Habitual Caffeine Consumption Research Articles

Intraocular Pressure, Glaucoma, and Dietary Caffeine Consumption: A Gene–Diet Interaction Study from the UK Biobank

Purpose:We examined the association of habitual caffeine intake with intraocular pressure (IOP) and glaucoma and whether genetic predisposition to higher IOP modified these associations. We also assessed whether genetic predisposition to higher coffee consumption was related to IOP.Design:Cross-sectional study in the UK Biobank.Participants:We included 121 374 participants (baseline ages, 39–73 years) with data on coffee and tea intake (collected 2006–2010) and corneal-compensated IOP measurements in 2009. In a subset of 77 906 participants with up to 5 web-based 24-hour-recall food frequency questionnaires (2009–2012), we evaluated total caffeine intake. We also assessed the same relationships with glaucoma (9286 cases and 189 763 controls).Methods:We evaluated multivariable-adjusted associations with IOP using linear regression and with glaucoma using logistic regression. For both outcomes, we examined gene–diet interactions using a polygenic risk score (PRS) that combined the effects of 111 genetic variants associated with IOP. We also performed Mendelian randomization using 8 genetic variants associated with coffee intake to assess potential causal effects of coffee consumption on IOP.Main Outcome Measures:Intraocular pressure and glaucoma.Results:Mendelian randomization analysis did not support a causal effect of coffee drinking on IOP (P > 0.1). Greater caffeine intake was associated weakly with lower IOP: the highest (≥232 mg/day) versus lowest (<87 mg/day) caffeine consumption was associated with a 0.10-mmHg lower IOP (Ptrend = 0.01). However, the IOP PRS modified this association: among those in the highest IOP PRS quartile, consuming > 480 mg/day versus < 80 mg/day was associated with a 0.35-mmHg higher IOP (Pinteraction = 0.01). The relationship between caffeine intake and glaucoma was null (P ≥ 0.1). However, the IOP PRS also modified this relationship: compared with those in the lowest IOP PRS quartile consuming no caffeine, those in the highest IOP PRS quartile consuming ≥ 321 mg/day showed a 3.90-fold higher glaucoma prevalence (Pinteraction = 0.0003).Conclusions:Habitual caffeine consumption was associated weakly with lower IOP, and the association between caffeine consumption and glaucoma was null. However, among participants with the strongest genetic predisposition to elevated IOP, greater caffeine consumption was associated with higher IOP and higher glaucoma prevalence.

Placebo Effect of Caffeine on Maximal Strength and Strength Endurance in Healthy Recreationally Trained Women Habituated to Caffeine.

Background: By using deceptive experimental designs, several investigations have observed that trained individuals may increase their performance when told they were given caffeine, when in fact they received a placebo (i.e., the placebo effect of caffeine). However, most of these investigations on the placebo effect of caffeine used individuals with low caffeine consumption or did not report habitual caffeine consumption, especially in studies analyzing resistance-based exercise. Hence, it is unknown if habitual caffeine consumers benefit from the placebo effect of caffeine on exercise performance. Thus, the aim of the present study was to analyze the placebo effect of caffeine on maximal strength and strength-endurance performance during the bench press exercise (BP) in women with mild–moderate daily consumption of caffeine. Methods: Thirteen resistance-trained women (BP one-repetition maximum (1RM) = 40.0 ± 9.7 kg) habituated to caffeine (4.1 ± 1.7 mg/kg/day) completed a deceptive randomized experimental design with two experimental trials. On one occasion, participants were told that they would receive 6 mg/kg of caffeine but received a placebo (PLAC), and on other occasions, participants did not receive any substance and were told that this was a control situation (CONT). In each experimental trial, participants underwent a 1RM BP test and a strength-endurance test consisting of performing the maximal number of repetitions at 50% of their 1RM. Results: In comparison to CONT, PLAC did not enhance 1RM (40.0 ± 10.5 kg vs. 41.0 ± 9.5 kg, respectively; p = 0.10), nor did it enhance the number of repetitions (32.2 ± 5.1 vs. 31.8 ± 4.5; p = 0.66) or mean power (130 ± 34 vs. 121 ± 26; p = 0.08) in the strength-endurance test. Conclusion: Informing participants that they were given caffeine, when in fact they received a placebo, did not modify any performance variable measured in this investigation. Thus, the use of the placebo effect of caffeine seemed an ineffective strategy to enhance muscle strength and strength endurance during the BP exercise in women with mild–moderate consumption of caffeine.

