4.6 Article

Vascular function in the aging human brain during muscle exertion

Journal

AGING-US
Volume 14, Issue 9, Pages 3910-3920

Publisher

IMPACT JOURNALS LLC

Keywords

frailty; vascular function; muscle strength; endothelial function; NIRS

Funding

  1. Body Composition Technologies Ltd Pte
  2. University of Taipei, Taipei, Taiwan

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The study found that cerebral oxygenation variability and brain hemodynamic variability increased during maximal voluntary muscle exertions, indicating vascular recruitment to maintain brain oxygen homeostasis. Interestingly, despite similar levels of cerebral oxygenation variability compared to young individuals, brain hemodynamic variability was significantly higher in adults aged over 50, suggesting a significant cost of amplifying hemodynamic oscillation to maintain stable oxygenation in the aging brain.
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 (alpha < 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 (alpha < 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.

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