JOURNAL ARTICLE

Quadriceps and respiratory muscle fatigue following high-intensity cycling in COPD patients

Damien Bachasson, Bernard Wuyam, Jean-Louis Pepin, Renaud Tamisier, Patrick Levy, Samuel Verges
PloS One 2013, 8 (12): e83432
24324843
Exercise intolerance in COPD seems to combine abnormal ventilatory mechanics, impaired O2 transport and skeletal muscle dysfunction. However their relative 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 (Q(tw)), transdiaphragmatic (P(di,tw)) and gastric (P(ga,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, Q(tw) (-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 Q(tw) correlated with the percentage reduction in P(di,tw) (r = 0.66; P<0.05). Percentage reductions in P(di,tw) and P(ga,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.

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