Usual Coffee Intake Research Articles

Coffee consumption and risk of renal cell carcinoma in the NIH-AARP Diet and Health Study.

Coffee consumption has been associated with a reduced risk of some cancers, but the evidence for renal cell carcinoma (RCC) is inconclusive. We investigated the relationship between coffee and RCC within a large cohort. Coffee intake was assessed at baseline in the National Institutes of Health-American Association of Retired Persons Diet and Health Study. Among 420 118 participants eligible for analysis, 2674 incident cases were identified. We fitted Cox-regression models to estimate hazard ratios (HRs) and 95% confidence intervals (CIs) for coffee consumption vs non-drinkers. We observed HRs of 0.94 (95% CI 0.81, 1.09), 0.94 (0.81, 1.09), 0.80 (0.70, 0.92) and 0.77 (0.66, 0.90) for usual coffee intake of <1, 1, 2-3 and ≥4 cups/day, respectively (Ptrend = 0.00003). This relationship was observed among never-smokers (≥4 cups/day: HR 0.62, 95% CI 0.46, 0.83; Ptrend = 0.000003) but not ever-smokers (HR 0.85, 95% CI 0.70, 1.05; Ptrend = 0.35; Pinteraction = 0.0009) and remained in analyses restricted to cases diagnosed >10 years after baseline (HR 0.65, 95% CI 0.51, 0.82; Ptrend = 0.0005). Associations were similar between subgroups who drank predominately caffeinated or decaffeinated coffee (Pinteraction = 0.74). In this investigation of coffee and RCC, to our knowledge the largest to date, we observed a 20% reduced risk for intake of ≥2 cups/day vs not drinking. Our findings add RCC to the growing list of cancers for which coffee consumption may be protective.

Abstract 4650: Coffee consumption and risk of renal cell carcinoma in the NIH-AARP Diet and Health Study

Abstract Background: Coffee consumption has been associated with lower all-cause mortality; however, its relationship to cancer risk is unclear. Evidence of inverse associations with cancers of the endometrium and liver were noted in a 2016 expert panel review convened by the International Agency for Research on Cancer, while findings for other malignancies were inconclusive. In the case of coffee and renal cell carcinoma (RCC), past studies have been limited by inadequate statistical power to detect modest effect sizes. To address this weakness in the existing literature, we investigated the relationship between coffee consumption and RCC risk in a large prospective cohort. Methods: Coffee intake was assessed at baseline with a food frequency questionnaire in the National Institutes of Health-AARP Diet and Health Study. Among 420,139 participants who were cancer-free at baseline, 2,674 incident cases of RCC were identified with a median of 16 years of follow-up. We fit multivariable-adjusted Cox proportional hazards models to estimate hazard ratios (HRs) and 95% confidence intervals (CIs) for coffee intake, with non-coffee drinkers as the reference group. We also conducted stratified analysis by sex, diabetes, and smoking status and subgroup analyses by consumption of predominately caffeinated vs. decaffeinated coffee. Results: We observed HRs for RCC of 0.95 (95% CI 0.82, 1.10), 0.95 (0.81, 1.10), 0.80 (0.70, 0.92) and 0.76 (0.65, 0.89) for usual coffee intake of &amp;lt;1, 1, 2-3 and 4+ cups per day respectively (Ptrend &amp;lt;0.00001). In sex-specific analyses the inverse relationship was observed among men (4+ cups per day: HR 0.70, 95% CI 0.58, 0.83; Ptrend &amp;lt;0.0001) but not women (HR 0.98, 95% CI 0.71, 1.35; Ptrend=0.12; Pinteraction=0.004). However, when restricting to non-smokers, we observed associations with coffee in both sexes (4+ cups per day: men: HR 0.68, 95% CI 0.48, 0.96, Ptrend = 0.002; women: HR 0.47, 95% CI 0.24, 0.91; Ptrend=0.0003). In other stratified analyses, the reduced risk for coffee remained in analyses restricted to those without a self-reported history of diabetes (HR 0.78, 95% CI 0.66, 0.92; Ptrend &amp;lt;0.0001) and was slightly stronger for usual caffeinated coffee drinkers (HR 0.66, 95% CI 0.54, 0.80; Ptrend &amp;lt;0.00001) than usual decaffeinated coffee drinkers (HR 0.76, 95% CI 0.57, 1.00; Ptrend=0.12), although a test of interaction was not significant (P=0.13). Our findings did not meaningfully change when we repeated our analyses excluding the first five years of follow-up. Conclusions: In this analysis of coffee consumption and RCC risk, to our knowledge the largest of its kind, we observed an approximately 20% reduced cancer risk for coffee consumption of 2 or more cups per day. Our findings provide the strongest epidemiologic evidence to date supporting an inverse association between coffee and RCC. Citation Format: Jongeun Rhee, Erikka Loftfield, Neal D. Freedman, Linda M. Liao, Rashmi Sinha, Mark P. Purdue. Coffee consumption and risk of renal cell carcinoma in the NIH-AARP Diet and Health Study [abstract]. In: Proceedings of the Annual Meeting of the American Association for Cancer Research 2020; 2020 Apr 27-28 and Jun 22-24. Philadelphia (PA): AACR; Cancer Res 2020;80(16 Suppl):Abstract nr 4650.

