In response to acute physiological stress, the sympathetic nervous system modifies neural outflow through increased firing frequency of lower-threshold axons, recruitment of latent sub-populations 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 yrs) and/or healthy aging without CAD (OH; n=14; 59±9 yrs) modified these recruitment strategies, that normally are observed in young healthy (YH; n=14; 25±3 yrs) 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: ∆6±4 APs/burst; EE: ∆10±6 APs/burst; both P<0.01) and OH (EI: ∆3±3 APs/burst; EE: ∆4±5 APs/burst; both P<0.01), but not in CAD (EI: ∆1±3 APs/burst; EE: ∆2±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: ∆5±2; EE: ∆6±4; both P<0.01), during EI-apnea only in OH (EI: ∆1±2; P<0.01; EE: ∆1±2; P=NS), and neither apnea in CAD (EI: ∆−2±2; EE: ∆−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.
- Coronary artery disease
- Sympathetic nervous system
- Sympathetic neural recruitment patterns
- Copyright © 2016, American Journal of Physiology-Heart and Circulatory Physiology