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Year : 2022  |  Volume : 2  |  Issue : 3  |  Page : 716-718

Retinal arterial occlusion following acute bout of intense exercise

Department of Vitreoretinal Diseases, Sankara Nethralaya, Chennai, Tamil Nadu, India

Date of Submission12-Nov-2021
Date of Acceptance10-Feb-2022
Date of Web Publication16-Jul-2022

Correspondence Address:
Dr. Dhanashree Ratra
Senior Consultant, Department of Vitreoretinal Diseases, Sankara Nethralaya, 41/18, College Road, Chennai - 600 006, Tamil Nadu
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/ijo.IJO_2845_21

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The various health benefits of physical exercise are well known. Regular, moderate exercise is included in every cardiovascular risk prevention program, as it has a protective effect on the cardiac vasculature. But intense, supramaximal exercise might have potentially adverse effects ranging from increased risk of vascular endothelial injury to sudden cardiac arrest. Acute bout of exercise at high-enough intensity can damage the endothelial cells in the systemic blood vessels. Exercise also affects the retinal and choroidal blood flow, but studies evaluating these effects are limited. Autoregulation, perfusion pressure, endothelial injury, hemoconcentration, and other systemic factors play a complex role in this. In a rare occurrence, we report two cases of sudden occlusion of retinal circulation involving the central retinal artery in one and the ophthalmic artery in the other, following acute, intense exercise in otherwise young, healthy persons. Extensive investigations revealed no other cause for the occlusion. Vision in the affected eye remained poor.

Keywords: Amaurosis Fugax, autoregulation, exercise, ophthalmic artery occlusion, retinal arterial occlusion

How to cite this article:
Ratra D, Khanna R. Retinal arterial occlusion following acute bout of intense exercise. Indian J Ophthalmol Case Rep 2022;2:716-8

How to cite this URL:
Ratra D, Khanna R. Retinal arterial occlusion following acute bout of intense exercise. Indian J Ophthalmol Case Rep [serial online] 2022 [cited 2022 Oct 6];2:716-8. Available from: https://www.ijoreports.in/text.asp?2022/2/3/716/351155

It is well known that regular exercise has a protective role on cardiac vasculature. Its effect on retinal and choroidal circulation is not clear.[1],[2] Complex interactions between various local and systemic factors along with autoregulation control the retinal blood flow after exercise. Retinal venous occlusions (RVOs) following exercise have been reported.[1] We report two cases of retinal arterial occlusion following intense exercise, possibly due to arterial vasoconstriction coupled with hemoconcentration.

  Case Reports Top

Case 1

A 25-year-old healthy Indian man noticed sudden diminution of vision in the right eye half an hour after a heavy weight training session in the gymnasium. He reported exercise-related episodes of transient vision loss for 5–10 seconds, since the past 3 years. He trained regularly at the gymnasium and denied intake of anabolic steroid. His medical and family histories were negative for any systemic diseases. The right eye showed central retinal artery occlusion with a cherry red spot at the macula, surrounding retinal whitening and arterial narrowing. The vision in the right eye was grossly reduced, and he could only count fingers close to face. The left eye was normal. His routine hemogram, blood sugar levels, glycosylated hemoglobin, coagulation profile, lipid profile, serum homocysteine levels, echocardiography, carotid Doppler, and computerized tomography angiography were within normal limits. No abnormal blood cells, sickle cells, or parasites were detected. Cardiology and neurology consultations revealed no abnormal findings. No specific treatment was given as the episode had taken place 5 days before the patient presented to us. Over a short follow-up of 1 month, no visual improvement was noted.

Case 2

A 15-year-old boy had experienced diminution of vision in the right eye just after an intense workout with heavy weightlifting. He had recently started training at a gymnasium. His medical history revealed meningitis 7 years ago and asthma for which he took occasional inhalational steroids. He reported to us 21 days after the onset. In the right eye, the visual acuity was counting fingers at 2 m. There was a relative afferent pupillary defect. The intraocular pressure was 14 mmHg. The optic nerve head (ONH) was pale with sclerosed vessels and pigments in all quadrants and an altered grayish appearance of the macula [Figure 1]. A fluorescein angiogram showed a delayed choroidal flush and delayed dye entry in the central retinal artery. Optical coherence tomography (OCT) showed loss of retinal architecture and thinning of retina with loss of ellipsoid zone. These features were suggestive of ophthalmic artery occlusion. The left eye was normal. His blood counts, glycosylated hemoglobin, coagulation profile, lipid levels, serum homocysteine levels, vitamin B12, and folic acid assays were normal. Vasculitis workup was negative. Digital subtraction angiography revealed a right central retinal artery attenuation with distal ophthalmic artery attenuation. Echocardiography and carotid Doppler were normal. Cardiology and neurology consultations revealed normal findings.
Figure 1: Images from Case 2. (a) Fundus photo of the right eye showing pale disk, narrowed arterioles, as well as veins and dull retina with pigmentary deposits. (b) In a late phase, montage fluorescein angiogram of the same eye showed delayed dye entry in the choroid as well as in the central retinal artery. The vessels were narrowed. Multiple small hyperfluorescent dots represent retinal pigment epithelial atrophy. A few blocked fluorescein areas are due to the subretinal pigment deposits. (c) The horizontal scan of the optical coherence tomography shows gross thinning of the retina and disorganization of the retinal architecture, where the layers are no longer distinguishable. A single cystoid lesion in the inner retina and a small defect in the ellipsoid zone below it are seen