MP64-08 THE EFFECT OF COFFEE INTAKE AND RS762551 GENOTYPE ON SURVIVAL FOLLOWING PROSTATE CANCER DIAGNOSIS

You have accessJournal of UrologyProstate Cancer: Epidemiology & Natural History II (MP64)1 Apr 2020MP64-08 THE EFFECT OF COFFEE INTAKE AND RS762551 GENOTYPE ON SURVIVAL FOLLOWING PROSTATE CANCER DIAGNOSIS Justin Gregg*, Peng Wei, Ganiraju Manyam, Jeri Kim, Carrie Daniel, and Practical Consortium Justin Gregg*Justin Gregg* More articles by this author , Peng WeiPeng Wei More articles by this author , Ganiraju ManyamGaniraju Manyam More articles by this author , Jeri KimJeri Kim More articles by this author , Carrie DanielCarrie Daniel More articles by this author , and Practical Consortium More articles by this author View All Author Informationhttps://doi.org/10.1097/JU.0000000000000939.08AboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissionsReprints ShareFacebookLinked InTwitterEmail Abstract INTRODUCTION AND OBJECTIVE: Higher coffee intake has been associated with lower risk of both localized and aggressive prostate cancer (PCa), and our group has shown that coffee intake may be associated with decreased disease progression in men on active surveillance. Furthermore, this effect may be modified by caffeine metabolism-related single nucleotide polymorphism (SNP), rs762551. As part of an international consortium we investigated coffee intake in relation to overall (OS) and PCa-specific (PCSS) survival; and examined whether associations varied by genotype. METHODS: We utilized data from the PRACTICAL consortium, which included 4,161 men with PCa from five U.S., Australian and European studies with: 1) genotype data for the SNP of interest, 2) data on usual coffee intake, 3) at least 6 months of follow-up, and 4) over 120 subjects. PCa cases were followed as per individual protocols and were censored at date of last follow-up or death. Study-specific, multivariable-adjusted Cox proportional hazards models were used to evaluate coffee intake (categorized as 0, 0.1-2.5 and >2.5 cups/day) in relation to OS and PCSS after accounting for patient and pathologic factors. Fixed-effects meta-analysis was used to assess associations in all patients and by genotype. RESULTS: The average age was 63.7 years (SD 8.0) and 2,681 (64%) men had confirmed localized disease. Median coffee consumption was 2.0 cups/day (range 0-14 cups/day) and 71% of men reported drinking coffee daily. Over a median follow-up of 5.6 years (SD 4.11), 618 (15%) men died, of whom 343 died of PCa. After accounting for clinical factors in each study, the highest tertile of coffee intake (>2.5 cups/day) was associated with longer OS compared with the lowest tertile (0 cups/day; Pooled estimated HR [peHR] 0.70, 95%CI 0.54-0.90, P<0.01). Further, higher coffee intake was associated with longer PCSS (peHR 0.47, 95%CI 0.35-0.63, P<0.01). The most pronounced association between coffee intake and OS was observed for men with the AA or fast caffeine metabolism genotype (peHR 0.49, 95%CI 0.36-0.65, P<0.01); a more modest association was observed for men with the AC or CC genotypes (peHR 0.74, 95%CI 0.50-1.10, P=0.14). Similarly, the AA genotype was associated with longer PCSS (peHR 0.12, 95%CI 0.11-0.14, P<0.01), but not in those with the AC or CC genotypes (peHR 1.54, 95%CI 0.56-4.28, P=0.41). As for coffee intake and SNP interaction analysis, there was no significant interaction for OS, though it was significant with respect to 0.1-2.5 cups/day (P=0.03) and >2.5 cups/day (P<0.01) for PCSS. CONCLUSIONS: In a large, pooled cohort of men with PCa, coffee intake of >2.5 cups per day was associated with longer OS and PCSS. This association appears most pronounced in men with a genotype indicative of fast caffeine metabolism. Further work is warranted to investigate and validate potential coffee- and caffeine-related mechanisms that may underlie PCa related deaths. Source of Funding: None © 2020 by American Urological Association Education and Research, Inc.FiguresReferencesRelatedDetails Volume 203Issue Supplement 4April 2020Page: e966-e966 Advertisement Copyright & Permissions© 2020 by American Urological Association Education and Research, Inc.MetricsAuthor Information Justin Gregg* More articles by this author Peng Wei More articles by this author Ganiraju Manyam More articles by this author Jeri Kim More articles by this author Carrie Daniel More articles by this author Practical Consortium More articles by this author Expand All Advertisement PDF downloadLoading ...

