Ventilatory responses to muscle metaboreflex activation in chronic obstructive pulmonary disease

Abstract

Key pointsr Recent evidence indicates a role for group III/IV muscle afferents in reflex control of the human ventilatory response to exercise.r Dyspnoea in chronic obstructive pulmonary disease (COPD) may be linked to this reflex response.r This study shows that activation of the muscle metaboreflex causes a ventilatory response in COPD patients but not in healthy controls.r This indicates abnormal involvement of muscle afferents in the control of ventilation in COPD which may be a contributing factor to exercise dyspnoea.Abstract Blockade of thin fibre muscle afferent feedback during dynamic exercise reduces exercise hyperpnoea in health and chronic obstructive pulmonary disease (COPD). Therefore, we hypothesised that activation of the muscle metaboreflex at rest would cause hyperpnoea. We evaluated the effect of muscle metaboreflex activation on ventilation, in resting COPD patients and healthy participants. Following a bout of rhythmic hand grip exercise, post exercise circulatory occlusion (PECO) was applied to the resting forearm to sustain activation of the muscle metaboreflex, in 18 COPD patients (FEV 1 /FVC ratio < 70%), 9 also classified as chronically hypercapnic, and 9 ageand gender-matched controls. The cardiovascular response to exercise and the sustained blood pressure elevation during PECO was similar in patients and controls. During exercise ventilation increased by 6.64 ± 0.84 in controls and significantly (P < 0.05) more, 8.38 ± 0.81 l min −1 , in patients. During PECO it fell to baseline levels in controls but remained significantly (P < 0.05) elevated by 2.78 ± 0.51 l min −1 in patients until release of circulatory occlusion, with no significant difference in responses between patient groups. Muscle metaboreflex activation causes increased ventilation in COPD patients but not in healthy participants. Chronic hypercapnia in COPD patients does not exaggerate this response. The muscle metaboreflex appears to be abnormally involved in the control of ventilation in COPD and may be a contributing factor to exercise dyspnoea.

Abnormal muscle metaboreflex control of ventilation in patients with chronic obstructive pulmonary disease: what mechanisms should be blamed?

“…However, the data from Bruce et al . () differ from data reported by previous studies that also investigated patients with COPD. For example, Nakamoto et al .…”

“…The results reported by Bruce et al . () certainly enlarge the knowledge about the contribution of muscle afferents sensitive to metabolites to the control of ventilation in patients with COPD. However, the data from Bruce et al .…”

“…In this context, a recent study published in The Journal of Physiology by Bruce et al . () sought to shed light on cardiorespiratory responses, with particular focus on the ventilatory response, in the face of isolated metaboreflex activation in patients with COPD. Patients with COPD with and without chronic hypercapnia and healthy controls were asked to perform a rhythmic handgrip task, which consisted of 1 s contraction at 50% of maximum voluntary contraction and 1 s relaxation, for 2 min.…”

“…Bruce et al . () showed that patients with COPD presented higher ventilation during metaboreflex activation, but it is not clear whether this was attributed to enhanced stimuli at the terminal endings on muscle afferents and/or alteration in the sensitivity of the neural arc per se . It is noteworthy, however, that ventilation was higher in patients with COPD as a result of exercise paired by relative intensity and duration.…”

Metaboreflex activation delays heart rate recovery after aerobic exercise in never‐treated hypertensive men

“…; Bruce et al . ). In the present study, however, responses to the occlusion session were similar between the NT and HT groups, denying any overactivation of the ventilatory arm of the metaboreflex in hypertension.…”