Habitual Caffeine Consumption Does Not Affect the Ergogenicity of Coffee Ingestion During a 5 km Cycling Time Trial.

There is growing evidence that caffeine and coffee ingestion prior to exercise provide similar ergogenic benefits. However, there has been a long-standing paradigm that habitual caffeine intake may influence the ergogenicity of caffeine supplementation. The aim of the present study was to investigate the effect of habitual caffeine intake on 5-km cycling time-trial performance following the ingestion of caffeinated coffee. Following institutional ethical approval, in a double-blind, randomized, crossover, placebo-controlled design, 46 recreationally active participants (27 men and 19 women) completed a 5-km cycling time trial on a cycle ergometer 60m in following the ingestion of 0.09g/kg coffee providing 3mg/kg of caffeine, or a placebo. Habitual caffeine consumption was assessed using a caffeine consumption questionnaire with low habitual caffeine consumption defined as <3 and ≥6mg · kg-1 · day-1 defined as high. An analysis of covariance using habitual caffeine intake as a covariant was performed to establish if habitual caffeine consumption had an impact on the ergogenic effect of coffee ingestion. Sixteen participants were classified as high-caffeine users and 30 as low. Ingesting caffeinated coffee improved 5-km cycling time-trial performance by 8 ± 12s; 95% confidence interval (CI) [5, 13]; p < .001; d = 0.30, with low, 9±14s; 95% CI [3, 14]; p = .002; d = 0.18, and high, 8 ± 10s; 95% CI [-1, 17]; p = .008; d = 0.06, users improving by a similar magnitude, 95% CI [-12, 12]; p = .946; d = 0.08. In conclusion, habitual caffeine consumption did not affect the ergogenicity of coffee ingestion prior to a 5-km cycling time trial.

CaffCo: A Valid and Reliable Tool to Assess Caffeine Consumption Habits, Caffeine Expectancies, and Caffeine Withdrawal Effects in Adults

Purpose: To develop and validate a questionnaire to evaluate caffeine consumption habits in adults. Methods: A caffeine habits and consumption questionnaire (CaffCo) was developed in three stages. ...

Coffee and Green Tea Decoction Intake in the Tunisian Population According to Genetic Polymorphisms of Genes Involved in Habitual Caffeine Intake

ABSTRACT The relationship between genetic variation and caffeinated beverages intake has been investigated in various human populations, but not among North Africans who have distinct caffeinated beverage dietary habits. Therefore, this study analysed the association between rs6968865 (AHR), rs382140 (NRCAM), rs9526558 (CAB39L), rs7754744 (PDSS2) and rs68157013 (TAS2R43) SNPs from previous GWASs on habitual caffeine consumption and caffeinated beverage intake in 568 healthy blood donors from the Tunisian population. The AHR caffeine metabolism gene SNP was associated with coffee intake but not with green tea decoction. However, the association of SNPs with caffeine metabolism (CAB39L and PDSS2), addiction to caffeine (NRCAM) and perceived caffeine bitterness (TAS2R43) genes was only observed or was stronger with the highest caffeine-containing beverage green tea decoction. The researchers further detected an opposite association of PDSS2 gene SNP with coffee and tea intake. The study provides additional data on caffeinated beverage intake genetics in a population with specific dietary habits

Habitual coffee intake and risk for nonalcoholic fatty liver disease: a two-sample Mendelian randomization study.

Epidemiological studies support a protective role of habitual coffee and caffeine consumption against the risk of non-alcoholic fatty liver disease (NAFLD). We aimed to investigate the causal relationship between coffee intake and the risk of NAFLD. We performed a two-sample Mendelian randomization (MR) analysis using SNPs associated with habitual coffee intake in a published genome-wide association study (GWAS) as genetic instruments and summary-level data from a published GWAS of NAFLD (1122 cases and 399,900 healthy controls) in the UK Biobank. The causal relationship was estimated with the inverse weighted method using a 4-SNP and 6-SNP instrument based on the single largest non-UK Biobank GWAS (n = 91,462) and meta-analysis (n = 121,524) of GWAS data on habitual coffee intake, respectively. To maximize power, we also used up to 77 SNPs associated with coffee intake at a liberal significance level (p ≤ 1e-4) as instruments. We observed a non-significant trend towards a causal protective effect of coffee intake on NAFLD based upon either the 4-SNP (OR: 0.76; 95% CI 0.51, 1.14, p = 0.19) or 6-SNP genetic instruments (OR: 0.77; 95% CI 0.48, 1.25, p = 0.29). The result also remains non-significant when using the more liberal 77-SNP instrument. Our findings do not support a causal relationship between coffee intake and NAFLD risk. However, despite the largest-to-date sample size, the power of this study may be limited by the non-specificity and moderate effect size of the genetic alleles on coffee intake.

