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Critical inspiratory constraints are postulated to lead to a plateau in tidal volume and increased dyspnea, limiting exercise tolerance in patients with moderate-to-severe COPD.
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Critical inspiratory constraints are proposed as a key mechanism for exercise intolerance and dyspnea in patients with moderate-to-severe COPD.
Exercise intolerance is characteristically multi-factorial in patients with chronic obstructive pulmonary disease (COPD) [1]. At least in symptomatic patients with moderate-to-severe airflow limitation, higher operating lung volumes assume a relevant role in decreasing patients’ tolerance to sustain “prolonged” exercise. As a consequence of the dynamic increase in the end-expiratory lung volume, tidal volume (VT) occurs close to total lung capacity (TLC), thereby reducing the room for further lung–chest wall expansion. The combination of low dynamic lung compliance and a severely reduced inspiratory reserve volume causes a mismatch between a growing respiratory neural drive and the resulting lung–chest wall displacement [2]. It has been postulated that such critical inspiratory constraints (CIC) lead to a plateau in VT, and a concomitant increase in dyspnoea as a function of ventilation ( V ′E) [3]. Accordingly, patients change their perception of the uncomfortable respiratory sensations from “laboured breathing” to “insufficient inspiration”, prompting early exercise termination [4]. The concept of critical inspiratory constraints is key to the modern understanding of exercise pathophysiology in patients with moderate-to-severe COPD
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Marillier et al. (2020) conducted an editorial in Chronic obstructive pulmonary disease (COPD). Critical inspiratory constraints was evaluated. Critical inspiratory constraints are postulated to lead to a plateau in tidal volume and increased dyspnea, limiting exercise tolerance in patients with moderate-to-severe COPD.
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