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The Impact of Nitrate Supplementation on the Peripheral Chemoreceptor Reflex to Hypoxia in Older Adults
Author(s) -
Bock Josh,
Limberg Jacqueline,
Hughes William,
Kruse Nicholas,
Ueda Kenichi,
Casey Darren
Publication year - 2017
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.31.1_supplement.867.1
Subject(s) - hypoxia (environmental) , cardiorespiratory fitness , carotid body , chemoreceptor , peripheral chemoreceptors , medicine , placebo , heart rate , anesthesia , hypoxic ventilatory response , bioavailability , reflex , peripheral , cardiology , crossover study , heart failure , ventilation (architecture) , blood pressure , pharmacology , respiratory system , chemistry , oxygen , electrophysiology , mechanical engineering , receptor , alternative medicine , organic chemistry , pathology , engineering
Peripheral chemoreceptors located within the carotid bodies activate cardiorespiratory reflexes in response to hypoxia. Carotid body chemoreceptor activity has been shown to be enhanced in conditions such as congestive heart failure, hypertension, and possibly aging. Nitric oxide (NO) has been proposed as an inhibitory modulator of carotid body chemosensitivity in response to hypoxia. Additionally, NO bioavailability is often reduced with cardiovascular risk factors such as aging. In the present study, we tested the hypothesis that increasing NO bioavailability via dietary nitrate (NO 3 ) supplementation would reduce cardiorespiratory responses to hypoxia in older adults. A double‐blind, randomized, placebo‐controlled, cross‐over study design was used to evaluate minute ventilation (V E ) and heart rate (HR) responses to acute hypoxia in 7 older adults (66±2 years; 5M/2F) before and after 4 weeks of NO 3 supplementation (beetroot powder) and placebo (beetroot powder devoid of NO 3 ). On each study visit, subjects underwent two separate isocapnic hypoxic tests (self‐regulating, partial rebreathing system with 10% O 2 ). Subjects remained on 10% O 2 until SpO 2 reached ≤80%. The hypoxic exposures were separated by a 15‐minute washout period with the subjects breathing room air. V E , HR, and SpO 2 were continuously monitored throughout each hypoxic exposure. Data were grouped together using a 7‐breath average with the slope of the linear regression line for each dependent variable (V E and HR) versus SpO 2 serving as a measure of peripheral chemosensitivity. The slopes for the two hypoxia tests on each study visit were averaged and used for statistical comparisons. On study day one (true baseline) acute hypoxia increased both V E and HR ( P <0.05 for both). Four weeks of NO 3 supplementation reduced the hypoxic ventilatory response (−0.16 ± −0.05 vs. −0.06 ± −0.03 L/minute/%SpO 2 , P <0.05), whereas no change was observed following the placebo phase of the study (−0.14 ± −0.07 vs. −0.14 ± −0.08 L/minute/%SpO 2 , P=0.67). Additionally, the heart rate responses to acute hypoxia were also reduced following NO 3 supplementation (−0.49 ± −0.08 vs. −0.30 ± −0.05 beats/minute/%SpO 2 , P <0.05), but not with placebo (−0.54 ± −0.11 vs. −0.45 ± −0.08 beats/minute/%SpO 2 , P=0.21). Our preliminary findings suggest that supplementation of NO 3 to boost NO bioavailability in older adults blunts the cardiorespiratory responses to hypoxia. Future studies should examine the therapeutic potential of NO 3 in patient populations exhibiting exaggerated peripheral chemosensitivity. Support or Funding Information Research supported by Neogenis Inc.