Abstract
Exercise intolerance in COPD seems to combine abnormal ventilatory mechanics, impaired O2 transport and skeletal muscle dysfunction. However their relatie contribution and their influence on symptoms reported by patients remain to be clarified. In order to clarify the complex interaction between ventilatory and neuromuscular exercise limiting factors and symptoms, we evaluated respiratory muscles and quadriceps contractile fatigue, dynamic hyperinflation and symptoms induced by exhaustive high-intensity cycling in COPD patients. Fifteen gold II-III COPD patients (age = 67±6 yr; BMI = 26.6±4.2 kg.m-2) performed constant-load cycling test at 80% of their peak workload until exhaustion (9.3±2.4 min). Before exercise and at exhaustion, potentiated twitch quadriceps strength (Qtw), transdiaphragmatic (Pdi,tw) and gastric (Pga,tw) pressures were evoked by femoral nerve, cervical and thoracic magnetic stimulation, respectively. Changes in operational lung volumes during exercise were assessed via repetitive inspiratory capacity (IC) measurements. Dyspnoea and leg discomfort were measured on visual analog scale. At exhaustion, Qtw (-33±15%, >15% reduction observed in all patients but two) and Pdi,tw (-20±15%, >15% reduction in 6 patients) were significantly reduced (P<0.05) but not Pga,tw (-6±10%, >15% reduction in 3 patients). Percentage reduction in Qtw correlated with the percentage reduction in Pdi,tw (r=0.66; P<0.05). Percentage reductions in Pdi,tw and Pga,tw negatively correlated with the reduction in IC at exhaustion (r=-0.56 and r=-0.62, respectively; P<0.05). Neither dyspnea nor leg discomfort correlated with the amount of muscle fatigue. In conclusion, high-intensity exercise induces quadriceps, diaphragm and less frequently abdominal contractile fatigue in this group of COPD patients. In addition, the rise in end-expiratory lung volume and diaphragm flattening associated with dynamic hyperinflation in COPD might limit the development of abdominal and diaphragm muscle fatigue. This study underlines that both respiratory and quadriceps fatigue should be considered to understand the complex interplay of factors leading to exercise intolerance in COPD patients.
Highlights
Dyspnea and leg discomfort are described by patients with chronic obstructive pulmonary disease (COPD) as the primary symptoms responsible for exercise limitation [1,2,3]
This study is the first to evaluate dynamic hyperinflation, symptoms, locomotor and respiratory muscle fatigue induced by exhaustive high intensity constant load cycling within the same group of patients with COPD
The main findings are as follows: i) significant reductions in evoked quadriceps and diaphragm responses were observed in most of the patients while only few patients had reduced abdominal contractility following exercise, ii) the reduction in inspiratory capacity (IC) during exercise negatively correlated with the percentage reduction in Pdi,tw and Pga,tw immediately after exhaustion and iii) no correlation was observed between the amount of muscle fatigue and symptoms of dyspnoea or leg discomfort
Summary
Dyspnea and leg discomfort are described by patients with chronic obstructive pulmonary disease (COPD) as the primary symptoms responsible for exercise limitation [1,2,3]. Pathophysiologic mechanisms involved in this limitation seem to combine abnormal ventilatory mechanics, impaired oxygen (O2) transport and skeletal muscle dysfunction [2,4]. Their relative contribution to exercise intolerance remains extensively debated [5]. Intrinsic muscle alterations (e.g. fiber type shift toward type II/IIX, reduced oxidative enzyme activities) contribute to higher exercise-induced contractile fatigue in patients with COPD [2,6]. Enhanced leg discomfort during exercise may be related to impaired quadriceps contractility [2,3]. Butcher et al [8] recently showed that patients with larger level of hyperinflation exhibit less quadriceps fatigue suggesting a relationship between respiratory muscle work and locomotor muscle fatigue [3]
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