The enhancing effect of 200 mg caffeine on mnemonic discrimination is at best small

ABSTRACT Mnemonic discrimination is the ability to discriminate among similar memories, which requires separable representations of similar information. The neurocomputational process that assumedly decorrelates representations during encoding and consolidation is referred to as pattern separation. Deficits in pattern separation contribute to age-related declines in mnemonic functioning, which has motivated the development of targeted interventions. We followed-up a recent report that one 200 mg-dose of caffeine administered post-study enhances mnemonic discrimination [Borota, D., Murray, E., Keceli, G., Chang, A., Watabe, J. M., Ly, M., Toscano, J. P., & Yassa, M. A. (2014). Post-study caffeine administration enhances memory consolidation in humans. Nature Neuroscience, 17(2), 201–203. https://doi.org/10.1038/nn.3623]. To test whether the reported enhancements are an artifact of performance-impairing withdrawal symptoms in the control group, we did not restrict preexperimental caffeine intake and statistically adjusted treatment effects for habitual caffeine consumption. We detected no effects of caffeine and nonsuperiority testing ruled out medium and large enhancements in both average (1200 mg per week) and low-consumers (50 mg per week). Our results raise doubts about a caffeine-mediated enhancement of mnemonic discrimination on two counts: If the effect exists, it (1) is substantially smaller than originally reported and (2) may reflect an offset of performance-impairing withdrawal symptoms rather than genuinely enhanced consolidation. We recommend that future studies employ an alternating exposure-abstinence protocol, use an active control group, and verify posttreatment caffeine abstinence via saliva or blood samples.

The Importance of Knowing Habitual Caffeine Consumption in Fatigue Risk Management Studies

The Importance of Knowing Habitual Caffeine Consumption in Fatigue Risk Management Studies

COFFEE VOLUME DOES NOT SUPPRESS APPETITE OR CHANGE PERCEIVED HUNGER IN HABITUAL CAFFEINE CONSUMERS

Caffeine is a heavily consumed substance that has several benefits, including appetite suppression and increased energy metabolism. PURPOSE: To determine the effect of caffeine amount and coffee volume on appetite profile, affective response, cognitive function, blood glucose levels and subsequent energy intake in female habitual caffeine consumers. METHODS: 19 healthy female (age: 24 ± 8, BF%: 24.9 ± 5.1) habitual caffeine consumers (255 ± 122 mg/day) ingested coffee of different volumes and caffeine amounts on four different occasions (C1: 237 ml/4 mg/kg; C2: 237 ml/6mg/kg; C3: 473 ml/4mg/kg; C4: 473 ml/6mg/kg) in a single blind, randomized, crossover design. Participants completed a visual analog scale (VAS) of appetite profile at pre, 0, 30 and 60 minutes. Affective response and cognitive function were assessed using the Activation-Deactivation Adjective Checklist (AD-ACL), Trail Making (TM) and Stroop tasks (ST) before and after the test drink. Blood glucose levels were measured at pre, 30 and 60 minutes. In addition, ad libitum breakfast was consumed at 60 minutes and 24-hour self-reported energy intake was recorded. A repeated measures ANOVA was used for analysis with significance accepted at p<0.05. RESULTS: A significant time (p<0.001), but not condition effect was observed in hunger (p=0.31), satiety (p=0.16), fullness (p=0.11), desire to eat (p=0.31) and prospective food consumption (p=0.19). No significant condition effect was observed in blood glucose levels (p=0.12), energy intake at breakfast (C1: 440 ± 213; C2: 400 ± 158; C3: 440 ± 226; C4: 386 ± 138 calories, p=0.43) or over 24-hours (C1: 16773 ± 532; C2: 1486 ± 434; C3: 1503 ± 321; C4: 1662 ± 505 calories, p=0.28). However, a significant interaction effect was observed in tiredness, calmness, energy and tension (p=0.02). In addition, a significant time (p<0.001) but not condition effect (p>0.05) was observed in TM, ST and state anxiety. Participants’ time to complete cognitive tasks decreased and state anxiety increased over time. CONCLUSIONS: Coffee volume may not have an effect on appetite suppression and perceived hunger, however, may modulate affective responses.

