Clinical importance of cross-sectional area of intercostal muscles in patients with chronic obstructive pulmonary disease.

INTRODUCTION: Limb muscle wasting is one of main systemic manifestation of chronic obstructive pulmonary disease (COPD). However, the change of respiratory muscle is unclear. OBJECTIVES: This study assessed the cross-sectional area (CSA) of the intercostal muscles (ICMs) in patients with COPD, using chest computed tomography (CT) and determined its association with the clinical characteristics of COPD. METHODS: They retrospectively reviewed 60 patients with stable COPD and compared them with 30 controls. CSA (mm2 ) of the ICM on chest CT was measured at the midline level of the lateral arch of the bilateral first rib with a 3-mm slice thickness by using CT histogram software. The association with the clinical characteristics of COPD and with the control groups was assessed. RESULTS: CSA of the ICM and the CSA/body mass index (BMI) were lower in the COPD group than in the control group. Patients with Global Initiative for Chronic Obstructive Lung Disease (GOLD) stage 4 had a significantly lower CSA of the ICM than patients with stage 1, 2, and 3. CSA of the ICM was positively associated with FEV1 , %FEV1 predicted, FEV1 /FVC ratio, and BMI and negatively associated with age. However, there were no associations with PaO2 , PaCO2 , smoking status, 6-minute walk test, frequency of acute exacerbation of COPD, and serum C-reactive protein level. CONCLUSION: Intercostal muscle atrophy occurs in COPD patients and is associated with severity of airway obstruction, BMI, and increasing age.

Physiological markers of exercise capacity and lung disease severity in cystic fibrosis.

BACKGROUND AND OBJECTIVE: Peak aerobic capacity (VO2 peak) is an important outcome measure in cystic fibrosis (CF), but measurement is not widely available and can be influenced by patient motivation, pain and fatigue. Alternative markers of disease severity would be helpful. Neural respiratory drive, measured using parasternal intercostal muscle electromyography (EMGpara), reflects the load to capacity balance of the respiratory system and provides a composite measure of pulmonary function impairment in CF. The aim of the study was to investigate the relationship between exercise capacity, EMGpara and established measures of pulmonary function in clinically stable adult CF patients. METHODS: Twenty CF patients (12 males, median (range) age: 22.3 (17.0-43.1) years) performed the 10-m incremental shuttle walk test (ISWT) maximally with contemporaneous measures of aerobic metabolism. EMGpara was recorded from second intercostal space at rest and normalized using peak electromyogram activity obtained during maximum respiratory manoeuvres and expressed as EMGpara%max (EMGpara expressed as a percentage of maximum). RESULTS: VO2 peak was strongly correlated with ISWT distance (r = 0.864, P < 0.0001). Lung gas transfer (TL CO) % predicted was best correlated with VO2 peak (r = 0.842, P < 0.0001) and ISWT distance (r = 0.788, P < 0.0001). EMGpara%max also correlated with VO2 peak (-0.757, P < 0.0001), while the relationships between exercise outcome measures and forced expiratory volume in 1 s (FEV1 ) % predicted and forced vital capacity (FVC) % predicted were less strong. A TL CO% predicted of <70.5% was the strongest predictor of VO2 peak <32 mL/min/kg (area under the curve (AUC): 0.96, 100% sensitivity, 83.3% specificity). ISWT distance and EMGpara%max also performed well, with other pulmonary function variables demonstrating poorer predictive ability. CONCLUSION: TL CO% predicted and EMGpara%max relate strongly to exercise performance markers in CF and may provide alternative predictors of lung disease progression.

Parasternal electromyography to determine the relationship between patient-ventilator asynchrony and nocturnal gas exchange during home mechanical ventilation set-up.

