Cross, Troy J.

During severe exercise, expiratory and inspiratory muscle fatigue develops by ∼50% of the tolerable exercise duration. The magnitude of expiratory and inspiratory muscle fatigue increases progressively toward exercise intolerance but is not different between muscle groups; this is despite the expiratory muscles being less fatigue-resistant. Inspecting esophageal and gastric twitches via cervical stimulation, we speculate that the progressive magnitude of exercise-induced inspiratory muscle fatigue is a function of recruitment and fatigue of the accessory inspiratory muscles.

Respiratory muscle fatigue could occur following involuntary breathing movements during maximal breath-holds. We measured respiratory muscle strength pre and post three preparatory and maximal breath-holds. We found significant reductions in diaphragm strength and total inspiratory and expiratory strength in some, but not all, divers. Divers that had respiratory muscle fatigue had a lower pseudo O 2 delivery (HR × [Formula: see text]) during the struggle phase. This suggests that reduced oxygen delivery may contribute to respiratory muscle fatigue during a breath-hold.

Exercise-induced respiratory muscle fatigue contributes to limiting exercise tolerance. Accordingly, better understanding the exercise conditions under which respiratory muscle fatigue occurs is warranted. Although heavy-intensity as well as short- and long-duration severe-intensity exercise performed to intolerance elicit diaphragm and expiratory muscle fatigue, we find, for the first time, that the relationship between exercise intensity, exercise duration, and the magnitude of exercise-induced fatigue is different for the diaphragm compared with the expiratory muscles.

ABSTRACT Introduction Measurement of the work of breathing (Wb) during exercise provides useful insights into the energetics and mechanics of the respiratory muscles across a wide range of minute ventilations. The methods and analytical procedures used to calculate the Wb during exercise have yet to be critically appraised in the literature. Purpose The aim of this systematic review was to evaluate the quality of methods used to measure the Wb during exercise in the available literature. Methods We conducted an extensive search of three databases for studies that measured the Wb during exercise in adult humans. Data were extracted on participant characteristics, flow/volume and pressure devices, esophageal pressure (P oes ) catheters, and methods of Wb analysis. Results A total of 120 articles were included. Flow/volume sensors used were primarily pneumotachographs ( n = 85, 70.8%), whereas the most common pressure transducer was of the variable reluctance type ( n = 63, 52.5%). Esophageal pressure was frequently obtained via balloon-tipped catheters ( n = 114, 95.0%). Few studies mentioned calibration, frequency responses, and dynamic compensation of their measurement devices. The most popular method of measuring the Wb was pressure–volume integration ( n = 51, 42.5%), followed by the modified Campbell ( n = 28, 23.3%) and Dean & Visscher diagrams ( n = 26, 21.7%). Over one-third of studies did not report the methods used to process their pressure–volume data, and the majority (60.8%) of studies used the incorrect Wb units and/or failed to discuss the limitations of their Wb measurements. Conclusions The findings of this systematic review highlight the need for the development of a standardized approach for measuring Wb, which is informative, practical, and accessible for future researchers.

The purpose of this study was to determine whether the longitudinal progression of decline in left ventricular ejection fraction (LVEF) in Duchenne muscular dystrophy (DMD) patients is moderated by ADRB1 genotype and whether the efficacy of ß-blocker therapy is influenced by genotype status. About 147 DMD patients (6-34 years.) were analyzed with a focus on β 1 adrenergic receptor (ADRB1) genotype variants. Patients were grouped by ADRB1 genotype resulting in Gly389 patients and Arg389 patients. A generalized additive mixed effects model was used to examine differences in the nonlinear trend of LVEF across patient ages between genotype groups and for ß-blocker use. Both genotype groups displayed a progressive decline in LVEF starting around the mean age of ambulation loss (~12 years). However, there was no difference between genotype groups in the progression of decline in LVEF. There was a significant effect of ß-blocker use on longitudinal LVEF, wherein patients on ß-blockers had systematically lower LVEF when compared to patients not on ß-blockers. However, the effect of ß-blocker therapy on LVEF was not affected by ADRB1 genotype. The current study did not demonstrate an influence of patient ADRB1 genotype on longitudinal LVEF in our cohort. Despite previous literature suggesting a positive influence of ß-blocker use on cardiac function in DMD patients and of an ADRB1 genotypic difference in responsiveness to ß-blocker use, we did not observe this in our cohort. Interestingly, our cohort did not demonstrate a positive influence of ß-blocker use on LVEF measures.

The measurement of the work of breathing (Wb) during exercise provides us with deep insights into respiratory (patho)physiology, and sheds light on the putative factors which lead to respiratory muscle fatigue. There are 4 popular methods available to determine the Wb. Our study demonstrates that no two of these methods produce identical values of Wb during exercise. This paper also discusses the practical and theoretical limitations of each method.