To the Editor,
I have read the article entitled "Effects of energy drinks on blood pressure, heart rate, and electrocardiographic parameters: an experimental study on healthy young adults" by Hajsadeghi et al. (1), which was recently published in the Anatolian Journal of Cardiology 2016; 16: 94-9, with great interest. The investigators reported that energy drink consumption could contribute to heart rate decrease and ST-T changes in healthy young adults. In addition, systolic and diastolic BP and other ECG parameters do not significantly change after the energy drink consumption (1).
There were conflicting results about the relationship between heart rate response and energy drink consumption (2, 3). Authors implied that the possible mechanism underlying the heart rate dec- rease was related to an increase in the stroke volume and enhancement of the myocardial contractility after the energy drink consumption (1). Authors claimed that excessive catecholamine release after energy drink consumption is the mechanism underlying the significant ST-T changes (1). It is well known that heart rate increase is an essential effect of catecholamine release. The possible reason underlying these conflicting results is related to the follow-up duration and amount of energy drink consumed (2, 3).
In addition, there was no data regarding smoking history or current smoking status. The vasopressor and tachycardia effects of smoking are associated with an increase in the plasma catecholamine concentration (4). Likewise, there was a strong relationship between heart rate variability and smoking (5).
In the light of this knowledge, authors should mention regarding the smoking habits of participants. Moreover, the follow-up duration and amount of energy drinks consumed should be standardized.
Levent Cerit
Department of Cardiology, Near East University, Nicosia-Turkish Republic of Northern Cyprus
References
1. Hajsadeghi S, Mohammadpour F, Manteghi MJ, Kordshakeri K, Tokazebani M, Rahmani E, et al. Effects of energy drinks on blood pressure, heart rate, and electrocardiographic parameters: An experimental study on healthy young adults. Anatol J Cardiol 2016; 16: 94-9.
2. Geiss KR, Jester I, Falke W, Hamm M, Waag KL. The effect of a taurine-containing drink on performance in 10 endurance-athletes. Amino Acids 1994; 7: 45-56. [Crossref]
3. Steinke L, Lanfear DE, Dhanapal V, Klaus JS. Effect of "energy drink" consumption on hemodynamic and electrocardiographic parameters in healthy young adults. Ann Pharmacother 2009; 43: 596-602.
4. Grassi G, Seravalle G, Calhoun DA, Bolla GB, Giannattasio C, Marabini M, et al. Mechanisms responsible for sympathetic activation by cigarette smoking in humans. Circulation 1994;90:248-53.
5. Bianchim MS, Sperandio EF, Martinhão GS, Matheus AC, Lauria VT, da Silva RP, et al. Correlation between heart rate variability and pulmonary function adjusted by confounding factors in healthy adults. Braz J Med Biol Res 2016 Mar 3. Epub ahead of print. [Crossref]
Address for Correspondence: Dr. Levent Cerit
Near East Hospital University Hospital, Nicosia-
Turkish Republic of Northern Cyprus
Phone: +90 392 675 10 00 E-mail: [email protected]
©Copyright 2016 by Turkish Society of Cardiology - Available online
at www.anatoljcardiol.com
DOI:10.14744/AnatolJCardiol.2016.7184
Author`s Reply
To the Editor,
We thank the authors for their great interest in our work entitled "Effects of energy drinks on blood pressure, heart rate, and electrocardiographic parameters: an experimental study on healthy young adults" published in Anatol J Cardiol 2016; 16: 94-9 (1). In addition to our discussion, they also notified the incoherent results of different studies on the heart rate (HR) response after energy drink consumption. Authors of the letter, however, stated that an HR increase is an essential effect of catecholamine release and then considered the combination of "HR decline" and "catecholamine release" as conflicting. Although we agree that an HR increase is an effect of situations with pure catecholamine release, it must be emphasized that a combination of "HR decline and catecholamine release" is also possible in some conditions, of which the most well-known is the Cushing reflex. As we supposed in the article, the HR decrease after energy drink consumption is possibly due to direct central stimulation of the vagus nerve by caffeine (2). A similar mechanism has been previously described for the Cushing reflex where concurrent hypertension (owing to sympathetic activation) and bradycardia (owing to the vagus nerve stimulation) are seen (3).
Given the known effects of smoking on sympathetic activation (4), as noted by the authors of the letter, we excluded all smokers from our study to avoid its possible confounding role on results. This was mentioned in the paper by excluding those with a history of "substance abuse." According to the valid definitions, including Diagnostic and Statistical Manual of Mental Disorders-Fifth Edition (DSM-5) (5), tobacco consumption is an example of substance abuse.
Finally, as we discussed in the abovementioned article (1), factors such as different types of energy drinks and durations of BP monitoring after energy drink consumption are among the possible reasons underlying the conflicting results of different studies on hemodynamic effects of energy drinks. Thus, we agree with the authors of the letter that considering follow-up duration and amount of energy drinks are of great importance in compa- ring the results of different investigations on energy drinks.
Shokoufeh Hajsadeghi
Department of Cardiology, Rasoul-e-Akram Hospital, Faculty of Medicine, Iran University of Medical Sciences; Tehran-Iran
References
1. Hajsadeghi S, Mohammadpour F, Manteghi MJ, Kordshakeri K, Tokazebani M, Rahmani E, et al. Effects of energy drinks on blood pressure, heart rate, and electrocardiographic parameters: An experimental study on healthy young adults. Anatol J Cardiol 2016; 16: 94-9.
2. Whitsett TL, Manion CV, Christensen HD. Cardiovascular effects of coffee and caffeine. Am J Cardiol 1984; 53: 918-22. [Crossref]
3. Hackett JG, Abboud FM, Mark AL, Schmid PG, Heistad DD. Coronary vascular responses to stimulation of chemoreceptors and baroreceptors:evidence for reflex activation of vagal cholinergic innervation. Circ Res 1972; 31: 8-17. [Crossref]
4. Grassi G, Seravalle G, Calhoun DA, Bolla GB, Giannattasio C, Marabini M, et al. Mechanisms responsible for sympathetic activation by cigarette smoking in humans. Circulation 1994; 90: 248-53.
5. Hasin DS, O'Brien CP, Auriacombe M, Borges G, Bucholz K, Budney A, et al. DSM-5 criteria for substance use disorders: recommendations and rationale. Am J Psychiatry 2013; 170: 834-51. [Crossref]
Address for Correspondence: Shokoufeh Hajsadeghi, MD,
Department of Neurology, Boston Children's Hospital
Harvard Medical School, 1 Autumn St, Boston, MA 02115-USA
Phone: (617) 919-6232 E-mail: [email protected]
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