Ventilatory responses to metaboreflex activation in chronic obstructive pulmonary disease

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Ventilatory responses to metaboreflex activation in chronic obstructive pulmonary disease. / Bruce, Richard; Turner, Alice; White, Michael.

In: The Journal of Physiology, Vol. 594, No. 20, 14.06.2016, p. 6025-6035.

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@article{9944dd6b10e64c24b8c52562ae024895,
title = "Ventilatory responses to metaboreflex activation in chronic obstructive pulmonary disease",
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. To evaluate 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 (FEV1/FVC ratio < 70%), 9 also classified as chronically hypercapnic, and 9 age and 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.",
author = "Richard Bruce and Alice Turner and Michael White",
year = "2016",
month = jun,
day = "14",
doi = "10.1113/JP272329",
language = "English",
volume = "594",
pages = "6025--6035",
journal = "The Journal of Physiology",
issn = "0022-3751",
publisher = "Wiley",
number = "20",

}

RIS

TY - JOUR

T1 - Ventilatory responses to metaboreflex activation in chronic obstructive pulmonary disease

AU - Bruce, Richard

AU - Turner, Alice

AU - White, Michael

PY - 2016/6/14

Y1 - 2016/6/14

N2 - 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. To evaluate 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 (FEV1/FVC ratio < 70%), 9 also classified as chronically hypercapnic, and 9 age and 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.

AB - 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. To evaluate 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 (FEV1/FVC ratio < 70%), 9 also classified as chronically hypercapnic, and 9 age and 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.

U2 - 10.1113/JP272329

DO - 10.1113/JP272329

M3 - Article

VL - 594

SP - 6025

EP - 6035

JO - The Journal of Physiology

JF - The Journal of Physiology

SN - 0022-3751

IS - 20

ER -