Caffeine and heart rate

Caffeine, Your Heart and Exercise

One of the most common comments that I receive in seeing a new patient with a heart rhythm disorder is “when my heart started racing (or skipping beats) I stopped drinking anything with caffeine.” There seems to be a general perception that caffeine can irritate the heart. The use of caffeine may be at an all-time high in today’s society as it is in many drinks, energy supplements, exercise regiments, coffee, and some teas.

Caffeine is a natural product that is extracted from the raw fruit of coffee plants (over sixty species), kola nuts, cocoa, yerba maté, guarana berries, coffee beans and teas. Caffeine is rapidly absorbed in about 30-60 minutes in our bodies after ingestion.

Caffeine and Your Heart

The question behind the comment I often encounter in clinic is “does caffeine effect my heart?” The simple answer is that it does. Caffeine in high doses raises your blood level of epinephrine. Epinephrine is also known as adrenalin. In pure forms, epinephrine can increase blood pressure, increase the contractility or force of the heart, and mildly increase the heart rate. In patients that are susceptable to abnormal heart rhythms, high doses can cause the heart to develop skipped beats from the upper or lower heart chambers or palpitations from a rapid heart rhythm (1).

In most patients that I meet, when high doses of caffeine are consumed, there can be an uncomfortable feeling of the heart beating. This is usually due to a mildly elevated heart rate and increased force of each heartbeat. These are normal responses of the heart when exposed to epinephrine, but they can lead to uncomfortable symptoms. With normal heart responses the symptoms typically improve when the body levels of caffeine diminish. Unfortunately, if the caffeine causes the heart to beat abnormally, the abnormal heart rhythm can persist even after the body levels of caffeine are very low or even absent.

For most people that enjoy caffeinated products our bodies develop tolerance to caffeine over time and the effects on the heart are lessened. Unfortunately for most patients that have consumed caffeine for many years without significant changes, the development of new abnormal heart rhythms is usually independent of the caffeine. However, it is always a good idea to consider a trial of stopping caffeinated products if you experience an abnormal heart rhythm or any new heart symptoms.

When considering your caffeine courses, caffeine that has been extracted or developed as a chemical, dry product, or pill appears to be more potent in our bodies compared to natural sources of caffeine. For example, the metabolism and exercise performance effects with caffeine are greater with caffeine pills compared to coffee that has a similar level of caffeine (2).

Caffeine and Exercise

There are many studies that have examined the impact of caffeine during exercise. When interpreting these studies you must take into account that they were performed in people that were often athletes with healthy hearts and may not apply to people with heart disease. Recently, the Journal of the International Society of Sports Nutrition summarized the effects of caffeine on exercise:

“1. Caffeine is effective for enhancing sport performance in trained athletes when consumed in low-to-moderate dosages (~3-6 mg·kgBM-1) and overall does not result in further enhancement in performance when consumed in higher dosages (= 9 mg·kgBM-1).

2. Caffeine exerts a greater ergogenic effect when consumed in an anhydrous state as compared to coffee.

3. Caffeine enhances alertness during periods of extended exhaustive exercise, as well as periods of sustained sleep deprivation.

4. Caffeine is ergogenic for sustained maximal endurance exercise, and has been shown to be highly effective for time-trial performance.

5. Caffeine supplementation is beneficial for high-intensity exercise, including team sports such as soccer and rugby, both of which are categorized by intermittent activity within a period of prolonged duration.

6. The literature is equivocal when considering the effects of caffeine supplementation on strength-power performance, and additional research in this area is warranted.

7. The scientific literature does not support caffeine-induced diuresis during exercise, or any harmful change in fluid balance that would negatively affect performance” (3,4).

When you look at the total evidence available, in low to moderate levels, caffeine will likely result in an improvement in both your aerobic exercise ability and tolerance and may also provide benefit in resistance exercise (4).

In conclusion, if you feel abnormal heart beats or rhythms if you start using caffeine or start using high doses then stop using it. You may have to wait days after the caffeine exposure for your heart to go back to normal. If it doesn’t or the symptoms are severe, you should contact your doctor. If you develop these symptoms after years of using similar levels of caffeine, then your heart symptoms are likely caused from other sources. If you use caffeine to improve your exercise ability, use relatively low doses. The accumulative evidence with low to moderate amounts of caffeine and exercise suggests it is beneficial and relatively safe. If you have prior heart disease or abnormal heart rhythms, talk to your physician before starting an endurance exercise program in which you want to also use caffeine to enhance your performance.

Aug. 1, 2002 — Like millions of Americans, self-described coffee addict Kathy Liebswager can’t quite function in the mornings until she has had her caffeine fix. She typically drinks eight to 10 cups throughout the day, and she says she believes the caffeine has a calming effect on her.

“When I worked, I literally couldn’t think until I had had my first cup of coffee,” the retired Navy counselor says. “There have been periods when I cut way down or mixed decaffeinated coffee with regular, but I definitely missed the caffeine.”

Liebswager is not alone in thinking of caffeine as a stress reliever, but a new study suggests the opposite is true. Researchers at Duke University Medical Center found that caffeine actually exaggerates stress and its effect lasts throughout the day.

Even more troubling, the researchers concluded that the equivalent of four cups of coffee raises blood pressure for many hours. Although the increases appear modest, they are large enough to affect heart attack and stroke risk, says lead author James D. Lane, PhD. The findings were reported in the July/August issue of the journal Psychosomatic Medicine.

“The level of blood pressure change we saw has been associated with an increased risk of heart disease,” Lane tells WebMD. “People consuming typical amounts of coffee and caffeinated soft drinks are probably raising their blood pressure by an amount equal to the beneficial reduction seen with antihypertensive drugs. So if you are taking blood pressure medication, it may not be doing you any good if you are drinking three or four cups of coffee a day.”

Caffeine is consumed daily by an estimated 85% of adults in the U.S. in the form of coffee, tea, and sodas. The average daily number of cups per coffee drinker is 3.3, and 64% of all coffee is consumed at breakfast.

To determine the impact of caffeine consumption during the morning and early afternoon, Lane and colleagues recruited 47 daily coffee drinkers for a two-day study. Half of the subjects were given caffeine capsules on the first day and the other half were given placebo pills. On the second study day, the two groups were switched; the previous day’s placebo group got the caffeine and the caffeine group got the placebo.

Coffee Consumption and Coronary Heart Disease in Men and Women

The relation between coffee consumption and cardiovascular disease has been studied extensively. Although many previous cohort studies found no significant association between coffee and coronary heart disease (CHD),1–4 more recent results have been inconsistent. Although case-control studies found a positive association between coffee consumption and risk of CHD,5,6 prospective cohort studies reported a lower risk among individuals with higher coffee consumption.7,8 In addition, other studies suggested that both high and low coffee intake were associated with an increase in the risk of CHD compared with moderate coffee consumption.9,10

Clinical Perspective p 2053

In view of these discrepancies and recent findings that coffee consumption may protect against diabetes mellitus,11–15 we extended our previous analysis4,16 and assessed the association between coffee consumption and risk of CHD in 2 ongoing large cohort studies of men and women. We also examined whether the association between coffee consumption and CHD was modified by the presence of type 2 diabetes mellitus, smoking, alcohol consumption, or obesity. The long duration of follow-up (14 years for men and 20 years for women) and the use of repeated measurements allowed us to assess both the short- and long-term effects of coffee.

Methods

Study Population

The Health Professionals Follow-up Study (HPFS) was established in 1986 and the Nurses’ Health Study (NHS) in 1976. Information on the cohorts has been updated every 2 years. Further details have been published elsewhere.17 In the present study, after excluding participants with cardiovascular disease or cancer at baseline, we obtained 44 005 men and 84 488 women who were followed up until 2000. The Harvard School of Public Health and Brigham and Women’s Hospital Human Subjects Committee Review Board approved the study protocol.

