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• W2944008093 abstract "Ageing is associated with skeletal muscle dysfunction extending to the striated muscles of the respiratory system, including the diaphragm, the principal muscle of breathing. Age-related diaphragm muscle sarcopenia is characterized by fibre-specific atrophy preferentially affecting myosin heavy chain type 2x/2b fibres, with consequential reductions in peak force generation (Greising, Mantilla, Gorman, Ermilov, & Sieck, 2013; Khurram et al., 2018). Accordingly, age-related impairments may limit the capacity of the diaphragm to perform high-force-dependent behaviours (e.g. coughing or sneezing), contributing to a compendium of change that culminates in increased risk of respiratory infection, progressing to pneumonia, which is a leading cause of morbidity and mortality in the elderly. In this issue of Experimental Physiology, Fogarty, Mantilla & Sieck (2019) extend a long-standing interest by this group in diaphragm muscle physiology, seeking to address two important questions. First, does age-related sarcopenia exacerbate intrinsic diaphragm muscle fatigue? Second, is force generation by old fatigued diaphragm sufficient to support ventilatory behaviours? Given that sarcopenia spares diaphragm type 1 and 2a fibres (Khurram et al., 2018), which are notably fatigue resistant, the authors hypothesized that ageing would not potentiate diaphragm fatigue. Moreover, given that basal ventilation is achieved with low force generating fibre recruitment, it was plausible to reason that residual forces generated even by fatigued sarcopenic diaphragm would be adequate to support ventilation. Force and fatigue were determined ex vivo in diaphragm muscle preparations from young (6-month-old) and old (24-month-old) male and female Fischer 344 rats. The group have previously demonstrated that age-related sarcopenia manifests equivalent outcomes in male and female mice (Greising, Mantilla, Medina-Martínez, Stowe, & Sieck, 2015) and rats (Khurram et al., 2018) upon consideration of diaphragm fibre size and distribution, ex vivo diaphragm force-generating capacity and peak transdiaphragmatic pressure generation in anaesthetized animals. Diaphragm muscle strips from young and old rats underwent one of three fatigue protocols, each involving repeated supramaximal activation of the muscle over a 2 min period at low (10 Hz), medium (40 Hz) or high (75 Hz) stimulation frequencies. Fatigue is defined as the temporal decline in force generation during repeated stimulation. A fatigue index is commonly calculated in studies by expressing the residual force at the termination of a fatigue protocol relative to the initial force. Although normalization in this manner is often useful, it can sometimes betray the full portfolio of performance measures, because improvements in fatigue index (i.e. apparent fatigue resistance) may relate more to differences in initial force generation between experimental groups, which are often not reported in studies. Fogarty et al. (2019) report the fatigue index in addition to the initial and residual diaphragm forces to provide a transparent composite portrait of the effect of sarcopenia on diaphragm performance. The authors confirmed type 2x/2b fibre-specific sarcopenia in old rats, revealed as a reduction in fibre cross-sectional area. Consistent with this observation, diaphragm force was lower in old compared with young rats in response to 40 and 75 Hz stimulation, but not 10 Hz stimulation. The fatigue index was increased after repeated muscle activation at 40 and 75 Hz (but not 10 Hz) in old compared with young diaphragms. However, of greater interest, the residual force generated by diaphragm muscle preparations was equivalent after all three fatigue protocols for both ages, reflecting the persistent contribution to force made by fatigue-resistant fibres of the diaphragm. Therefore, the authors demonstrate clearly that age-related sarcopenia results in a weaker but not more fatiguable diaphragm, with a fast-to-slow shift in the relative contribution to force generation by muscle fibres in aged muscle. With reference to an impressive and extensive portfolio of studies by this group exploring neuromechanical control of breathing throughout the lifespan, the authors provide a model of fibre-type contribution to diaphragm muscle specific force and transdiaphragmatic pressure generation in non-fatigued and fatigued conditions for young and old rats. Reasonably, the authors conclude that residual force generation by fatigued young and old diaphragm is adequate to generate the transdiaphragmatic pressures required for ventilatory behaviours; thus, a ‘breather’ of sorts for the elderly from the frailties exacted by ‘Father Time’. However, as highlighted by the model, sarcopenia-related weakness has a considerable limiting effect on expulsive non-ventilatory behaviours, such as coughing, entirely consistent with observations of impaired maximal inspiratory and expiratory pressures in the elderly sarcopenic population (Ohara et al., 2018). The findings of Fogarty et al. (2019) are relevant to additional stressors known to cause diaphragm muscle atrophy and weakness, such as mechanical ventilation, sepsis, respiratory disease and hypoxia (Greising, Ottenheijm, O'Halloran, & Barreiro, 2018). An additional important issue is the implication of generalized atrophy of the diaphragm for ventilatory performance. For example, pan-fibre atrophy of the diaphragm is a feature of cancer cachexia (Roberts et al., 2013). Indeed, many contributory factors, such as sepsis, respiratory loading and steroids, at the confluence of disease states, particularly in critically ill elderly people, have the potential in combination for devastating consequences on respiratory performance across all motor behaviours. None declared. Both authors approved the final version of the manuscript and agree to be accountable for all aspects of the work in ensuring that questions related to the accuracy or integrity of any part of the work are appropriately investigated and resolved. All persons designated as authors qualify for authorship, and all those who qualify for authorship are listed." @default.
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• W2944008093 date "2019-05-27" @default.
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• W2944008093 title "Diaphragm muscle performance in ageing: A new perspective on an old story" @default.
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• W2944008093 doi "https://doi.org/10.1113/ep087758" @default.
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