Contractile Properties of the Human Diaphragm during Chronic Hyperinflation

Similowski, Thomas; Shi, Yan; Gauthier, Alain P.; Macklem, Peter T.; Bellemare, F.

doi:10.1056/nejm199109263251304

Cited by 402 publications

(240 citation statements)

References 27 publications

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“…The idea that nearly complete length adaptations of the diaphragm occur in humans was supported for many years by an observation that diaphragm twitch force in hyperinflated chronic obstructive pulmonary disease (COPD) patients is similar to that of the normal population when normalized to lung volume (83). However, whether diaphragm fiber lengths physically shorten by deletion of sarcomeres in series in chronically hyperinflated humans has never been clearly established, in part because of the difficulty in accurately measuring sarcomere length in vivo, at FRC.…”

Section: Length Plasticitymentioning

confidence: 98%

Respiratory muscle fiber remodeling in chronic hyperinflation: dysfunction or adaptation?

Clanton¹,

Levine²

2009

Journal of Applied Physiology

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Clanton TL, Levine S. Respiratory muscle fiber remodeling in chronic hyperinflation: dysfunction or adaptation? J Appl Physiol 107: 324 -335, 2009. First published April 9, 2009 doi:10.1152/japplphysiol.00173.2009.-The diaphragm and other respiratory muscles undergo extensive remodeling in both animal models of emphysema and in human chronic obstructive pulmonary disease, but the nature of the remodeling is different in many respects. One common feature is a shift toward improved endurance characteristics and increased oxidative capacity. Furthermore, both animals and humans respond to chronic hyperinflation by diaphragm shortening. Although in rodent models this clearly arises by deletion of sarcomeres in series, the mechanism has not been proven conclusively in human chronic obstructive pulmonary disease. Unique characteristics of the adaptation in human diaphragms include shifts to more predominant slow, type I fibers, expressing slower myosin heavy chain isoforms, and type I and type II fiber atrophy. Although some laboratories report reductions in specific force, this may be accounted for by decreases in myosin heavy chain content as the muscles become more oxidative and more efficient. More recent findings have reported reductions in Ca 2ϩ sensitivity and reduced myofibrillar elastic recoil. In contrast, in rodent models of disease, there is no consistent evidence for loss of specific force, no consistent shift in fiber populations, and atrophy is predominantly seen only in fast, type IIX fibers. This review challenges the hypothesis that the adaptations in human diaphragm represent a form of dysfunction, secondary to systemic disease, and suggest that most findings can as well be attributed to adaptive processes of a complex muscle responding to unique alterations in its working environment. diaphragm; fiber type; sarcomere; skeletal muscle; emphysema THIS REVIEW IS INTENDED TO bring readers up to date with accumulating evidence that the diaphragm undergoes remarkable adaptations to chronic hyperinflation and chronic lung obstruction. Some of these adaptations are expected, based on well known responses of limb muscle to chronic changes in length and mechanical load, but others appear to be surprisingly unique, revealing aspects of muscle plasticity and pathology that are not anticipated from known basic science concepts. We will concentrate this review on what has been observed, primarily at the muscle fiber level in both animals and humans, with primary emphasis on the diaphragm. There have been several excellent previous reviews of this area, and the reader is encouraged to refer to these (13,41,58,65,66). Where possible, we will attempt to complement, update, and at times challenge current concepts with the purpose of furthering dialogue and promoting further inquiry. LENGTH PLASTICITYThe diaphragm, like all other muscles, exhibits a characteristic length-tension relationship analogous to the Frank-Starling curve for the heart. As length is increased in the relaxed muscle, a passive length-tension cu...

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Section: Length Plasticitymentioning

confidence: 98%

Respiratory muscle fiber remodeling in chronic hyperinflation: dysfunction or adaptation?

Clanton¹,

Levine²

2009

Journal of Applied Physiology

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“…With experimental emphysema, the diaphragm remodels to better match its length-tension relationship to its foreshortened resting length (31,32). Similarly, patients with COPD may have better inspiratory muscle function than normal subjects at equal lung volumes (33). If LVRS countermands such adaptive mechanisms, then the expected improvements due to decreased lung volume alone may be attenuated.…”