Assessment of Coffee Consumption

Dietary questionnaires were sent to the HPFS participants in 1986, 1990, 1994, and 1998 and to the NHS participants in 1980, 1984, 1986, 1990, 1994, and 1998. On each questionnaire, participants were asked how often on average during the previous year they had consumed coffee and tea. The participants could choose from 9 responses. The method of coffee preparation was assessed only in 1990 in both studies. Decaffeinated coffee and different types of caffeinated soft drinks were first assessed in 1986 in the HPFS and in 1984 in the NHS. In addition, we also inquired in the NHS questionnaire of 1980 whether the participant’s consumption for each beverage had greatly increased or decreased over the past 10 years. Using the US Department of Agriculture food composition sources, supplemented with other sources, we estimated that the caffeine content was 137 mg per cup of coffee, 47 mg per cup of tea, 46 mg per can or bottle of cola beverage, and 7 mg per serving of chocolate candy. We assessed the total intake of caffeine by summing the caffeine content for a specific amount of each food during the previous year (1 cup for coffee or tea, one 12-ounce bottle or can for carbonated beverages, and 1 ounce for chocolate) multiplied by a weight proportional to the frequency of its use. In our validation study, we obtained high correlations between consumption of coffee and other caffeinated beverages estimated from the food frequency questionnaire and consumption estimated from repeated 1-week diet records (coffee, r=0.78; tea, r=0.93; and caffeinated sodas, r=0.85).18

Assessment of Nonfatal Myocardial Infarction and Fatal CHD

The primary end point for this analysis was CHD, which included symptomatic nonfatal myocardial infarction (MI) or fatal CHD that occurred after the return of the 1986 questionnaire in men and the 1980 questionnaire in women but before June 1, 2000. We requested permission to review medical records from subjects who reported having a nonfatal MI on a follow-up questionnaire. Physicians unaware of the self-reported risk factor status systematically reviewed the records. MI was classified as confirmed if the criteria of the World Health Organization were met, specifically, symptoms and either ECG changes or elevated cardiac enzyme levels.19 We included confirmed and probable cases for the analyses. Deaths were identified from state vital statistics records and the National Death Index or reported by the families and the postal system. Fatal CHD was considered to have occurred if fatal MI was confirmed by hospital records or an autopsy or if CHD was listed as the cause of death on the death certificate, if it was listed as an underlying and the most plausible cause of death, and if evidence of previous CHD was available.

Assessment of Medical History, Anthropometric Data, and Lifestyle Factors

On the baseline questionnaires, we requested information about age, weight, and height; smoking status; parental history of MI; use of hormone therapy in women; and personal history of MI and other diseases. This information, with the exception of height and parental history of MI, has been updated on the biennial follow-up questionnaires. Body mass index (BMI) was calculated as weight in kilograms divided by the square of height in meters. Physical activity was assessed biennially. In the HPFS, participants were queried about the average time spent per week during the preceding year in specific activities (eg, walking outdoors, jogging, and bicycling).20 The time spent in each activity in hours per week was multiplied by its typical energy expenditure, expressed in metabolic equivalent tasks (METs) and then summed over all activities to yield a METs/h score. In the NHS, physical activity was reported in hours per week of moderate (eg, brisk walking) and vigorous (eg, strenuous sports and jogging) exercise.21 Standard portion sizes for alcoholic drinks were specified as a can/bottle or glass for beer, 4-oz glass for wine, and 1 drink or shot for liquor. Detailed information on the validity and reproducibility of the questionnaire has been reported elsewhere.18,22–25

Statistical Analyses

Participants were classified according to levels of coffee consumption. Person-years of exposure were calculated from the date of return of the baseline questionnaire to the date of nonfatal MI, fatal CHD, or June 1, 2000, whichever came first. For individuals who developed a nonfatal MI and later died of fatal CHD during the follow-up, we only included follow-up time to the nonfatal event in the overall analysis to avoid double counting. Participants who had a nonfatal MI and later died of CHD within the same 2-year period were counted only for the fatal event.

Sex-specific Cox regression models were used to investigate the association between coffee consumption and incidence of CHD events. Hazard ratios were used to estimate relative risks (RRs). To reduce within-subject variation and best represent long-term diet, we used the cumulative average of dietary intakes from all available dietary questionnaires up to the start of each 2-year follow-up interval26; for example, the average of the 1986 and 1990 intake was used for the follow-up between 1990 and 1994, and the average of the 1986, 1990, and 1994 intake was used for the follow-up between 1994 and 1998. In alternative analyses, we also used simple updating (the most recent information on coffee consumption before the event) to study short-term effects of coffee on CHD.

Physical activity, alcohol intake, BMI, smoking status, and use of hormone therapy, aspirin, multivitamin supplements, and vitamin E supplements were also updated during follow-up with the most recent data for each 2-year interval. Models were first adjusted for age and smoking status. Furthermore, we adjusted for BMI, physical activity, alcohol intake, use of hormone therapy for women, parental history of MI, aspirin use, multivitamin use, vitamin E supplement use, and history of hypertension, hypercholesterolemia, and diabetes mellitus at baseline. To test for linear trends across categories, we modeled coffee consumption as a continuous variable in the models with the median value of each level of coffee consumption. Stratified analyses were conducted according to smoking status, alcohol consumption, history of diabetes mellitus, and BMI. We studied the association between caffeine intake, decaffeinated coffee and tea consumption, and CHD. We also examined separately the effect of filtered and non–paper-filtered (espresso/percolator) coffee on CHD.

As a complementary study, we examined the association of caffeinated and decaffeinated coffee and plasma levels of total, low-density lipoprotein (LDL), and high-density lipoprotein (HDL) cholesterol. We conducted these analyses in men and women who were selected as control subjects in 2 previous nested case-control studies of MI.27 Blood samples were collected in 1990 in women and 1994 in men; therefore, we used dietary information from the 1990 food frequency questionnaire for women and from the 1994 food frequency questionnaire for men. We calculated multivariable-adjusted means of plasma cholesterol levels across categories of consumption. All analyses were performed with SAS software, version 8.2 (SAS Institute Inc, Cary, NC).

The authors had full access to the data and take responsibility for its integrity. All authors have read and agree to the manuscript as written.

Results

During 14 years of follow-up in the HPFS, we documented 2173 cases of CHD, including 1449 nonfatal MIs and 724 fatal CHD events. During 20 years of follow-up in the NHS, we documented 2254 cases of CHD (1561 nonfatal MIs and 693 fatal CHD events). Characteristics of the population are presented by levels of coffee consumption in Table 1. Frequent coffee consumption was strongly associated with smoking: 30% of the men and more than half of the women who drank ≥6 cups/d also smoked cigarettes. In addition, individuals who drank more coffee were more likely to drink alcohol and to use aspirin and less likely to drink tea, to exercise, and to use multivitamin and vitamin E supplements.

In age-adjusted analyses, we found no significant association between long-term coffee consumption and risk of CHD for men but a positive association for women (Table 2). However, when we further adjusted for smoking status, the positive association in women disappeared, which suggests that the age-adjusted results were strongly confounded by smoking. After multivariable adjustment, the RRs were somewhat attenuated. Additional adjustment for total energy intake, glycemic load, cereal fiber, folate, and polyunsaturated, saturated, trans, and n-3 fatty acids did not appreciably alter the results. Interestingly, the consumption of ≥6 cups/d of coffee was associated with a slightly lower risk of fatal CHD in both men (RR 0.60, 95% confidence interval 0.26 to 1.36) and women (RR 0.61 95% CI 0.37 to 1.02); the pooled RRs across categories of coffee consumption were 1.0, 1.06 (95% CI 0.90 to 1.26), 1.04 (95% CI 0.89 to 1.21), 0.93 (95% CI 0.79 to 1.09), 1.01 (95% CI 0.81 to 1.28), and 0.61 (95% CI 0.39 to 0.93).