Association between Coffee Consumption and Its Polyphenols with Cardiovascular Risk Factors: A Population-Based Study.

Epidemiological studies have examined the effect of coffee intake on cardiovascular disease, but the benefits and risks for the cardiovascular system remain controversial. Our objective was to evaluate the association between coffee consumption and its polyphenols on cardiovascular risk factors. Data came from the “Health Survey of São Paulo (ISA-Capital)” among 557 individuals, in São Paulo, Brazil. Diet was assessed by two 24-h dietary recalls. Coffee consumption was categorized into <1, 1–3, and ≥3 cups/day. Polyphenol intake was calculated by matching food consumption data with the Phenol-Explorer database. Multiple logistic regression models were used to assess the associations between cardiovascular risk factors (blood pressure, total cholesterol, low-density lipoprotein cholesterol (LDL-c), high-density lipoprotein cholesterol (HDL-c), triglycerides, fasting glucose, and homocysteine) and usual coffee intake. The odds were lower among individuals who drank 1–3 cups of coffee/day to elevated systolic blood pressure (SBP) (Odds Ratio (OR) = 0.45; 95% Confidence Interval (95% CI): 0.26, 0.78), elevated diastolic blood pressure (DBP) (OR = 0.44; 95% CI: 0.20, 0.98), and hyperhomocysteinemia (OR = 0.32; 95% CI: 0.11, 0.93). Furthermore, significant inverse associations were also observed between moderate intake of coffee polyphenols and elevated SBP (OR = 0.46; 95% CI: 0.24, 0.87), elevated DBP (OR = 0.51; 95% CI: 0.26, 0.98), and hyperhomocysteinemia (OR = 0.29; 95% CI: 0.11, 0.78). In conclusion, coffee intake of 1–3 cups/day and its polyphenols were associated with lower odds of elevated SBP, DBP, and hyperhomocysteinemia. Thus, the moderate consumption of coffee, a polyphenol-rich beverage, could exert a protective effect against some cardiovascular risk factors.

The effect of coffee intake on lysophosphatidylcholines: A targeted metabolomic approach

Lysophosphatidylcholines (lysoPC) are known to be a pathological component of oxidized-LDL, and several studies demonstrate its pro-inflammatory properties invitro. Nevertheless, bioactive compounds found in coffee, such as phenolic acids might inhibit LDL oxidation. The relationship between coffee consumption and lysoPC has not been described previously in humans. The aim of the present study was to assess the association between coffee intake and plasma lysoPC levels in adults. Data was from the "Health Survey of Sao Paulo (ISA-Capital)", a cross-sectional population-based survey in Sao Paulo, among 169 individuals aged 20 years or older. This population was categorized into three groups: non-coffee consumers (0mL/day-G1), low coffee consumers (≤100mL/day-G2), and high coffee consumers (>100mL/day-G3). Usual coffee intake was estimated by two 24HR and one FFQ, using Multiple Source Method. Quantification of the metabolites was performed by mass spectrometry (FIA-MS/MS and HPLC-MS/MS) and 14 lysoPC species were identified. The association between coffee intake and lysoPC was analyzed by multiple linear regression adjusted for age, sex, household per capita income, smoking, physical activity, body mass index, total energy intake, use of drugs, vegetables and fruit consumption and caffeine intake. LysoPC levels were significantly lower in G3 than in G1, for the lysoPC a C16:1 (β=-0.56; p=0.014), lysoPC a C18:1 (β=-2.57; p=0.018), and lysoPC a C20:4 (β=-1.14; p=0.037). In opposition, the ratios of C16:0/C16:1 and C18:0/18:1 was higher in G3 (β=5.04; p=0.025 and β=0.28; p=0.003, respectively). LysoPC profile differed according to coffee intake, showing a possible beneficial health effect of this beverage on inflammatory and oxidative processes.

