Key result
Aging and coronary artery disease impaired sympathetic neural recruitment during apnea, with CAD patients showing no significant increase in mean action potentials per burst.
Why the study?
Do aging and coronary artery disease alter sympathetic neural recruitment strategies during end-inspiratory and end-expiratory apnea?
Cross-Sectional (n=42)
Do aging and coronary artery disease alter sympathetic neural recruitment strategies during end-inspiratory and end-expiratory apnea?
Aging and coronary artery disease are associated with inherent dysregulation in the central features of apnea-related sympathetic outflow.
Sympathetic recruitment during apnea is preserved with aging but blunted in CAD; leaves open whether this reflects disease-specific neural dysregulation.
In response to acute physiological stress, the sympathetic nervous system modifies neural outflow through increased firing frequency of lower-threshold axons, recruitment of latent subpopulations of higher-threshold axons, and/or acute modifications of synaptic delays. Aging and coronary artery disease (CAD) often modify efferent muscle sympathetic nerve activity (MSNA). Therefore, we investigated whether CAD (n = 14; 61 ± 10 yr) and/or healthy aging without CAD (OH; n = 14; 59 ± 9 yr) modified these recruitment strategies that normally are observed in young healthy (YH; n = 14; 25 ± 3 yr) individuals. MSNA (microneurography) was measured at baseline and during maximal voluntary end-inspiratory (EI) and end-expiratory (EE) apneas. Action potential (AP) patterns were studied using a novel AP analysis technique. AP frequency increased in all groups during both EI- and EE-apnea (all P < 0.05). The mean AP content per integrated burst increased during EI- and EE-apnea in YH (EI: Δ6 ± 4 APs/burst; EE: Δ10 ± 6 APs/burst; both P < 0.01) and OH (EI: Δ3 ± 3 APs/burst; EE: Δ4 ± 5 APs/burst; both P < 0.01), but not in CAD (EI: Δ1 ± 3 APs/burst; EE: Δ2 ± 3 APs/burst; both P = NS). When APs were binned into "clusters" according to peak-to-peak amplitude, total clusters increased during EI- and EE-apnea in YH (EI: Δ5 ± 2; EE: Δ6 ± 4; both P < 0.01), during EI-apnea only in OH (EI: Δ1 ± 2; P < 0.01; EE: Δ1 ± 2; P = NS), and neither apnea in CAD (EI: Δ -2 ± 2; EE: Δ -1 ± 2; both P = NS). In all groups, the AP cluster size-latency profile was shifted downwards for every corresponding cluster during EI- and EE-apnea (all P < 0.01). As such, inherent dysregulation exists within the central features of apnea-related sympathetic outflow in aging and CAD.
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Badrov et al. (2016) conducted a cross-sectional in Coronary artery disease and aging (n=42). Aging and coronary artery disease vs. Young healthy individuals was evaluated on Mean action potential (AP) content per integrated burst during end-inspiratory and end-expiratory apnea. Aging and coronary artery disease impaired sympathetic neural recruitment during apnea, with CAD patients showing no significant increase in mean action potentials per burst.
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