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PubMed1999

Early occurrence of respiratory muscle deoxygenation assessed by near-infrared spectroscopy during leg exercise in patients with chronic heart failure.

The mechanisms of respiratory muscle deoxygenation during incremental leg exercise with expired gas analysis were investigated in 29 patients with chronic heart failure and 21 normal subjects. The deoxygenation and blood volume of the respiratory muscle and exercising leg muscle were assessed by near-infrared spectroscopy (NIRS). To evaluate the influence of the leg exercise on the blood volume of the respiratory muscle, 10 normal subjects also underwent a hyperventilation test with NIRS. The respiratory muscle deoxygenation point (RDP), at which oxygenated hemoglobin starts to decrease, was observed in both groups during exercise. The oxygen consumption (VO2) and the minute ventilation at the RDP in the patients was lower (p<0.01). At the same VO2, the respiratory rate was higher in patients (p<0.01). During exercise, the blood volume of the leg muscle increased, while that of the respiratory muscle decreased. During a hyperventilation test, the minute ventilation was higher than that of the RDP during exercise, the blood volume of the respiratory muscle did not decrease, and the RDP was not detectable. In conclusion, a limited ability to increase perfusion of respiratory muscles during exercise combined with the greater work of breathing results in early respiratory muscle deoxygenation in patients with chronic heart failure.

Blood Volume↗
PubMed2004

[Effect of dead space loading on ventilation, respiratory muscle and exercise performance in chronic obstructive pulmonary disease].

OBJECTIVE: To evaluate the effect of dead space (V(D)) loading on ventilation and respiratory muscle function, to test a novel measurement of oxygen consumption of respiratory muscle, and to analyze the effect of oxygen consumption of respiratory muscle on exercise performance. METHODS: Twenty-six patients with moderate chronic obstructive pulmonary disease (COPD) and 29 age-matched healthy control subjects underwent 30 W or 55 W constant work (CW) exercise in a standard protocol and under 300 ml (46 cm in length) dead space loading. Pulmonary function test (PFT) was measured pre- and post-exercise both in the dead space loading and unloading. RESULTS: The addition of 300 ml V(D) did not significantly affect FVC, FEV(1), and FEV(1)/FVC in both COPD patients and the healthy controls at rest or after CW exercise. The values of FVC, FEV(1), and FEV(1)/FVC with V(D) loading in COPD were (3.03 +/- 0.15) L, (1.95 +/- 0.09) L and (64.9 +/- 2.5)%, respectively; after 55 W CW exercise, those values were (3.03 +/- 0.18) L, (2.00 +/- 0.13) L, and (66.3 +/- 3.2)%, respectively (P > 0.05). Minute ventilation (V.(E)) and oxygen uptake (V.O(2)) significantly went up with V(D) loading and dropped with unloading at rest and during exercise in every subject. The enhancement of V.O(2) under V(D) loading (DeltaV.O(2)) was not significantly different between COPD and the control at rest or during lower intensity CW (30 W) exercise. However, DeltaV.O(2) was significantly higher in COPD than in the control during moderate intensity CW (55 W) exercise [(272 +/- 24) ml/min vs (194 +/- 19) ml/min, P < 0.05]. CONCLUSIONS: Lengthening respiratory tube to 46 cm (300 ml dead space) combined with moderate constant work exercise does not worsen the airflow obstructive in COPD,or results in respiratory muscle fatigue both in the COPD patients and the healthy controls. The enhancement of V.O(2) under V(D) loading can be considered as oxygen consumption of respiratory muscle working for increased ventilation. An advantage of oxygen consumption in respiratory muscle during moderate intensity exercise in COPD implies that maintaining the balance of oxygen supplying to both respiratory and limb muscles might be the key point in performing moderate to heavy exercise.

Adult↗
PubMed1996

[Acute effect of lorazepam on respiratory muscles in stable patients with chronic obstructive pulmonary disease].