The null association between coffee and CHD was independent of smoking status (Table 3; Figure; P for interaction=0.51 in men and P=0.96 in women) and alcohol consumption (P for interaction=0.32 in men and P=0.90 in women). The association was also similar for participants with and without type 2 diabetes mellitus and for obese (BMI ≥30 kg/m2) and nonobese participants (Table 3).

RRs (with 95% CIs) of CHD from 1986 to 2000 in men and from 1980 to 2000 in women, by levels of coffee consumption and smoking status (never and past combined). Reference category was nonsmokers who drank <1 cup of coffee per month. Data were adjusted for variables in Table 2, except for smoking.

Alternative analyses with the most recent coffee consumption data showed no association between shorter-term intake (2- to 4-year interval) and CHD (multivariable RRs for men were 1.0, 0.88, 0.91, 0.93, 0.96, and 0.80 ; the corresponding RRs for women were 1.0, 0.96, 1.09, 0.98, 0.96, and 0.98 ). When we stopped updating coffee consumption after the person developed angina, hypertension, hypercholesterolemia, cancer, or type 2 diabetes mellitus, it did not change the results. We also tried excluding participants who reported a change in their coffee consumption during the 10 years before baseline and excluding the first 4 years of follow-up to avoid latent disease; these exclusions did not appreciably affect the association between coffee consumption and risk of CHD. Finally, we excluded from the analyses participants who reported hypertension, hypercholesterolemia, or diabetes mellitus at baseline, as well as those who developed these diseases during the follow-up, again obtaining similar results. The multivariable adjusted means of total, LDL, and HDL cholesterol across categories of caffeinated and decaffeinated coffee are presented in Table 5. No significant associations were observed between coffee consumption and blood lipids.

Discussion

In this large prospective study, we did not find a detrimental effect of coffee consumption on risk of CHD in either men or women. No association was observed for total caffeine intake, decaffeinated coffee, or tea. These results provide strong evidence against the hypothesis that coffee consumption increases the risk of CHD.

Coffee is one of the most widely consumed beverages in the United States and worldwide.28 The health effects of coffee consumption have been studied and debated extensively. In an earlier meta-analysis,2 cohort studies did not support an association between coffee intake and risk of CHD (pooled RR=1.05, 95% CI 0.99 to 1.12 for drinking 5 or more cups/d versus none), whereas case-control studies tended to suggest a positive association (RR=1.63, 95% CI 1.50 to 1.78). Several biases could explain the difference. For instance, recall bias in case-control studies may explain a positive association if individuals who developed CHD were more likely to overreport coffee intake than healthy controls.

Results from recent epidemiological studies are mixed. Woodward and Tunstall-Pedoe7 followed a Scottish population for 8 years. Their results suggested that higher coffee consumption was associated with lower risk of cardiovascular disease among men but not among women. Kleemola et al8 assessed coffee consumption in a Finnish population 3 times during 10 years of follow-up and found a lower risk of nonfatal MI in men with high coffee consumption (>7 cups/d); however, they also observed a slightly increased CHD mortality in the same group. Additionally, in a case-control study, Hammar et al6 reported that daily consumption of 7 to 9 dL of filtered coffee was associated with an increased risk of CHD in men compared with a daily consumption of 3 dL or less; however, this association was not observed for women. Two other studies suggested a J-shaped relationship between coffee consumption and risk of CHD.9,10 The present analyses, which used repeated measures of coffee consumption over 14 to 20 years of follow-up, found no evidence of either short-term (2 to 4 years) or long-term effects. Likewise, we found no association with decaffeinated coffee or total caffeine intake. Repeated measurement of diet was a unique advantage in the present study because our analysis using a cumulative average of intake was able to best represent long-time diet and reduce within-subject variations.

Coffee is a major source of caffeine. Caffeine is an adenosine-receptor antagonist,29 and all tissues with adenosine receptors may be affected by caffeine exposure. Caffeine stimulates fat oxidation in muscle30 and increases basal energy expenditure.31 Also, caffeine stimulates free fatty acid release from peripheral tissues32 and decreases insulin sensitivity in skeletal muscle.33 In addition, caffeine might impair insulin action by stimulating the release of epinephrine, which is a potent inhibitor of insulin activity.34 Finally, caffeine increases blood pressure35 and homocysteine levels36 in short-term studies. However, the above effects of caffeine could be transient, because partial tolerance might develop after several days of use.37 Thus, some of these mechanisms cannot be extrapolated to long-term use,15 whereas others mechanisms could counterbalance the effects of caffeine. For instance, substances in coffee such as potassium, niacin, and magnesium have previously been shown to be beneficial for glucose and insulin metabolism.38 In addition, antioxidants in coffee such as chlorogenic acid and other phenolic compounds might improve insulin sensitivity.39 These mechanisms may explain the recent findings that habitual coffee intake is associated with a lower risk of developing type 2 diabetes mellitus.11–15 In the present study, coffee consumption had no adverse or beneficial effect on CHD in participants with or without diabetes mellitus. In both men and women, there was some suggestion that heavy consumption (6 cups or more per day) was associated with a lower risk of fatal CHD (Table 2); however, the number of fatal CHD cases was relatively small, and the results should be interpreted with caution.

Coffee consumption was strongly correlated with smoking; thus, it is not surprising that coffee intake was positively associated with CHD in age-adjusted analyses in the NHS cohort, in which smoking was more prevalent. However, this association disappeared after adjustment for smoking and in analyses stratified by smoking status. A recent study suggested a synergistic detrimental effect of acute smoking and caffeine (200 mg) on aortic stiffness.40 However, we did not find an interaction between smoking and coffee consumption in relation to CHD risk. Although smoking was strongly correlated with coffee consumption, the detrimental effects of smoking on CHD were the same among coffee drinkers and nondrinkers.

Finally, most participants in the present study consumed filtered coffee. Neither filtered caffeinated coffee nor filtered decaffeinated coffee was substantially associated with plasma levels of total, LDL, and HDL cholesterol. Among those who reported consuming non–paper-filtered coffee, we did not find an increased risk of CHD. Boiled coffee increases serum cholesterol,41,42 and some evidence suggests that high consumption of this beverage is related to CHD risk.6,43 The lack of association between non–paper-filtered coffee in the HPFS and the NHS I cohorts is likely to be due in part to (1) the inclusion of espresso in this category, which has lower concentrations of the cholesterol-increasing components kahweol and cafestol,44 and (2) the modest consumption even in the highest categories (≥2 cup/d), compared with intervention studies such as Bak and Grobbee’s work,45 which examined the effect of the consumption of 4 to 6 cups of boiled coffee per day. The results of the present study do not exclude a relation between high nonfiltered coffee consumption and CHD risk.

In conclusion, in these 2 large cohorts, after a follow-up of 14 years for men and 20 years for women, we found no evidence of an adverse association between coffee intake and the risk of developing CHD. Likewise, we found no association for consumption of total caffeine, decaffeinated coffee, or tea. These data do not provide any evidence that coffee consumption increases the risk of CHD.

This study was supported by National Institutes of Health research grants CA87969, DK55523, DK58845, and HL34594. Dr Lopez-Garcia’s research is supported by a fellowship from the Secretaria de Estado de Educacion y Universidades (Ministerio de Educacion y Cultura de España) and Fondo Social Europeo. Dr Hu’s research is supported in part by an American Heart Association Established Investigator Award.

