Inspiratory resistance decreases limb blood flow in COPD patients with heart failure.

The inspiratory muscles, in particular, are characteristically overloaded in COPD plus CHF, with greater elastic and resistive work of breathing. Moreover, these muscles might be functionally weakened as ventilation increases during exercise in patients with COPD [2]. It has been postulated that fatiguing contractions would stimulate diaphragmatic thinly myelinated group III and unmyelinated group IV fibres, thereby increasing limb sympathetic outflow and vascular resistance. The so-called respiratory muscle metaboreflex would then redirect blood flow from locomotor to respiratory muscles to avoid, or at least postpone, the impending failure of the ‘‘vital pump’’ [3, 4]. In this context, we previously found marked blood flow reduction to nonactive and active limbs during inspiratory resistive loading in CHF [5]. Work from our laboratory also showed improved peripheral muscle oxygen delivery after respiratory muscle unloading (under stable cardiac output and arterial oxygen content) in CHF-free COPD [6] and COPD-free CHF [7]. It is therefore conceivable that the coexistence of CHF would potentiate the respiratory muscle metaboreflex in patients with a primary diagnosis of COPD.