Benzodiazepines are known to cause muscle hypotonia, but their effects on respiratory muscle function, particularly on diaphragm, have not yet been studied. Our aim was to look for any effect of lorazepam on respiratory muscle function in patients with chronic obstructive pulmonary disease (COPD). Nine stable COPD patients (mean +/- SD forced expiratory volume in one second (FEV1) 0.91 +/- 0.31 l) were included in the study. The following measurements were performed before and 1 hour after lorazepam administration (doses: 1.5 to 2 mg) by sublingual route: forced vital capacity (FVC), FEV1, maximal voluntary ventilation (MVV), arterial oxygen tension (PaO2), arterial carbon dioxide tension (PaCO2), minute ventilation (Ve), tidal volume (Vt), respiratory rate (f), inspiratory time/inspiratory plus expiratory time (Ti/Ttot)-, mean inspiratory flow (Vi), maximal inspiratory (MIP) and expiratory (MEP) pressures, maximal pleural pressure (Pplmax), transdiaphragmatic pressures (Pdi) and skeletal muscle strength and endurance. As expected, no change was noted in FVC, FEV1, FEV1/FVC (Table-1). Besides stability of expiratory flows, this denotes no change in collaboration in spite of the sedative effects of lorazepam. There was a 20% decrease in Ve, due to a Vt reduction and a small increase in PaCO2. These could be explained by the central effects of benzodiazepines. Skeletal muscle strength and endurance decreased significantly (22 and 50% respectively-Table 2), in accordance with the previously reported muscular actions of this pharmacological group. Respiratory muscle function parameters, MIP, MEP, MVV and Ppl showed significant reductions (10 to 20 per cent), as was the case with diaphragmatic function measured by Pdi (Muller maneuver with abdominal protrussion and maximal open-glottis expulsive maneuver) (Table 3). This study demonstrates that a single lorazepam dose reduces strength and endurance of respiratory muscle in chronic stable COPD patients.

Female↗
PubMed1986

Intermittent positive pressure breathing in patients with respiratory muscle weakness. Alterations in total respiratory system compliance.

Intermittent positive pressure ventilation (IPPB) is reported to improve lung compliance and decrease the work of breathing in subjects with kyphoscoliosis. These results suggest that IPPB may improve chest wall and lung compliance in patients with neuromuscular disease. We studied the short-term effects of IPPB on total respiratory system compliance in 14 subjects with neuromuscular disease. Seven were quadriplegics, and seven had muscular dystrophy. Vital capacity was reduced to 38 +/- 14 percent of the predicted normal values. Baseline measurements of total respiratory system compliance were 57 +/- 18 percent when compared to normal control values. After a 20 minute treatment of IPPB delivered with inspiratory pressures of 20 to 25 cm H2O that more than tripled resting tidal volume, there was no significant change in total respiratory system compliance in either group of patients. These findings indicate that patients with quadriplegia or muscular dystrophy do not derive immediate improvement in ventilatory mechanics from IPPB treatments.

Adolescent↗
PubMed1996

Mechanical significance of respiratory muscle activity in humans during halothane anesthesia.

BACKGROUND: Prior human studies have shown that halothane attenuates activity in the parasternal intercostal muscle and enhances phasic activity in respiratory muscles with expiratory actions. This expiratory muscle activity could contribute to reductions in the functional residual capacity produced by anesthesia. Termination of this activity could contribute to the maintenance of inspiratory rib cage expansion. The purpose of this study was to estimate in humans the mechanical significance of expiratory muscle activity during halothane anesthesia and to search for the presence of scalene muscle activity during halothane anesthesia that might contribute to inspiratory rib cage expansion. METHODS: Six subjects (3 males, 3 females) were studied while awake and during 1.2 MAC halothane anesthesia, both during quiet breathing and during carbon dioxide rebreathing. Respiratory muscle activity was measured using fine-wire electromyography electrodes. Chest wall configuration was determined using images of the thorax obtained by three-dimensional, fast computed tomography and respiratory impedance plethysmography. Functional residual capacity was measured by a nitrogen dilution technique. Measurements were obtained after paralysis with 0.1 mg/kg vecuronium and mechanical ventilation. RESULTS: Phasic inspiratory activity was present in the scalene muscle of four anesthetized subjects during quiet breathing and all anesthetized subjects during rebreathing. Phasic inspiratory activity was present in the parasternal intercostal muscle during halothane anesthesia in only the three female subjects and was enhanced by rebreathing; parasternal intercostal muscle activity was never present in anesthetized males. During anesthesia with quiet breathing, phasic expiratory activity was observed in the transversus abdominis muscles of only the three male subjects. Despite these differences in the pattern of respiratory muscle use, the pattern of chest wall responses to rebreathing was similar between males and females. When expiratory muscle activity was present, paralysis increased the end-expiratory thoracic volume by expanding the rib cage, demonstrating that this activity reduced thoracic volume in these subjects. Changes in thoracic blood volume were significant determinants of the change in functional residual capacity produced by paralysis. CONCLUSIONS: In humans anesthetized with 1.2 MAC end-tidal halothane, there are marked interindividual differences in respiratory muscle use during quiet breathing that may be related to sex; phasic inspiratory scalene muscle and parasternal intercostal muscle activity may contribute to inspiratory rib cage expansion in some subjects; and when present, expiratory muscle activity significantly constricts the rib cage and contributes to reductions in functional residual capacity caused by halothane anesthesia.

