Erik Konrad Grasser

Cardiovascular and cerebrovascular effects in response to Red Bull consumption combined with mental stress

The sale of energy drinks is often accompanied by a comprehensive and intense marketing with claims of benefits during periods of mental stress. As it has been shown that Red Bull negatively impacts human hemodynamics at rest, we investigated the cardiovascular and cerebrovascular consequences when Red Bull is combined with mental stress. In a randomized cross-over study, 20 young healthy humans ingested either 355 ml of a can Red Bull or water and underwent 80 minutes after the respective drink a mental arithmetic test for 5 minutes. Continuous cardiovascular and cerebrovascular recordings were performed for 20 minutes before and up to 90 minutes after drink ingestion. Measurements included beat-to-beat blood pressure (BP), heart rate, stroke volume, and cerebral blood flow velocity. Red Bull increased systolic BP (+7 mm Hg), diastolic BP (+4 mm Hg), and heart rate (+7 beats/min), whereas water drinking had no significant effects. Cerebral blood flow velocity decreased more in response to Red Bull than to water (-9 vs -3 cm/s, p <0.005). Additional mental stress further increased both systolic BP and diastolic BP (+3 mm Hg, p <0.05) and heart rate (+13 beats/min, p <0.005) in response to Red Bull; similar increases were also observed after water ingestion. In combination, Red Bull and mental stress increased systolic BP by about 10 mm Hg, diastolic BP by 7 mm Hg, and heart rate by 20 beats/min and decreased cerebral blood flow velocity by -7 cm/s. In conclusion, the combination of Red Bull and mental stress impose a cumulative cardiovascular load and reduces cerebral blood flow even under a mental challenge.

Cardiovascular and metabolic responses to tap water ingestion in young humans: does the water temperature matter?

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.

Cardiovascular responses to the ingestion of sugary drinks using a randomised cross-over study design: does glucose attenuate the blood pressure-elevating effect of fructose?

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 blood pressure-elevating effect of Red Bull energy drink is mimicked by caffeine but through different hemodynamic pathways

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 drinks 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 RBs 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.

Energy Drinks and Their Impact on the Cardiovascular System: Potential Mechanisms

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.

The thermic effect of sugar-free Red Bull: do the non-caffeine bioactive ingredients in energy drinks play a role?

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.

Postprandial hypotension in older adults: Can it be prevented by drinking water before the meal?

BACKGROUND & AIMS An important consequence of ageing is a tendency for postprandial blood pressure to decline, which can lead to fainting. As a possible countermeasure, we investigated in healthy older adults the impact of drinking water before a breakfast meal on postprandial cardiovascular and autonomic functions. METHODS After a stable cardiovascular baseline recording for at least 20 min, twelve older adult (67 ± 1 y) test subjects ingested, in a crossover study design, either 100 mL or 500 mL of tap water over 4 min, which was followed by the consumption of the test breakfast meal (1708 kJ) over a period of 15 min. Then, cardiovascular recordings were resumed for 90 min after the meal. Eleven young (25 ± 1 y) and healthy subjects served as a control group. Measurements included beat-to-beat blood pressure, heart rate, impedance cardiography and autonomic variables. RESULTS In older adults, systolic and diastolic blood pressure started to decline around 30 min after the meal, with the lowest values around 60 min; these effects were not observed in the young control group. Postprandial systolic blood pressure decreased between 30 and 90 min to a greater extent in response to 100 mL than to 500 mL (-6.4 vs. -3.3 mmHg, P < 0.05). Drinking 500 mL of water tended to increase stroke volume, cardiac output and vagal markers to a greater extent than 100 mL. CONCLUSIONS Our data suggest that drinking a large volume (500 mL) of water before a meal may attenuate postprandial hypotension in older adults.

It is likely that the drinking of cold and room temperature water decreases cardiac workload

