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Background: Media have anecdotally reported that drinking energy drinks in combination with alcohol and exercise could cause sudden cardiac death. This study investigated changes in the electrocardiogram (ECG) and heart rate variability after intake of an energy drink, taken in combination with alcohol and exercise.
Methods: Ten healthy volunteers (five men and five women aged 19–30) performed maximal bicycle ergometer exercise for 30 min after: (i) intake of 0·75 l of an energy drink mixed with alcohol; (ii) intake of energy drink; and, (iii) no intake of any drink. ECG was continuously recorded for analysis of heart rate variability and heart rate recovery.
Results: No subject developed any clinically significant arrhythmias. Post-exercise recovery in heart rate and heart rate variability was slower after the subjects consumed energy drink and alcohol before exercise, than after exercise alone.
Conclusion: The healthy subjects developed blunted cardiac autonomic modulation after exercising when they had consumed energy drinks mixed with alcohol. Although they did not develop any significant arrhythmia, individuals predisposed to arrhythmia by congenital or other rhythm disorders could have an increased risk for malignant cardiac arrhythmia in similar situations.
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During the 1990s, several beverage companies introduced energy drinks containing caffeine, taurine and carbohydrates. These drinks have become very popular not only as sport drinks, but also in a mix with alcohol. Three Swedish sudden deaths after consuming energy drinks and then exercising (Finnegan, 2003; Lehtihet et al., 2006) has been reported and the question has been raised whether the intake of energy drinks together with physical exercise, and possibly also in combination with alcohol, could increase the risk of sudden death – presumably by an arrhythmic origin. However, no empirical link has been found between the intake of energy drink and the time of death, or between the intake of energy drink and the mechanisms responsible for the deaths.
Few studies have examined how energy drinks combined with alcohol affects the heart (Baum & Weiss, 2001; Ferreira et al., 2004). To our knowledge no previous study has investigated the possible arrhythmogenic effects of this combined intake. Increased risk of cardiac arrhythmia could be manifested by changes in the morphology of the electrocardiogram (ECG) or by changes in the mechanisms that trigger individual heartbeats. In particular, malignant cardiac arrhythmia can also be caused by autonomic imbalance with low parasympathetic activity and high sympathetic activity (Task Force of the European Society of Cardiology and the North American Society of Pacing and Electrophysiology, 1996). Several studies in clinical settings correlate reduced cardiac autonomic modulation, as reflected by the beat-to-beat changes in heart rate (heart rate variability, HRV) with the risk of sudden death (Wolf et al., 1978; Ewing et al., 1985; Every et al., 2002). Several studies have also shown that the decrease of heart rate after peak exercise, also called Heart Rate Recovery (HRR), can be used as a marker of parasympathetic activity and also as a predictor of mortality (Cole et al., 1999; Gorelik et al., 2006).
The aim of this study was to examine ECG changes in healthy subjects after the consumption of energy drink combined with alcohol followed by exercise. In particular, our aim was to investigate if the combined intake of energy drink and alcohol caused abnormal patterns in post-exercise HRR or in HRV. Such changes could contribute to an increased risk of cardiac arrhythmia.
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The study was carried out in 10 healthy volunteers – five men and five women aged 19–30. Their background anthropometrical data are listed in Table 1. The investigations were performed in several steps with at least a 1-week wash out period. All tests included sequential laboratory tests (electrolytes, caffeine and glucose), 12-lead ECGs, and Holter monitoring. All subjects gave informed consent, and the local ethical committee of Umeå University approved the study protocol.
Table 1. Baseline values for the healthy volunteers.
| ||Men (n = 5)||Women (n = 5)|
|Mean (SD)||Mean (SD)|
|Age (years)||26·2 (1·5)||26·8 (4·7)|
|BMI (kg m−2)||23·9 (1·8)||23·5 (2·4)|
|Systolic blood pressure (mmHg)||122·8 (7·7)||116·8 (8·1)|
|Diastolic blood pressure (mmHg)||68·6 (10·0)||72·4 (13·5)|
|Heart rate (beats/minute)||73·6 (11·8)||66·4 (8·0)|
|S-Mg (mmol l−1)||0·8 (1·1)||0·8 (3·0)|
|S-Glucose (mmol l−1)||5·0 (0·4)||4·7 (0·7)|
|S-K (mmol l−1)||4·1 (0·5)||3·9 (0·3)|
|S-Na (mmol l−1)||141·8 (1·0)||140·0 (1·6)|
|S-Creatinine (mmol l−1)||80·8 (10·5)||84·8 (10·7)|
|S-Albumin (g l−1)||41·8 (2·8)||36·6 (3·0)|
|PQ time (ms)||157·2 (21·7)||130·0 (16·9)|
|QRS duration (ms)||95·6 (8·6)||87·6 (12·4)|
|QT time (ms)||387·2 (25·4)||406·4 (27·8)|
|QT time, corrected (ms)||417·0 (16·9)||417·4 (18·9)|
The subjects performed a physical and laboratory baseline screening, followed by four tests, all performed in the same order with 1–3 months between each test:
Consumption of 0·75 l of energy drink (three cans of RedBull®, containing 0·4% of taurine, 0·032% of caffeine, totally 3000 mg of taurine and 240 mg of caffeine) after an overnight fast.
