Publication
Initial Assessment of Lactate as Mediator of Exercise-Induced Retinal Protection
Downloadable Content
- Persistent URL
- Last modified
- 05/21/2025
- Type of Material
- Authors
- Language
- English
- Date
- 2019-01-01
- Publisher
- Springer International Publishing A.G.
- Publication Version
- Copyright Statement
- © Springer Nature Switzerland AG 2019, Corrected Publication 2020.
- Final Published Version (URL)
- Title of Journal or Parent Work
- Volume
- 1185
- Start Page
- 451
- End Page
- 455
- Grant/Funding Information
- NIH R01EY028859, R01EY028450, R01EY021592, T32EY07092, and P30EY006360; and an unrestricted grant from Research to Prevent Blindness, Inc.
- The Abraham J. & Phyllis Katz Foundation; VA RR&D Center Grant C9246C,
- Research Career Scientist Award C9257, Merit Award I01RX002806, and SPiRE Award Number I21RX001924;
- Abstract
- Physical exercise is protective in rodent models of retinal injury and disease. Data suggest that this is in part mediated by brain-derived neurotrophic factor (BDNF) signal transduction. It has been hypothesized that exercised-induced neuroprotection may be mediated by increases in circulating lactate that in turn alter BDNF secretion. We therefore tested whether mice undergoing a treadmill running regimen previously shown to be protective in a mouse model of retinal degeneration (RD) have increased serum levels of lactate. Lactate levels in exercised and non-exercised mice were statistically indistinguishable. A role for circulating lactate in exercise-induced retinal protection is unsupported.
- Author Notes
- Keywords
Tools
- Download Item
- Contact Us
-
Citation Management Tools
Relations
- In Collection:
Items
| Thumbnail | Title | File Description | Date Uploaded | Visibility | Actions |
|---|---|---|---|---|---|
|
|
Publication File - vp4n8.pdf | Primary Content | 2025-05-01 | Public | Download |