Adult↗
PubMed1994

[Postoperative pulmonary complications in patients undergoing thoracic surgery with special reference to preoperative respiratory muscle strength and nutrition].

Postoperative pulmonary complications in patients undergoing thoracic surgery were examined along with their preoperative respiratory muscle strength and nutrition. Respiratory muscle strength was assessed by maximum inspiratory (MIP) and expiratory (MEP) pressures. Nutrition was assessed by serum levels of albumin and total cholesterol. The examined cases include 51 cases of lung tumors, 8 cases of mediastinal tumors, 9 cases of empyema, 3 cases of esophageal cancer, 2 cases of chest wall tumors, and 2 cases of giant bulla. Preoperative respiratory muscle training increased both MIP and MEP significantly (p < 0.01). Thirteen patients who had postoperative pulmonary complications had significantly lower values (p < 0.01), and did not show significant increases in either MIP or MEP even after training. The cases which experienced complications also showed significantly lower preoperative serum levels of albumin and total cholesterol (p < 0.01). Therefore, patients with respiratory muscle weakness and poor nutrition have a higher risk of postoperative pulmonary complications.

Adult↗
PubMed1999

Respiratory muscle strength in Cushing's syndrome.

The effect of Cushing's syndrome on respiratory muscle strength is unknown. Therefore, we studied 10 consecutive patients with severe Cushing's syndrome. The respiratory muscles were assessed using maximal inspiratory and expiratory mouth pressures (MIP, MEP), maximal sniff transdiaphragmatic pressures (max sniff Pdi), and maximal sniff esophageal pressures (max sniff Pes). Maximal quadricep strength was also assessed. The patients demonstrated an overall mean MIP 92 cm H(2)O, SD 19 (mean 105% of predicted; SD, 23%), mean MEP 134 cm H(2)O, SD 35 (mean 99% of predicted; SD, 25%), mean max sniff Pdi 107 cm H(2)O, SD 12 (mean 78% of predicted; SD, 10%) and mean max sniff Pes of 92 cm H(2)O, SD 11 (mean 92% of predicted; SD, 11%). Quadriceps muscle strength was reduced in all 10 patients: mean 26 kg, SD 9 (mean 49% of predicted strength, SD 21%). Respiratory muscle weakness was not found, despite the presence of severe quadriceps impairment. We conclude that major weakness of the respiratory muscles is not usual in Cushing's syndrome.

Adult↗
PubMed1982

The sensation of respiratory muscle force.

The sensation of respiratory muscle force was examined in 8 normal subjects using the direct scaling method of magnitude production. At the end of a normal expiration, at functional residual capacity (FRC), subjects generated an inspiratory effort against a closed airway to produce a force that correspond to specific numerical values for sensation magnitude. Thereafter, at lung volumes of 2 L above FRC and 1 L below FRC, subjects attempted to reproduce the same force as that previously generated at FRC. Diaphragm electromyographic activity, recorded with an esophageal electrode, was used as a measure of central respiratory motor output. The difference between the mouth pressure during relaxation against a closed shutter and the peak airway pressure during the static inspiratory maneuver (Pmus) was employed as an index of muscle tension. The exponent for the magnitude production of force during maneuvers at FRC, i.e., the slope of the line relating log airway pressure and log sensation magnitude was 1.60 +/- SE 0.15. The exponent for force scaling was 1.47 +/- SE 0.17 after correcting for differences in inspiratory duration during maneuvers of different force. During inspiratory maneuvers at FRC plus 2 L, diaphragm EMG was 441 +/- SE 70%, but Pmus was 111 +/- SE 11% of the respective values during subjectively equal efforts at FRC. During inspiratory maneuvers at FRC minus 1 L, diaphragm EMG was 54 +/- SE 5%, but Pmus was 94 +/- SE 4% of the respective values during efforts at FRC perceived to be of equal force. These results suggest that the sensation of respiratory muscle force depends primarily on signals related to the tension generated by the contracting muscles rather than on the sensation of innervation associated with the central nervous system motor command.

