Sucrose dampens caffeine-induced blood pressure elevations - A randomized crossover pilot study in healthy, non-obese men.

Purpose: Sales for sugar-sweetened and caffeinated beverages are still rising globally and their consumption has been linked to the development of cardiovascular diseases. However, direct evidence from human interventional studies in response to such beverages is still scarce. Methods: Seven young, non-obese men participated in a randomized crossover study where four test drinks [60 g sucrose + 50 mg caffeine, 60 g sucrose + caffeine-placebo, 50 mg caffeine, and caffeine-placebo] were investigated. Each drink was brought to a total volume of 500 mL with water. Continuous and beat-to-beat hemodynamic monitoring was conducted for 30 min baseline and continued for 90 min after the ingestion of each drink. Measurements included blood pressure, heart rate, stroke volume, cardiac output, total peripheral resistance, index of contractility, and double product. Results: Two-factor ANOVA analysis revealed significant treatment-by-time effects for diastolic blood pressure, heart rate, stroke volume, cardiac output, total peripheral resistance, index of contractility, and double product (all p < 0.01). Diastolic blood pressure and total peripheral resistance increased significantly to caffeine-only (all p < 0.05), while sucrose + caffeine-placebo and sucrose + caffeine both decreased resistance responses (all p < 0.05). Cardiac output increased significantly to sucrose + caffeine-placebo and sucrose + caffeine (all p < 0.05), and on trend for heart rate, stroke volume, and index of contractility (all p between 0.05 and 0.09). Conclusion: In young, non-obese men, a caffeinated and sucrose-sweetened beverage at concentrations similar to classical commercial Cola products exhibited distinct hemodynamic actions where the presence of sucrose dampened caffeine-induced blood pressure elevations, but at the expense of a tendency to increase cardiac work.

Dose-dependent heart rate responses to drinking water: a randomized crossover study in young, non-obese males.

PURPOSE: The aim of the study was to explore a potential dose effect of water on heart rate responses and markers of vagal tone modulation. METHODS: This was a randomized crossover study involving eight men whose heart rate and heart rate variability parameters were continuously measured following ingestion of different volumes of still mineral water (200, 400, 600, and 800 mL). RESULTS: A significant volume by time effect for heart rate (p < 0.005) was observed. Ingestion of all volumes of drink water of more 200 mL significantly decreased the heart rate. Significant time effects for heart rate variability parameters were observed. CONCLUSION: Ingestion of a mineral water drink affected the heart rate in men in a time-dependent manner, possibly by changes in cardiac vagal modulation.

Cardiovascular responses to a glucose drink in young male individuals with overweight/obesity and mild alterations in glucose metabolism, but without impaired glucose tolerance.

PURPOSE: Little is known about whether mild aberrations in glucose metabolism, which are seen in overweight/obese subjects (OW/OB) without impaired glucose tolerance, affect regulator control elements for blood pressure homeostasis. METHODS: Hence, we measured in age-matched male subjects with normal weight (n = 16; BMI = 22.4 kg m-2) and OW/OB (n = 11; BMI = 28.6 kg m-2) continuous beat-to-beat blood pressure, heart rate, stroke volume, myocardial contractility and baroreflex sensitivity during a 30 min baseline and for 120 min after the ingestion of 75 g glucose dissolved in 300 mL tap water (OGTT). Blood samples for the assessment of plasma glucose and insulin were collected at baseline and every 30 min after the drink and homeostatic model assessment of insulin resistance (HOMA-IR) was calculated. RESULTS: At baseline, glucose (5.3 ± 0.4 SD vs 5.0 ± 0.4 mmol L-1; p = 0.01), insulin (7.4 ± 0.4 vs 3.7 ± 2.7 mU L-1; p = 0.02) and HOMA-IR (1.8 ± 1.3 vs 0.8 ± 0.6; p = 0.01) were significantly higher in subjects with OW/OB, but none classified as having impaired glucose tolerance (plasma glucose levels < 7.8 mmol L-1 at 120 min post-OGTT) or hypertension (all < 130/80 mmHg at baseline). In response to the glucose drink, and in comparison to subjects with normal weight, we observed in subjects with OW/OB a trend towards increased plasma insulin levels (+7445 ± 4858 vs. +4968 ± 1924 mU h L-1; p = 0.08), which was not seen for blood glucose (p = 0.59). Moreover, subjects with OW/OB showed impaired peripheral vasodilation, diminished heart rate and myocardial contractility responses but increased peripheral pulse pressure (all p < 0.05). CONCLUSIONS: Young male subjects with OW/OB, but without glucose intolerance or hypertension, showed attenuated peripheral vasodilation and diminished cardiac responses to a glucose drink.

Perspective: Cardiovascular Responses to Sugar-Sweetened Beverages in Humans: A Narrative Review with Potential Hemodynamic Mechanisms.

Cardiovascular diseases are still the primary cause of mortality worldwide, with high blood pressure and type 2 diabetes as major promoters. Over the past 3 decades, almost in parallel with the rise in cardiovascular disease incidence, the consumption of sugar-sweetened beverages (SSBs) has increased. In this context, SSBs are potential contributors to weight gain and increase the risk for elevations in blood pressure, type 2 diabetes, coronary heart disease, and stroke. Nevertheless, the mechanisms underlying the cardiovascular and metabolic responses to SSBs, in particular on blood pressure, are poorly understood. We discuss and propose potential mechanisms underlying differential effects of sugars on postprandial blood pressure regulation; provide evidence for additional molecular contributors, i.e., fibroblast growth factor 21, towards sugar-induced cardiovascular responses; and discuss potential cardiovascular neutral sugars. Furthermore, we explore whether pre-existing glucose intolerance in humans exacerbates the cardiovascular responses to SSBs, thus potentially aggravating the cardiovascular risk in already-susceptible individuals.

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.

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.

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.

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.

Time course of cardiovascular responses induced by mental and orthostatic challenges.

Cardiovascular responses to single stressors diminish over time. Interaction of different stressors influencing hemodynamic variables, indicative of stress-induced reactivity and physiological responses are, however, poorly understood. We investigated time course of mental (using mental arithmetic, MA) and orthostatic (using head up tilt, HUT) challenges induced responses in 16 males. Three protocols were used: HUT, MA and MA+HUT, with sessions randomized and two weeks apart. Hemodynamic responses were compared for 30s epochs of stress application (stress(T1), stress(T2)...). Compared to baseline, HUT, HUT+MA and MA applications affected heart rate (HR) (+15.1+/-8.0 bpm, +20.0+/-9.2 bpm, +11.9+/-7.2 bpm, all p's<.001, respectively) and stroke volume (SV) (-22.3+/-8.1 ml, -22.0+/-10.4 ml, -7.6+/-8.7 ml, all p's<.001, respectively). HUT and MA+HUT induced HR increases were higher in stress(T2) compared to stress(T1) (p<.05) and reached maximum at stress(T2). HUT and MA+HUT further reduced SV in stress(T2) as compared to stress(T1) (p<.001); lowest SV was in stress(T2). Mean arterial pressure reached its minimum in stress(T1) during HUT and MA+HUT (-6.0+/-8.5mm Hg, p<.001, -4.4+/-9.7 mm Hg, p<.01, respectively) but increased in MA (+4.3+/-3.7 mm Hg, p<.01). Combination of MA+HUT resulted in different time courses of blood pressure responses as compared to HUT alone. We conclude that application of single or combined stress challenges lead to stressor- and time dependent-initial changes in cardiovascular responses. Our findings provide novel insights regarding the duration a stressor must be applied to elicit maximal cardiovascular responses.