INTRODUCTION: Patient-ventilator asynchrony (PVA) can adversely affect the successful initiation of non-invasive home mechanical ventilation (HMV). The aim of this observational study was to quantify the prevalence of PVA during initiation of HMV and to determine the relationship between PVA and nocturnal gas exchange. METHOD: Type and frequency of PVA were measured by surface parasternal intercostal muscle electromyography, thoracoabdominal plethysmography and mask pressure during initiation of HMV. Severe PVA was defined, as previously, as asynchrony affecting ≥10% of breaths. RESULTS: 28 patients (18 male) were enrolled aged 61±15 years and with a body mass index of 35±9 kg/m(2). Underlying diagnoses were neuromuscular disease with or without chest wall disease (n=6), obesity related chronic respiratory failure (n=12) and COPD (n=10). PVA was observed in all patients with 79% of patients demonstrating severe PVA. Triggering asynchrony was most frequent, observed in 24% (IQR: 11-36%) of breaths, with ineffective efforts accounting for 16% (IQR: 4-24%). PVA types were similar between disease groups, with the exception of auto-triggering, which was higher in patients with COPD (12% (IQR: 6-26%)). There was no correlation observed between PVA and time spent with oxygen saturations ≤90%, mean oxygen saturations or transcutaneous carbon dioxide levels during overnight ventilation. CONCLUSIONS: Severe PVA was identified in the majority of patients, irrespective of pathophysiological disease state. This was not associated with ineffective ventilation as evidenced by gas exchange.

Daily acute intermittent hypoxia elicits functional recovery of diaphragm and inspiratory intercostal muscle activity after acute cervical spinal injury.

A major cause of mortality after spinal cord injury is respiratory failure. In normal rats, acute intermittent hypoxia (AIH) induces respiratory motor plasticity, expressed as diaphragm (Dia) and second external intercostal (T2 EIC) long-term facilitation (LTF). Dia (not T2 EIC) LTF is enhanced by systemic adenosine 2A (A2A) receptor inhibition in normal rats. We investigated the respective contributions of Dia and T2 EIC to daily AIH-induced functional recovery of breathing capacity with/without A2A receptor antagonist (KW6002, i.p.) following C2 hemisection (C2HS). Rats received daily AIH (dAIH: 10, 5-min episodes, 10.5% O2; 5-min normoxic intervals; 7 successive days beginning 7days post-C2HS) or daily normoxia (dNx) with/without KW6002, followed by weekly (reminder) presentations for 8weeks. Ventilation and EMGs from bilateral diaphragm and T2 EIC muscles were measured with room air breathing (21% O2) and maximum chemoreceptor stimulation ( MCS: 7% CO2, 10.5% O2). dAIH increased tidal volume (VT) in C2HS rats breathing room air (dAIH+vehicle: 0.47±0.02, dNx+vehicle: 0.40±0.01ml/100g; p<0.05) and MCS (dAIH+vehicle: 0.83±0.01, dNx+vehicle: 0.73±0.01ml/100g; p<0.001); KW6002 had no significant effect. dAIH enhanced contralateral (uninjured) diaphragm EMG activity, an effect attenuated by KW6002, during room air breathing and MCS (p<0.05). Although dAIH enhanced contralateral T2 EIC EMG activity during room air breathing, KW6002 had no effect. dAIH had no statistically significant effects on diaphragm or T2 EIC EMG activity ipsilateral to injury. Thus, two weeks post-C2HS: 1) dAIH enhances breathing capacity by effects on contralateral diaphragm and T2 EIC activity; and 2) dAIH-induced recovery is A2A dependent in diaphragm, but not T2 EIC. Daily AIH may be a useful in promoting functional recovery of breathing capacity after cervical spinal injury, but A2A receptor antagonists (e.g. caffeine) may undermine its effectiveness shortly after injury.

Measurement of parasternal intercostal electromyogram during an infective exacerbation in patients with cystic fibrosis.

The parasternal intercostal muscle electromyogram (sEMGpara) is a measure of neural respiratory drive and reflects lung disease severity in stable cystic fibrosis (CF). The aim of the study was to measure sEMGpara in acute infective exacerbations of CF and compare changes in sEMGpara with those in conventional lung function measures. 12 patients with CF admitted to hospital with an acute chest infection were studied. There was a significant reduction in mean ± SD sEMGpara (ΔsEMGpara -38 ± 19%, p<0.001) between admission and discharge. Spirometery also improved significantly from admission to discharge; Δforced expiratory volume in 1 s % predicted 39 ± 30%, p<0.001 and Δvital capacity % pred 22 ± 18%, p<0.001. sEMGpara has potential value as a nonvolitional measure of change in respiratory function in CF.

Airway management of tetanus after the Haitian earthquake: new aspects of old observations.