Disclosures

None.

Footnotes

Reprint requests to Dr Frank B. Hu, Departments of Nutrition and Epidemiology, Harvard School of Public Health, 665 Huntington Ave, Boston, MA 02115. E-mail

  • 1 Myers MG, Basinski A. Coffee and coronary heart disease. Arch Intern Med. 1992; 152: 1767–1772.CrossrefMedlineGoogle Scholar
  • 2 Kawachi I, Colditz GA, Stone CB. Does coffee drinking increase the risk of coronary heart disease? Results from a meta-analysis. Br Heart J. 1994; 72: 269–275.CrossrefMedlineGoogle Scholar
  • 3 Greenland S. A meta-analysis of coffee, myocardial infarction, and coronary death. Epidemiology. 1993; 4: 366–374.CrossrefMedlineGoogle Scholar
  • 4 Willett WC, Stampfer MJ, Manson JE, Colditz GA, Rosner BA, Speizer FE, Hennekens CH. Coffee consumption and coronary heart disease in women: a ten-year follow-up. JAMA. 1996; 275: 458–462.CrossrefMedlineGoogle Scholar
  • 5 Tavani A, Bertuzzi M, Negri E, Sorbara L, La Vecchia C. Alcohol, smoking, coffee and risk of non-fatal acute myocardial infarction in Italy. Eur J Epidemiol. 2001; 17: 1131–1137.CrossrefMedlineGoogle Scholar
  • 6 Hammar N, Andersson T, Alfredsson L, Reuterwall C, Nilsson T, Hallqvist J, Knutsson A, Ahlbom A. Association of boiled and filtered coffee with incidence of first nonfatal myocardial infarction: the SHEEP and the VHEEP study. J Intern Med. 2003; 253: 653–659.CrossrefMedlineGoogle Scholar
  • 7 Woodward M, Tunstall-Pedoe H. Coffee and tea consumption in the Scottish Heart Health Study follow up: conflicting relations with coronary risk factors, coronary disease, and all cause mortality. J Epidemiol Community Health. 1999; 53: 481–487.CrossrefMedlineGoogle Scholar
  • 8 Kleemola P, Jousilahti P, Pietinen P, Vartiainen E, Tuomilehto J. Coffee consumption and the risk of coronary heart disease and death. Arch Intern Med. 2000; 160: 3393–3400.CrossrefMedlineGoogle Scholar
  • 9 Panagiotakos DB, Pitsavos C, Chrysohoou C, Kokkinos P, Toutouzas P, Stefanadis C. The J-shaped effect of coffee consumption on the risk of developing acute coronary syndromes: the CARDIO2000 case-control study. J Nutr. 2003; 133: 3228–3232.CrossrefMedlineGoogle Scholar
  • 10 Happonen P, Voutilainen S, Salonen JT. Coffee drinking is dose-dependently related to the risk of acute coronary events in middle-aged men. J Nutr. 2004; 134: 2381–2386.CrossrefMedlineGoogle Scholar
  • 11 van Dam RM, Feskens EJ. Coffee consumption and risk of type 2 diabetes mellitus. Lancet. 2002; 360: 1477–1478.CrossrefMedlineGoogle Scholar
  • 12 Tuomilehto J, Hu G, Bidel S, Lindstrom J, Jousilahti P. Coffee consumption and risk of type 2 diabetes mellitus among middle-aged Finnish men and women. JAMA. 2004; 291: 1213–1219.CrossrefMedlineGoogle Scholar
  • 13 Rosengren A, Dotevall A, Wilhelmsen L, Thelle D, Johansson S. Coffee and incidence of diabetes in Swedish women: a prospective 18-year follow-up study. J Intern Med. 2004; 255: 89–95.CrossrefMedlineGoogle Scholar
  • 14 Carlsson S, Hammar N, Grill V, Kaprio J. Coffee consumption and risk of type 2 diabetes in Finnish twins. Int J Epidemiol. 2004; 33: 616–617.CrossrefMedlineGoogle Scholar
  • 15 Salazar-Martinez E, Willett WC, Ascherio A, Manson JE, Leitzmann MF, Stampfer MJ, Hu FB. Coffee consumption and risk for type 2 diabetes mellitus. Ann Intern Med. 2004; 140: 1–8.CrossrefMedlineGoogle Scholar
  • 16 Grobbee DE, Rimm EB, Giovannucci E, Colditz G, Stampfer M, Willett W. Coffee, caffeine, and cardiovascular disease in men. N Engl J Med. 1990; 323: 1026–1032.CrossrefMedlineGoogle Scholar
  • 17 Willett WC, Green A, Stampfer MJ, Speizer FE, Colditz GA, Rosner B, Monson RR, Stason W, Hennekens CH. Relative and absolute excess risks of coronary heart disease among women who smoke cigarettes. N Engl J Med. 1987; 317: 1303–1309.CrossrefMedlineGoogle Scholar
  • 18 Salvini S, Hunter DJ, Sampson L, Stampfer MJ, Colditz GA, Rosner B, Willett WC. Food-based validation of a dietary questionnaire: the effects of week-to-week variation in food consumption. Int J Epidemiol. 1989; 18: 858–867.CrossrefMedlineGoogle Scholar
  • 19 Rose GA BH. Cardiovascular Survey Methods. Geneva, Switzerland: World Health Organization; 1982. WHO Monograph Series, No. 58.Google Scholar
  • 20 Koh-Banerjee P, Chu NF, Spiegelman D, Rosner B, Colditz G, Willett W, Rimm E. Prospective study of the association of changes in dietary intake, physical activity, alcohol consumption, and smoking with 9-y gain in waist circumference among 16 587 US men. Am J Clin Nutr. 2003; 78: 719–727.CrossrefMedlineGoogle Scholar
  • 21 Rockhill B, Willett WC, Manson JE, Leitzmann MF, Stampfer MJ, Hunter DJ, Colditz GA. Physical activity and mortality: a prospective study among women. Am J Public Health. 2001; 91: 578–583.CrossrefMedlineGoogle Scholar
  • 22 Willett WC, Sampson L, Stampfer MJ, Rosner B, Bain C, Witschi J, Hennekens CH, Speizer FE. Reproducibility and validity of a semiquantitative food frequency questionnaire. Am J Epidemiol. 1985; 122: 51–65.CrossrefMedlineGoogle Scholar
  • 23 Rimm EB, Stampfer MJ, Colditz GA, Colditz GA, Litin LB, Willett WC. Validity of self-reported waist and hip circumferences in men and women. Epidemiology. 1990; 1: 466–473.CrossrefMedlineGoogle Scholar
  • 24 Giovannucci E, Colditz G, Stampfer MJ, Rimm EB, Litin L, Sampson L, Willett WC. The assessment of alcohol consumption by a simple self-administered questionnaire. Am J Epidemiol. 1991; 133: 810–817.CrossrefMedlineGoogle Scholar
  • 25 Chasan-Taber S, Rimm EB, Stampfer MJ, Spiegelman D, Colditz GA, Giovannucci E, Ascherio A, Willett WC. Reproducibility and validity of a self-administered physical activity questionnaire for male health professionals. Epidemiology. 1996; 7: 81–86.CrossrefMedlineGoogle Scholar
  • 26 Hu FB, Stampfer MJ, Rimm E, Ascherio A, Rosner BA, Spiegelman D, Willett WC. Dietary fat and coronary heart disease: a comparison of approaches for adjusting for total energy intake and modeling repeated dietary measurements. Am J Epidemiol. 1999; 149: 531–540.CrossrefMedlineGoogle Scholar
  • 27 Mukamal KJ, Jensen MK, Gronbaek M, Stampfer MJ, Manson JE, Pischon T, Rimm EB. Drinking frequency, mediating biomarkers, and risk of myocardial infarction in women and men. Circulation. 2005; 112: 1406–1413.Google Scholar
  • 28 National Coffee Association. Coffee consumption in the USA. Coffee Research Institute Web site. Available at: http://www.coffeeresearch.org/market/usa.htm. Accessed December, 2004.Google Scholar
  • 29 Van Soeren MH, Graham TE. Effect of caffeine on metabolism, exercise endurance, and catecholamine responses after withdrawal. J Appl Physiol. 1998; 85: 1493–1501.CrossrefMedlineGoogle Scholar
  • 30 Spriet LL, MacLean DA, Dyck DJ, Hultman E, Cederblad G, Graham TE. Caffeine ingestion and muscle metabolism during prolonged exercise in humans. Am J Physiol. 1992; 262 (part 1): E891–898.CrossrefMedlineGoogle Scholar
  • 31 Astrup A, Toubro S, Cannon S, Hein P, Breum L, Madsen J. Caffeine: a double-blind, placebo-controlled study of its thermogenic, metabolic, and cardiovascular effects in healthy volunteers. Am J Clin Nutr. 1990; 51: 759–767.CrossrefMedlineGoogle Scholar
  • 32 Ryu S, Choi SK, Joung SS, Suh H, Cha YS, Lee S, Lim K. Caffeine as a lipolytic food component increases endurance performance in rats and athletes. J Nutr Sci Vitaminol (Tokyo). 2001; 47: 139–146.CrossrefMedlineGoogle Scholar
  • 33 Keijzers GB, De Galan BE, Tack CJ, Smits P. Caffeine can decrease insulin sensitivity in humans. Diabetes Care. 2002; 25: 364–369.CrossrefMedlineGoogle Scholar
  • 34 Thong FS, Graham TE. Caffeine-induced impairment of glucose tolerance is abolished by beta-adrenergic receptor blockade in humans. J Appl Physiol. 2002; 92: 2347–2352.CrossrefMedlineGoogle Scholar
  • 35 Hartley TR, Lovallo WR, Whitsett TL. Cardiovascular effects of caffeine in men and women. Am J Cardiol. 2004; 93: 1022–1026.CrossrefMedlineGoogle Scholar
  • 36 Verhoef P, Pasman WJ, Van Vliet T, Urgert R, Katan MB. Contribution of caffeine to the homocysteine-raising effect of coffee: a randomized controlled trial in humans. Am J Clin Nutr. 2002; 76: 1244–1248.CrossrefMedlineGoogle Scholar
  • 37 Lovallo WR, Wilson MF, Vincent AS, Sung BH, McKey BS, Whitsett TL. Blood pressure response to caffeine shows incomplete tolerance after short-term regular consumption. Hypertension. 2004; 43: 760–765.Google Scholar
  • 38 Natella F, Nardini M, Giannetti I, Dattilo C, Scaccini C. Coffee drinking influences plasma antioxidant capacity in humans. J Agric Food Chem. 2002; 50: 6211–6216.CrossrefMedlineGoogle Scholar
  • 39 Arnlov J, Vessby B, Riserus U. Coffee consumption and insulin sensitivity. JAMA. 2004; 291: 1199–1201.CrossrefMedlineGoogle Scholar
  • 40 Vlachopoulos C, Kosmopoulou F, Panagiotakos D, Ioakeimidis N, Alexopoulos N, Pitsavos C, Stefanadis C. Smoking and caffeine have a synergistic detrimental effect on aortic stiffness and wave reflections. J Am Coll Cardiol. 2004; 44: 1911–1917.CrossrefMedlineGoogle Scholar
  • 41 Zock PL, Katan MB, Merkus MP, van Dusseldorp M, Harryvan JL. Effect of a lipid-rich fraction from boiled coffee on serum cholesterol. Lancet. 1990; 335: 1235–1237.CrossrefMedlineGoogle Scholar
  • 42 Jee SH, He J, Appel LJ, Whelton PK, Suh I, Klag MJ. Coffee consumption and serum lipids: a meta-analysis of randomized controlled clinical trials. Am J Epidemiol. 2001; 153: 353–362.CrossrefMedlineGoogle Scholar
  • 43 Tverdal A, Stensvold I, Solvoll K, Foss OP, Lund-Larsen P, Bjartveit K. Coffee consumption and death from coronary heart disease in middle aged Norwegian men and women. BMJ. 1990; 300: 566–569.CrossrefMedlineGoogle Scholar
  • 44 Gross G, Jaccaud E, Huggett AC. Analysis of the content of the diterpenes cafestol and kahweol in coffee brews. Food Chem Toxicol. 1997; 35: 547–554.CrossrefMedlineGoogle Scholar
  • 45 Bak AA, Grobbee DE. The effect on serum cholesterol levels of coffee brewed by filtering or boiling. N Engl J Med. 1989; 321: 1432–1437.CrossrefMedlineGoogle Scholar