Consumption of 0·75 l of energy drink mixed with vodka, corresponding to 0·4 g of ethanol per kg body weight, and a maximal bicycle ergometer exercise 30 min later. This trial, laboratory analysis also included s-ethanol (ED/ET).
Consumption of 0·75 l of energy drink and a maximal bicycle ergometer exercise 30 min later (ED).
Maximal bicycle ergometer exercise after 30 min rest (EX).
The subjects consumed the amount of energy drink within 30 min. The maximal bicycle ergometer exercise was designed to be maximal and last for up to 15 min, following the protocol suggested by Nordenfelt et al. (Nordenfelt et al., 1985). The subjects returned to the supine position directly after exercise. They stayed in the supine position at least for 1 h in all tests and remained in the laboratory up to 6 h after the bicycle ergometer exercise test (Tests ED/ET and ED).
The local laboratory performed analyses (s-glucose, s-potassium, s-sodium, s-creatinine, s-magnesium, ionised s-calcium) using routine biochemical methods. Caffeine and ethanol were analysed at the Department of Forensic Chemistry, National Board of Forensic Medicine, Linköping, Sweden. A standard ECG recorder (Siemens-Elema AB, Solna, Sweden) was used to record twelve-lead ECGs to calculate PQ and QT/QTc times, and QRS duration. QT was corrected for heart rate according to Bazett (Bazett, 1920).
During the tests, ECG was recorded with an ambulatory recorder unit (Braemer DL 700; Braemer inc. Burnsville, MN, USA) with a sample rate of 128 Hz. Cardiac conduction and rhythm disturbances were automatically analysed by a Holter-ECG system (Danica Holter Replay Unit, Danica Biomedical, Borlänge, Sweden). One investigator examined all recordings, confirmed pathological events, and corrected detection errors. ECG and R-R intervals were exported from the Holter-ECG system. HRR and HRV were analysed with custom-designed software using the Matlab software (Mathworks, Natick, MA, USA).
HRR was determined by fitting a first order exponential decay curve to the post-exercise heart rate recovery according to Javorka et al. (Javorka et al., 2003):
where the decay constant (T), peak heart rate (HRPeak) and final heart rate (HRRest) were determined by using the simplex search method (Lagarias et al., 1998), with data from the first 300 s after the maximal bicycle exercise.
The R-R interval data were transformed to an evenly sampled (2 Hz) time series by cubic spline interpolation before HRV was analysed. Spurious arrhythmic beats and artefacts were replaced using interpolation. Recordings from Test 1 were analysed as non-overlapping 10-min sequences. Data from Tests 2 to 4 were analysed as 2-min sequences because of the non-stationary HRV during the recovery after exercise. The mean heart rate was calculated for each sequence. Data were detrended by removing the mean value and the linear trend.
Heart rate variability was analysed in the frequency domain: the power spectral density was estimated by auto-regressive modelling using the Burg algorithm with 30 parameters. HRV was measured by calculating the total spectral power (PTOT), the power of the low-frequency component (PLF; 0·04–0·15 Hz), and the power of the high-frequency component (PHF; 0·15–0·50 Hz). Often, the low-frequency (LF) component is associated with baroreceptor mediated blood-pressure control, reflecting both sympathetic and parasympathetic activity. In most subjects, the high-frequency (HF) component peaks at the respiration frequency, reflecting parasympathetic activity (Task Force of the European Society of Cardiology and the North American Society of Pacing and Electrophysiology, 1996). The ratio PLF/PHF was calculated as an indicator of sympathovagal balance. All spectral indices were logarithmically transformed.
Data were analysed by repeated measures analysis of variance (ANOVA) with time and test as factors. Statistically significant main effects were analysed with a simple contrast, where, e.g. the first sequence (baseline) was compared with the other sequences. Data from Test 1 were analysed using paired t-tests. Statistical significance was defined as a P-value <0·05 (two-sided).
