The impact of chronic obstructive pulmonary disease (COPD) upon respiratory mechanics was described elegantly in the 1940s by Rahn and coworkers (Rahn et al., 1946). Thereafter, the mechanical repercussions of COPD were largely overlooked until a Renaissance of interest in the 1980s focussed attention upon the repercussions of COPD for the respiratory muscles. By the 1990s, a clear understanding had emerged that expiratory flow limitation, hyperinflation and dyspnoea were interlinked phenomena that contributed to exercise intolerance (O’Donnell, 2001). The influence of hyperinflation upon the work of breathing is profound, especially during exercise, when end expiratory lung volume increases dynamically as part of a strategy to maximise expiratory flow generating capacity. Whilst this strategy is effective in mitigating the influence of expiratory flow limitation upon minute ventilation, it does so at great cost to the inspiratory muscles, which must overcome both greater elastance, and the effects of intrinsic positive end expiratory pressure. In the late 1990s, evidence also emerged that the increased inspiratory work imposed by COPD induces considerable remodelling of the diaphragm. Not only is there an increase in the proportion of fatigue resistant type I muscle fibres (Levine et al., 1997), but oxidative enzyme activities and capillarity also increase. These adaptations are consistent with a shift towards an endurance-trained phenotype, which has led to the perception that the diaphragms of patients with COPD are well adapted to chronic loading. This assumption is supported by the observation that patients with COPD showed no evidence of low-frequency diaphragm fatigue following treadmill exercise to the limit of tolerance . However, in recent years, it has been recognised that the diaphragm remodelling of COPD is imperfect. Inspiratory muscle weakness is a prominent feature of COPD (Decramer, 2001), but like so much of the pathophysiology of COPD, its aetiology is complex. Weakness has two primary sources, both of which contribute to impaired function, 1) muscle fibre myopathy due to systemic manifestations of COPD, corticosteroids and changes in physical activity patterns; 2) functional weakening due to the interaction of hyperinflation and the pressure-volume relationship. As explained above, these decrements in the capacity of the inspiratory muscles to deliver ventilation are paralleled by a considerable increase in the work of breathing due to hyperinflation. Furthermore, during exercise, inefficiencies of breathing pattern, and the early onset of metabolic acidosis, also serve to increase the ventilatory requirement of exercise, exacerbating the demands placed upon the inspiratory muscles. Thus, patients with COPD experience a “double-whammy” of an increase in the demand for inspiratory muscle work, and a reduction in the capacity to meet that demand. This mismatch has serious implications for dyspnoea and exercise tolerance. The functional imbalance within the respiratory pump of patients with COPD makes the respiratory muscles an obvious therapeutic target. A number of recent systematic reviews and meta-analyses support a beneficial influence of inspiratory muscle training (IMT) upon inspiratory muscle function, dyspnoea and exercise tolerance (Gosselink et al., 2011). There is evidence that IMT elicits beneficial structural adaptation within the accessory inspiratory musculature of patients with COPD, as well as diaphragm hypertrophy in healthy individuals. Furthermore, evidence is also emerging from healthy individuals that IMT improves exercise tolerance, at least in part, via an increase in the activation threshold of the inspiratory muscle metaboreflex (McConnell & Lomax, 2006). When activated by high intensity inspiratory muscle work, this reflex has been shown to induce limb muscle vasoconstriction, and impaired fatigue resistance (McConnell & Lomax, 2006). Following IMT, the delayed onset of the reflex, preserves limb blood flow, enhances oxygen delivery , and exercise tolerance (Romer et al., 2002; McConnell & Lomax, 2006). Replication of these observations in patients with COPD is awaited, but there is every reason to believe that IMT elicits similar changes to metaboreflex activation.