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PubMed1997

Cross-bridge kinetics in respiratory muscles.

In respiratory muscles, force generation and shortening depend on the cyclical interaction of actin and myosin (cross-bridge cycling). During cross-bridge cycling, adenosine triphosphate (ATP) is hydrolysed. The globular head region of the myosin heavy chain (MyHC) possesses both the binding site to actin and the site for ATP hydrolysis. Therefore, the MyHC is both a structural and enzymatic protein. Different isoforms of MyHC are expressed in skeletal muscle fibres, and these MyHC isoforms provide mechanical and metabolic diversity. In the present study, the relationships between MyHC isoform expression in single rat diaphragm muscle fibres and their mechanical and energetic properties were evaluated. The expression of MyHC isoforms in single diaphragm muscle fibres was identified using electrophoretic and immunohistochemical techniques. Cross-bridge cycling kinetics in diaphragm muscle fibres clearly depend on MyHC isoform expression, and these differences are interpreted in the context of Huxley's two-state cross-bridge model. It is concluded that the unique mechanical and energetic properties of myosin heavy chain isoforms are designed to accomplish different motor behaviours of the diaphragm muscle, and that, as a result of these unique properties, a selective recruitment of diaphragm muscle fibres is essential to avoid fatigue.

Actins↗
PubMed1977

Respiratory muscle fatigue: a cause of respiratory failure?

1. The question whether respiratory muscle fatigue ever causes respiratory failure is over 40 years old, but we still have no definitive answer to this question. Skeletal muscle fatigue occurs when the rate of energy consumption of the muscle is greater than the energy supplied, so that energy stores are utilized and eventually become depleted. 2. Five factors which are important in the development of muscle fatigue (a, the tension developed by the muscle; b, the maximum tension the muscle can develop; c, the energy stored within the muscle; d, the energy supplied to the muscle; e, the efficiency of the muscle). These can be affected in many diseases, so disposing to fatigue, thus respiratory muscle fatigue is likely to be a common occurrence. 3. Respiratory muscle fatigue can in principle easily be diagnosed at the bedside by application of a simple electromyographic technique used to detect fatigue in other skeletal muscles.

Electromyography↗
PubMed2006

[Neuromuscular disorders - assessment of the respiratory muscles].

Involvement of respiratory muscles is a nearly constant feature of neuromuscular disorders, leading to respiratory failure. A careful respiratory follow up adapted to the variable time course of each disease is therefore mandatory. As the first step, a systematic clinical evaluation is essential to detect the subtle respiratory symptoms and signs related to respiratory muscle failure. Dyspnea and orthopnea are often late findings in patients with a usually severe functional impairment due to peripheral muscle weakness. Nocturnal respiratory events (obstructive sleep apnea syndrome and hypoventilation) are strongly suggested by daytime hypersomnolence and frequent morning headaches. Physical evaluation is essential to detect accessory muscle recruitment, supine abdominal paradox, and encumbrance of upper or lower airways. Vital capacity (VC) is the most classical lung function test. The major limitation of spirometry is its poor sensitivity to detect a moderate inspiratory muscle weakness. Supine VC may improve the detection of diaphragmatic involvement. Peak expiratory flow during cough (cough PEF) gives an overall evaluation of cough efficiency, values below 160 to 270 L/min suggesting poor airway clearance. Arterial blood gases are performed in case of clinical signs, significant deterioration of lung function tests, or sleep desaturations. Hypercapnia is weakly related to lung function results in patients with Steinert dystrophy and those with bulbar involvement. A specific evaluation of respiratory muscle strength is mandatory, as these tests are both sensitive and highly prognostic. Possible discrepancies (particularly in bulbar patients) between maximal inspiratory pressure (PImax) and sniff nasal inspiratory pressure (SNIP) justify to perform both measurements and to select the highest pressure. A maximal expiratory pressure (PEmax) below 45 cm H2O may indicate a compromised cough efficiency but the correlation with cough PEF may be poor. A screening nocturnal oxymetry is useful to detect sleep apneas and hypoventilation. Criteria defining significant desaturations remain however controversial. Suspicion of obstructive sleep apnea syndrome on clinical grounds or oxymetry findings should be confirmed by a conventional polysomnography.

