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At least 253 records · Page 14Linked to original sources

PubMed2002

Effect of posture on oxygenation and respiratory muscle strength in convalescent infants.

OBJECTIVE: To determine if differences in respiratory muscle strength could explain any posture related effects on oxygenation in convalescent neonates. METHODS: Infants were examined in three postures: supine, supine with head up tilt of 45 degrees, and prone. A subsequent study was performed to determine the influence of head position in the supine posture. In each posture/head position, oxygen saturation (SaO2) was determined and respiratory muscle strength assessed by measurement of the maximum inspiratory pressure (PIMAX). PATIENTS: Twenty infants, median gestational age 34.5 weeks (range 25-43), and 10 infants, median gestational age 33 weeks (range 30-36), were entered into the first and second study respectively. RESULTS: Oxygenation was higher in the prone and supine with 45 degrees head up tilt postures than in the supine posture (p<0.001), whereas PIMAX was higher in the supine and supine with head up tilt of 45 degrees postures than in the prone posture (p<0.001). Head position did not influence the effect of posture on PIMAX or oxygenation. CONCLUSION: Superior oxygenation in the prone posture in convalescent infants was not explained by greater respiratory muscle strength, as this was superior in the supine posture.

Female↗

PubMed1991

Respiratory muscle recruitment in awake ponies during exercise and CO2 inhalation.

We measured respiratory muscle electromyograms (EMG), inspiratory (I) and expiratory (E) airflow patterns and functional residual capacity (FRC) in six ponies at rest, during treadmill walking at 1.8 mph-5, 10, and 15% grades, and during 2, 4, and 6% CO2 inhalation. There were several similarities in the responses to exercise and CO2 inhalation. The shapes of the I and E flow patterns were not changed appreciably from the respective control patterns during either condition. Mean diaphragm EMG increased from control (P less than 0.05) at 1.8 mph-10 and 15% grades, and during 4 and 6% inhalation. However, mean transversus abdominis EMG did not change significantly from control (P greater than 0.10) during either condition. Exercise did not have an effect (P greater than 0.05) on FRC, and there was only a slight (P less than 0.05) increase in FRC (100 ml or 2%) during 6% CO2 inhalation. Based on the fact that we did not find major differences between exercise and CO2 inhalation in mean diaphragm and transversus abdominis EMG, I and E flow patterns, and FRC we conclude that factor(s) other than the ventilatory stimulus and the non-ventilatory functions of the respiratory muscles are important determinants of the pony's respiratory muscle recruitment pattern under these conditions.

Animals↗

PubMed1994

Respiratory muscle function in patients with asbestos-related pleural disease.

The effect of asbestos-related pleural disease (ARPD) on the generation of maximum respiratory pressure was investigated in 11 male patients with ARPD mean age 57 years, range 45-74, and mean duration of asbestos exposure of 9.9 years, range 5-16. There were three smokers, seven ex-smokers and one non-smoker. Breathlessness ranged from grade 1-3 on the MRC score. The extent of pleural disease was calculated using a score based on the ILO score for pleural disease. Full respiratory function tests, global respiratory muscle strength and diaphragmatic strength were assessed. Respiratory muscle strength, including diaphragm strength, was normal. Recoil pressure was high or at the upper limit of normal in four patients and correlated with chest radiograph score for pleural disease (r = 0.65, P < 0.02). There was no difference in either global respiratory muscle or diaphragmatic strength between patients with and without involvement of one or both costophrenic angles or between patients with mild or severe breathlessness. We conclude that respiratory muscle strength is not importantly reduced in ARPD, and it is unlikely that weakness contributes to breathlessness in these patients. By contrast reduced chest wall compliance is likely to be an important factor in breathlessness in some cases.

Aged↗

PubMed1994

Corticosteroid-induced myopathy of the respiratory muscles.

Corticosteroids may cause myopathy of both skeletal and respiratory muscles. This is of specific clinical importance in patients with chronic obstructive pulmonary disease (COPD), who already have impaired respiratory muscle function. After treatment with fluorinated steroids, side-effects occur more frequently and are worse compared to treatment with non-fluorinated steroids. Acute myopathy and atrophy are caused by short-term high-dose corticosteroid administration, resulting in rhabdomyolysis, diffuse muscle weakness and severe dyspnoea. In contrast, chronic myopathy occurs after prolonged treatment with corticosteroids, and results in proximal muscle weakness and type IIb fibre atrophy. The pathophysiology of steroid myopathy is unknown, but reduction in protein synthesis and increased glycogen accumulation may play a major role. Animal models have demonstrated weakening of the diaphragm and a decrease in body and diaphragm mass after corticosteroid administration. In humans, a reduction in respiratory and peripheral muscle strength, an elevation of urinary creatine excretion and selective type IIb fibre atrophy may be observed. Treatment of corticosteroid-induced myopathy consists of tapering the dose of steroids or switching to non-fluorinated steroids.

