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Ventilation Inhibits Sympathetic Neural Recruitment During Severe Chemoreflex Stress
Author(s) -
Badrov Mark B,
Barak Otto F,
Mijacika Tanja,
Drvis Ivan,
Dujic Zeljko,
Shoemaker J Kevin
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.867.5
Subject(s) - medicine , apnea , heart rate , microneurography , ventilation (architecture) , anesthesia , blood pressure , functional residual capacity , cardiology , respiratory rate , baroreflex , lung , lung volumes , mechanical engineering , engineering
The current study investigated the effects of ventilation on sympathetic neural recruitment during severe chemoreflex stress. We measured, in six trained breath‐hold divers (one female; 35±11 yrs, 181±11 cm, 74±13 kg), muscle sympathetic nerve activity (MSNA; microneurography), heart rate (HR; electrocardiogram), blood pressure (BP; Finometer), and arterial hemoglobin saturation (HbSat; pulse oximetry) at baseline (2 mins) and during alternating periods (30 s) of functional residual capacity (FRC) apnea and asphyxic rebreathing, a protocol designed to elicit severe chemoreflex activation in the absence and presence of ventilation, respectively. Subjects were instructed to stop when they achieved ~85% of their self‐perceived ‘maximal’ tolerance for the protocol. The final FRC apnea and rebreathe periods were used for analysis. Sympathetic action potential (AP) discharge patterns were studied using a novel AP detection and analysis technique. This technique quantifies not only the number and morphology of APs within the integrated burst at rest, but also the emergence of latent (and larger) APs as stress develops. Compared to baseline, HbSat decreased to similar levels during FRC apnea and rebreathe (80±3 and 78±11%, respectively; P >0.05). Compared to baseline (18±7 bursts/min), MSNA burst frequency increased during FRC apnea (Δ35±6 bursts/min; P <0.01), but not rebreathe (Δ1±4 bursts/min; P >0.05), whereas burst amplitude (54±12 AU) increased during both FRC apnea (Δ82±30 AU) and rebreathe (Δ26±16 AU; both P <0.05), although the increase was greater during FRC apnea ( P <0.01). Compared to baseline (9±3 APs/burst), the mean AP content per integrated burst increased during both FRC apnea (Δ20±6 APs/burst) and rebreathe (Δ7±5 APs/burst; both P <0.01). Similarly, the number of active AP clusters per integrated burst (5±1 clusters/burst) increased during both FRC apnea (Δ4±1 clusters/burst) and rebreathe (Δ2±1 clusters/burst; both P <0.01). However, in both cases, the magnitude of increase was greater during FRC apnea (both P <0.01). Finally, when APs were binned according to peak‐to‐peak amplitude (i.e., into clusters), the number of total AP clusters detected (12±2 total clusters) increased during FRC apnea (Δ6±1 total clusters; P <0.01), but not rebreathe (Δ0±1 total clusters; P >0.05). As such, ventilation restrains sympathetic neural recruitment during severe chemoreflex stimulation. While the increased within‐burst firing frequency of previously active, lower‐threshold sympathetic axons appears preserved, but diminished, in the presence of ventilation (i.e., rebreathe), the recruitment of previously silent, higher‐threshold sub‐populations of larger‐sized sympathetic axons appears specific to apnea, and inhibited by ventilation. Support or Funding Information Supported by Natural Sciences and Engineering Research Council of Canada.