Caffeine Intake Does Not Negatively Affect Heart Rate Variability in Physically Active University Students: Preliminary Findings

Abstract Objectives Caffeine is a widely consumed stimulant on the beverage market. It is known to affect the autonomic nervous system (ANS), influencing the balance of parasympathetic versus sympathetic drive. This can be measured by heart rate variability (HRV) – fine scale changes in normal sinus rhythm. However, there has been little research done regarding the influence caffeinated drinks have on HRV in active university students. The purpose of this observational study is to examine the relationship between habitual caffeine intake and morning HRV readings in this population. It is hypothesized that higher intakes of caffeine will be associated with lower, more sympathetic HRV scores. Methods Healthy participants (N = 24, 18–25y) were drawn from two related investigations. Subjects were free of stimulant medications and recreationally active, but not part of an organized sports team. Subjects were given a daily diet log over 3–4 d to record food and drink intake, which was analyzed for caffeine (mg) using the Food Processor software (ESHA Research, Salem OR). Simultaneously, daily fasted HRV (100-scale composite score) was observed with a Holter-type sensor and software (ithlete, Southampton, UK) shortly after waking. Results Average caffeine intake did not significantly correlate with average HRV (r = 0.269; P = 0.204). Comparisons of caffeine intake with individual-day HRV measures were similarly weakly positive and non-significant with the exception of the final day of recording, which was more robust (r = 0.543; P = 0.036). Conclusions The data failed to support our hypothesis that habitual intakes of caffeine would be negatively associated with early morning, fasted HRV scores. Habitual caffeine consumption was not a significant contributor to sub-chronic sympathetic drive. Rather, the relationship tended to be positive (greater vagal tone), not negative (a more “stressed” ANS) as predicted. Future research should investigate the acute and chronic effects of specific caffeine sources on specific catecholamines and their relationship to HRV in young, physically active populations. Funding Sources University of Mount Union Inter-Science Research Club.

Inconsistency in the Ergogenic Effect of Caffeine in Athletes Who Regularly Consume Caffeine: Is It Due to the Disparity in the Criteria That Defines Habitual Caffeine Intake?

Caffeine is the most popular psychoactive substance in the world, and data suggests that it is widely used by athletes before competition to enhance physical and mental performance. The high number of athletes that regularly use caffeine suggests the need to investigate the effect of acute caffeine ingestion in athletes habituated to caffeine. However, most of the studies supporting this claim have used samples of athletes who do not consume caffeine on a regular basis, and with caffeine intake withdrawal prior to the experiments. A search through 19 databases conducted on habitual caffeine users was performed. The results of the studies regarding the ergogenic effect of caffeine in naïve vs. habitual caffeine consumers are contradictory. The diversity of results are likely associated with the use of different thresholds to categorize individuals as naïve or high caffeine consumers. There are no valid and standardized methods to accurately estimate the amount of caffeine ingested per day in athletes. We proposed a classification of athletes that habitually consume caffeine by using dietary questionnaires, and ultimately, to reduce the likelihood of discrepancies caused by the improper qualification of daily caffeine intake in studies directed at the assessment of acute caffeine intake in habitual caffeine consumers.

Three consecutive nights of sleep loss: Effects of morning caffeine consumption on subjective sleepiness/alertness, reaction time and simulated driving performance

Caffeinated products are often consumed as a popular countermeasure to the effects of sleep loss. However, the efficacy of caffeine to exert these effects after consecutive nights of sleep loss is poorly understood. The aim of this study was to investigate the effects of three consecutive nights of restricted sleep and morning caffeine consumption on subjective ratings of sleepiness/alertness, reaction time, and simulated driving performance. Twenty healthy, habitual caffeine consumers (11 females; age: 23.3 ± 5.7 y; BMI: 22.3 ± 3.5 kg⋅m−2; caffeine intake: 204 ± 89 mg⋅day−1; Mean ± SD) who had normal sleeping patterns (≥8 h⋅night−1) participated in this double-blind, placebo-controlled, randomised study. Following one night of normal sleep (≥8 h time in bed (TIB)), participants underwent three consecutive nights of restricted sleep (5 h TIB). Participants received caffeine (200 mg; n = 10) or placebo (n = 10) capsules each morning and all participants received caffeine (100 mg) capsules each afternoon. Subjective ratings of alertness, concentration and tiredness were measured before and 1 h after morning capsule administration. Choice Reaction Time (CRT) was examined 1 h after morning capsule administration, with response speed and accuracy as outcome variables. Driving performance was assessed using a 30 min simulated driving task, with lateral (standard deviation of lane position [SDLP]; total number of line crossings [LC]) and longitudinal (standard deviation of speed [SDSP]) measures of vehicle control as outcome variables. Alertness and concentration significantly decreased, and tiredness increased across the three days of sleep loss. Caffeine only marginally alleviated these effects. No differences were observed between treatments or across trial days for response speed and accuracy on the CRT task. Likewise, no significant differences were observed between groups or across trial days for any measures of simulated driving performance. Overall, results from this study indicate that three consecutive days of sleep loss influence subjective ratings of alertness, concentration and tiredness, but does not alter CRT or simulated driving performance. Caffeine may alleviate some of the negative subjective effects imposed by restricted sleep, but the efficacy of caffeine to attenuate performance changes in CRT and driving performance were unable to be observed.