Usual Coffee Intake among Adults in the United States

BackgroundDespite widespread popularity and possible health effects, the prevalence and distribution of coffee in US adults is poorly characterized.ObjectiveOur aim was to estimate usual daily coffee consumption among US adults according to demographic, socioeconomic, and other health‐related factors.MethodsDietary intake data was obtained from a food frequency questionnaire (FFQ) and two nonconsecutive 24‐hour dietary recalls administered during the National Health and Nutrition Examination Survey (NHANES) from 2003 to 2006. Analyses were weighted so that estimates were representative of the US adult population, aged ≥20 years, (n=6,219; weighted n=206,574,330). The NCI method, incorporating FFQ and dietary recall data, was used to estimate both the probability of consumption and the amount of coffee consumed by gender, age, race/ethnicity, education, income, cigarette smoking, alcohol drinking, and general health condition. Trends in coffee intake over time were evaluated using linear regression to model day one intake from NHANES 2003 to 2012 (n=24,950) adjusted for gender, age, and race/ethnicity.ResultsAn estimated 154 million adults or 75% of the US population over 20 years of age drink coffee, and 65% of these coffee consumers drink coffee daily. Prevalence of coffee drinking did not differ by gender or general health condition, but was lower among non‐Hispanic blacks, adults earning less than $20,000 per year, never smokers, and non‐drinkers of alcohol. Additionally, prevalence was higher among older age groups with 86% of adults ≥60 years but only 59% of adults &lt;30 years drinking coffee. Overall, usual median ± SE coffee consumption was 7 ± 0.3 fl oz/day or 0.9 cups/day with the highest daily intake among men, older age groups, non‐Hispanic Whites, current smokers, and heavy drinkers of alcohol. Among consumers, usual median intake was 11 ± 0.4 fl oz/day or 1.4 cups/day. Population mean coffee intake did not significantly change from 2003 to 2012 (P for trend=0.10); furthermore, no significant changes were observed by gender, age, or racial/ethnic group over time.ConclusionsCoffee is a common dietary exposure particularly among older age groups, smokers, and alcohol drinkers who are also at higher risk of chronic disease and mortality. The data suggest that the probability of coffee drinking increases with age, but longitudinal studies are needed to understand lifetime changes in coffee drinking.Support or Funding InformationThis work was supported by the Intramural Research Program of the National Institutes of Health, Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, and Department of Health and Human Services.

Abstract 1880: Associations of coffee drinking with systemic immune and inflammatory markers