Cough↗
PubMed1993

Effect of global inspiratory muscle fatigue on ventilatory and respiratory muscle responses to CO2.

We evaluated the effect of global inspiratory muscle fatigue on ventilation and respiratory muscle control during CO2 rebreathing in normal subjects. Fatigue was induced by breathing against a high inspiratory resistance until exhaustion. CO2 response curves were measured before and after fatigue. During CO2 rebreathing, global fatigue caused a decreased tidal volume (VT) and an increased breathing frequency but did not change minute ventilation, duty cycle, or mean inspiratory flow. Both esophageal and transdiaphragmatic pressure swings were significantly reduced after global fatigue, suggesting decreased contribution of both rib cage muscles and diaphragm to breathing. End-expiratory transpulmonary pressure for a given CO2 was lower after fatigue, indicating an additional decrease in end-expiratory lung volume due to expiratory muscle recruitment, which leads to a greater initial portion of inspiration being passive. This, combined with the reduction in VT, decreased the fraction of VT attributable to inspiratory muscle contribution; therefore the inspiratory muscle elastic work and power per breath were significantly reduced. We conclude that respiratory control mechanisms are plastic and that the respiratory centers alter their output in a manner appropriate to the contractile state of the respiratory muscles to conserve the ventilatory response to CO2.

Adult↗
PubMed2005

Lung and respiratory muscle function at discharge from a respiratory intensive care unit.

BACKGROUND: The purpose of this prospective observational study was to describe lung and respiratory muscle function at Respiratory Intensive Care Unit (RICU) discharge after a severe exacerbation of Chronic Obstructive Pulmonary Disease (COPD). METHODS: The study was conducted in 42 consecutive COPD patients in whom arterial blood gases, dynamic and static lung volumes, maximal inspiratory pressure (MIP) were assessed at discharge from the RICU and compared with values measured 6 months previously when they were in a stable state. The same measurements were performed at 6-month interval in 42 comparable stable COPD patients not requiring any hospitalisation for at least 6 months used as controls. RESULTS: 24% of patients in the study group were discharged with hypercapnia whereas they were normocapnic before the acute episode. Compared to prior to exacerbation, patients of study group showed a significant worsening in mean values of PaCO2 (p=0.005), MIP (p=0.005) and FEV1 (p=0.041). Predefined criteria of worsening in PaCO2, MIP and FEV1 were observed in 47%, 33% and 28% of patients in study respectively. Neither lung nor respiratory muscle function in last stable state did predict post RICU functional worsening. In a period of 6 months controls showed no change in the studied parameters. CONCLUSIONS: After a severe acute exacerbation requiring admission to a RICU and immediately before discharge 1) a large proportion of COPD patients still show preserved lung and respiratory muscle function 2) more than one third of them would require further care and rehabilitative attempts to restore functional derangements.

Aged↗
PubMed2002

A novel clinical test of respiratory muscle endurance.

Impaired respiratory muscle endurance (RME) could reduce exercise tolerance and contribute to ventilatory failure. The aim of the present study was to develop a clinically-feasible method to measure RME using negative-pressure inspiratory-threshold loading. It was hypothesized that endurance time (tlim) could be predicted by normalizing oesophageal pressure-time product (PTP) per total breath cycle (PTPoes) for maximum oesophageal pressure (Poes,max); the load/capacity ratio. The corresponding mouth pressures, PTPmouth and Pmouth,max were also measured. The RME test was performed on 30 healthy subjects exposed to the same target pressure (70% of Poes,max). Eight patients with systemic sclerosis/interstitial lung disease were studied to assess the validity and acceptability of the technique. Normal subjects showed a wide intersubject variation in tlim (coefficient of variation, 69%), with a linear relationship demonstrated between log tlim and PTPoes/Poes,max (r=0.88). All patients with systemic sclerosis/interstitial lung disease had normal respiratory muscle strength, but six out of eight had a reduction in RME. In conclusion, endurance time can be predicted from the load/capacity ratio, over a range of breathing strategies; this relationship allows abnormal respiratory muscle endurance to be detected in patients. Oesophageal and mouth pressure showed a close correlation, thus suggesting that the test could be applied noninvasively.