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  Discussion Top

A few cases of RVO following intense exercise have been described in the literature, which were attributed to dehydration.[1] One of these cases also had branch arteriolar occlusion, thought to be due to increased back pressure in the capillary bed.[1] Long-term effects of consistent exercise have demonstrated a protective role by causing an increase in the ONH capillary flow and decrease in the size of foveal avascular zone (FAZ).[2] But acute effects of intense exercise training on retinal circulation are not known. Retinal circulation is autoregulated. During exercise, there is a rise in the systolic blood pressure. However, the retinal circulation remains unaffected to this change probably due to the myogenic response (Bayliss effect), which is retinal vasoconstriction in response to the increased intramural pressure.[3] This is demonstrated by the fact that the area of FAZ and vessel density at the level of the deep capillary plexus remain unchanged following submaximal physical exertion.[3] But the increased metabolic demand created by the exercise leads to shunting of blood toward the cardiac and skeletal muscles. This leads to a decrease in blood flow to the ONH. With higher-intensity workouts, hypocapnia, a potent stimulus for vasoconstriction, coupled with an increase in the blood viscosity due to dehydration further decrease the blood flow.[4] Following cessation of exercise, there occurs dilation of the retinal vessels to maintain a steady blood flow. This response appears to be age and intensity dependent.[3] The response is better in younger age group and at submaximal exercise intensity. Various studies have found that the intraocular pressure increases following certain weightlifting and yogic postures due to valsalva maneuver and increased hydrostatic pressure that accompany these activities.[5] This would cause a further decrease in the perfusion pressure of the retina and the ONH.

Intense supramaximal bouts of exercise have known to cause vascular injury. Adams opines that acute bout of exercise at a high-enough intensity damages the endothelial cells in the blood vessels demonstrated by the reduced flow-mediated vasodilation and increased circulatory markers of endothelial injury seen immediately afterward.[5] But very often, this endothelial injury is undetected as repair of the endothelial injury takes place by an hour. However, increase in blood concentration of various markers of endothelial damage, namely, microRNA-126, endothelial microparticle (EMP), von Willebrand factor (vWF), thrombomodulin (TM), and circulating endothelial cells (CECs), has been noted.[6]

Exercise-induced vasospastic amaurosis fugax seen in the first case has been reported before and is postulated to be due to hypersensitivity reaction to the mediators secreted during exercise or due to inappropriately high release of mediators such as catecholamines, endothelin-1, and neuropeptide Y.[6],[7] Two case series have reported this peculiar phenomenon. Some patients are seen to respond to nifedipine or calcium channel blockers with reduction in these vascular events.[7],[8]

  Conclusion Top

In conclusion, we report here occurrence of retinal vascular occlusion in two healthy young adults, which can be attributed to intense exercise. The fact that no abnormality could be detected even after extensive investigations and that the episodes occurred within a few minutes of the exercise leads us to believe that the supramaximal exercise might be directly responsible for these vascular occlusions. The complex interplay between the vasodilatory and pressor responses and the loss of autoregulation at exhaustion may have played a role. Considering the widespread acceptance of high-intensity training programs as a tool for physical fitness among the young generation, its role in retinal vascular occlusions should be further evaluated.

Ethics approval

No formal approval is required for case reports by the Ethics Committee of Medical Research Foundation, Sankara Nethralaya.

Consent to participate

Written informed consent was given by all the participants.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

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Conflicts of interest

There are no conflicts of interest.

  References Top

Coca M, Tecle N, Amde W, Mehta A. Combined central retinal vein and branch retinal artery occlusion post intense physical activity. Cureus 2017;9:1-5.  Back to cited text no. 1
Schmitz B, Nelis P, Rolfes F, Alnawaiseh M, Klose A, Krüger M, et al. Effects of high-intensity interval training on optic nerve head and macular perfusion using optical coherence tomography angiography in healthy adults. Atherosclerosis 2018;274:8-15.  Back to cited text no. 2
Nussbaumer M, Donath L, Fischer M, Schäfer J, Faude O, Zahner L, et al. Effects of acute bouts of endurance exercise on retinal vessel diameters are age and intensity dependent. Age (Dordr) 2014;36:9650.  Back to cited text no. 3
Ikemura T, Hayashi N. Ocular circulatory responses to exhaustive exercise in humans. Eur J Appl Physiol 2012;112:3313-8.  Back to cited text no. 4
Qureshi IA, Xi XR, Huang YB, Wu XD. Magnitude of decrease in intraocular pressure depends upon intensity of exercise. Korean J Ophthalmol 1996;10:109-15.  Back to cited text no. 5
Adams V. CrossTalk proposal: Acute exercise elicits damage to the endothelial layer of systemic blood vessels in healthy individuals. J Physiol 2018;596:537-9.  Back to cited text no. 6
Jehn A, Frank Dettwiler B, Fleischhauer J, Sturzenegger M, Mojon DS. Exercise-induced vasospastic amaurosis fugax. Arch Ophthalmol 2002;120:220-2.  Back to cited text no. 7
Imes RK, Hoyt WF. Exercise-induced transient visual events in young healthy adults. J Clin Neuroophthalmol 1989;9:178-80.  Back to cited text no. 8


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