Two men developed severe tetanus after the 2010 Haitian earthquake. They were admitted to the United States Naval Ship Comfort, a hospital ship sent to provide humanitarian relief. Severe masseter and intercostal muscle spasm impaired airway access and ventilation. Propofol and sevoflurane relieved the tetany, allowing airway control and ventilation without intubation or neuromuscular blocking drugs during wound debridement. Presynaptic impairment of inhibitory neurotransmitter release by tetanospasmin toxin is countered by enhancement of spinal cord postsynaptic inhibitory receptor activity by general anesthetics. Avoidance of tracheal intubation and mechanical ventilation during anesthesia may be desirable in the settings of limited resources in which tetanus usually presents.

Neural respiratory drive, pulmonary mechanics and breathlessness in patients with cystic fibrosis.

BACKGROUND: Neural respiratory drive (NRD) measured from the diaphragm electromyogram (EMGdi) reflects the load/capacity balance of the respiratory muscle pump and is a marker of lung disease severity. EMGdi measurement is invasive, but recording the EMG from the parasternal intercostal muscles using surface electrodes (sEMGpara) could provide a non-invasive method of assessing NRD and disease severity. Objectives To test the hypothesis that NRD measured by sEMGpara correlates with EMGdi, to provide an index of disease severity in cystic fibrosis (CF) and to relate to exercise-induced breathlessness. METHODS: 15 patients with CF (mean forced expiratory volume in 1 s (FEV(1)) 53.5% predicted) and 15 age-matched healthy controls were studied. sEMGpara and EMGdi were recorded at rest and during exercise. sEMGpara was recorded using surface electrodes and EMGdi using a multipair oesophageal electrode catheter. Signals were normalised using the peak EMG recorded during maximum respiratory manoeuvres and expressed as EMG%max. The respiratory pattern, metabolic data, oesophageal and gastric pressures and Borg scores were also recorded. RESULTS: Mean (SD) resting sEMGpara%max and EMGdi%max were higher in patients with CF than in controls (13.1 (7)% and 18.5 (7.5)% vs 5.8 (3)% and 7.5 (2)%, respectively, p<0.001). In the patients with CF, resting sEMGpara%max and EMGdi%max were related to the degree of airways obstruction (FEV(1)) (r = -0.91 and r = -0.82, both p<0.001), hyperinflation (r = 0.63 and r = 0.56, both p<0.001) and dynamic lung compliance (r = -0.53 and r = -0.59, both p<0.001). During exercise, sEMGpara%max and EMGdi%max were strongly correlated with breathlessness in the patients with CF before (r = 0.906, p<0.001) and after (r = 0.975, p<0.001) the onset of neuromechanical dissociation. CONCLUSION: sEMGpara%max provides a non-invasive marker of neural drive, which reflects disease severity and exercise-induced breathlessness in CF.

[Activation of satellite cells in the intercostal muscles of patients with chronic obstructive pulmonary disease]. / Activación de células satélite en el músculo intercostal de pacientes con EPOC.

OBJECTIVE: The respiratory muscles of patients with chronic obstructive pulmonary disease (COPD) display evidence of structural damage in parallel with signs of adaptation. We hypothesized that this can only be explained by the simultaneous activation of satellite cells. The aim of this study was to analyze the number and activation of those cells along with the expression of markers of microstructural damage that are frequently associated with regeneration. PATIENTS AND METHODS: The study included 8 patients with severe COPD (mean [SD] forced expiratory volume in 1 second, 33% [9%] of predicted) and 7 control subjects in whom biopsies were performed of the external intercostal muscle. The samples were analyzed by light microscopy to assess muscle fiber phenotype, electron microscopy to identify satellite cells, and real-time polymerase chain reaction to analyze the expression of the following markers: insulin-like growth factor 1, mechano growth factor, and embryonic and perinatal myosin heavy chains (MHC) as markers of microstructural damage; Pax-7 and m-cadherin as markers of the presence and activation of satellite cells, respectively; and MHC-I, IIa, and IIx as determinants of muscle fiber phenotype. RESULTS: The patients had larger fibers than healthy subjects (54 [6] vs 42 [4] microm(2); P< .01) with a similar or slightly increased proportion of satellite cells, as measured by ultrastructural analysis (4.3% [1%] vs 3.7% [3.5%]; P>.05) or expression of Pax-7 (5.5 [4.1] vs 1.6 [0.8] arbitrary units [AU]; P< .05). In addition, there was greater activation of satellite cells in the patients, as indicated by increased expression of m-cadherin (3.8 [2.1] vs 1.0 [1.2] AU; P=.05). This was associated with increased expression of markers of microstructural damage: insulin-like growth factor 1, 0.35 (0.34) vs 0.09 (0.08) AU (P< .05); mechano growth factor, 0.45 (0.55) vs 0.13 (0.17) AU (P=.05). CONCLUSIONS: The intercostal muscles of patients with severe COPD show indirect signs of microstructural damage accompanied by satellite cell activation. This suggests the presence of ongoing cycles of lesion and repair that could partially explain the maintenance of the structural properties of the muscle.