Abstract Background: Coffee drinking has been inversely associated with mortality as well as cancers of the endometrium, colon, skin and liver. Improved insulin sensitivity and reduced inflammation are among the hypothesized mechanisms by which coffee drinking may affect cancer risk. The association between coffee drinking and systemic levels of immune and inflammatory markers has not been well characterized. Objective: To explore the associations of coffee drinking with levels of a wide range of immune and inflammatory markers. Design: Luminex bead-based assays were used to measure serum levels of 77 immune and inflammatory markers in 1728 older non-Hispanic Whites from three case-control studies nested within the Prostate, Lung, Colorectal, and Ovarian Cancer Screening Trial. Usual coffee intake was self-reported using a semi-quantitative food frequency questionnaire. We used weighted multivariable logistic regression models to examine the associations between coffee drinking and dichotomized marker levels. We conducted statistical trend tests by assigning each coffee category its median value and modeling as a continuous variable. We applied a 20% false discovery rate criterion to the P-values for trend. Results: Ten of the 77 examined markers were nominally associated (P-value&amp;lt;0.05) with coffee drinking. The five markers that withstood correction for multiple comparisons included various aspects of the host response namely chemotaxis of monocytes/macrophages (IFNγ, CX3CL1/fractalkine, CCL4/MIP-1β), pro-inflammatory cytokines (sTNFRII) and regulators of cell growth (FGF-2). Heavy coffee drinkers had lower circulating levels of IFNγ (OR = 0.35; 95% CI 0.16, 0.75; P-trend = 0.0003), CX3CL1/fractalkine (OR = 0.25; 95% CI 0.10, 0.64; P-trend = 0.0031), CCL4/MIP-1β (OR = 0.48; 95% CI 0.24, 0.99; P-trend = 0.0050), FGF-2 (OR = 0.62; 95% CI 0.28, 1.38; P-trend = 0.0080) and sTNFRII (OR = 0.34; 95% CI 0.15, 0.79; P-trend = 0.0112) than non-coffee drinkers. Conclusions: Coffee drinking was associated with lower circulating levels of inflammatory markers, which may partially mediate previously observed associations of coffee drinking with lower mortality and morbidity. Validation studies, ideally controlled feeding trials, and prospective studies, such as nested case-control studies, are needed to confirm these associations. Citation Format: Erikka Loftfield, Meredith S. Shiels, Barry I. Graubard, Hormuzd A. Katki, Anil Chaturvedi, Britton Trabert, Ligia Pinto, Troy Kemp, Fatma M. Shebl, Susan T. Mayne, Nicolas Wentzensen, Mark P. Purdue, Allan Hildesheim, Rashmi Sinha, Neal D. Freedman. Associations of coffee drinking with systemic immune and inflammatory markers. [abstract]. In: Proceedings of the 106th Annual Meeting of the American Association for Cancer Research; 2015 Apr 18-22; Philadelphia, PA. Philadelphia (PA): AACR; Cancer Res 2015;75(15 Suppl):Abstract nr 1880. doi:10.1158/1538-7445.AM2015-1880

Associations of Coffee Drinking with Systemic Immune and Inflammatory Markers.

Coffee drinking has been inversely associated with mortality as well as cancers of the endometrium, colon, skin, prostate, and liver. Improved insulin sensitivity and reduced inflammation are among the hypothesized mechanisms by which coffee drinking may affect cancer risk; however, associations between coffee drinking and systemic levels of immune and inflammatory markers have not been well characterized. We used Luminex bead-based assays to measure serum levels of 77 immune and inflammatory markers in 1,728 older non-Hispanic Whites. Usual coffee intake was self-reported using a food frequency questionnaire. We used weighted multivariable logistic regression models to examine associations between coffee and dichotomized marker levels. We conducted statistical trend tests by modeling the median value of each coffee category and applied a 20% false discovery rate criterion to P values. Ten of the 77 markers were nominally associated (P trend < 0.05) with coffee drinking. Five markers withstood correction for multiple comparisons and included aspects of the host response namely chemotaxis of monocytes/macrophages (IFNγ, CX3CL1/fractalkine, CCL4/MIP-1β), proinflammatory cytokines (sTNFRII), and regulators of cell growth (FGF-2). Heavy coffee drinkers had lower circulating levels of IFNγ [odds ratios (OR), 0.35; 95% confidence intervals (CI), 0.16-0.75], CX3CL1/fractalkine (OR, 0.25; 95% CI, 0.10-0.64), CCL4/MIP-1β (OR, 0.48; 95% CI, 0.24-0.99), FGF-2 (OR, 0.62; 95% CI, 0.28-1.38), and sTNFRII (OR, 0.34; 95% CI, 0.15-0.79) than non-coffee drinkers. Lower circulating levels of inflammatory markers among coffee drinkers may partially mediate previously observed associations of coffee with cancer and other chronic diseases. Validation studies, ideally controlled feeding trials, are needed to confirm these associations.