Section: Respiratory Muscle Functionmentioning

confidence: 99%

Physiologic Basis for Improved Pulmonary Function after Lung Volume Reduction

Fessler¹,

Scharf²,

Ingenito³

et al. 2008

Proceedings of the American Thoracic Society

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It is not readily apparent how pulmonary function could be improved by resecting portions of the lung in patients with emphysema. In emphysema, elevation in residual volume relative to total lung capacity reduces forced expiratory volumes, increases inspiratory effort, and impairs inspiratory muscle mechanics. Lung volume reduction surgery (LVRS) better matches the size of the lungs to the size of the thorax containing them. This restores forced expiratory volumes and the mechanical advantage of the inspiratory muscles. In patients with heterogeneous emphysema, LVRS may also allow space occupied by cysts to be reclaimed by more normal lung. Newer, bronchoscopic methods for lung volume reduction seek to achieve similar ends by causing localized atelectasis, but may be hindered by the low collateral resistance of emphysematous lung. Understanding of the mechanisms of improved function after LVRS can help select patients more likely to benefit from this approach.Keywords: lung mechanics; emphysema surgery; lung recoil; airflow limitation; respiratory muscles PHYSIOLOGIC BASIS FOR IMPAIRMENT WITH EMPHYSEMAInflammatory changes associated with chronic obstructive pulmonary disease (COPD) initiate the changes in lung mechanical properties that characterize emphysema. Inflammation leads to destruction of elastin, which contributes to lung elasticity, and collagen, which provides tensile strength. Although recent interest has focused on the cellular and molecular mechanisms contributing to emphysema, the study of lung mechanical stresses, one of the earliest postulated causes of emphysema (1), has received less attention. Weakened lung parenchyma is more likely to fracture during respiratory stress, and coalescence of a few alveoli can increase stress on adjacent units in a way that favors formation of large, localized cysts similar to the pattern seen in patients with advanced emphysema (2-4). Effects of Emphysema on Expiratory FlowThese sequelae of inflammation ultimately decrease lung elastic recoil and small airway caliber, contributing to characteristic airflow limitation. The three classic determinants of expiratory flow limitation are lung elastic recoil, the propensity for airways to close, and airway resistance (5). Loss of elastic recoil in emphysema decreases the upstream pressure that drives expiratory flow, thereby decreasing maximal flows at any lung volume. Loss of elastic recoil also increases the unstressed volume of the lung (the volume remaining when elastic recoil is zero). Loss of radial traction on airways from lung parenchyma contributes to airway closure at higher lung volumes (increased trapped volume) because a higher transmural pressure is required to maintain airway patency. In addition, airway caliber at any lung volume is decreased (6). Coexisting small airway inflammation and fibrosis further increase airway resistance (7,8). These changes collectively reduce the rate of lung emptying.The rate of lung emptying may be expressed as its time constant, the time necessary for approximately 63% o...

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“…Other investigators consider that because compensatory adaptation occurs in the diaphragm of patients with COPD failure of transdiaphragmatic pressure (Pdi) generation is not a clinically important problem [5]. Respiratory muscle recruitment during exercise in COPD has been previously examined during treadmill exercise [6,7], but these studies examined only the amplitude of the pressure swings and did not address the impact of positive pressure ventilation (PPV).…”

mentioning

confidence: 99%

Respiratory muscle activity in patients with COPD walking to exhaustion with and without pressure support

Kyroussis¹,

Polkey²,

Hamnegärd³

et al. 2000

Eur Respir J

115

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The function of the diaphragm and other respiratory muscles during exercise in chronic obstructive pulmonary disease (COPD) remains controversial and few data exist regarding respiratory muscle pressure generation in this situation.The inspiratory pressure/time products of the oesophageal and transdiaphragmatic pressure, and the expiratory gastric pressure/time product during exhaustive treadmill walking in 12 patients with severe COPD are reported. The effect of noninvasive positive pressure ventilation during treadmill exercise was also examined in a subgroup of patients (n=6).During free walking, the inspiratory pressure/time products rose early in the walk and then remained level until the patients were forced to stop because of intolerable dyspnoea. In contrast, the expiratory gastric pressure/time product increased progressively throughout the walk. When patients walked the same distance assisted by noninvasive positive pressure ventilation, a substantial reduction was observed in the inspiratory and expiratory pressure/time products throughout the walk. When patients walked with positive pressure ventilation for as long as they could, the pressure/time products observed at exercise cessation were lower than those observed during exercise cessation after free walking.It is concluded that, in severe chronic obstructive pulmonary disease, inspiratory muscle pressure generation does not increase to meet the demands imposed by exhaustive exercise, whereas expiratory muscle pressure generation rises progressively. Inspiratory pressure support was shown to substantially unload all components of the respiratory muscle pump. Eur Respir J 2000; 15: 649±655.

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Contractile Properties of the Human Diaphragm during Chronic Hyperinflation

Cited by 402 publications

References 27 publications

Respiratory muscle fiber remodeling in chronic hyperinflation: dysfunction or adaptation?

Respiratory muscle fiber remodeling in chronic hyperinflation: dysfunction or adaptation?

Physiologic Basis for Improved Pulmonary Function after Lung Volume Reduction

Respiratory muscle activity in patients with COPD walking to exhaustion with and without pressure support

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