To the Editor: Recently, we have provided indirect evidence for a decreased cardiac workload in young and healthy subjects in response to ingestion of 500 mL cold (3 C)or room (22 C)-tempered water, but not to body-tempered (37 C) water. This conclusion was based on the observation of a reduced heart rate and a decreased rate-pressure double product, a marker for myocardial oxygen consumption. Our view has been challenged by the letter to editor written by Dr. McMullen on the basis that ingestion of water is expected to elicit an enhanced sympathetic drive to the heart and thereby increasing cardiac contraction force, which would in turn lead to an increased cardiac workload. However, a careful analysis of our data does not support this argument. Dr. McMullen challenges our observation and raises two issues about our recent publication (Girona et al. 2014). Firstly, Dr. McMullen points out that we have not measured the rate of blood pressure changes (dP/ dt). He claims that a possible increase in dP/dt, elicited by a water-induced enhanced sympathetic drive to the heart, would increase stroke volume and thus blood pressure, which in turn would load baroreceptors to decrease heart rate. This increased dP/dt would then increase cardiac workload. Secondly, Dr. McMullen claims that we had no control condition and raises the issue of stationarity, thereby questioning the reliability of our measurements after the first 30 min postingestion. Before rebutting these two issues, we would like to point out that in the study by McMullen et al. (2014) cardiac contraction force was estimated from dP/dt measured at the finger level via infrared plethysmography, which is not the best method to evaluate cardiac contraction force (Sharman et al. 2007). The assessment of cardiac contractility even by measuring ventricular dP/dt with a high-fidelity catheter should be considered with some caution as it is influenced by preload (Carabello 2002). In addition, there are many differences between our study (Girona et al. 2014) and that by McMullen et al. (2014) besides subjects’ age (23 vs. 43 years on average) and amount of water ingested (500 vs. 100 mL). Firstly, their study subjects abstained from food and drink, excepting water, for only 2 h before the experimental session, a situation which could add variability in the baseline values. In contrast, our subjects came to the lab after an overnight fasting to ensure standardized conditions. Secondly and most importantly for baseline determination, McMullen’s participants ‘. . . moved to a sitting position and a 120 s pre-ingestion period was followed by . . . the presentation and ingestion of the interventions. . . .’ (McMullen et al. 2014). In contrast, in our study, we had no posture change and we waited 20–30 min after instrumentation before starting a 30 min baseline to ensure stable cardiovascular and metabolic parameters. As we did not measure dP/dt, one can merely speculate on a possible augmented dP/dt in response to drinking water. However, a risen dP/dt value does not necessarily reflect cardiac sympathetic activation as it is influenced by many other variables (Carabello 2002). An increased preload due to a longer filling time could also increase cardiac contraction force through distension of sarcomeres and contribute to the increased stroke volume. Moreover, our changes in stroke volume were rather small (+5–6% in the peak response) and less pronounced than the changes in heart rate, which explains the trend for a lower cardiac output. We would like to stress that cardiac workload cannot be derived from an averaged single beat (based on an increased stroke volume or an increased dP/dt), but we should consider instead the total cardiac workload over 1 min. A marked decrease in heart rate would then offset the increased workload of a single beat. The observed decrease in double product, which correlates with the oxygen consumption of the myocardium (Van Vliet & Montani 1999), is thus consistent with a diminished cardiac workload. We acknowledge that we did not include a no-drink control but the purpose of our study was to compare the responses across water drinks at different temperatures using a randomized cross-over design, which provides sufficient statistical power to draw concrete conclusions. Dr. McMullen also raises the issue of parameter stationarity after 30 min post-drink. Our results were presented as changes from a 30-min stable baseline with baseline values set to 0, explaining the low standard error of the mean (SEM) during the baseline period. An increased SEM after an intervention is expected due to the dynamic of the post-drink situation and that not all study subjects are expected to respond identically, but rather with individual variability in the

Water ingestion decreases cardiac workload time-dependent in healthy adults with no effect of gender

Ingestion of water entails a variety of cardiovascular responses. However, the precise effect remains elusive. We aimed to determine in healthy adults the effect of water on cardiac workload and to investigate potential gender differences. We pooled data from two controlled studies where blood pressure (BP) and heart rate (HR) were continuously recorded before and after the ingestion of 355 mL of tap water. Additionally, we calculated double product by multiplying systolic BP with HR and evaluated spectral parameters referring to vagal tone. All parameters were investigated for potential differences based on gender. In response to water, HR, systolic BP, and double product decreased significantly during the first 30 min. However, these effects were attenuated for HR and double product and even abolished for systolic BP over the subsequent 30 min. Over the entire post-drink period (60 min), decreases in HR and double product (all P < 0.05) were observed. Spectral markers for vagal tone increased with the on-set of the water drink and remained elevated until the end (P < 0.005). No significant gender difference in cardiac workload parameters was observed. We provide evidence that drinking water decreases, in a time-dependent fashion, cardiac workload and that these responses appear not to be influenced by gender.

Substantial inter-subject variability in blood pressure responses to glucose in a healthy, non-obese population

Aim: A large inter-subject variability in the blood pressure (BP) response to glucose drinks has been reported. However, the underlying factors remain elusive and we hypothesized that accompanying changes in glucose metabolism affect these BP responses. Methods: Cardiovascular and glycemic changes in response to a standard 75 g oral-glucose-tolerance-test were investigated in 30 healthy, non-obese males. Continuous cardiovascular monitoring, including beat-to-beat BP, electrocardiographically deduced heart rate and impedance cardiography, was performed during a 30 min baseline and continued up to 120 min after glucose ingestion. Blood samples were taken at baseline, 30, 60, 90, and 120 min for the assessment of glucose, insulin and c-peptide. Additionally, we evaluated body composition by using validated bioelectrical impedance techniques. Results: Individual overall changes (i.e., averages over 120 min) for systolic BP ranged from −4.9 to +4.7 mmHg, where increases and decreases were equally distributed (50%). Peak changes (i.e., peak averages over 10 min intervals) for systolic BP ranged from −1.3 to +9.5 mmHg, where 93% of subjects increased systolic BP above baseline values (similar for diastolic BP) whilst 63% of subjects increased peak systolic BP by more than 4 mmHg. Changes in peak systolic BP were negatively associated with the calculated Matsuda-index of insulin sensitivity (r = −0.39, p = 0.04) but with no other evaluated parameter including body composition. Moreover, besides a trend toward an association between overall changes in systolic BP and total fat mass percentage (r = +0.32, p = 0.09), no association was found between other body composition parameters and overall BP changes. Conclusion: Substantial inter-subject variability in BP changes was observed in a healthy, non-obese subpopulation in response to an oral glucose load. In 63% of subjects, peak systolic BP increased by more than a clinically relevant 4 mmHg. Peak systolic BP changes, but not overall BP changes, correlated with insulin sensitivity, with little influence of body composition.