Three consecutive nights of restricted sleep: effects of morning caffeine consumption on mood, reaction time and simulated driving performance

Introduction: Sleep is a fundamental biological requirement, essential for optimal health. Individuals unable to achieve adequate amounts of sleep may experience a range of negative behavioural and psychological consequences (e.g. increased daytime sleepiness, altered mood, reduced cognitive performance, driving impairment). Caffeinated products are often consumed as a popular countermeasure to reduce sleepiness, enhance mood, and improve cognitive functioning. However, the efficacy of caffeine to exert these effects after consecutive nights of restricted sleep is poorly understood, particularly in relation to performance on complex applied tasks (e.g. driving a motor vehicle). Therefore, the aim of this study was to investigate the effects of three consecutive nights of restricted sleep on subjective ratings of mood, cognitive function, and simulated driving performance and assess the ability of a morning dose of caffeine to attenuate any effects associated with sleep restriction. Materials and methods: Twenty healthy habitual caffeine consumers (11 females; age: 23.3±5.7 y; BMI: 22.3±3.5 kg·m-2; caffeine intake: 204±89 mg·day-1; Mean±SD) who had normal sleeping patterns (≥8 h sleep/night) participated in this double-blind, placebo-controlled, randomised study. Following one night of normal sleep (Day 0: ≥8 h time in bed (TIB)), participants underwent three consecutive nights of restricted sleep (Day 1, 2, 3: 5 h TIB). Participants received caffeine (200 mg; n=10) or placebo (n=10) capsules, together with a decaffeinated coffee and standardised breakfast each morning. All participants received caffeine (100 mg) capsules to consume in the afternoon of each trial day. On Day 0, 1 and 3, participants completed visual analog scales to measure subjective ratings of alertness, concentration and tiredness, before and 1 h after capsule administration. Cognitive function was examined 1 h after capsule administration using a computerised Choice Reaction Time (CRT) task. Response speed and accuracy were the outcome variables. Analysis of response speed was conducted using both traditional central tendency measures (comparing mean and variance) and ex-Gaussian distributional analysis. Driving performance was assessed using a 30 min simulated driving task. Lateral (standard deviation of lane position [SDLP] and total number of line crossings [LC]) and longitudinal (standard deviation of speed [SDSP]) measures of vehicular control were the outcome variables. Results: Alertness and concentration significantly decreased, and tiredness increased across the three days of sleep restriction (all p's< 0.001). Caffeine only marginally alleviated these effects. No differences were observed between treatments or across trial days for response speed and accuracy on the CRT task, irrespective of the analytical approach employed. Likewise, no significant differences were observed between groups or across trial days for lateral (SDLP, LC) and longitudinal (SDSP) measures of simulated driving performance. Conclusion: Overall, results from this study indicate that three consecutive days of sleep restriction may influence subjective ratings of alertness, concentration and tiredness, but does not appear to impact CRT or simulated driving performance. Caffeine may alleviate some of the negative subjective effects imposed by restricted sleep, but the efficacy of caffeine to attenuate performance changes in cognitive function and driving performance were unable to be observed in this study.

The Effects of High Doses of Caffeine on Maximal Strength and Muscular Endurance in Athletes Habituated to Caffeine.