Caffeine and Heart Rate: What Is the Effect of Caffeine on Heart Rate?

Problem:

What effect does caffeine have on human heart rate?

Materials:

  • 10 Adults or more (We want to test as many as possible. Why do you think this is?)
  • Mp3 player loaded with relaxing music
  • Clock and stopwatch (a cell phone usually has both of these functions)
  • Eye mask
  • 5 cans of a caffeinated version of a drink
  • 5 cans of a non-caffeinated version of the same drink
  • Paper and tape
  • Notebook

Procedure:

  1. Spend some time learning how to accurately take a person’s pulse. There are plenty of good resources online that can teach you how. Using a stopwatch, make sure to practice taking somebody else’s pulse until you’re sure you can get an accurate reading every time.

  1. Mask your drinks using your paper and tape and label each can with a number.
  2. Make sure that you record whether each number is caffeinated or non-caffeinated in your notebook.
  3. Arrange a time to test each adult. It will take around 30 minutes to perform the test. Test each person at around the same time of day, in the same circumstances (same chair, same song, etc.). Be sure to test each adult one at a time. Ask each person to refrain from eating or drinking for two hours before the test. Why do you think we want to make sure all of these things are the same from one test to the next?
  4. Ask each subject what his or her caffeine consumption habits are. Record the subject’s answers on a sheet of paper dedicated to that subject, and be sure to keep your records confidential.
  5. Have your subject put the mask over his or her eyes. Have the subject put the headphones on, listen to the music, and relax.
  6. After five minutes have passed, take and record your subject’s starting pulse without disturbing them.
  7. Provide your subject with a randomly selected drink. Record the drink’s number in your notebook. Ask your subject to drink it as quickly as possible.
  8. Wait five minutes, and then take and record your subject’s pulse. Continue taking the subject’s pulse at 5-minute intervals until 15 minutes have passed.
  9. Graph the data you recorded.
  10. Do people who consume caffeine regularly react to the caffeine? To the placebo? To both? Is there a correlation between habitual caffeine consumption and the change in pulse rate? Try to think of as many questions as you can, and keep an eye out for surprising results. After you are satisfied with your analysis, look up the effects of caffeine on the body and see if your study agrees with what other scientists have found.

Results:

The results you get will depend strongly on what subjects you used for your study.

Why?

Caffeine is a stimulant, a class of drugs that increase your heart rate and make you more energetic. However, the effects of caffeine are not identical between subjects. Plenty of people are born with a natural tolerance to caffeine, meaning that the caffeine’s effects aren’t so pronounced when such people consume it. People without a natural tolerance may also develop one over time simply by drinking caffeine.

