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| LETTER TO EDITOR |
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| Year : 2022 | Volume
: 22
| Issue : 3 | Page : 117-118 |
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Can long-term post-COVID-19 fainting syndrome explain why a US artist swimmer Anita Alvarez has recurrent fainting attacks after diving during a swimming competition? Does interleukin-6 play a role?
Amr Ahmed1, Neveen Refaey2
1 Department of Public Health, Tuberculosis Program, First Health Cluster, Ministry of Health, Riyadh, Saudi Arabia
2 Department of Physical Therapy for Women's Health, Faculty of Physical Therapy, Cairo University, Giza, Egypt
| Date of Submission | 28-Sep-2022 |
| Date of Acceptance | 09-Oct-2022 |
| Date of Web Publication | 15-May-2023 |
Correspondence Address:
Amr Ahmed
Department of Public Health, Tuberculosis Program, First Health Cluster, Ministry of Health, Riyadh
Saudi Arabia
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/sjsm.sjsm_22_22
How to cite this article:
Ahmed A, Refaey N. Can long-term post-COVID-19 fainting syndrome explain why a US artist swimmer Anita Alvarez has recurrent fainting attacks after diving during a swimming competition? Does interleukin-6 play a role?. Saudi J Sports Med 2022;22:117-8 |
How to cite this URL:
Ahmed A, Refaey N. Can long-term post-COVID-19 fainting syndrome explain why a US artist swimmer Anita Alvarez has recurrent fainting attacks after diving during a swimming competition? Does interleukin-6 play a role?. Saudi J Sports Med [serial online] 2022 [cited 2023 Jun 8];22:117-8. Available from: https://www.sjosm.org/text.asp?2022/22/3/117/377101 |
Dear Editor,
At the 19th International Swimming Federation World Aquatic Championships held in Budapest, Hungary, American swimmer Anita Alvarez lost consciousness, experienced recurrent fainting attacks after diving during a swimming competition and had to be pulled from the bottom of the pool by her coach. Moreover, this happens for the second time.[1]
Five (0.6%) of the 789 elite athletes in an observational study who tested positive for COVID-19 had cardiovascular magnetic resonance evidence of inflammatory cardiac disease (myocarditis or pericarditis).[2]
Concern has been expressed by a number of authors on the effect of neurologic and neuromuscular problems on return to play. As they recover from COVID-19 disease, athletes may experience tiredness, decreased neuromuscular function, and decreased muscle strength. Several additional COVID-related problems, such as general weariness, cognitive impairment, and coagulopathy, can occur in recovering athletes.[3],[4]
The most common chronic cardiovascular dysautonomia in young- and middle-aged people, primarily women, is postural orthostatic tachycardia syndrome. Chronic orthostatic intolerance, an abnormal increase in heart rate upon standing, and deconditioning are its defining characteristics. Postviral autoimmune activation has been proposed as a potential cause of the condition.[5]
Interleukin-6 (IL) is crucial for athletes, particularly after arduous activity and after submerging in cold water. Immersion in cold water is linked to a little increase in IL-6 levels from postexercise values.[6] Two studies described a syncopal episode in COVID-19 survivors 3–4 weeks after diagnosis, at the postacute COVID-19 stage. This increases the likelihood that syncope had a role, not just during the illness's acute stage but also as a long-term consequence. Patients in both of these cases underwent analysis for postural orthostatic tachycardia disorder, a part of the autonomic dysfunctions. As previously stated, unexplained presyncope accounted for 87.9% (531/604) of the detailed scenes and was the most frequent cause of the temporary loss of awareness. Reflex presyncope occurred 7.8% of the time overall (47/604). Orthostatic hypotension made up 2.2% (13/604) of the cases and 2.2% (13/604) of the cases likely had cardiac presyncope.[7],[8]
IL-6 is a localized energy sensor that is supplied to active skeletal muscle and can explain why there is an increase in plasma IL-6 during the exercise. The length and intensity of the workout have an impact on the creation of IL-6, and moo muscle glycogen material supports this production. The discovery of abnormally elevated levels of IL-6 following arduous exercise has consistently been observed in several studies. After 6 min of vigorous exercise, a 2-fold increase in plasma IL-6 was seen. After 30 min of running by the treadmill, the blood level of IL-6 had significantly increased, reaching its peak after 2.5 h. In other studies, when IL-6 levels were not monitored during the running workout, but rather a few hours later, peak IL-6 levels were discovered right away after the workout, followed by a rapid decline. In this manner, maximal IL-6 levels (100-fold increment) were assessed immediately following the 3–3.5 h race.[9]
Peak IL-6 levels are attained at the conclusion of the workout or soon after. Chronic IL-6 elevations cause hyperinsulinemia, lower body mass, and impaired insulin control of skeletal muscle glucose absorption. The level of circulating IL-6 is two to three times higher in senior patients with type 2 diabetes mellitus than it is in younger, healthy people.[10]
As stated by the National Institute for Health and Care Excellence, a significant proportion of acute COVID-19 survivors experience long-term physical and neuropsychiatric symptoms, which are categorized as “ongoing symptomatic COVID-19” (symptoms that continue for 4–12 weeks after the onset of the illness) and “post-COVID-19 syndrome” or “long COVID” (symptoms that continue for more than 12 s). We hypothesize that inflammatory cytokines such as IL-6 may be involved in the neuro-immune cross-talk that results in these chronic COVID-19 symptoms (IL-6). This hypothesis is supported by a number of research lines, including population-based cohort and genetic Mendelian randomization studies, which suggest that inflammation and weariness are related and that IL-6 may play a causal role in both symptoms. In particular, clinical epidemiology studies are necessary to determine whether IL-6 and/or other inflammatory cytokine levels are elevated.[11]
Finally, this letter of the editor is an alarming pill for saving athletes all over the world and evaluating recurrent attacks of syncopal or cardiac arrest or other cardiovascular problems nowadays post-COVID-19 pandemic long-term sequelae, and more clinical studies are needed.
Financial support and sponsorship
Nil.
Conflicts of interest
There are no conflicts of interest.
| References | |  |
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| 5. | Johansson M, Ståhlberg M, Runold M, Nygren-Bonnier M, Nilsson J, Olshansky B, et al. Long-haul Post-COVID-19 symptoms presenting as a variant of postural orthostatic tachycardia syndrome: The Swedish experience. JACC Case Rep 2021;3:573-80. |
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| 7. | Kanjwal K, Jamal S, Kichloo A, Grubb BP. New-onset postural orthostatic tachycardia syndrome following coronavirus disease 2019 infection. J Innov Card Rhythm Manag 2020;11:4302-4. |
| 8. | Miglis MG, Prieto T, Shaik R, Muppidi S, Sinn DI, Jaradeh S. A case report of postural tachycardia syndrome after COVID-19. Clin Auton Res 2020;30:449-51. |
| 9. | Pedersen BK, Steensberg A, Schjerling P. Muscle-derived interleukin-6: Possible biological effects. J Physiol 2001;536:329-37. |
| 10. | Reihmane D, Dela F. Interleukin-6: Possible biological roles during exercise. Eur J Sport Sci 2014;14:242-50. |
| 11. | Kappelmann N, Dantzer R, Khandaker GM. Interleukin-6 as potential mediator of long-term neuropsychiatric symptoms of COVID-19. Psychoneuroendocrinology 2021;131:105295. |
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