CrossTalk opposing view: Respiratory muscle training does improve exercise tolerance

In the vast majority of healthy human beings exercising at sea level, there is no respiratory limitation to oxygen uptake. This fact leads inevitably to the question, how can respiratory muscle training (RMT) possibly improve exercise tolerance? Resolution of this conundrum lies in thinking beyond the obvious, and in an appreciation of the role of respiratory muscle work in perfusion and neural fatigue mechanisms. In a recent systematic review and metaanalysis of RMT, Illi and colleagues (Illi et al. 2012) undertook a detailed analysis of some 46 original studies of RMT. The analysis included both strength and endurance RMT, and sought to (1) identify factors that influence changes in exercise tolerance after RMT and (2) undertake a meta-analysis of a sample of placebo and controlled trials (n = 8). The meta-analysis revealed ‘significant improvement in performance after RMT, which was detected by constant load tests, time trials and intermittent incremental tests, but not by [continuous] incremental tests’; standardised mean differences were 0.66, 1.85, 2.96 and 0.3, respectively (Illi et al. 2012). Of course, one can contend the validity of the conclusions of any meta-analysis on the basis of the rigour applied to inclusion criteria, and the relevance/validity of the key outcome variables (Polkey et al. 2011). The argument that RMT simply makes people better at doing volitional tests of respiratory muscle function has been invoked previously (Polkey et al. 2011); indeed, my adversary has argued strongly that the inability to measure significant increases in diaphragm twitch pressures (Tw Pdi) following RMT divests the intervention of all credibility, stating that, ‘234 subjects would need to be randomized to definitively refute the hypothesis that [RMT] improves Tw Pdi and we argue that such a study is required’ (Hart et al. 2001). In addition to the obvious limitation of Tw Pdi for assessing the outcome of RMT (i.e. poor between-day reliability), recent advances in the understanding of exercise limiting factors (see below) also highlight the inadequacy of reductionist approaches to evaluating complex, integrative physiological phenomena. Thus, if one accepts the robustness of Illi and colleagues’ methods (Illi et al. 2012), their recent meta-analysis provides strong, objective support for the contention that RMT improves exercise tolerance. Notwithstanding this, the credibility of RMT resides ultimately in the provision of convincing underlying mechanisms for resulting changes in exercise tolerance. In this regard, I contend that RMT has also achieved a critical threshold of credibility (McConnell, 2007). As mentioned previously, the key to understanding how RMT influences exercise tolerance is an appreciation of the role of respiratory muscle work in perfusion, and in central and spinal mechanisms of fatigue. The role of respiratory muscle work in exercise limitation has been studied extensively by Dempsey and colleagues who have made an outstanding contribution to our understanding of interactions between muscle afferents (respiratory and locomotor), and a range of factors that limit exercise tolerance. Specifically, Dempsey’s group has elucidated the respiratory muscle metaboreflex, which elicits sympathetically mediated vasoconstriction (Harms et al. 1997; Dempsey et al. 2006). Above a critical threshold of inspiratory muscle work, the accumulation of metabolites within exercising respiratory muscles stimulates group III and IV afferents, inducing sympathoexcitation (Sheel et al. 2002). Functional repercussions include accelerated time to fatigue during exercise (Harms et al. 2000; McConnell & Lomax, 2006), and exacerbation of exercise-induced locomotor muscle fatigue (Romer et al.