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Vascular function in the aging human brain during muscle exertion

To determine how brain oxygenation is stably maintained during advancing age, cerebral oxygenation and hemoglobin were measured real-time at 10 Hz using near-infrared spectroscopy (NIRS) at rest (30 seconds) and during a 10-repeated handgrip strength test (30 seconds) for 834 adults (M/F = 45/55%) a...

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Detalles Bibliográficos
Autores principales: Zhu, Maijian, Lee, Tania Xu Yar, Hsieh, Yu-Wen, Lai, Li-Fan, Condello, Giancarlo, Donnelly, Cyril J., Smith, Marc, Hamzah, Sareena Hanim, Lim, Boon-Hooi, Huang, Chih-Yang, Chi, Nai-Fang, Kuo, Chia-Hua
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Impact Journals 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9134944/
https://www.ncbi.nlm.nih.gov/pubmed/35500246
http://dx.doi.org/10.18632/aging.204052
Descripción
Sumario:To determine how brain oxygenation is stably maintained during advancing age, cerebral oxygenation and hemoglobin were measured real-time at 10 Hz using near-infrared spectroscopy (NIRS) at rest (30 seconds) and during a 10-repeated handgrip strength test (30 seconds) for 834 adults (M/F = 45/55%) aged 20–88 y. The amplitude of cerebral hemodynamic fluctuation was reflected by converting 300 values of % oxygen saturation and hemoglobin of each 30-second phase to standard deviation as indicatives of brain oxygenation variability (BOV) and brain hemodynamic variability (BHV) for each participant. Both BOV (+21–72%) and BHV (+94–158%) increased during the maximal voluntary muscle exertions for all age levels (α < 0.05), suggesting an increased vascular recruitment to maintain oxygen homeostasis in the brain. Intriguingly, BHV was >100 folds for both resting and challenged conditions (α < 0.001) in >80% of adults aged above 50 y despite similar BOV compared with young age counterparts, indicating a huge cost of amplifying hemodynamic oscillation to maintain a stable oxygenation in the aging brain. Since vascular endothelial cells are short-lived, our results implicate a hemodynamic compensation to emergence of daily deficits in replacing senescent endothelial cells after age 50 y.