Background: The main goal of this study was to assess the acute effects of the intake of 9 and 11 mg/kg/ body mass (b.m.) of caffeine (CAF) on maximal strength and muscle endurance in athletes habituated to caffeine. Methods: The study included 16 healthy strength-trained male athletes (age = 24.2 ± 4.2 years, body mass = 79.5 ± 8.5 kg, body mass index (BMI) = 24.5 ± 1.9, bench press 1RM = 118.3 ± 14.5 kg). All participants were habitual caffeine consumers (4.9 ± 1.1 mg/kg/b.m., 411 ± 136 mg of caffeine per day). This study had a randomized, crossover, double-blind design, where each participant performed three experimental sessions after ingesting either a placebo (PLAC) or 9 mg/kg/b.m. (CAF-9) and 11 mg/kg/b.m. (CAF-11) of caffeine. In each experimental session, participants underwent a 1RM strength test and a muscle endurance test in the bench press exercise at 50% 1RM while power output and bar velocity were measured in each test. Results: A one-way repeated measures ANOVA revealed a significant difference between PLAC, CAF-9, and CAF-11 groups in peak velocity (PV) (p = 0.04). Post-hoc tests showed a significant decrease for PV (p = 0.04) in the CAF-11 compared to the PLAC group. No other changes were found in the 1RM or muscle endurance tests with the ingestion of caffeine. Conclusion: The results of the present study indicate that high acute doses of CAF (9 and 11 mg/kg/b.m.) did not improve muscle strength nor muscle endurance in athletes habituated to this substance.

No association between coffee consumption and risk of atrial fibrillation: A Mendelian randomization study

Background and aimsSome observational studies have found that habitual coffee and caffeine consumption might reduce the risk of atrial fibrillation (AF). We conducted a two-sample Mendelian randomization study to explore the potential association between coffee consumption and AF. Methods and resultsThis study was based on summary-level data from the Atrial Fibrillation Consortium, including 588 190 individuals (65 446 cases and 522 744 non-cases). Nine single-nucleotide polymorphisms associated with coffee consumption at significance level of P < 5 × 10−8 were used as instrumental variables and were obtained from a genome-wide association study that included up to 375 833 individuals.The odds ratio of AF per genetically-predicted 50% increase of coffee consumption was 0.98 (95% confidence interval, 0.88, 1.10; P = 0.80) in the standard inverse-variance weighted analysis. Results were consistent in sensitivity analyses using the weighted median and MR-Egger methods, and no directional pleiotropy (P = 0.37) was observed. Moreover, complementary analyses that separated the coffee-related single-nucleotide polymorphisms based on their association with blood levels of caffeine metabolites (lower, higher, unrelated or unknown association) revealed no association with AF. ConclusionsThis study does not support a causal association between habitual coffee consumption and risk of AF.

The Acute Effect of Various Doses of Caffeine on Power Output and Velocity during the Bench Press Exercise among Athletes Habitually Using Caffeine.

Background: Previously studies confirm ergogenic effects of caffeine (CAF); however there is no available scientific data regarding the influence of acute CAF intake on power output in athletes habitually consuming CAF. The main goal of this study was to assess the acute effect of 3, 6, 9 mg/kg/b.m. doses of CAF intake on power output and bench press bar velocity in athletes habitually consuming CAF. Methods: The study included 15 healthy strength-trained male athletes (age = 26.8 ± 6.2 years, body mass = 82.6 ± 9.7 kg; BMI = 24.8 ± 2.7; bench press 1RM = 122.3 ± 24.5 kg). All participants were habitual caffeine consumers (5.2 ± 1.2 mg/kg/b.m.; 426 ± 102 mg of caffeine per day). This study had a randomized, crossover, double-blind study design where each participant performed four different experimental sessions, with one week interval between each trial. In every experimental session participants performed bench press, three sets of five repetitions at 50% 1RM. The power output and bar velocity assessments under four different conditions: a placebo (PLAC), and three doses of caffeine ingestion: 3 mg/kg/b.m. (CAF-3), 6 mg/kg/b.m. (CAF-6) and 9 mg/kg/b.m. (CAF-9). Results: The statistical significance was set at p < 0.05. The repeated measures ANOVA between PLAC and CAF-3; CAF-6; CAF-9 revealed no statistically significant differences in power output and velocity of the bar during the bench press exercise. A large effect size (ES) in mean power-output was found between PLAC and CAF-9 in Sets 1 and 2. A large ES in peak power-output was found between PLAC and CAF-6 in Set 2, and between PLAC and CAF-9 in Sets 1 and 2. A large ES in peak velocity was found between PLAC and CAF-9 in Sets 1–3. Conclusion: The results of the present study indicate that acute doses of CAF before exercise does not have a significant effect on power output and bar velocity in a group of habitual caffeine users.

