The authors would like to express their gratitude to Mr. Andre Benedito da Silva for animal care, Mr. Bruno Paredes for his help with flow cytometry analysis, Mrs. Ana Lucia Neves da Silva

for her help with microscopy, and Mrs. Moira Elizabeth Schöttler and Ms. Claudia Buchweitz for their Pictilisib assistance in editing the manuscript. “
“The publisher regrets the original print of this publication incorrectly contains a table of model data that are not relevant to the study as it is described (Table 4). Because the data in this table does not form part of the model description or discussion in the paper, it should not be considered accurate, and should not be cited by other publications. Supplementary material that is referred to in the article was not initially made available with the printed article. The supplementary material can AT13387 now be found online. Figures S1–S3 illustrate the trends of normalised slope (Sn) against lung turnover for the three scenarios of airway constriction. Each show a generally modest increase in Sn with constriction, except for 80% constriction in Figure S1 and 60% and 80% constriction in Figure S3 which have unrealistic shape and rate of increase in comparison to the experimental literature.

Figure S4 shows locations of convective pendelluft during the breath transition from inspiration to expiration. Note that the flows are of small magnitude and are only observed over about 0.10 s in the baseline model. Although retrograde flow at very low levels can be observed in the model throughout

expiration in highly constricted regions these flows are of very small magnitude. Figure S1.  Normalised slopes plotted against lung turnover when only the terminal units in the region are constricted. The publisher would like to apologise for any inconvenience caused. “
“The main symptoms of chronic heart failure (CHF) are dyspnea and fatigue (Jefferies and Towbin, 2010 and Pina, 2003). Various studies have pointed out how these symptoms are related to abnormalities in respiratory muscles (Drexler et al., 1992 and Coats, 1996) and the presence Ceramide glucosyltransferase of cardiomegaly (Olson et al., 2006). Inspiratory muscle dysfunction has been reported as a reduction in the capacity to generate inspiratory muscle pressure and strength, a functional decline which can be attributed to histological and biochemical changes. Diaphragm biopsies from CHF patients have demonstrated the occurrence of muscle fiber regeneration/transformation. Other mechanisms might include proinflammatory cytokine activation and decreased blood flow associated with the endothelial dysfunction characterizing CHF syndrome (Mancini et al., 1994 and Mitch and Goldberg, 1996). Some CHF patients exhibit lower maximal inspiratory pressure (MIP) and inspiratory muscle endurance, factors known to result in exercise limitation and deterioration in quality of life, in addition to worsening patient prognosis (Dall’Ago et al., 2006).