The possibility that certain people may have a tolerance to caffeine while others may not is one example of a variable—something that has a direct influence on the information we gather. Here’s an example of how this variable might work: you may find yourself testing two people that just happen to be naturally very tolerant to caffeine. If these happened to be the only two people you tested, you may not have seen a significant change in heart rate. This data may have led you to a misleading conclusion about caffeine’s effect on the human body! This is why you were instructed to test as many subjects as possible and why you were told to ask your subjects about their caffeine habits. When you take these steps, you can collect more useful data that lets you control the variable of tolerance by identifying the people that are more likely to have a similar tolerance to the drug.

1. This effect applies to the researchers, too. If researchers know they’re administering a drug as opposed to a placebo, there’s a chance they may look extra carefully for signs that the drug is doing something. This introduces bias into the experiment and can distort the results! A Double-Blind Study is one in which even the people administering the test don’t know what option they’re testing. This helps prevent bias from affecting the study’s results.

How does your caffeine intake influence exercise?

Surveys show that approximately 90 percent of Americans consume caffeine daily. In fact, more than half of American adults ingest over 300 milligrams of caffeine every day (i.e., approximately two and a half cups of regular coffee).

Most people consume caffeine to give them a daytime boost or keep them awake longer at night. What is caffeine’s influence on exercise? This column will try to shed some light on that question.

More about caffeine

Caffeine is not synonymous with coffee. It comes in various forms, including coffee, tea, cola, chocolate, medications, etc. According to the National Soft Drink Association, most 12-ounce cans of soda contain approximately 45 milligrams of caffeine. By comparison, a seven-ounce cup of coffee has approximately 100 milligrams of caffeine.

A cardiovascular stimulant, caffeine affects the heart directly by causing andrenergic nerve terminals in the heart and adrenal medulla to release more catecholamines. It has both positive inotropic (i.e., strength of contraction) and chronotropic (i.e., increased heart rate) effects.

Caffeine is also a powerful central nervous system stimulant, acting particularly on the brain and skeletal muscles. It also delays fatigue and acts as a smooth muscle relaxant and vasodilator. Blood concentrations of caffeine peak within 15 to 45 minutes of ingestion. However, its metabolic effects may last over an hour. The liver metabolizes almost 100 percent of caffeine, but some residual may appear in the urine.

No solid evidence indicates moderate caffeine consumption is a risk factor for any type of cancer, cardiovascular disease or decreased fertility in women. In 1987, the FDA affirmed that moderate quantities of caffeine have no adverse effects.

However, studies have shown caffeine can cause high blood pressure and increase heart rate. At least one study concluded that long-term coffee consumption decreased bone mineral density in women.

Probably the most important long-term health side-effect is caffeine’s effect on sleep. Studies have shown that as little as one strong cup of coffee (150 to 200 milligrams of caffeine), consumed 30 to 60 minutes before sleeping, can cause restlessness, difficulty falling asleep, increased body movements, decreased quality of sleep and a tendency to be awakened by sudden noises.

Ceasing caffeine consumption five to six hours prior to sleeping, thus allowing more time for the body to metabolize the caffeine, will lessen these side-effects.

Caffeine’s effect on exercise

Numerous studies have researched the effect of caffeine ingestion on exercise performance. Most of them generally conclude that caffeine consumption prior to working out seems to extend endurance performance during moderately strenuous aerobic exercise.

The main proposed mechanism for this improvement is the increased use of fat as fuel. However, there seems to be benefit discrepancies between habitual caffeine users and nonhabitual users. Once a certain level of tolerance is reached, the ergogenic effect of caffeine may be reduced.

Another commonly reported benefit of caffeine ingestion prior to exercise is a decreased sense of overall exertion (i.e., reduced RPE), which may lead to improved enjoyment of exercise. However, since caffeine is often used as an appetite suppressant, some individuals may not consume the calories needed to sustain exercise.

Keep in mind, caffeine’s effects vary from person to person. Following caffeine ingestion, some might notice tremendous benefits during exercise, while others may not.

Conclusion

Caffeine ingestion prior to exercise seems to have metabolic, musculoskeletal and central nervous system stimulant effects. However, there is no consistent evidence on its ability to delay fatigue.

Caffeine appears to offer ergogenic benefits during prolonged exercise, but not during short-burst, high-intensity activities.

However, caffeine ingestion in the range of 400 to 500 milligrams may cause nausea, abdominal discomfort and irritability. It elevates heart rate and blood pressure, which may affect the ability to accurately monitor training intensity.

Withdrawal from regular caffeine ingestion also produces an array of negative side effects, including headaches, irritability and drowsiness.

Many people do not realize how much caffeine they ingest daily. Some people drink coffee in the morning, sodas throughout the day and a piece of chocolate here and there. It could take all day and part of the night for the body to rid its systems of caffeine. It is important to assess your current caffeine habits to get an idea of your daily caffeine intake.

You may need to modify your exercise sessions if you discover youre consuming too much caffeine prior to exercise or are withdrawing from caffeine. For example, you may want to decrease the intensity or duration of exercise after you decide to make changes in your caffeine consumption patterns.

If youve consumed too much caffeine, the intensity and duration may need to be lowered for that day. If youre withdrawing from caffeine use, your training heart rate should be re-evaluated and exercise duration modified, since you may not have the same level of energy or motivation as before.

In addition, it is important to reevaluate resting heart rates prior to exercise to see if they have changed due to any changes in caffeine consumption.

As always, its important to consult a fitness professional doctor, personal trainer, sports nutritionist if you plan to try to modify your caffeine intake for health or exercise reasons.

Search Active and register online for an event in your area!

Get fit with top coaches! Check out Training Bible

Does Caffeine Increase Heart Rate?

Does your mom or dad like to have a cup or two of coffee in the morning? Does your sister have a cola habit? If so, they can help you with this experiment, aimed at discovering whether caffeine affects the rate at which a heart beats.

The basics of your experiment would be to measure and record the resting heart rate of your subject. You’d then have that person drink a cup of coffee, some soda, or other beverage containing caffeine. You can determine the amount of caffeine they’ll be ingesting by reading the label of the soda or coffee can.

Wait for 20 minutes after the beverage has been consumed, and then recheck the resting heart rate. Just be sure that your subject sits quietly during and after the time he or she is consuming the caffeine. Exercising would cause the heart rate to increase, with or without the benefit of caffeine.

Ideally, you could do this with three or four different people, and conduct three trials for each person. Record your results, and see whether the caffeine affected their heart rates.

What’s Causing Me to Wake Up with a Racing Heart, and How Do I Treat It?

There are many possible causes of a fast heart rate in the morning. Here’s a look at some common ones and other symptoms to watch out for.

Anxiety

Stress and anxiety trigger the release of stress hormones, which in turn increase your heart rate and blood pressure. The more anxious you feel, the more pronounced your symptoms can be.

If you have depression or anxiety, or are under a lot of stress, you may wake up with a racing heart from time to time.

Other common symptoms of anxiety include:

  • rapid breathing or shortness of breath
  • trouble concentrating
  • restlessness
  • excessive worry
  • difficulty sleeping

Drinking alcohol the night before

If you’re waking up with your heart racing after drinking, chances are you’ve had too much.

Drinking alcohol increases your heart rate. The more you drink, the faster your heart beats. A recent study confirmed that binge drinking and long-term heavy alcohol use are associated with different types of cardiac arrhythmia, especially sinus tachycardia.

You may also have other symptoms, such as a headache, muscle aches, nausea, and dizziness. These symptoms should clear up as your hangover subsides.

Sugar

The sugar you consume is absorbed into your bloodstream after passing through your small intestine. Having too much sugar can cause a blood sugar spike. This signals your pancreas to release insulin and convert what it can to energy.

The increase in blood sugar and energy is interpreted by your body as stress, which triggers the release of stress hormones. Along with a racing heart, you may also begin to sweat. Some people also get what’s known as a “sugar headache.”