Oxidative stress in the external intercostal muscles of patients with obstructive sleep apnoea.

BACKGROUND: The external intercostal muscles are chronically exposed to increased inspiratory loading and to continuous hypoxia-reoxygenation cycles in patients with obstructive sleep apnoea syndrome (OSAS). It was therefore hypothesised that oxidative stress levels would be increased in these muscles, and that treatment with continuous positive airway pressure (CPAP) would modify the oxidative stress levels and improve muscle dysfunction. METHODS: A case-control study and a case-case study were conducted on the external intercostal muscles of 12 patients with severe OSAS (before and after 6 months of treatment with CPAP) and 6 control subjects. Reactive carbonyl groups, malondialdehyde (MDA)-protein and hydroxynonenal (HNE)-protein adducts, antioxidant enzyme levels, 3-nitrotyrosine and fibre type proportions were measured using immunoblotting and immunohistochemistry. RESULTS: Compared with controls, the intercostal muscles of patients with OSAS had higher levels of protein carbonylation (median values 3.06 and 2.45, respectively, p = 0.042), nitration (median values 1.64 and 1.05, respectively, p = 0.019) and proportions of type I fibres (median values 57% and 48%, respectively, p = 0.035) and reduced respiratory muscle endurance (median values 3.2 and 9.5 min, respectively, p = 0.001). Positive correlations were found between MDA-protein and HNE-protein adducts (r = 0.641, p = 0.02 and r = 0.594, p = 0.05, respectively) and 3-nitrotyrosine (r = 0.625, p = 0.03) and the apnoea-hypopnoea index (AHI) in all the patients with OSAS. Although treatment with CPAP significantly improved the AHI and oxygen desaturation, muscle oxidative stress levels and respiratory muscle endurance were not affected. CONCLUSIONS: This study suggests that inspiratory muscle performance is not completely restored after long-term treatment with CPAP.

Is excitation-contraction coupling impaired in myasthenia gravis?

OBJECTIVE: To investigate whether excitation-contraction (E-C) coupling of muscle is impaired in patients with myasthenia gravis (MG). METHODS: In 51 patients with generalized MG and 35 normal subjects, compound muscle action potentials (CMAPs) of the abductor pollicis brevis, and movement-related potentials using an accelerometer placed at the thumb tip were simultaneously recorded after median nerve stimulation at the wrist. The E-C coupling time (ECCT) was estimated by a latency difference between CMAP and movement-related potential. Antibodies against acetylcholine receptor (AChR), ryanodine receptor (RyR), and muscle specific receptor tyrosine kinase (MuSK) were measured by immunoassays. RESULTS: The mean ECCT was significantly longer in patients with MG (mean+/-SEM; 2.79+/-0.1 ms; p=0.002) than in normal controls (2.52+/-0.1 ms). Among MG patients, the mean ECCT was longer for patients with thymoma than for those without it (P=0.04), and was shorter for patients treated with FK506 (an immunosuppressant and also an enhancer of RyR related Ca(2+) release) than for those not receiving this treatment (p=0.04). ECCT had no significant correlation with anti-AChR, anti-RyR, or anti-MuSK antibodies. CONCLUSIONS: In MG, E-C coupling appears to be impaired, particularly in patients with thymoma, and FK506 possibly facilitates E-C coupling. SIGNIFICANCE: The functional implication of impaired E-C coupling is not established, but it may contribute to muscle weakness in patients with MG.

