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

Abstract

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.

Conflict of interest statement

Competing Interests: The authors have declared that no competing interests exist.

Figures

Figure 1. End-expiratory (EELV) and end-inspiratory (EILV) lung volumes as a percentage of total lung capacity (TLC), tidal volume (VT) and inspiratory capacity (IC) before (Baseline), 5 minutes after the start of constant-load cycling (5 min) and at exhaustion (Exh) (Panel A).

Changes in IC during the same conditions (Panel B). *, significant differences from Baseline (P

Figure 2. Individual changes in quadriceps strength evoked by femoral magnetic stimulation (Qtw; Panel A), transdiaphragmatic pressure evoked by cervical magnetic stimulation (Pdi,tw; Panel B) and gastric pressure evoked by thoracic magnetic stimulation (Pga,tw; Panel C) from before (Baseline) the constant-load cycling to immediately after exhaustion (Exh).

The thick line indicates the group average reduction. The dotted line indicates the 15% reduction threshold for significant amount of muscle fatigue. *, significant group difference from Baseline (P

Figure 3. Correlation of the percentage reduction from baseline in transdiaphragmatic pressure evoked during cervical magnetic stimulation (ΔPdi,tw) with the percentage reduction from Baseline in quadriceps strength evoked during femoral magnetic stimulation immediately after exhaustive constant load cycling (ΔQtw; Panel A).

Correlation of ΔPdi,tw (Panel B) and the percentage reduction from Baseline of gastric pressure evoked during thoracic magnetic stimulation immediately after exhaustive constant load cycling (ΔPga,tw ; Panel C) with the reduction in IC at exhaustion (ΔIC).