Exercise Slows Retinal Aging, but Which of the Many Mechanisms Involved are Important?
As researchers note here, there is evidence for exercise to slow retinal aging and the progression of conditions involving retinal degeneration. Exercise affects many aspects of aging, not to the same degree as the practice of calorie restriction, but likely through an overlapping set of mechanisms related to cellular stress response upregulation, including increased autophagy and mitochondrial quality control. There is is a vast forest of interacting metabolic changes to explore, however, and the research community has yet to come to a solid grasp of which of the effects of exercise are the most relevant in any given tissue type in the body.
Physical activity and exercise have long been known to be beneficial to the human body. The benefits of exercise range from being critical for maintaining health and wellbeing, to ameliorating and preventing disease pathogenesis. Exercise has been demonstrated to improve the pathology of several chronic diseases including cardiovascular disease, type 2 diabetes, obesity, and cancer. Regular exercise is now also being "prescribed" at a clinical level as a non-pharmacological therapeutic intervention for complex neurodegenerative diseases such as Alzheimer's disease (AD) and Parkinson's disease (PD). Ultimately this begs the question: Is exercise actually beneficial, or is mammalian physiology not evolutionarily suited to lead a sedentary lifestyle?
Given the broad beneficial effects of exercise observed across disorders of the central nervous system (CNS), it is assumed that exercise provides similar non-pharmacological benefits to retinal degenerative diseases including, but not limited to, diabetic retinopathy (DR), retinitis pigmentosa (RP), glaucoma, and age-related macular degeneration (AMD). These complex neurodegenerative diseases all have varying pathophysiological properties and given these and the limited therapeutic options available, the benefits of exercise in potentially mitigating retinal disease pathologies may be of considerable interest in the field of ophthalmology.
There has been some clinical data that demonstrates both the preventative and rehabilitative effects of exercise to retinal health. Physical activity has been shown to both lower the risk of AMD development and improved visual outcomes. Further, fundamental research into exercise using pre-clinical animal models has demonstrated protection against retinal degeneration including in glaucoma, DR, RP, and AMD. A major question is what is happening at the molecular level in exercise to provide this protection to retinal degeneration? Although the evidence for exercise being of benefit to human physiology is clear, the underlying molecular mechanisms underpinning its benefit, particularly in the CNS, remain largely unknown.