Bidirectional causality of physical exercise in retinal neuroprotection

Abstract

Physical exercise is recognized as an effective intervention to improve mood, physical performance, and general well-being. It achieves these benefits through cellular and molecular mechanisms that promote the release of neuroprotective factors. Interestingly, reduced levels of physical exercise have been implicated in several central nervous system diseases, including ocular disorders. Emerging evidence has suggested that physical exercise levels are significantly lower in individuals with ocular diseases such as glaucoma, age-related macular degeneration, retinitis pigmentosa, and diabetic retinopathy. Physical exercise may have a neuroprotective effect on the retina. Therefore, the association between reduced physical exercise and ocular diseases may involve a bidirectional causal relationship whereby visual impairment leads to reduced physical exercise and decreased exercise exacerbates the development of ocular disease. In this review, we summarize the evidence linking physical exercise to eye disease and identify potential mediators of physical exercise-induced retinal neuroprotection. Finally, we discuss future directions for preclinical and clinical research in exercise and eye health.

Figure 1

Impact of physical exercise–induced neuroprotective factors on various ocular diseases. *PE increases/potentially increases the level of adiponectin (APN), BDNF, and IGF-1. For the other neurotropic factors, PE potentially influences their levels however there is no direct mention of whether PE causes an increase or decrease in their levels. Created with BioRender.com. AMD: Age-related macular degeneration; BDNF: brain-derived neurotrophic factor; CNTF: ciliary neurotrophic factor; FGF-21: fibroblast growth factor-21; GDNF: glial cell line–derived neurotrophic factor; IGF-1: insulin-like growth factor-1; PE: physical exercise; ROP: retinopathy of prematurity; RP: retinitis pigmentosa; VEGF-A: vascular endothelial growth factor-A.