Adult↗
PubMed2004

Walking modality affects respiratory muscle action and contribution to respiratory effort.

We hypothesized that walking at increased speed or increasing gradient might have different effects on chest wall kinematics and respiratory muscle power components, and contribute differently to respiratory effort sensation. We measured the volumes of chest wall compartments by optoelectronic plethysmography, esophageal, gastric and transdiaphragmatic ( P(di)) pressures, and the sensation of the respiratory effort by a Borg scale in five normal subjects walking both at ascending gradient with constant speed (AG) and at ascending speed with constant gradient (AS). Chest wall kinematics, evaluated by displacement of chest wall compartments, did not show any significant difference between AS and AG. Muscle power, calculated as the product of mean flow and mean pressure, increased similarly, but its partitioning into pressure and velocity of shortening differed in the two modes. A greater increase in the pressure developed by the abdominal muscles ( P(abm)) (4.06-fold), and in the velocity of shortening of both rib cage inspiratory muscles ( v(rcm,i)) (2.01-fold) and the diaphragm ( v(di)) (1.90-fold) was associated with a lower increase in the pressure developed by the rib cage inspiratory muscles ( P(rcm,i)) (1.24-fold) and P(di) (0.99-fold) with AG. Instead, with AS, a lower increase in P(abm) (2.12-fold), v(rcm,i) (1.66-fold) and v(di) (1.54-fold) was associated with a greater increase in P(rcm,i) (1.56-fold) and P(di) (1.97-fold). A combination of P(abm) and v(di) during AG (Wald chi(2)=23.19, P<0.0000), with the addition of P(rcm,i) during AS (Wald chi(2)=29.46, P<0.0000), was the best predictor of Borg score. In conclusion, the general strategy adopted by respiratory centers during different walking modes does not differ in terms of ventilation, chest wall kinematics, and respiratory muscle power production, whereas it does in terms of partitioning of power into pressure and velocity of shortening, and respiratory muscle contribution to respiratory effort sensation. Combinations of different patterns of flow and pressure generation made the respiratory effort sensation similar during AS and AG modes.

Adult↗
PubMed1990

Respiratory muscle insufficiency in acute respiratory failure of subjects with severe COPD: treatment with intermittent negative pressure ventilation.

Nine subjects with severe chronic obstructive pulmonary disease (COPD) in acute respiratory failure (ARF) and with marked weakness of the respiratory muscles (Group A) underwent intermittent negative pressure ventilation by means of an iron lung (8 h daily for 7 days). Seven subjects with COPD in stabilized chronic respiratory failure (Group B) were studied as controls and submitted to the same medical therapy without ventilator treatment. Functional respiratory tests were performed before and after 7 days of treatment. After ventilatory treatment, Group A showed an increase of maximum inspiratory pressure (PImax), maximum expiratory pressure (PEmax), vital capacity (VC), arterial oxygen tension (PaO2), pH and a decrease of residual volume (RV), total lung capacity of (TLC) and arterial carbon dioxide tension (PaCO2) (all statistically significant). No improvement was ascertained in the functional parameters of Group B. The expiratory muscles seem to play a determining role in ARF. We conclude that the iron lung is a useful therapeutic defence in removing muscular fatigue and in restoring a good level of respiratory compensation of ARF in severe COPD.

Female↗
PubMed2006

Respiratory muscle activity and respiratory obstruction after abdominal surgery.