Adrenal Cortex Hormones↗

PubMed1991

Improved respiratory muscle endurance of highly trained cyclists and the effects on maximal exercise performance.

Insufficient respiratory muscle endurance (RME) may be one of the factors limiting ventilation during peak athletic performance. Our purpose was to determine whether the RME of highly trained cyclists could be enhanced and if so, to determine the effects of improved RME on their maximal exercise performance. Ten male cyclists (maximal oxygen consumption (VO2max) greater than 60 ml/kg-1) began the study by performing 3 tests. These were VO2max, RME measured as maximal sustainable ventilatory capacity (MSVC) and maximal exercise endurance (tlim) measured by an endurance cycling test to exhaustion at 90% of their maximal power output. Five subjects then completed 4 weeks of isocapnic hyperpnea training (16 session) and 5 subjects were controls. Following this training interval, each subject repeated the initial tests. After the RME training, the MSVC increased from 155 +/- 11 to 174 +/- 12 l/min (p = 0.004) for the training subjects while there was no change in the controls (155 +/- 26 and 150 +/- 34 l/min). There were no changes for any of the 10 subjects in either the maximal exercise performance (VO2max = 66.1 +/- 4.7 to 66.5 +/- 4.8 ml.kg-1) or the maximal exercise endurance (tlim = 335 +/- 79 to 385 +/- 158 sec). In conclusion, 4 weeks of respiratory muscle endurance training increased respiratory muscle endurance but had no effect on the maximal cycling performance of highly trained cyclists.

Adult↗

PubMed1994

Respiratory muscle compensation for unilateral or bilateral hemidiaphragm paralysis in awake canines.

In humans and some animals, the surviving respiratory muscles are able to compensate fully for unilateral, and partially for bilateral, hemidiaphragm paralysis. To examine differential activity of individual respiratory muscles after unilateral or bilateral diaphragm paralysis, length and electromyogram (EMG) of left costal and crural diaphragm segments, parasternal intercostal, and transversus abdominis were measured directly in five awake canines after implantation with sonomicrometry transducers and bipolar EMG electrodes under three conditions: during normal breathing (NOFRZ), after infusion of local anesthetic (bupivacaine) through a cervical phrenic nerve cuff to induce reversible contralateral hemidiaphragm (CNFRZ), and after bilateral diaphragm (BIFRZ) paralysis. From NOFRZ to CNFRZ, costal, crural, parasternal, and transversus abdominis increased shortening and EMG activity to compensate for contralateral diaphragm paralysis, but the increase in activity was not equivalent for each muscle. With BIFRZ, parasternal and transversus abdominis showed further increases in activity, coordinated between both inspiration and expiration. Normalized intrabreath profiles revealed dynamic differences in development of muscle activity within each breath as paralysis worsened. Review of simultaneous muscle activities showed coordinated interactions among the compensating muscles: passive shortening of transversus, and lengthening of costal and crural, coincided with increased active inspiratory shortening of parasternal. We conclude that an integrated strategy of respiratory muscle compensation for unilateral or bilateral diaphragm paralysis occurs among chest wall, abdominal, and diaphragm segmental muscles, with relative contributions of individual muscles adjusted according to the degree of diaphragm dysfunction.

Animals↗

PubMed1988

Pharmacotherapy of respiratory muscles.

This article assesses the role of pharmacotherapy in the management of respiratory muscle dysfunction. It focuses on two classes of drugs, the methylxanthines and the sympathomimetic agents. A prospective section focuses also on the particularities of the diaphragm among the skeletal striated muscles. In addition, a new approach to respiratory pharmacotherapy, which may be beneficial in patients with respiratory muscle dysfunction, is suggested.

Animals↗

PubMed1988

Similarities between behavior of respiratory muscles in breath-holding and in elastic loading.

Breath-holding subjects often exhibit involuntary contractions of respiratory muscles which are much stronger and faster than the efforts they would make during unrestricted breathing at the same level of CO2 and O2. To gain a better understanding of the genesis of these contractions, we compared them with the respiratory response to external elastic loading. Normal men rebreathed a mixture of 8% CO2 in oxygen against no load, elastic loads of 25 and 75 cm H2O/L, and held their breath, equivalent to an elastic load of 226 cm H2O/L. At iso-CO2, increasing loads led to progressively smaller tidal volumes, inspiratory flow rates and ventilation. However, respiratory muscles were progressively activated by the loads, as indicated by increasing occlusion pressure, so that inspiratory flow rate and ventilation were defended much better than could be expected if no neural compensation occurred. The pattern of respiratory muscle activity in breath-holding was qualitatively similar to that in elastic loading, and seemed quantitatively to be an extreme form of reaction to a large load. The reduction in inspiratory time and therefore of peak inspiratory pressure and ratio of inspiratory to total time with very large loads could be viewed as an adaptive response to limit respiratory muscle fatigue.

