Cardiorespiratory responses to high-intensity skeletal muscle metaboreflex activation in chronic obstructive pulmonary disease.

Abstract

Augmented skeletal muscle metaboreflex activation may accompany chronic obstructive pulmonary disease (COPD). The maintained metaboreflex control of mean arterial pressure (MAP) that has been reported may reflect limited evaluation using only one moderate bout of static handgrip (HG) and following postexercise ischaemia (PEI). We tested the hypothesis that cardiovascular and respiratory responses to high-intensity static HG and isolated metaboreflex activation during PEI are augmented in COPD patients. Ten patients with moderate to severe COPD and eight healthy age- and BMI-matched controls performed two-minute static HG at moderate (30% maximal voluntary contraction; MVC) and high (40% MVC) intensity followed by PEI. Despite similar ratings of perceived exertion, arm muscle mass and strength, COPD patients demonstrated lower MAP responses during both HG intensities compared with controls (time×group interaction, p<.05). Indeed, during high-intensity HG at 40% MVC, peak MAP responses were significantly lower in COPD patients (ΔMAP: COPD 41±9mmHg vs. controls 56±14mmHg, p<.05). Notably, no group differences in MAP were observed during PEI (e.g. 40% MVC PEI: ΔMAP COPD 33±9mmHg vs. controls 33±6mmHg, p>.05). We found no between-group differences in heart rate, respiratory rate, or estimated minute ventilation during HG or PEI. These results suggest that the pressor response to high-intensity HG is blunted in COPD patients. Moreover, despite inducing a strong cardiovascular and respiratory stimulus, skeletal muscle metaboreflex activation evoked similar responses in COPD patients and controls.