to the ingestion of energy drinks are best explained by the actions of caffeine and sugar, with little influence from other ingredients. However, a role for other active constituents, such as taurine and glucuronolactone, cannot be ruled out. This article reviews the potentially adverse hemodynamic effects of energy drinks, particularly on blood pressure and heart rate, and discusses the mechanisms by which their active ingredients may interact to adversely affect the cardiovascular system. Research areas and gaps in the literature are discussed with particular reference to the use of energy drinks among high-risk individuals. Adv Nutr 2016;7:950-60.

Overconsumption of sugar-sweetened beverages has been implicated in the pathogenesis of CVD. The objective of the present study was to elucidate acute haemodynamic and microcirculatory responses to the ingestion of sugary drinks made from sucrose, glucose or fructose at concentrations similar to those often found in commercial soft drinks. In a randomised cross-over study design, twelve young healthy human subjects (seven men) ingested 500 ml tap water in which was dissolved 60 g of either sucrose, glucose or fructose, or an amount of fructose equivalent to that present in sucrose (i.e. 30 g fructose). Continuous cardiovascular monitoring was performed for 30 min before and at 60 min after ingestion of sugary drinks, and measurements included beat-to-beat blood pressure (BP) and impedance cardiography. Additionally, microvascular endothelial function testing was performed after iontophoresis of acetylcholine and sodium nitroprusside using laser Doppler flowmetry. Ingestion of fructose (60 or 30 g) increased diastolic and mean BP to a greater extent than the ingestion of 60 g of either glucose or sucrose (P, 0·05). Ingestion of sucrose and glucose increased cardiac output (CO; P,0·05), index of contractility (P,0·05) and stroke volume (P, 0·05), but reduced total peripheral resistance (TPR; P,0·05), which contrasts with the tendency of fructose (60 and 30 g) to increase resistance. Microvascular endothelial function did not differ in response to the ingestion of various sugary drinks. In conclusion, ingestion of fructose, but not sucrose, increases BP in healthy human subjects. Although sucrose comprises glucose and fructose, its changes in TPR and CO are more related to glucose than to fructose.

The energy drink Red Bull (RB) has recently been shown to elevate resting blood pressure (BP) and double product (reflecting increased myocardial load). However, the extent to which these effects can be explained by the drink's caffeine and sugar content remains to be determined. We compared the cardiovascular impact of RB to those of a comparable amount of caffeine, and its sugar-free version in eight young healthy men. Participants attended four experimental sessions on separate days according to a placebo-controlled randomized crossover study design. Beat-to-beat hemodynamic measurements were made continuously for 30 min at baseline and for 2 h following ingestion of 355 mL of either (1) RB + placebo; (2) sugar-free RB + placebo; (3) water + 120 mg caffeine, or (4) water + placebo. RB, sugar-free RB, and water + caffeine increased BP equally (3–4 mmHg) in comparison to water + placebo (P < 0.001). RB increased heart rate, stroke volume, cardiac output, double product, and cardiac contractility, but decreased total peripheral resistance (TPR) (all P < 0.01), with no such changes observed following the other interventions. Conversely, sugar-free RB and water + caffeine both increased TPR in comparison to the water + placebo control (P < 0.05). While the impact of RB on BP is the same as that of a comparable quantity of caffeine, the increase occurs through different hemodynamic pathways with RB's effects primarily on cardiac parameters, while caffeine elicits primarily vascular effects. Additionally, the auxiliary components of RB (taurine, glucuronolactone, and B-group vitamins) do not appear to influence these pathways.