Adult↗
PubMed1984

Reversible hypercapnic respiratory insufficiency in scleroderma caused by respiratory muscle weakness.

A patient with scleroderma presented with hypercapnic respiratory failure. Evaluation of pulmonary mechanics revealed severe restriction caused in part by respiratory muscle weakness. Treatment with prednisone corrected hypoventilation, improved symptoms, increased lung volumes, returned respiratory muscle strength to normal range, but did not change the degree of lung stiffness. This case demonstrates that restrictive patterns in scleroderma can be due to either lung or chest wall disease and that the latter may be reversible. If respiratory muscle weakness is present with restrictive ventilatory patterns in patients with scleroderma, a therapeutic trial of corticosteroid is warranted.

Humans↗
PubMedDate not supplied

Typology of the respiratory muscles in normal men and in patients with moderate chronic respiratory diseases.

Histochemical muscle fibre composition was studied in biopsies from the diaphragm, the external and internal intercostal muscles in the fifth intercostal space and horizontal and vertical parts of the serratus in 8 subjects with normal lung function and in 18 patients with abnormal lung function (6 restrictive and 12 obstructive). Muscle fibres were classified as type I (slow twitch) or type II (fast twitch) on the basis of their myofibrillar ATPase pH lability. All the muscles studied showed a mosaic pattern with the two fibre types. In every respiratory muscle, the percentage of type I fibres was higher than 50%. There was no significant difference between the three groups (normal, restrictive and obstructive) for each of the six muscles studied. The fibre diameters were similar for all types and muscles (range of means: 41-63 micron), except for the diaphragm in which the diameters of type I and type II fibres were significantly higher in the normal subjects as compared to the obstructive and restrictive patients. Moreover, there was a significant linear correlation between the diameter of the diaphragmatic fibres and vital capacity and FEV1. A low "atrophy factor" was found for each muscle studied with a large intra-individual variation. The results support the idea that the increased respiratory loading due to disease do not hypertrophy the respiratory muscles and suggest that the effect of the disease on the respiratory muscles is more related to the increased mechanical impedance of the respiratory system rather than to the changes in thoracic configuration.

Adenosine Triphosphatases↗
PubMed1994

Respiratory muscles during ventilatory support.

Knowledge of the fate and behaviour of the respiratory muscles during ventilatory support is important for the guidance of clinical care. Full support facilitates muscle metabolic repletion, but exposes them to the risk of disuse atrophy. The effect of partial support varies according to the selected mode: assisted mechanical ventilation (AMV) and synchronized intermittent mechanical ventilation (SIMV) result in much less respiratory muscle rest than generally anticipated. On the other hand, inspiratory pressure support (IPS) is able to rest the respiratory muscles and to prevent fatiguing contractions. Opposite interventions have been proposed in case of difficult weaning: either to unload the respiratory muscles by using partial support, or to overload them according to a training programme. The optimal strategy is not known and may combine both approaches.

Humans↗
PubMed1999

[Respiratory muscle force and resistance in patients with SAHS. The effect of using nighttime CPAP].

UNLABELLED: During nighttime episodes of obstructive apnea in patients with sleep apnea-hypopnea syndrome (SAHS), repeated and progressive inspiratory efforts are made. Such intense nighttime activity can have a deleterious effect on daytime function of respiratory muscles. OBJECTIVE: The objective of this study was to evaluate daytime respiratory muscle function in a group of SAHS patients before and after two months of treatment with nighttime continuous positive airway pressure (CPAP). METHODS: We enrolled 12 patients with SAHS and 10 normal subjects (control group). To evaluate respiratory muscle strength we measured maximum esophageal pressure (Pesmax), transdiaphragmatic pressure (Pdimax) and inspiratory pressure in the mouth (PM). Respiratory muscle resistance was assessed using peak pressure in the mouth (PMPeak), time of tolerance (Tlim) and maximum inspiratory pressure-time index (PTimax). We also analyzed the nighttime function of respiratory muscles during apneic episodes in 10 of the 12 SAHS patients. We propose and define an index of nighttime respiratory muscle activity (RMian) as the product of the tension-time index for the diaphragm observed at the end of nighttime apneic episodes (TTdiapnea) and the apnea-hypopnea index (AHI). RESULTS: Respiratory muscle strength was similar in the two groups and no changes were observed in SAHS patients after treatment with nighttime CPAP. However, tolerance was lower in SAHS patients (PMpeak--30%, Tlim--31% and PTimax--49%). Two months of nighttime CPAP normalized all three variables in these patients. MRian was related to percent improvement in PMpeak after treatment with nighttime CPAP in SAHS patients (r = 0.66, p < 0.04). CONCLUSION: SAHS has an adverse effect on the daytime endurance of respiratory muscles that is proportional to the increase of nighttime mechanical muscle activity. The application of nighttime CPAP is restorative, probably because it allows respiratory muscles to rest.

