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PubMed2006

Mechanisms of dyspnoea and its language in patients with asthma.

This study hypothesises that regardless of the global score of dyspnoea intensity, different descriptors may be selected by asthmatic patients during short cardiopulmonary exercise test (sCPET) and methacholine (Mch) inhalation. It also examines whether different qualitative dyspnoea sensations can help explain the underlying mechanisms of the symptom. Minute ventilation (V'E), tidal volume (VT) and inspiratory capacity (IC) were measured in 22 stable asthmatic patients, and the sensation of dyspnoea during Mch inhalation and sCPET was quantitatively (Borg scale) and qualitatively (descriptors) assessed. The work rate and oxygen uptake (V'O2) were also measured during sCPET. Airway obstruction and hyperinflation, as measured by IC reduction, were the best correlates for dyspnoea with Mch. During sCPET, changes in WR, V'O2, V'E and VT significantly correlated with Borg score, with V'E being the best predictor of dyspnoea; IC decreased in eight patients. Furthermore, chest tightness (68%) was the highest reported descriptor during Mch inhalation, whereas work/effort (72%) was the highest during sCPET. In conclusion, obstruction/hyperinflation and work rate are highly reliable predictors of Borg rating of dyspnoea during methacholine inhalation and short cardiopulmonary exercise testing, respectively. Regardless of the global score of intensity dyspnoea, different descriptors may be selected by patients during short cardiopulmonary exercise testing and methacholine inhalation. Various qualities of dyspnoea result from different pathophysiological abnormalities.

Administration, Inhalation↗

PubMedDate not supplied

Exercise physiology in COPD.

Multiple mechanisms contribute to exercise limitation in chronic obstructive pulmonary disease (COPD). The ability to increase ventilation during exercise is reduced; the more advanced the disease, the more impaired the exercise tolerance is. However, factors other than ventilatory limitation play an important role in reducing the exercise capacity in COPD. Data implicating peripheral muscle atrophy and muscle weakness as cofactors have been reported in individuals with advanced disease. At this stage daily activities are curtailed to avoid exertional respiratory discomfort. Recent studies have demonstrated that the muscle aerobic capacity of stable hypoxemic COPD patients is impaired; oxygen uptake (V'O2) kinetics and 31P magnetic resonance spectroscopy studies have shown that these patients rely heavily on non-aerobic energy sources even during moderate, sustained workloads. Finally, early occurrence of metabolic acidosis has been demonstrated in patients with mild to severe COPD during exercise. Inadequate tissue oxygenation appears to result from a defect in peripheral oxygen utilization rather than from a reduction in O2 bulk flow. Peripheral factors may include: a) impaired diffusive conductance for O2 between red cells and mitochondria; b) heterogeneous distribution of O2 bulk flow within the exercising muscle fibers; c) inertia of the oxidative processes at the cellular level; d) changes in distribution of muscle fibers, e) reduction in muscle aerobic enzymes; and f) poor nutritional status. Since muscle dysfunction has an important role in the development of exercise intolerance, physical rehabilitation is more and more used as part of the treatment of COPD. The aim of this review is to briefly discuss current views on the mechanisms responsible for the reduced ability to exercise and the rationale for exercise rehabilitation in COPD patients.

Exercise↗