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.

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.

Objective: Consumption of energy drinks is increasing amongst athletes and the general public. By virtue of their bioactive ingredients (including caffeine, taurine, glucuronolactone, and B-group vitamins) and paucity of calories, sugar-free "diet" versions of these drinks could be a useful aid for weight maintenance. Yet little is known about the acute influence of these drinks, and specifically the role of the cocktail of non-caffeine ingredients, on resting energy expenditure (REE) and substrate oxidation. Therefore, the metabolic impact of sugar-free Red Bull (sfRB) to a comparable amount of caffeine was compared. Methods: REE and respiratory quotient (RQ) were measured in eight healthy young men by ventilatedhood indirect calorimetry for 30 min baseline and 2 h following ingestion of 355 ml of either: sfRB 1 placebo, water 1 120 mg caffeine, or water 1 placebo, according to a randomized cross-over design. Results: sfRB and water 1 caffeine both increased REE to the same degree (14%). Additionally, sfRB briefly increased RQ. Water 1 caffeine had no effect on RQ relative to water 1 placebo. Conclusions: sfRB enhanced thermogenesis and marginally shifted RQ to favor carbohydrate oxidation. The stimulatory effects of sfRB on REE are mimicked by water 1 caffeine, indicating that the auxiliary ingredients do not influence this thermic effect. The metabolic effects of sfRB are primarily due to caffeine alone.

1Conclusions Galactose thus presents the interesting characteristics of a low-glycemic sugar with mild cardiovascular effects. Further studies are warranted to confirm the clinical relevance of the milder cardiovascular effects of galactose than other sugars for insulin resistant obese and/ or diabetic patients with cardiac insufficiency.

Background/Objectives:Drinking large amounts of water is often recommended for weight control. Whether water intake stimulates energy and fat metabolism is, however, controversial with some studies reporting that drinking half a litre or more of water increases resting energy expenditure (REE) by 10–30% and decreases respiratory quotient (RQ), whereas others report no significant changes in REE or RQ. The aim here was to reassess the concept of water-induced thermogenesis and fat oxidation in humans, with particular focus on interindividual variability in REE and RQ responses, comparison with a time-control Sham drink, and on the potential impact of gender, body composition and abdominal adiposity.Subjects/Methods:REE and RQ were measured in healthy young adults (n=27; body mass index range: 18.5–33.9 kg m−2), by ventilated hood indirect calorimetry for at least 30 min before and 130 min after ingesting 500 ml of purified (distilled) water at 21–22 °C or after Sham drinking, in a randomized cross-over design. Body composition and abdominal fat were assessed by bioimpedance techniques.Results:Drinking 500 ml of distilled water led to marginal increases in REE (<3% above baseline), independently of gender, but which were not significantly different from Sham drinking. RQ was found to fall after the water drink, independently of gender, but it also diminished to a similar extent in response to sham drinking. Interindividual variability in REE and RQ responses was not associated with body fatness, central adiposity or fat-free mass.Conclusions:This study conducted in young men and women varying widely in adiposity, comparing the ingestion of distilled water to Sham drinking, suggests that ingestion of purified water per se does not result in the stimulation of thermogenesis or fat oxidation.