Rebuttal from Alison K. McConnell

The good news is that Dr Patel and I agree that, ‘Interpreting a limited number of trials…is hazardous’ (Patel et al. 2012, this issue). Unfortunately, this is precisely what he and his colleagues have done; having identified over 130 papers, a handful of trials have been ‘cherry picked’ to support their argument. This is simply not good enough, particularly when a number of meta-analyses exist, all of which conclude that respiratory muscle training (RMT) improves exercise tolerance (Geddes et al. 2008; Shoemaker et al. 2009; Gosselink et al. 2011; Illi et al. 2012). Furthermore, when citing the meta-analysis by Gosselink et al. (2011) to support their contention that RMT provides no additional benefit to pulmonary rehabilitation, Patel et al. disingenuously neglect to mention its main conclusion: standalone RMT improves exercise tolerance.

Patel et al. have also misrepresented the literature elsewhere. For example, Sperlich et al. (2009) and Lomax et al. (2010) are cited as evidence that RMT does not improve exercise tolerance. However, Sperlich et al. utilised an exercise outcome shown repeatedly to be insensitive to RMT (for good physiological reasons, Romer et al. 2007), whilst Lomax et al. did not assess exercise tolerance.

Furthermore, most scientists will be mystified by the arbitrary selection of 50 as an optimal sample size. Sample size is determined by effect size and reliability. For reliable outcomes with moderate to large effects (e.g. exercise tolerance), 10 participants per group provide adequate power. Thus, discounting 127 studies containing fewer than 50 participants requires clear justification. For those wondering about the conclusion of these 127 studies, I refer to the meta-analyses cited above.

In their only foray into mechanistic debate, Patel et al. ponder why improvements in exercise tolerance and inspiratory muscle function do not correlate. Why would they? Maximal inspiratory pressure (MIP) is merely a surrogate of one aspect of inspiratory muscle function; MIP is not only one step removed from the contractile properties of the inspiratory muscles, it's also remote from an important underlying mechanism. This is exemplified by the fact that endurance RMT does not improve MIP, but does improve exercise tolerance (Verges et al. 2008); the underlying mechanism is slowing the rate of intramuscular metabolite accumulation, not increasing MIP per se.

In closing, I offer a question to ponder: ‘Why do so many scientists and clinicians continue to study RMT?’ Are they all misguided, or is it perhaps because the objective evidence indicates it ‘works’?

Call for comments

Readers are invited to give their views on this and the accompanying CrossTalk articles in this issue by submitting a brief comment. Comments must not exceed 250 words, with a maximum of six references from peer reviewed publications only. To submit a comment, use the online form available in the centre panel on the HighWire site. If other responses have already been submitted, a ‘view comments’ link will be visible.

All comments will be moderated, and those deemed to add significantly to the discussion will be published online-only as footnotes to the articles. Comments may be posted up to 6 weeks after publication of the article, at which point the discussion will close and authors will be invited to submit a ‘final word’.

Questions about this call should be directed to Jerry Dempsey at jdempsey@wisc.edu.

To submit a comment, go to: http://jp.physoc.org/letters/submit/jphysiol;590/15/3401

Conflict of interest

The author is an inventor of two inspiratory muscle training products and acknowledges a beneficial interest in the form of a share of licence income to the University of Birmingham and Brunel University. She also acts as a consultant to POWERbreathe International Ltd.