Processed sugar isn’t the only cause. Refined carbohydrates, such as white bread or pasta, can have the same effect, especially in people with diabetes.

Atrial fibrillation

Atrial fibrillation (AFib) is the most common type of irregular heartbeat. It happens when the heart’s upper chambers beat out of coordination with the lower chambers.

AFib usually causes a fast heart rate, but some people feel a fluttering or thumping in the chest. AFib itself isn’t usually life-threatening. In some cases, it can increase the risk of heart failure and may require treatment.

If you have AFib, you may also experience:

  • dizziness
  • shortness of breath
  • anxiety
  • weakness
  • feeling faint or lightheaded

Sleep apnea

Sleep apnea is a sleep disorder in which breathing repeatedly stops and starts.

Obstructive sleep apnea is the most common type. It occurs when your throat muscles relax, causing your airway to narrow or close.

Research shows that sleep apnea increases the risk of irregular heart rate. The sudden drops in your blood oxygen levels raise your blood pressure and strain your cardiovascular system.

Some symptoms of sleep apnea are:

  • loud snoring
  • gasping for air during sleep
  • trouble sleeping through the night
  • dry mouth on waking
  • morning headaches

Caffeine

Caffeine is a natural stimulant commonly found in coffee, tea, and cacao plants. It stimulates your brain and central nervous system, which increases alertness. In some people, too much caffeine can increase heart rate and blood pressure and cause anxiety and nervousness.

Consuming a large amount of products containing caffeine, such as coffee, tea, soda, and energy drinks can cause your heart to race. Other side effects of too much caffeine include:

  • feeling jittery
  • irritability
  • trouble sleeping
  • shakiness
  • frequent urination

Diabetes

Diabetes causes high blood glucose levels, which can damage the walls of your arteries and cause a rapid heart rate, high blood pressure, and other heart-related complications. In 2015, researchers also discovered that a rapid heart rate increases the risk of diabetes.

Other symptoms of diabetes include:

  • frequent urination
  • excessive thirst
  • extreme hunger
  • fatigue
  • tingling or numbness in the hands and feet
  • blurred vision

Medications that contain stimulants

Just like caffeine, other stimulants can cause your heart to race. Certain over-the-counter (OTC) and prescription medications can include such stimulants.

These include:

  • inhaled steroids
  • amphetamine
  • thyroid medication, such as levothyroxine
  • OTC cough and cold medications that contain pseudoephedrine, such as Sudafed
  • attention deficit hyperactivity disorder (ADHD) drugs

Hypoglycemia (low blood sugar)

Rapid heart rate is just one of the possible effects of low blood sugar on your body. Going a long time without eating can cause low blood sugar as well as certain conditions, like:

  • diabetes
  • liver disease
  • kidney disease
  • adrenal gland disorders
  • heavy alcohol use

Other symptoms of low blood sugar include:

  • headache
  • mood swings
  • trouble concentrating
  • visual disturbances

Nightmares or night terrors

Nightmares and night terrors can cause you to wake up with a racing heart. Nightmares are disturbing dreams that can wake you up. Night terrors are a type of sleep disorder in which a person awakens partially in a state of terror.

If you wake up after an upsetting dream or night terror with your heart racing, your heart rate should slow as you calm down.

Cold or fever

Any drastic change in your body temperature can cause changes in your heart rate.

Your body reacts to a change in temperature by triggering processes to try to regulate your body temperature. This includes expanding and constricting your skin’s blood vessels to help keep heat in or carry it to your skin’s surface, causing muscle contractions and shivering.

Your heart rate can increase as a result of your body working harder to maintain its normal temperature. For many people, this is around 98.6°F (37°C).

Overactive thyroid

Also called hyperthyroidism, this condition occurs when your thyroid gland produces too much of the hormone thyroxine. It can accelerate your metabolism and cause a rapid or irregular heartbeat as well as unintentional weight loss.

Other symptoms you may notice include:

  • increased appetite
  • sweating and night sweats
  • heat intolerance
  • menstrual irregularities

Lack of sleep

Along with a number of other negative effects on your body, there’s evidence that sleep deprivation can also increase your heart rate.

Aim to sleep seven to nine hours every night. Not getting enough sleep can lead to clumsiness and a higher risk of accidents. It also causes daytime drowsiness, concentration problems, and headaches.

Anemia

Anemia occurs when there are too few healthy red blood cells in your body to carry the amount of oxygen your body’s organs and tissues need to work properly.

Anemia can occur when your body doesn’t make enough or destroys red blood cells. People with heavy periods have a higher risk for anemia, too.

Along with abnormal heart rhythms, anemia can also cause:

  • fatigue
  • weakness
  • shortness of breath
  • headaches

Dehydration

Dehydration is the result of your body losing more fluid than it takes in. When your body loses too much water, your cells and organs aren’t able to function properly. Dehydration can be mild or severe. If left untreated, it can cause serious complications.

Common symptoms of mild dehydration are:

  • dry mouth
  • increased thirst
  • decreased urination
  • headache

Symptoms of severe dehydration include:

  • excessive thirst
  • rapid heart rate
  • rapid breathing
  • low blood pressure
  • confusion

Periods, pregnancy, and menopause

Fluctuating hormone levels related to menstruation, pregnancy, and menopause can trigger the feelings of a racing heart.

During the menstrual cycle, estrogen and progesterone levels rise and fall. This has been linked to episodes of a faster-than-normal heart rate called supraventricular tachycardia.

Heart palpitations during pregnancy are caused by the increased amount of blood in the body, which can cause your heart to beat 25 percent faster than usual.

In perimenopause and menopause, the decrease in estrogen production is associated with an increase in heart rate. This can cause frequent palpitations and nonthreatening arrhythmias.

Hot flashes can also trigger palpitations in menopause and cause your heart rate to increase by 8 to 16 beats.

Binge drinking could trigger abnormal heart rhythms

“Why Oktoberfest could be damaging your heart” is the somewhat strange headline in The Times.

Researchers who attended the annual Bavarian beer and folk festival found binge drinkers were more likely to have abnormal heart rhythm patterns.

This could be of potential concern – in extreme cases, abnormal heart rhythms (arrhythmias) can trigger serious complications, such as stroke. No complications of this type were found in the study.

Researchers included more than 3,000 people who attended Oktoberfest in Germany and used a smartphone app to take recordings of the heart, while a breathalyser was used to measure alcohol levels.

The findings were compared with those of another study involving more than 4,000 people believed to represent the general public.

A novel feature of this approach is it provided “real-time” measurements of alcohol consumption, rather than relying on people recalling how much alcohol they’d drunk, which is often unreliable.

The researchers found binge drinking was linked with an increased risk of having an irregular heartbeat, but this was mainly a type called sinus tachycardia. This is not life threatening, but involves the heart beating at an abnormally fast rate of over 100 beats a minute, which can be very unpleasant.

While these findings do not prove there’s a significant link between alcohol and dangerous heart problems, less serious irregularities were found. It’s unclear whether this would cause problems further down the line.

To reduce health risks associated with drinking alcohol, government guidelines advise having no more than 14 units a week and spreading your drinking over three or more days if you regularly drink as much as 14 units a week.

Where did the story come from?

The study was carried out by researchers from University Hospital Munich and the German Cardiovascular Research Centre.

Funding was provided by University Hospital Munich and the European Commission’s Horizon 2020 research and innovation programme.

The researchers also used data from the KORA study, which was funded by the Helmholtz Zentrum München, the German Research Centre for Environmental Health, the German Federal Ministry of Education and Research, and the State of Bavaria.

The study was published in the peer-reviewed European Heart Journal.

