title: Coronary artery disease affects cortical circuitry associated with brain-heart integration during volitional exercise.
abstract: This study tested the hypothesis that coronary artery disease (CAD) alters the cortical circuitry associated with exercise. Observations of changes in heart rate (HR) and in cortical blood oxygenation level-dependent (BOLD) images were made in 23 control subjects [control; 8 women; 63 ± 11 yr; mean arterial pressure (MAP): 90 ± 9 mmHg] (mean ± SD) and 17 similarly aged CAD patients (4 women; 59 ± 9 yr; MAP: 87 ± 10 mmHg). Four repeated bouts each of 30%, 40%, and 50% of maximal voluntary contraction (MVC) force (LAB session), and seven repeated bouts of isometric handgrip (IHG) at 40% MVC force (fMRI session), were performed, with each contraction lasting 20 s and separated by 40 s of rest. There was a main effect of group (P = 0.03) on HR responses across all IHG intensities. Compared with control, CAD demonstrated less task-dependent deactivation in the posterior cingulate cortex and medial prefrontal cortex, and reduced activation in the right anterior insula, bilateral precentral cortex, and occipital lobe (P < 0.05). When correlated with HR, CAD demonstrated reduced activation in the bilateral insula and posterior cingulate cortex, and reduced deactivation in the dorsal anterior cingulate cortex, and bilateral precentral cortex (P < 0.05). The increased variability in expected autonomic regions and decrease in total cortical activation in response to the IHG task are associated with a diminished HR response to volitional effort in CAD. Therefore, relative to similarly aged and healthy individuals, CAD impairs the heart rate response and modifies the cortical patterns associated with cardiovascular control during IHG.
authors.affiliation: Neurovascular Research Laboratory, School of Kinesiology, University of Western Ontario, London, Ontario, Canada;
authors.forename: Katelyn N
authors.initials: KN
authors.lastname: Norton
authors.affiliation: Neurovascular Research Laboratory, School of Kinesiology, University of Western Ontario, London, Ontario, Canada;
authors.forename: Mark B
authors.initials: MB
authors.lastname: Badrov
authors.affiliation: Neurovascular Research Laboratory, School of Kinesiology, University of Western Ontario, London, Ontario, Canada;
authors.forename: Carly C
authors.initials: CC
authors.lastname: Barron
authors.affiliation: Lawson Health Research Institute, University of Western Ontario, London, Ontario, Canada; Cardiac Rehabilitation Program, Division of Cardiology, University of Western Ontario, London, Ontario, Canada;
authors.forename: Neville
authors.initials: N
authors.lastname: Suskin
authors.affiliation: Brain Innovation, Maastricht, Netherlands; and.
authors.forename: Armin
authors.initials: A
authors.lastname: Heinecke
authors.affiliation: Neurovascular Research Laboratory, School of Kinesiology, University of Western Ontario, London, Ontario, Canada; Department of Physiology and Pharmacology, The University of Western Ontario, London, Ontario, Canada kshoemak@uwo.ca.
authors.forename: J Kevin
authors.initials: JK
authors.lastname: Shoemaker
mesh_terms: D001921:Brain / Q000503:physiopathology*; D001931:Brain Mapping; D002560:Cerebrovascular Circulation / Q000502:physiology; D003324:Coronary Artery Disease / Q000503:physiopathology*; D015444:Exercise / Q000502:physiology*; D005080:Exercise Test; D005260:Female; D006225:Hand / Q000502:physiology; D018737:Hand Strength; D006339:Heart Rate / Q000502:physiology*; D006801:Humans; D008279:Magnetic Resonance Imaging; D008297:Male; D008875:Middle Aged; D009119:Muscle Contraction / Q000502:physiology; D010100:Oxygen / Q000097:blood; D014836:Volition
chemical_list: D010100:Oxygen
keywords: compensation hypothesis; coronary artery disease; cortical autonomic network; handgrip exercise