Adult↗

PubMed1981

Contractile function and fatigue of the respiratory muscles in man.

Ventilation depends on the proper functioning of the respiratory muscles. These muscles, like other skeletal muscles, can endure high work loads for only short time periods. The work of breathing in patients with lung disease in increased and it has therefore been argued that respiratory muscle fatigue may develop and contribute to respiratory failure. We have studied the contractile function and fatigue of the sternomastoid muscle and the diaphragm in normal subjects and found that these respiratory muscles have the same contractile properties as limb muscles. If subjected to a high load they develop similar patterns of fatigue. Studies on the sternomastoid muscle in patients with lung disease also confirmed that respiratory stress produces fatigue.

Action Potentials↗

PubMed1990

[Chronic kidney insufficiency and respiratory muscle function. Changes induced by treatment with 1,25(OH)2D3].

A myopathy basically involving proximal respiratory muscles can develop in uremia. To evaluate respiratory muscle force in uremia, maximal inspiratory pressure (MIP) was measured in 27 patients with renal failure. MIP was very limited in patients with a creatinine clearance (Crc) lower than 10/ml/min 1.73 m2 not treated with hemodialysis (HD) and in patients on HD who were not treated with 1.25 (OH)2D3 (45 +/- 9 and 43 +/- 5 cm H2O, respectively), moderately reduced in patients on HD treated with 1.25 (OH)2D3 (58 +/- 5 cmH2O) and normal in patients with Crc higher than 10 ml/min 1.73 m2 (86 +/- 6 cmH2O). The treatment with 1.25 (OH)2D3 during 3 months promoted a significant increase in MIP and serum calcium level and a reduction in parathyroid hormone in patients with Crc lower than 10 ml/min. It was concluded that, in uremia, a respiratory muscle weakness partially reversible with vitamin D therapy may be found.

Adult↗

PubMed1984

Respiratory muscle function in health.

Normally both quiet breathing and augmented ventilation during physical exercise are sustained by the inspiratory muscles around the chest wall. Among these, the diaphragm is most important. The inspiratory muscles of the upper airways must also contract to permit inspiration to occur. The expiratory muscles of the chest wall and abdomen do not normally participate in breathing per se, but are critically important for coughing. The strength of respiratory muscle contraction, as estimated from maximum static inspiratory and expiratory pressures, depends on neural drive, the length at which the muscles contract, and the velocity with which they shorten during contraction. The intrinsic strength of the respiratory muscles also depends on whether they are hypertrophied, or atrophied consequent to weight loss. As a result of the structural and biochemical properties of their muscle fibers and their blood supply, normal respiratory muscles have a high level of endurance. However, even well-trained normal subjects may develop inspiratory muscle fatigue if they are subjected to severe inspiratory resistive loads, hypoxia, high levels of physical exercise at normal atmospheric pressure, or work under hyperbaric conditions. The respiratory muscles of normal subjects respond to training. Strength training regimens enhance respiratory muscle but not ventilatory endurance, and vice versa.(ABSTRACT TRUNCATED AT 250 WORDS)

Body Weight↗

PubMed1985

Respiratory muscle and organ blood flow with inspiratory elastic loading and shock.

Since respiratory muscles fail when blood flow is inadequate, we asked whether their blood flow would be maintained in severe hypotensive states at the expense of other vital organs (brain, heart, kidney, gut, spleen). We measured blood flow (radiolabeled microspheres) to respiratory muscles and vital organs in 11 dogs breathing against an inspiratory elastic load, first with normal blood pressure (BP) and then hypotension produced by cardiac tamponade. With the elastic load alone, there was no change in BP or cardiac output; diaphragmatic blood flow (Qdi) increased from 12.8 +/- 7.0 to 34.1 +/- 15.6 ml/100 g, and total respiratory muscle flow (QTR) increased from 56.5 +/- 19.1 to 97.4 +/- 36.5 ml/100 g, but except for the brain, there was no change in blood flow to other organs. With tamponade (mean BP = 79 +/- 16 mmHg), flow decreased to all organs, whereas Qdi (39.0 +/- 19.4) did not change. QTR decreased, but not significantly, to 88.6 +/- 49.5. With more tamponade (mean BP = 53 +/- 13 mmHg), flow to all vital organs decreased as well as QTR (57.9 +/- 47.18), but Qdi did not significantly decrease and had the same relationship to respiratory force as with normal BP. Thus, with severe inspiratory elastic loading and severe hypotension, the diaphragm and external intercostal muscles did most of the respiratory work, and their flow was maintained at the expense of other vital organs.

