| Autor: |
Aranda LC; Pulmonary Function and Clinical Exercise Physiology Unit (SEFICE), Division of Respiratory Medicine, Department of Medicine, Federal University of São Paulo (UNIFESP), São Paulo, Brazil.; Department of Physiology, UNIFESP, São Paulo, Brazil., Ribeiro IC; Pulmonary Function and Clinical Exercise Physiology Unit (SEFICE), Division of Respiratory Medicine, Department of Medicine, Federal University of São Paulo (UNIFESP), São Paulo, Brazil.; Department of Physiology, UNIFESP, São Paulo, Brazil., Freitas TO; Pulmonary Function and Clinical Exercise Physiology Unit (SEFICE), Division of Respiratory Medicine, Department of Medicine, Federal University of São Paulo (UNIFESP), São Paulo, Brazil.; Department of Physiology, UNIFESP, São Paulo, Brazil., Degani-Costa LH; Pulmonary Function and Clinical Exercise Physiology Unit (SEFICE), Division of Respiratory Medicine, Department of Medicine, Federal University of São Paulo (UNIFESP), São Paulo, Brazil., Dias DS; Department of Physiology, UNIFESP, São Paulo, Brazil., De Angelis K; Department of Physiology, UNIFESP, São Paulo, Brazil., Paixão AO; School of Physical Education and Sport, University of São Paulo, São Paulo, Brazil., Brum PC; School of Physical Education and Sport, University of São Paulo, São Paulo, Brazil., Oliveira ASB; Department of Neurology and Neurosurgery, UNIFESP, São Paulo, Brazil., Vianna LC; NeuroV̇ASQ̇-Integrative Physiology Laboratory, Faculty of Physical Education, University of Brasilia, Brasilia, Brazil., Nery LE; Pulmonary Function and Clinical Exercise Physiology Unit (SEFICE), Division of Respiratory Medicine, Department of Medicine, Federal University of São Paulo (UNIFESP), São Paulo, Brazil., Silva BM; Pulmonary Function and Clinical Exercise Physiology Unit (SEFICE), Division of Respiratory Medicine, Department of Medicine, Federal University of São Paulo (UNIFESP), São Paulo, Brazil.; Department of Physiology, UNIFESP, São Paulo, Brazil. |
| Abstrakt: |
We investigated the locomotor muscle metaboreflex control of ventilation, circulation, and dyspnea in patients with chronic obstructive pulmonary disease (COPD). Ten patients [forced expiratory volume in 1 second (FEV1; means ± SD) = 43 ± 17% predicted] and nine age- and sex-matched controls underwent 1 ) cycling exercise followed by postexercise 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. In addition, 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. NEW & NOTEWORTHY This study's integrative physiology approach provides evidence for a specific alteration in locomotor muscle metaboreflex control of ventilation in patients with COPD. Furthermore, molecular analyses of a skeletal muscle biopsy suggest that the amount of muscle metaboreceptor stimuli derived from type II skeletal myocytes and redox imbalance overcame a downregulation of metabolically sensitive muscle afferents. |