Plethysmographic estimation of thoracic gas volume in apneic mice.

Electrical stimulation of intercostal muscles was employed to measure thoracic gas volume (TGV) during airway occlusion in the absence of respiratory effort at different levels of lung inflation. In 15 tracheostomized and mechanically ventilated CBA/Ca mice, the value of TGV obtained from the spontaneous breathing effort available in the early phase of the experiments (TGVsp) was compared with those resulting from muscle stimulation (TGVst) at transrespiratory pressures of 0, 10, and 20 cmH2O. A very strong correlation (r2= 0.97) was found, although with a systematically (approximately 16%) higher estimation of TGVst relative to TGVsp, attributable to the different durations of the stimulated (approximately 50 ms) and spontaneous (approximately 200 ms) contractions. Measurements of TGVst before and after injections of 0.2, 0.4, and 0.6 ml of nitrogen into the lungs in six mice resulted in good agreement between the change in TGVst and the injected volume (r2= 0.98). In four mice, TGVsp and TGVst were compared at end expiration with air or a helium-oxygen mixture to confirm the validity of isothermal compression in the alveolar gas. The TGVst values measured at zero transrespiratory pressure in all CBA/Ca mice [0.29 +/- 0.05 (SD) ml] and in C57BL/6 (N = 6; 0.34 +/- 0.08 ml) and BALB/c (N = 6; 0.28 +/- 0.06 ml) mice were in agreement with functional residual capacity values from previous studies in which different techniques were used. This method is particularly useful when TGV is to be determined in the absence of breathing activity, when it must be known at any level of lung inflation or under non-steady-state conditions, such as during pharmaceutical interventions.

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.

Detection of pneumonia among children under six years by clinical evaluation.

To determine the most useful clinical symptoms and signs for detection of pneumonia in children, we carried out a prospective clinical study at Queen Alia Hospital, Amman, on 147 children admitted between August 2002 and January 2003 with clinical pneumonia. All the children had chest X-rays, which were read by the same radiologist. The most sensitive and specific signs and symptoms for prediction of pneumonia were coughing, tachypnoea (respiratory rate > 50/min) and chest wall indrawing. We found that presence of tachypnoea and lower chest wall indrawing can detect most cases of pneumonia. If all clinical signs are negative, chest X-ray findings are unlikely to be positive.

Lung function and surface electromyography of intercostal muscles in cement mill workers.

Impairment of pulmonary function in cement mill workers has been previously reported without considering a variety of parameters that can help evaluate more thoroughly the effect of cement dust on the respiratory system. In addition, an integrated approach has not been considered to assert the involvement of respiratory muscles. Therefore, in the present study spirometry and surface electromyography (SEMG) of intercostal muscles were used for indicating pulmonary impairment. In this study, a group of 50, apparently healthy volunteers, male cement mill workers aged 20-60 years with exposure of 13 years on average, were randomly selected. They were matched with another group of 50 control healthy male subjects in terms of age, height, weight and socioeconomic status. Both groups met the standard exclusion criteria. Spirometry was performed on an electronic spirometer, while SEMG of intercostal muscles was performed by using a chart recorder. The results demonstrated statistically significant reduction in lung function parameters i.e., force vital capacity (FVC) (p < 0.0005); force expiratory volume in first second (FEV1) (p < 0.0005); peak expiratory flow (PEF) (p < 0.005); and maximum voluntary ventilation (MVV) (p < 0.0005) in cement mill workers, when compared with controls. However, the FEV1/FVC ratio was significantly higher (p < 0.025) in cement mill workers. Similarly, the parameters obtained from SEMG of intercostal muscles, i.e. number of peaks (NOP) (p < 0.0005); maximum peak amplitude (MPA) (p < 0.0005); peak to peak amplitude (PPA) (p < 0.0005); duration of response (DOR) (p < 0.0005) and maximum peak duration (MPD) (p < 0.0005), were significantly lower in cement mill workers than in controls. It is concluded that exposure to cement dust not only impairs lung function but also affects costal muscle performance, thus possibly indicating the decreased lung and thoracic compliance.

Rnx deficiency results in congenital central hypoventilation.

