TY - JOUR
T1 - Impaired adrenergic- and corticotropic-axis outflow during exercise in chronic obstructive pulmonary disease
AU - Iranmanesh, Ali
AU - Rochester, Dudley F.
AU - Liu, Jing
AU - Veldhuis, Johannes D.
N1 - Funding Information:
We thank Samuel Rudolph and Jill Smith for support of manuscript preparation; Ashley Bryant for data analysis and graphics; and Salem Veterans Affairs Hormone Laboratory for assay assistance. Supported in part via the Center for Translational Science Activities grant 1 UL 1 RR024150 from the National Center for Research Resources (Rockville, MD) and DK073148 and DK050456 ( Metabolic Studies Core of the Minnesota Obesity Center ) from the National Institutes of Health (Bethesda, MD) .
PY - 2011/11
Y1 - 2011/11
N2 - Exercise stimulates coordinated release of the sympathoadrenal hormones adrenocorticotropic hormone (ACTH), cortisol, norepinephrine (NE), and epinephrine (Epi). The study hypothesis was that chronic obstructive pulmonary disease (COPD) is marked by heightened sympathoadrenal outflow at comparable relative workloads. The location of the study was at a clinical research unit. Eight healthy men and 9 men with stable COPD (forced expiratory volume at 1 second <75% predicted) were studied. Volunteers rested (baseline) or exercised at individual submaximal (35% ± 5%) or maximal oxygen consumption. Blood was sampled every 2 minutes for 40 minutes concurrently. Two-way analysis of covariance was applied to examine group (healthy/COPD) and exercise (3 levels) effects on ACTH, cortisol, NE, and Epi release and regularity (estimable by approximate entropy). The timing of peak hormone concentrations was Epi, 14 minutes; NE, 16 minutes; ACTH, 22 minutes; and cortisol, 34 minutes in both cohorts. Type of exercise regimen influenced all 4 hormones (each P <.001), and subject group (control vs COPD) affected cortisol (P <.001) and Epi (P =.048) responses. Exercise regimen and group together controlled ACTH, cortisol, and Epi (each P <.001), but not NE, responses. In particular, endocrine responses were attenuated in COPD compared with control subjects. Approximate entropy analysis also identified loss of maximal exercise-induced ACTH-secretory regularity in COPD patients (P =.042). These outcomes demonstrate impaired rather than augmented exercise-associated sympathocorticotropic-axis outflow in patients with COPD even when outcomes are normalized to maximal oxygen consumption, suggesting that factors other than fitness are at work.
AB - Exercise stimulates coordinated release of the sympathoadrenal hormones adrenocorticotropic hormone (ACTH), cortisol, norepinephrine (NE), and epinephrine (Epi). The study hypothesis was that chronic obstructive pulmonary disease (COPD) is marked by heightened sympathoadrenal outflow at comparable relative workloads. The location of the study was at a clinical research unit. Eight healthy men and 9 men with stable COPD (forced expiratory volume at 1 second <75% predicted) were studied. Volunteers rested (baseline) or exercised at individual submaximal (35% ± 5%) or maximal oxygen consumption. Blood was sampled every 2 minutes for 40 minutes concurrently. Two-way analysis of covariance was applied to examine group (healthy/COPD) and exercise (3 levels) effects on ACTH, cortisol, NE, and Epi release and regularity (estimable by approximate entropy). The timing of peak hormone concentrations was Epi, 14 minutes; NE, 16 minutes; ACTH, 22 minutes; and cortisol, 34 minutes in both cohorts. Type of exercise regimen influenced all 4 hormones (each P <.001), and subject group (control vs COPD) affected cortisol (P <.001) and Epi (P =.048) responses. Exercise regimen and group together controlled ACTH, cortisol, and Epi (each P <.001), but not NE, responses. In particular, endocrine responses were attenuated in COPD compared with control subjects. Approximate entropy analysis also identified loss of maximal exercise-induced ACTH-secretory regularity in COPD patients (P =.042). These outcomes demonstrate impaired rather than augmented exercise-associated sympathocorticotropic-axis outflow in patients with COPD even when outcomes are normalized to maximal oxygen consumption, suggesting that factors other than fitness are at work.
UR - http://www.scopus.com/inward/record.url?scp=80055005681&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=80055005681&partnerID=8YFLogxK
U2 - 10.1016/j.metabol.2011.03.018
DO - 10.1016/j.metabol.2011.03.018
M3 - Article
C2 - 21632072
AN - SCOPUS:80055005681
SN - 0026-0495
VL - 60
SP - 1521
EP - 1529
JO - Metabolism: Clinical and Experimental
JF - Metabolism: Clinical and Experimental
IS - 11
ER -