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The study investigated whether consumption of energy drinks – alone or in combination with maximal bicycle ergometer exercise with and without consumption of alcohol – caused any changes in the ECG or in HRV in healthy volunteers. No signs of any clinically significant arrhythmia were found in any of the tests, but small ECG changes were found that may be related to the consumption of energy drink and alcohol. The main finding was that consumption of energy drink mixed with alcohol influenced both the post-exercise recovery in heart rate and in HRV.
We have not found any previous studies linking the combination of taurine, caffeine and alchohol to changes in HRV. Taurine moderates the flow of cations, especially calcium, across the cell membranes, protecting the heart muscle from both high and low serum calcium concentrations (Huxtable, 1992; Schaffer & Azuma, 1992). Caffeine increases vagal autonomic nerve activity in resting subjects (Hibino et al., 1997; Yeragani et al., 2005). The intake of caffeine before exercise has also been associated with exaggerated vagal withdrawal during post-exercise recovery because of higher baseline level of vagal activity before exercise(Yeragani et al., 2005) There is also evidence that caffeine can improve physical performance (Doherty, 1998; Laurent et al., 2000; Cox et al., 2002). Our study showed a decreased PLF/PHF and a tendency to increased PHF, most likely reflecting an increased vagal modulation, when subjects were resting after consuming energy drinks.
Physical exercise reduces HRV, noted as a decreased parasympathetic and an increased sympathetic activity (Javorka et al., 2003), leading to an increase of heart rate, stroke volume, and myocardial contractility. After cessation of exercise, heart rate rapidly declines due to a vagal reactivation, which also results in successively increased HRV (Imai et al., 1994). In our study, all subjects had a reduced HRV during recovery after maximal bicycle ergometer exercise, independent of heart rate, as compared with HRV during the rest period. This reduction – signalling a reduced parasympathetic tone or the predominance of sympathetic over vagal stimulation – was enhanced when energy drink and alcohol was consumed before exercise.
Although no subject developed any significant arrhythmias during post-exercise recovery, we hypothesise that in predisposed individuals the blunted vagal reactivation, caused by the combined intake of energy drink and alcohol, might be arrhythmogenic. Reduced HRV has been linked to the degree of autonomic neuropathy in diabetic patients and linked with the risk for sudden death (Ewing et al., 1985, 1991). The relative risk of sudden cardiac death (SCD) is increased following vigorous physical exercise (Kohl et al., 1992; Alberti et al., 2000). Therefore, subjects having an inability to increase vagal activity could have an increased risk for sudden death during post-exercise recovery (Jouven et al., 2005). The majority of people who die because of SCD have a pre-existing disease; more than half of these cases have hypertrophic cardiomyopathy or coronary anomalies (Maron et al., 1996). A substantial number, however, die without receiving a definite diagnosis. In these cases, a genetic disorder causing a fatal arrhythmia could have existed. As most of these diagnoses only can be made by ECG analysis ante-mortem, it is not known whether the reported deaths after energy drink intake were afflicted by any of these diseases.
Intake of an energy drink alone appeared to increase vagal activity during rest in the supine position: On the other hand, intake of energy drink resulted in slower vagal reactivation after exercise, as compared to exercise alone. Although the pattern in post-exercise HRR mainly has been associated with vagal reactivation, the time constant of the exponential decay has been associated with sympathetic withdrawal (Buchheit et al., 2007). Therefore, our findings could also reflect delayed sympathetic withdrawal, probably due to stimulant effect of the energy drink.
The results showed changes in the standard ECG. The consumption of energy drink and alcohol caused an increase in PQ time. This finding indicates that electrophysiological changes are induced by the amount of energy drink and alcohol consumed. As the impact on the heart from the combination energy drink/alcohol/exercise was unknown, for ethical reasons, the limit of blood alcohol concentration was decided to not exceed 0·5%. Moreover, because this pilot study included only 10 healthy volunteers, further larger studies are needed to confirm our results.
In conclusion, we found no clinically significant arrhythmias in any part of our studies. Maximal bicycle ergometer exercise after consuming an energy drink and alcohol, led to delayed heart rate recovery with decreased HRV, as compared to recovery after only exercise. Physical exercise causes a parasympathetic withdrawal and an increased sympathetic activity, and the risk of arrhythmias is increased after physical exercise. This risk could be further accentuated with the intake of an energy drink and alcohol as this causes a blunted cardiac autonomic control. The arrhythmia risk is probably of most concern for predisposed individuals – such as individuals with congenital or other arrhythmia-causing disorders or for individuals with cardiac autonomic dysfunction.