Adult↗
PubMed2004

Endurance training of respiratory muscles improves cycling performance in fit young cyclists.

BACKGROUND: Whether or not isolated endurance training of the respiratory muscles improves whole-body endurance exercise performance is controversial, with some studies reporting enhancements of 50% or more, and others reporting no change. Twenty fit (VO2 max 56.0 ml/kg/min), experienced cyclists were randomly assigned to three groups. The experimental group (n = 10) trained their respiratory muscles via 20, 45 min sessions of hyperpnea. The placebo group (n = 4) underwent "sham" training (20, 5 min sessions), and the control group (n = 6) did no training. RESULTS: After training, the experimental group increased their respiratory muscle endurance capacity by 12%. Performance on a bicycle time trial test designed to last about 40 min improved by 4.7% (9 of 10 subjects showed improvement). There were no test-re-test improvements in either respiratory muscle or bicycle exercise endurance performance in the placebo group, nor in the control group. After training, the experimental group had significantly higher ventilatory output and VO2, and lower PCO2, during constant work-rate exercise; the placebo and control groups did not show these changes. The perceived respiratory effort was unchanged in spite of the higher ventilation rate after training. CONCLUSIONS: The results suggest that respiratory muscle endurance training improves cycling performance in fit, experienced cyclists. The relative hyperventilation with no change in respiratory effort sensations suggest that respiratory muscle training allows subjects to tolerate the higher exercise ventilatory response without more dyspnea. Whether or not this can explain the enhanced performance is unknown.

Adolescent↗
PubMed1997

Hyperinflation and respiratory muscle interaction.

Hyperinflation clearly affects respiratory muscle interaction. It commonly increases the rib cage contribution to chest wall motion, whilst it reduces the abdominal contribution. This change is thought to result from the fact that hyperinflation severely reduces the mechanical advantage of the diaphragm, whilst it affects the mechanical advantage of the neck and rib cage muscles to a lesser extent. The mechanical disadvantage in the diaphragm induced by hyperinflation is presumably primarily the result of the length changes undergone by the diaphragm in acute hyperinflation. Changes in diaphragmatic geometry are generally considered to be less important in the reduction of the diaphragm's force-generating capacity. Further factors contributing to the mechanical disadvantage in the diaphragm include a reduction in the appositional component of diaphragmatic action (through reduction in the zone of apposition), and a reduction in the insertional component (through a shift in the alignment of the diaphragmatic fibres from axial to radial). In chronic hyperinflation, the diaphragm adapts to the chronically hyperinflated state. This adaptation to chronic foreshortening is similar to the adaptation occurring in the skeletal muscle. It is caused by a dropout of sarcomeres in series along the muscle fibres. It restores the force-generating capacity of the muscle, in part, but it reduces the capacity of the muscle to undergo length changes. The mechanical advantage of the parasternal intercostals and the scalenes is possibly less affected, because the length changes undergone by these muscles during hyperinflation are smaller. The factors determining the mechanical advantage of the parasternal intercostals are complex. Variables related to the mechanical advantage of the parasternal intercostals include: length changes; changes in angle between the parasternal intercostals and the sternum and between rib and sternum; and changes in mechanical arrangement among different parasternals. At present, it is difficult to develop an integrated view of these factors and of their change with hyperinflation. Finally, hyperinflation commonly results in recruitment of expiratory muscles. The functional significance of this expiratory muscle recruitment in patients is still debated.

Diaphragm↗