4.5 Article

High-intensity exercise impairs extradiaphragmatic respiratory muscle perfusion in patients with COPD

Journal

JOURNAL OF APPLIED PHYSIOLOGY
Volume 130, Issue 2, Pages 325-341

Publisher

AMER PHYSIOLOGICAL SOC
DOI: 10.1152/japplphysiol.00659.2020

Keywords

COPD; exercise; NIRS; perfusion; respiratory muscles

Funding

  1. Research Foundation Flanders (FWO) [G0A4516N - ZKC9570 - C22/15/035]
  2. ERS fellowship [LTRF 2016-6686]
  3. Coordination for the Improvement of Higher Education Personnel (CAPES), Brazil [88881.188754/2018-01]
  4. Chiang Mai University's scholarship, Chiang Mai, Thailand [6392 (7)/0807]
  5. Research Foundation Flanders [FWO - 12U5618N]

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The study found that high-intensity exercise impairs extradiaphragmatic respiratory muscle perfusion in patients with COPD, and the insufficient adjustment in respiratory muscle perfusion during high-intensity exercise may partly explain the increased sensations of dyspnea. There are differences in respiratory muscle perfusion between high-intensity constant-load cycling and voluntary normocapnic hyperpnea in COPD patients.
The study investigated whether high-intensity exercise impairs inspiratory and expiratory muscle perfusion in patients with chronic obstructive pulmonary disease (COPD). We compared respiratory local muscle perfusion between constant-load cycling[sustained at 80% peak work rate (WRpeak)] and voluntary normocapnic hyperpnea reproducing similar work of breathing (WoB) in 18 patients [forced expiratory volume in the first second (FEV1): 58 +/- 24% predicted]. Local muscle blood flow index (BFI), using indocyanine green dye, and fractional oxygen saturation (%StiO(2)) were simultaneously assessed by near-infrared spectroscopy (NIRS) over the intercostal, scalene, rectus abdominis, and vastus lateralis muscles. Cardiac output (impedance cardiography), WoB (esophageal/gastric balloon catheter), and diaphragmatic and extradiaphragmatic respiratory muscle electromyographic activity (EMG) were also assessed throughout cycling and hyperpnea. Minute ventilation, breathing pattern, WoB, and respiratory muscle EMG were comparable between cycling and hyperpnea. During cycling, cardiac output and vastus lateralis BFI were significantly greater compared with hyperpnea [by +4.2 (2.6-5.9) L/min and +4.9 (2.2-7.8) nmol/s, respectively] (P < 0.01). Muscle BFI and %StiO(2) were, respectively, lower during cycling compared with hyperpnea in scalene [by -3.8 (-6.4 to -1.2) nmol/s and -6.6 (-8.2 to -5.1)%], intercostal [by -1.4 (-2.4 to -0.4) nmol/s and -6.0 (-8.6 to -3.3)%], and abdominal muscles [by -1.9 (-2.9 to -0.8) nmol/s and -6.3 (-9.1 to -3.4)%] (P < 0.001). The difference in respiratory (scalene and intercostal) muscle BFI between cycling and hyperpnea was associated with greater dyspnea (Borg CR10) scores (r = -0.54 and r = -0.49, respectively, P < 0.05). These results suggest that in patients with COPD, 1) locomotor muscle work during high-intensity exercise impairs extradiaphragmatic respiratory muscle perfusion and 2) insufficient adjustment in extradiaphragmatic respiratory muscle perfusion during high-intensity exercise may partly explain the increased sensations of dyspnea. NEW & NOTEWORTHY We simultaneously assessed the blood flow index (BFI) in three respiratory muscles during hyperpnea and high-intensity constant-load cycling sustained at comparable levels of work of breathing and respiratory neural drive in patients with COPD. We demonstrated that high-intensity exercise impairs respiratory muscle perfusion, as intercostal, scalene, and abdominal BFI increased during hyperpnea but not during cycling. Insufficient adjustment in respiratory muscle perfusion during exercise was associated with greater dyspnea sensations in patients with COPD.

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