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The muscle metaboreflex during exercise in chronic obstructive pulmonary disease Sherman, Megan F. B.

Abstract

Chronic obstructive pulmonary disease (COPD) is characterised by deteriorating lung and airway function. Altered peripheral skeletal muscle properties, favouring glycolytic metabolism, are also well-documented in this population. Skeletal muscle properties such as those found in COPD patients may have significant effects on the magnitude of the muscle metaboreflex. Hypotheses: It was hypothesized that the muscle metaboreflex would be magnified in people with COPD compared to healthy controls, and that disease severity and exercise capacity would be correlated with the magnitude of the muscle metaboreflex. Methods: Eleven people with mild-to-severe COPD (FEV₁.₀ = 56.3 ± 7.4% predicted) and 11 age- and gender- matched controls performed isometric handgrip exercise (IHG) for 2.5 minutes, at 35% MVC, followed by 2 minutes of post-exercise circulatory occlusion (PECO). Hemodynamic changes were measured throughout the protocol to assess the magnitude of the metaboreflex. Participants also performed a progressive cycle test to volitional exhaustion. Results: Heart rate, mean arterial pressure (MAP), leg blood flow and leg vascular resistance responses were similar between the COPD group and controls throughout IHG and PECO (% change from baseline) (p > 0.05). Heart rate was highest at minute 2.5 of IHG (COPD 18 ± 4%, control 18 ± 3%) and returned to baseline during PECO, while MAP peaked at minute 2.5 of IHG (COPD 29 ± 5%, control 30 ± 3%) and remained elevated throughout PECO (COPD 25 ± 3%, control 21 ± 2%). Total peripheral resistance rose more in the COPD group throughout the protocol and approached significance at minute 2 of PECO (COPD 39 ± 9, control 18 ± 4%, p = 0.09). Cardiac output remained significantly higher throughout IHG and PECO in the control group (IHG 2.5 min: COPD 0.08 ± 7, control 17 ± 4%, p = 0.01). There was no association between disease severity (r = -0.22, p = 0.32) or exercise capacity (r = -0.02, p=0.92) and the magnitude of the muscle metaboreflex. Conclusions: The muscle metaboreflex is preserved in people with COPD. The mechanisms responsible remain unclear, however, unchanged upper limb skeletal muscle properties and desensitization of peripheral afferents to metabolites are plausible explanations.

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