The genes Tlx1 (Hox11), Enx (Hox11L2, Tlx-2) and Rnx (Hox11L2, Tlx-3) constitute a family of orphan homeobox genes. In situ hybridization has revealed considerable overlap in their expression within the nervous system, but Rnx is singularly expressed in the developing dorsal and ventral region of the medulla oblongata. Tlx1-deficient and Enx-deficient mice display phenotypes in tissues where the mutated gene is singularly expressed, resulting in asplenogenesis and hyperganglionic megacolon, respectively. To determine the developmental role of Rnx, we disrupted the locus in mouse embryonic stem (ES) cells. Rnx deficient mice developed to term, but all died within 24 hours after birth from a central respiratory failure. The electromyographic activity of intercostal muscles coupled with the C4 ventral root activity assessed in a medulla-spinal cord preparation revealed a high respiratory rate with short inspiratory duration and frequent apnea. Furthermore, a coordinate pattern existed between the abnormal activity of inspiratory neurons in the ventrolateral medulla and C4 motorneuron output, indicating a central respiratory defect in Rnx mice. Thus, Rnx is critical for the development of the ventral medullary respiratory centre and its deficiency results in a syndrome resembling congenital central hypoventilation.

Acquired slow-channel syndrome: a form of myasthenia gravis with prolonged open time of the acetylcholine receptor channel.

A 32-year-old female presented with a 2-year history of fluctuating generalized weakness including extraocular, bulbar, and limb muscles, suggesting myasthenia gravis, but with poor response to pyridostigmine and unusual electromyographic findings. After rest, power increased on repeated maximal contractions, followed by progressive weakness. There were decremental responses at low-frequency stimulation, but incremental responses at high frequencies, and single stimuli evoked repetitive compound muscle action potentials. Plasmapheresis was ineffective. In a conventional assay, antibodies against acetylcholine receptors (AChRs) were borderline. However, in an assay using cells expressing mainly adult-type human AChRs, the patient's serum was positive. Thymectomy revealed a hyperplastic thymus. An intercostal muscle specimen revealed small miniature end-plate potentials, 0.22+/-0.02 mV instead of 0.56+/-0.05 mV in controls. The number of 125I-alpha-bungarotoxin binding sites was normal. The decay time constant of end-plate potentials was increased from 5.3+/-0.6 msec in controls to 23+/-3.6 msec in the patient. Ultrastructurally, there was no destruction of the end plate. Transfer of the patient's plasma to mice in vivo produced similar physiological changes in their diaphragms. We conclude that the patient has an immune-mediated disorder, in which an antibody specific to the adult form of the AChRs alters the channel properties, reducing total current and slowing the closure. We propose the name "acquired slow-channel syndrome" for this variant of myasthenia gravis.

Patterns of inspiratory muscle shortening during hypoxia and hypercapnia in dogs.

The shortening of parasternal intercostal muscles (Para) and crural (Cru) and costal diaphragms (Cos) are not precisely understood. We therefore examined shortening patterns of these inspiratory muscles by using chronically implanted sonomicrometers in dogs. To avoid acute effects of surgery, measurements were performed 3 weeks after implanting the sonomicrometers. Patterns of length changes of Para, Cru, and Cos were measured during hypoxia and hypercapnia under two levels of anaesthesia. Respiratory length change (delta L) was assessed as a percentage change relative to the resting length at functional residual capacity (LFRC). Peak tidal shortening was defined as the maximal change from LFRC (delta L/LFRC). Under light anesthesia, the delta L/LFRC was the same among the three muscle groups at all tidal volumes (VT). Under deep anaesthesia, the delta L/LFRC both of Cru and Cos exceeded that of Para. Under light anaesthesia, the maximal shortening velocity ((delta L/LFRC)/delta t) of Cru was greater than that of Para. Under deep anaesthesia, the (delta L/LFRC)/delta t of Para was exceeded by that both of Cru and Cos. Furthermore, the (delta L/LFRC)/delta t of each inspiratory muscle was greater during hypoxia than during hypercapnia at equal volume. We conclude that: 1) the contribution of the diaphragm to ventilation increases during deep anaesthesia; 2) the muscle shortening velocity during hypoxia or hypercapnia is lower in parasternal intercostal muscles than in the diaphragm; and 3) there is no difference in the shortening pattern between crural and costal diaphragms.