Serum biomarkers of habitual coffee consumption may provide insight into the mechanism underlying the association between coffee consumption and colorectal cancer

Coffee intake may be inversely associated with colorectal cancer; however, previous studies have been inconsistent. Serum coffee metabolites are integrated exposure measures that may clarify associations with cancer and elucidate underlying mechanisms. Our aims were 2-fold as follows: 1) to identify serum metabolites associated with coffee intake and 2) to examine these metabolites in relation to colorectal cancer. In a nested case-control study of 251 colorectal cancer cases and 247 matched control subjects from the Prostate, Lung, Colorectal, and Ovarian Cancer Screening Trial, we conducted untargeted metabolomics analyses of baseline serum by using ultrahigh-performance liquid-phase chromatography-tandem mass spectrometry and gas chromatography-mass spectrometry. Usual coffee intake was self-reported in a food-frequency questionnaire. We used partial Pearson correlations and linear regression to identify serum metabolites associated with coffee intake and conditional logistic regression to evaluate associations between coffee metabolites and colorectal cancer. After Bonferroni correction for multiple comparisons (P = 0.05 ÷ 657 metabolites), 29 serum metabolites were positively correlated with coffee intake (partial correlation coefficients: 0.18-0.61; P < 7.61 × 10(-5)); serum metabolites most highly correlated with coffee intake (partial correlation coefficients >0.40) included trigonelline (N'-methylnicotinate), quinate, and 7 unknown metabolites. Of 29 serum metabolites, 8 metabolites were directly related to caffeine metabolism, and 3 of these metabolites, theophylline (OR for 90th compared with 10th percentiles: 0.44; 95% CI: 0.25, 0.79; P-linear trend = 0.006), caffeine (OR for 90th compared with 10th percentiles: 0.56; 95% CI: 0.35, 0.89; P-linear trend = 0.015), and paraxanthine (OR for 90th compared with 10th percentiles: 0.58; 95% CI: 0.36, 0.94; P-linear trend = 0.027), were inversely associated with colorectal cancer. Serum metabolites can distinguish coffee drinkers from nondrinkers; some caffeine-related metabolites were inversely associated with colorectal cancer and should be studied further to clarify the role of coffee in the cause of colorectal cancer. The Prostate, Lung, Colorectal, and Ovarian trial was registered at clinicaltrials.gov as NCT00002540.

Coffee intake and breast cancer risk in the NIH‐AARP diet and health study cohort

There are several biologic mechanisms whereby coffee might reduce breast cancer risk. Caffeine and caffeic acid, major coffee constituents, have been shown to suppress mammary tumor formation in animal models and to inhibit DNA methylation in human breast cancer cells, respectively. Coffee may also reduce risk through decreasing inflammation and influencing estrogen metabolism. However, epidemiologic studies have been inconsistent and few studies have examined the association by estrogen and progesterone receptor (ER/PR) status. We evaluated coffee intake for its effect on incident breast cancer in the National Institutes of Health-AARP Diet and Health Study cohort, which included 198,404 women aged 50-71 with no history of cancer, who in 1995-1996 completed a questionnaire capturing usual coffee intake over the past year. State cancer registry and mortality index linkage identified 9,915 primary incident breast carcinomas through December 2006; available information on hormone receptor (HR) status identified 2,051 ER+/PR+ and 453 ER-/PR- cancers. In multivariable proportional hazards models, coffee intake was not associated with breast cancer risk (p-value for trend = 0.38; relative risk = 0.98, 95% confidence interval: 0.91-1.07, for four or more cups per day as compared to women who never drank coffee), and results did not vary by body mass index or history of benign breast biopsy (p-value for interaction > 0.10). We found no evidence of a relationship with either caffeinated or decaffeinated coffee. Null findings persisted for risk of both HR-positive and -negative breast cancers. These findings from a large prospective cohort do not support a role of coffee intake in breast carcinogenesis.

Caffeine Supplementation Had No Effect on Endurance Capacity in Elderly Subjects Who Had Abstained from Caffeine-Containing Nutrition for 8 Hours

Background: In this study, we investigated the effect of acute caffeine ingestion on physical performance after only 8 hours of caffeine abstinence. Methods: The study was a randomized, double-blind, cross-over study and included 30 healthy subject aged ≥70 years who had been recruited by their general practitioner. The participants abstained from caffeine for 8 hours (overnight) and the next morning they received placebo and then caffeine (6 mg/kg), or caffeine and then placebo at an interval of 1 week. One hour after the intervention we measured cycling endurance (ergometer), perceived effort during cycling (Borg scale), postural stability (force platform), and maximal isometric arm flexion strength and endurance (dynamometer chair). Blood samples were taken before the intervention, before cycling, after 5 minutes of cycling, and at exhaustion. Results: The participants had a usual coffee intake of six cups/day and after 8 hours of caffeine abstinence the plasma concentration of caffeine was 4.1 μM. Caf...