BACKGROUND: Respiratory movements in patients after abdominal surgery are frequently abnormal, with associated disturbances in the pattern of inspiratory pressure generation. The reasons for these abnormalities are not clear and have been attributed to impaired action of the diaphragm. However, an alternative is that partial airway obstruction could trigger reflex activation of the inspiratory ribcage muscles, which would cause a similar pattern of inspiratory pressure change. Direct measurement of electrical activity can indicate if reflex activation of inspiratory muscles occurs when partial airway obstruction is present. METHODS: In an open study, we implanted electrodes to measure the EMG of scalene, intercostal and external oblique abdominal muscles in patients after lower abdominal surgery. Analgesia was with morphine i.v. by patient control. We used nasal cannulae to measure nasal airflow and compared EMG activity when airway obstruction was present with activity when breathing was not obstructed. RESULTS: The pattern of activity of the different muscles was distinct. Intercostal activity reached a maximum during inspiration, before the scalene muscles, whereas scalene activity increased in phase with increasing lung volume. Abdominal muscle activity commenced when expiratory flow had ceased and continued until the next inspiration. In all three muscle groups, partial airway obstruction did not alter muscle activity. CONCLUSIONS: Partial airway obstruction does not activate inspiratory ribcage muscles, in patients receiving morphine for postoperative analgesia after lower abdominal surgery. Changes in respiratory pressures and abnormalities of chest wall movement described in previous studies cannot be attributed to reflex responses and probably result from increased airway resistance and abdominal muscle action.

Abdomen↗
PubMed1989

Respiratory muscle weakness and fatigue.

Respiratory muscle weakness can result from a variety of neuromuscular disorders, and it is now possible to identify different patterns of weakness and quantify the extent of this weakness using reliable, sensitive tests of respiratory muscle strength. However the quantification of respiratory muscle 'fatigue' has proved more difficult, and it is now recognized that there is unlikely to be one single index of fatigue, rather a whole sequence of changes that occur in response to loading. It is likely that in practice, a close interplay between respiratory pump capacity, demands on the pump and more especially, adaptive changes in respiratory drive, protect the respiratory muscles from overt peripheral contractile failure, and that the fall in tension following prolonged muscular activity involves many different closely inter-related processes. Investigation of these processes is likely to be more rewarding than attempts to develop a single 'test of fatigue', and may lead to an improved understanding of the role of respiratory muscle dysfunction in ventilatory failure.

Fatigue↗
PubMed1999

Respiratory muscle involvement in multiple sclerosis.

Respiratory complications are common in the terminal stages of multiple sclerosis and contribute to mortality in these patients. When respiratory motor pathways are involved, respiratory muscle weakness frequently occurs. Although it is well established that weakness of the respiratory muscles produces a restrictive ventilatory defect, the degree of muscle weakness and pulmonary function are poorly related. Respiratory muscle weakness was observed in patients with normal or near normal pulmonary function. Expiratory muscle weakness is more prominent than inspiratory muscle weakness and may impair performance of coughing. Subsequently, in addition to bulbar dysfunction, respiratory muscle weakness may contribute to ineffective coughing, pneumonia, and sometimes even acute ventilatory failure may ensue. Respiratory muscle weakness may also occur early in the course of the disease. Recent studies suggest that the respiratory muscles can be trained for both strength and endurance in multiple sclerosis patients. Whether respiratory muscle training delays the development of respiratory dysfunction and subsequently improves exercise capacity and cough efficacy, prevents pulmonary complications or prolongs survival in the long-term remains to be determined.

Humans↗
PubMed1988

Respiratory muscles in disease.

The respiratory muscles play an important role in the clinical manifestations of different disease states. Respiratory muscle dysfunction plays a primary role in the development of ventilatory failure in patients with neuromuscular disorders. Although the respiratory muscles are placed at a mechanical disadvantage in patients with obstructive lung disease, there is little clinical evidence to suggest that respiratory muscle dysfunction plays a primary role in the development of ventilatory failure.

Asthma↗
PubMed2005

Respiratory muscle plasticity.

Plasticity of respiratory muscles must be considered in the context of their unique physiological demands. The continuous rhythmic activation of respiratory muscles makes them among the most active in the body. Respiratory muscles, especially the diaphragm, are non-weight-bearing, and thus, in contrast to limb muscles, are not exposed to gravitational effects. Perturbations in normal activation and load known to induce plasticity in limb muscles may not cause similar adaptations in respiratory muscles. In this review, we explore the structural and functional properties of the diaphragm muscle and their response to alterations in load and activity. Overall, relatively modest changes in diaphragm structural and functional properties occur in response to perturbations in load or activity. However, disruptions in the normal influence of phrenic innervation by frank denervation, tetrodotoxin nerve block and spinal hemisection, induce profound changes in the diaphragm, indicating the substantial trophic influence of phrenic motoneurons on diaphragm muscle.

Adaptation, Physiological↗