Simulated apneas significantly increased sympathetic burst incidence from 29 to 49 bursts/100 heartbeats and activated a cortical network including the insular cortex and anterior cingulate.
Observational (n=16)
Randomized order
No
Do simulated apneas (breath-holds and Mueller manoeuvres) alter cortical BOLD-fMRI signals and peripheral sympathoneural firing in healthy humans?
Simulated apneas activate and inhibit specific cortical networks involved in generating sympathetic outflow, providing a neuroanatomical basis for understanding elevated sympathetic responses in conditions like sleep apnea and heart failure.
Tasa de eventos absoluta: 49% vs 29%
valor p: p=<0.001
End-expiratory breath-holds (BH) and Mueller manoeuvres (MM) elicit large increases in muscle sympathetic nerve activity (MSNA). In 16 healthy humans (9♀, 35 ± 4 years) we used functional magnetic resonance imaging with blood oxygen level-dependent (BOLD) contrast to determine the cortical network associated with such sympathoexcitation. We hypothesized that increases in MSNA evoked by these simulated apneas are accompanied by BOLD contrast changes in the insular cortex, thalamus and limbic cortex. A series of 150 whole-brain images were collected during 3 randomly performed 16-second end-expiratory BHs and MMs (-30 mmHg). The identical protocol was repeated separately with MSNA recorded from the fibular nerve. The time course of the sympathoexcitatory response to both breathing tasks were correlated with whole-brain BOLD signal changes. Brain sites demonstrating both positive (activation) and negative (deactivation) correlations with the MSNA time course were identified. Sympathetic burst incidence increased (p<0.001) from 29 ± 6 (rest) to 49 ± 6 (BH) and 47 ± 6 bursts/100 heartbeats (MM). Increased neural activity (Z-scores) was identified in the right posterior and anterior insular cortices (3.74, 3.64), dorsal anterior cingulate (3.42), fastigial and dentate cerebellar nuclei (3.02, 3.34). Signal intensity decreased in the left posterior insula (3.28) and ventral anterior cingulate (3.01). Apnea both activates and inhibits elements of a cortical network involved in the generation of sympathetic outflow. These findings identify a neuroanatomical substrate to guide future investigations into central mechanisms contributing to disorders characterized by elevated basal MSNA and exaggerated sympathetic responses to simulated apneas such as sleep apnea and heart failure.
Kimmerly et al. (Mon,) conducted a observational in Healthy volunteers (n=16). End-expiratory breath-holds (BH) and Mueller manoeuvres (MM) vs. Rest (baseline) was evaluated on Sympathetic burst incidence (bursts/100 heartbeats) (p=<0.001). Simulated apneas significantly increased sympathetic burst incidence from 29 to 49 bursts/100 heartbeats and activated a cortical network including the insular cortex and anterior cingulate.