Liliane C. Aranda, Indyanara C. Ribeiro, Tiago O. Freitas, Luiza H. Degani-Costa, Danielle S. Dias, Katia De Angelis, Ailma O. Paixão, Patricia C. Brum, Acary S.B. Oliveira, Lauro C. Vianna, Luiz E. Nery, Bruno M. Silva

ALTERED LOCOMOTOR MUSCLE METABOREFLEX CONTROL OF VENTILATION IN PATIENTS WITH COPD

  • Physiology (medical)
  • Physiology
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We investigated the locomotor muscle metaboreflex control of ventilation, circulation, and dyspnea in patients with chronic obstructive pulmonary disease (COPD). Ten patients [FEV1 (mean ± SD) = 43 ± 17% predicted] and nine age- and sex-matched controls underwent: 1) cycling exercise followed by post-exercise circulatory occlusion (PECO) to activate the metaboreflex or free circulatory flow to inactivate it; 2) cold pressor test to interpret whether any altered reflex response was specific to the metaboreflex arc; and 3) muscle biopsy to explore the metaboreflex arc afferent side. We measured airflow, dyspnea, heart rate, arterial pressure, muscle blood flow, and vascular conductance during reflexes activation. Additionally, we measured fiber types, glutathione redox balance, and metaboreceptor-related mRNAs in the vastus lateralis. Metaboreflex activation increased ventilation versus free flow in patients (⁓15%, P < 0.020) but not in controls (P > 0.450). In contrast, metaboreflex activation did not change dyspnea in patients (P = 1.000) but increased it in controls (⁓100%, P < 0.001). Other metaboreflex-induced responses were similar between groups. Cold receptor activation increased ventilation similarly in both groups (P = 0.46). Patients had greater type II skeletal myocyte percentage (14%, P = 0.010), lower glutathione ratio (-34%, P = 0.015), and lower nerve growth factor (NGF) mRNA expression (-60%, P = 0.031) than controls. Therefore, COPD altered the locomotor muscle metaboreflex control of ventilation. It increased type II myocyte percentage and elicited redox imbalance, potentially producing more muscle metaboreceptor stimuli. Moreover, it decreased NGF expression, suggesting a downregulation of metabolically-sensitive muscle afferents.

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