Generally, the UK media’s reporting of the study was accurate. BBC News helpfully explained: “These odds are very low, which meant there was no significant link between alcohol and dangerous heart arrhythmias in the study. But there was a significant link between alcohol consumption and more benign arrhythmias.”

What kind of research was this?

This cross-sectional study aimed to investigate the link between alcohol and having an irregular heart rhythm.

Volunteers at Oktoberfest (who were expected to binge drink to some extent) had their heart rate and rhythm recorded using a smartphone-based electrocardiogram (ECG). The amount of alcohol in their system was measured using a breathalyser.

The researchers contrasted these findings with findings from another study involving people from the general population taking part in a community-based study about long-term diseases.

They also had an ECG, but their alcohol levels were assessed using a questionnaire asking how much they had drunk over the past week.

Acute excessive alcohol consumption, or binge drinking, has been associated with so-called “holiday heart syndrome”, which causes irregularities in the heart rhythm in people without any history of cardiac issues.

The researchers thought an increase in breath alcohol concentration would be associated with a higher level of irregular heart rhythms (arrhythmias), and wanted to compare this with day-to-day alcohol intake.

As this was a cross-sectional study where the measurements were only taken at one point in time, this type of study isn’t able to prove that alcohol intake causes abnormal heart rhythms.

What did the research involve?

Adults visiting Oktoberfest in Munich between September and October 2015 volunteered to take part in the study as part of the acute alcohol group (people likely to drink a lot in a short space of time).

Participants of the community-based KORA study, Co-operative Health Research in the Region of Augsburg, were also recruited to represent the chronic alcohol group (people likely to drink at an “everyday” level).

Electrocardiogram (ECG) recordings lasting 30 seconds were taken from the acute alcohol group using a smartphone-based AliveCor device.

The device wirelessly communicates with a software application, and was held in both hands by the participant. The KORA group had a 10-second digital ECG.

Two cardiologists, who were unaware which group the participants were in, analysed the ECG recordings to identify and classify the arrhythmias.

To assess alcohol consumption, a handheld device called Alcotest 7510 was used in the acute alcohol group – this accounts for any remaining alcohol in the mouth. The KORA group was assessed using a validated seven-day recall method.

Details of other possible confounding factors were collected:

Acute group (self-reported)

  • age
  • sex
  • country of origin
  • history of heart disease
  • use of cardiovascular and anti-arrhythmic drugs
  • active smoking status

KORA (standardised interview)

  • age
  • sex
  • history of heart disease
  • smoking status
  • diabetes
  • stroke
  • use of cardiovascular and anti-arrhythmic drugs

What were the basic results?

There were 3,028 volunteers in the acute alcohol cohort, with an average age of 34.4 (29% female).

The findings for this group were as follows:

  • average breath alcohol level was 0.85g per kg, considered to be a moderate intake – 3g per kg is considered “disabled due to intoxication” under German law
  • heart arrhythmias occurred in 30.5% of the group – sinus tachycardia, where the heart beats at over 100 beats per minute, occurred in 25.9%; other arrhythmias were present in 5.4% of the group
  • breath alcohol concentration was significantly associated with heart arrhythmias overall, with a 75% increase in the chance of having a heart arrhythmia for each additional 1g per kg of breath alcohol (odds ratio per unit change 1.75, 95% confidence interval 1.50 to 2.05)
  • each increase in breath alcohol of 1g per kg doubled the risk of sinus tachycardia (OR 1.96, 95%CI 1.66 to 2.31)

There were 4,131 people in the KORA group, with an average age of 49.1 (51% female). The findings were:

  • average alcohol consumption was 15.8g per day, equivalent to about 2 units
  • each additional 1g per kg consumed was associated with increased risk of sinus tachycardia – but this increase was quite small (OR 1.03, 95%CI 1.01 to 1.05)

How did the researchers interpret the results?

The researchers concluded that acute alcohol consumption is associated with heart arrhythmias and sinus tachycardia in particular.

They say this may lead to more serious heart rhythms problems, such as atrial fibrillation, though this was only present in less than 1% of each group.

The researchers also didn’t follow the people over time to see who developed more serious arrhythmias that could lead to further complications.

Conclusion

This cross-sectional study found binge drinking is associated with an increased risk of having an irregular heartbeat.

However, the type of irregular heartbeat found was mainly sinus tachycardia, which isn’t life threatening but involves the heart beating at an abnormally fast rate of over 100 heartbeats a minute.

This research also has some notable limitations:

  • The ECG recordings from the acute alcohol group were taken using a smartphone application operated outside the manufacturer’s recommended environment. The lively atmosphere within the beer tent may have caused inaccurate recordings.
  • The population recruited from Oktoberfest was varied in ethnic origin and only 69% were from Germany – it may not be appropriate to compare them with the KORA community population, where more than 99.5% were of German descent.
  • The volunteers in the acute alcohol group were self-selected and might not be representative of the average binge drinker in terms of potential confounding factors like health background. They also provided details of their age, sex, heart disease history and use of heart medications, which may not be accurate because of recall bias and alcohol consumption.
  • But the main limitation is the study design – cross-sectional studies cannot prove cause and effect.

These findings do not prove there is a significant link between alcohol and dangerous heart arrhythmias, but the researchers did find less serious heart irregularities.

To reduce the risk of any health risks associated with drinking alcohol:

  • drink no more than 14 units a week on a regular basis
  • spread drinking over at least three days a week if you regularly drink 14 units a week

Better still, cut down and aim to have several alcohol-free days a week.

Analysis by Bazian
Edited by NHS Website

Links to the headlines

How binge drinking disrupts your heartbeat: Consuming large amounts found to cause an irregular rhythm that can lead to serious health problems in later life

Mail Online, 26 April 2017

Alcohol binge can upset heart’s rhythm, say researchers

BBC News, 26 April 2017

Links to the science

Brunner S, Herbel R, Drobesch C, et al.

Alcohol consumption, sinus tachycardia, and cardiac arrhythmias at the Munich Octoberfest: results from the Munich Beer Related Electrocardiogram Workup Study (MunichBREW)

European Heart Journal. Published online April 25 2017

0 shares 1 min

Alcohol is a frequent trigger of a common type of rapid heartbeat called supraventricular tachycardia (SVT). This is a benign (non-harmful) arrhythmia (irregular heartbeat). “Tachycardia” means rapid heartbeat and “supraventricular” means that the rapid beats come from the upper chambers or the middle region of the heart. It is also called “paroxysmal,” meaning it comes on suddenly.

The rapid heartbeats that you’ve been experiencing after drinking alcohol aren’t unusual. Many people experience the same thing. In fact, having an extra drink or two at celebrations or during the holidays can cause rapid heartbeats that are often called “Holiday Heart.” Red wine is often a particular culprit.

The same type of rapid heartbeat can occur as a result of drinking caffeinated beverages, eating chocolate, and using other stimulants. Lack of sleep can cause you to have episodes as well.

The best way to deal with your rapid heartbeat is to learn to stop it as soon as it starts. You can do this by practicing my breathing exercises. You also might consider eliminating alcohol and caffeine from your diet and taking supplemental magnesium. Start with 250 mg and increase the dose up to 500 mg daily. If you find that the magnesium has a laxative effect, take calcium along with it (the dosage should be about twice the amount of magnesium but no more than 700 milligrams a day for women, I don’t recommend that men take calcium supplements.)

If your rapid heartbeat goes on for hours, or you get weak, dizzy or develop pain, be sure to call your doctor and get evaluated. You should have an electrocardiogram while you’re having the rapid heartbeat to make sure that it is benign SVT. This kind of rapid heartbeat rarely requires medical attention, and you can usually eliminate or minimize its occurrence by making changes in your habits.

Andrew Weil, M.D.

About the author

Leave a Reply

Your email address will not be published. Required fields are marked *