Influence of caffeine upon tolerance to a simulated hemorrhagic challenge in habituated users

Caffeine is an adenosine receptor antagonist and its consumption in caffeine naïve individuals is associated with increased blood pressure. However, the influence of caffeine consumption upon blood pressure in individuals habituated to caffeine is less clear. Approximately 300mg of caffeine is consumed daily by 80% of the United States active duty military yet the influence of caffeine upon tolerance to a simulated hemorrhagic challenge in habituated users is unknown. Our aim was to examine the influence of caffeine consumption upon tolerance to a simulated hemorrhagic challenge (Lower Body Negative Pressure; LBNP) in habitual caffeine consumers. Eight healthy participants (age: 27 ± 6 yrs, Ht: 179 ± 10 cm, Wt: 76.0 ± 14.4 kg) completed three double blinded, counterbalanced trials (Caffeine, Decaffeinated and Water). Following baseline measures of cardiovascular control (including mean arterial pressure, MAP; mmHg and total peripheral resistance, TPR; mmHg/l/min) participants drank (6.25ml/kg body mass) either water (Water; volume control), decaffeinated coffee (Decaffeinated; placebo control) or caffeinated coffee (Caffeine; 4 mg caffeine/kg body mass). Participants were measured again following the ingestion of the drink (pre LBNP) and then underwent a graded LBNP protocol (−20mmHg, −30mmHg, etc.) until pre‐syncope. LBNP tolerance was quantified as cumulative stress index (CSI; mmHg*min). Data are presented at baseline (pre drink), prior to LBNP (pre LBNP and post drink), a common time point during LBNP tolerated by all individuals in all trials (−30mmHg) and at pre syncope. MAP increased from baseline to pre LBNP in all trials (Caffeine: from 84 ± 7 to 98 ± 7 mmHg; Decaffeinated: from 90 ± 10 to 94 ± 7 mmHg and Water: from 89 ± 9 to 97 ± 6 mmHg; P &lt; 0.05 in all trials). MAP was reduced at pre syncope in all trials (Caffeine: 59 ± 4 mmHg; Decaffeinated: 57 ± 4 and Water: 60 ± 7 mmHg; all P &lt; 0.05 relative to pre LBNP). MAP was not different between trials at any time point (P &gt; 0.05). TPR was not different from baseline during LBNP in the Water and Decaffeinated trials (from: 13 ± 2 and 14 ± 2 to −30mmHg: 16 ± 3 and 16 ± 2 mmHg/l/min, respectively both P &gt; 0.05 vs. baseline) but increased during LBNP in the Caffeine trial (from: 13 ± 2 to −30mmHg: 18 ± 3 mmHg/l/min; P = 0.004 vs. baseline). LBNP Tolerance was greater in the Caffeine trial (941 ± 376 mmHg*min, 19.2 ± 4.8 min) relative to the Decaffeinated trial (686 ± 382 mmHg*min, 15.7 ± 5.1 min; CSI: P = 0.021), but was not different relative to the Water trial (Water: 816 ± 383 mmHg*min, 17.5 ± 5.0 min; CSI: P = 0.093). Caffeine consumption alters cardiovascular control during a simulated hemorrhagic challenge and may influence LBNP tolerance in habitual caffeine users, although this affect appears to be small. This may have implications for the treatment of a hemorrhagic insult in individuals who are habitual caffeine users and whom have an elevated risk of hemorrhagic injury (e.g. soldiers).This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

Abstract P298: Normotensive Habitual Caffeine Consumers Experience No Change in Blood Pressure or Pulse Wave Velocity Following the Combined Consumption of Caffeine and Dietary Nitrate

Intro: Caffeine intake may elevate blood pressure (BP), while habitual consumption leads to developed tolerance, providing conflicting evidence for incurred changes in BP. Dietary nitrate consumption decreases BP and reduces arterial stiffness in patients with atherosclerosis and hypertension due to increased plasma nitrite and enhanced bioavailability of nitric oxide. However, a decline in BP for a healthy cohort could be an unwanted side effect for normotensive individuals. Less is known about the combined effects of dietary nitrate and caffeine on resting hemodynamics in a healthy population. Hypothesis: We hypothesized that caffeine supplementation would increase systolic blood pressure (SBP) and pulse wave velocity (PWV) while combined dietary nitrate consumption would attenuate this rise. Methods: In a randomized, double-blind, counterbalanced study, eight healthy, young adults who typically consumed some but not more than 500 mg caffeine/day completed 4 separate visits to the laboratory, each visit separated by one week. Prior to each visit, participants consumed a 4-day supplementation regimen of either dietary nitrate (12.4 mmol, NIT) or a placebo nitrate (PLN) combined with either caffeine (3 mg/kg, CAF) or placebo caffeine (PLC); this comprised 1 of 4 treatments. The final dose of NIT or PLN was consumed 2.5 hours prior to assessments while CAF or PLC was consumed 1 hour prior. Participants minimized consumption of dietary nitrate rich foods and caffeine during the 4 days leading up to their scheduled visit. Each visit consisted of measurements of peripheral SBP and diastolic blood pressure (DBP) with aortic central systolic and diastolic blood pressure (cSBP and cDBP, respectively) assessed noninvasively using pulse wave analysis. Measurement of arterial stiffness via applanation tonometry determined PWV. A linear mixed effects model analysis was performed to determine if supplementation regimen influenced hemodynamic parameters. Results: SBP of NIT+CAF (115±6 mmHg), PLN+CAF (117±9 mmHg), NIT+PLC (115±6 mmHg) and PLN+PLC (115±6 mmHg)(p=0.591) and PWV of NIT+CAF (5.5±1.1 m/s), PLN+CAF (5.8±0.7 m/s), NIT+PLC (5.8±0.6 m/s) and PLN+PLC (5.6±1.0 m/s) (p=0.353) were not statistically different between treatments. In addition, DBP (p=0.496), cSBP (p=0.656), cDBP (p=0.548), aortic augmentation index (p=0.054), and resting heart rate (p=0.646) were not different between treatments. Conclusion: Following 4 days of caffeine supplementation, habitual caffeine users did not experience any changes in resting hemodynamics when compared to a placebo supplement. In addition, dietary nitrate did not incur any changes in resting metrics whether or not it was consumed alongside caffeine. In this regard, habitual caffeine users are not affected by 3mg/kg doses of caffeine, and dietary nitrate (12.4 mmol/day) does not further reduce the BP of healthy normotensive adults.

Influence of genetic polymorphisms and habitual caffeine intake on the changes in blood pressure, pulse rate, and calculation speed after caffeine intake: A prospective, double blind, randomized trial in healthy volunteers

The aim of this study was to investigate the contribution of gene polymorphisms, in combination with habitual caffeine consumption, to the effect of caffeine intake on hemodynamic and psychoactive parameters. A double-blind, prospective study was conducted with 201 healthy volunteers randomly allocated 2:1 to the caffeinated group (150 mL decaffeinated coffee with additional 200 mg caffeine) or decaffeinated group (150 mL decaffeinated coffee). We measured the changes in blood pressure (BP) and calculation speed upon coffee intake, stratifying with gene polymorphisms, e.g., those in adenosine A2A receptor (ADORA2A) and cytochrome P450 (CYP) 1A2, and daily caffeine consumption (≤90 mg/day and >90 mg/day). Overall, caffeine intake independently increased BP and calculation speed (p-values < 0.05), irrespective of the polymorphisms. In stratified analysis, a statistical significance within the caffeinated group was observed for the change in systolic BP in the stratum of CYP1A2 polymorphism with daily caffeine consumption ≤90 mg/day: change in systolic BP in the CYP1A2 rs762551 CC group (mean ± SD = 11.8 ± 5.9) was higher than that in the AA/CA group (4.1 ± 5.5). Gene polymorphisms may limitedly modify the effect of caffeine intake on hemodynamic parameters in combination with habitual caffeine consumption.

Relationships between use of dietary supplements, caffeine and sensation seeking among college students

Objective: Caffeine and dietary supplement (DS) use by college students is not well-documented. Given reported associations between energy drink consumption and sensation seeking, we used the Sensation Seeking Scale Form V (SSS-V) to assess relationships between sensation-seeking, caffeine, and DS use. Participants: Data from 1,248 college students from five US institutions were collected from 2009 to 2011. Methods: Linear regression was used to examine relationships between scores on the SSS-V and caffeine and DS use, demographic, and lifestyle characteristics. Results: Male sex, nonHispanic race-ethnicity, higher family income, tobacco use, consuming caffeinated beverages, more than 400 mg caffeine per day, and energy drinks with alcohol at least 50% of the time, were significantly associated with higher total SSS-V scores (P < 0.001). Those using protein DSs had higher total, disinhibition, and boredom susceptibility SSS-V scores (Ps < 0.001). Conclusions: Results demonstrate a positive correlation between sensation-seeking attitudes and habitual caffeine, energy drink, and DS consumption.