Animals↗

PubMed1982

Respiratory muscle strength and maximal voluntary ventilation in undernourished patients.

To assess the effect of chronic debilitation on respiratory muscle function, we studied 16 poorly nourished (PN) patients without pulmonary disease, and 16 well-nourished (WN) subjects matched for age and sex. Body weight, vital capacity (VC), maximal voluntary ventilation (MVV), and maximal static inspiratory and expiratory pressures (PImax and PEmax) were measured and expressed as percent predicted. Respiratory muscle strength (RMS) was calculated as (% PImax + % PEmax)2. Body weight was 71% predicted in the PN group and 104% in the WN group. The RMS, MVV, and VC were 37%, 41%, and 63%, respectively, of the values in the WN group (p less than 0.001). The 60% reduction in RMS was shared almost equally among inspiratory and expiratory muscles, and PEmax was linearly related to body weight. Because malnutrition reduces both respiratory muscle strength and MVV, it may well impair respiratory muscle capacity to handle increased ventilatory loads in thoracopulmonary disease.

Adolescent↗

PubMed2003

Respiratory muscle electromyogram and mouth pressure during isometric contraction.

When extra-diaphragmatic muscles are activated progressively under approximately isometric conditions, we expect a corresponding increase in respiratory muscle output. Therefore, we examined relative recruitment shown as the latency to onset of EMG activity, and the relationship between mouth pressure and electromyogram activity of the neck accessory and transversus abdominis (TRANS) muscles during respiratory maneuvers against occlusion. Fine wire electrodes were inserted into the scalene (SCLN), sternocleidomastoid (STERNO), trapezius (TRAPZ) and TRANS in six awake, healthy subjects. Mouth pressure, raw and moving average EMG signals were recorded during gradual production of expiratory or inspiratory mouth pressure to maximum (MPmax) at FRC in the standing posture. Group mean linear regression lines of EMG activity versus mouth pressure were strongly significant for SCLN and TRANS, less for STERNO, and least for TRAPZ. The SCLN and STERNO showed EMG activities with low, and TRAPZ showed EMG activity only with high, mouth pressure. At 90% MPmax, TRAPZ was much less active compared with TRANS, SCLN, or STERNO. These results suggest that over a wide range of respiratory effort there is a significant difference in the relationship between mouth pressure and EMG activity in the accessory muscles, with differential recruitment of individual respiratory muscles.

Adult↗

PubMed1994

Control of breathing and respiratory muscle strength in patients with multiple sclerosis.

In 11 patients with moderately severe multiple sclerosis, lasting 11.2 +/- 7.3 years, in stable condition, and in 10 age- and sex-matched control subjects, we investigated lung function, respiratory muscle strength, and ventilatory control system. Respiratory muscle strength was assessed by measuring maximal inspiratory and expiratory mouth pressures (Pimax and Pemax, respectively). Respiratory central drive was evaluated in terms of neuromuscular (P0.1) and ventilatory (Ve) output, breathing room air and during CO2 rebreathing. In the absence of any significant impairment of lung function, patients showed a reduction of Pimax and Pemax amounting to about 40 percent and 60 percent of the predicted value at functional residual capacity (FRC), respectively; a significant, inverse correlation was found between both Pimax and Pemax at FRC and the severity score of the disease. While at rest Ve was similar to that of control subjects, baseline P0.1 was significantly higher in patients (1.97 +/- 0.79 vs 0.97 +/- 0.20 cm H2O, p < 0.005). Compared with the control group, during CO2 rebreathing P0.1/PetCO2 slope, although less steep, was not dissimilar in patients (0.34 +/- 0.13 vs 0.46 +/- 0.19 cm H2O/mm Hg, NS); on the other hand, Ve/PetCO2 slope was much lower in the patient group (1.93 +/- 0.91 vs 3.27 +/- 1.11 L/min/mm Hg, p < 0.01) and was significantly related to the functional stage of disease and to Pimax and Pemax values at FRC. These results indicate that in patients with clinically stable, moderately severe multiple sclerosis, the respiratory muscle function is abnormal. Moreover, the inspiratory drive at rest is increased and the drive response to CO2 appears normal, while the ventilatory response to CO2 is significantly impaired. Respiratory muscle weakness (and/or lack of coordination) could explain, at least in part, the lower ventilatory response in these patients, whereas the mechanism of increased rate of the initial inspiratory force generation remains unclear.

Adult↗

PubMed1997

The role of respiratory muscles in the impairment of the respiratory system function in the workers of a chemical plant division producing pesticides.

Workers of a chemical plant department producing dust and liquid pesticides (37 males and 17 females) exposed to dust containing free silica, organic solvents and active substances, among others: organophosphate compounds, pyrethroids, triazines, carbamates and dithiocarbamates, 2,4-D, captan, carboxine, carbendazim and dodine were studied. Spirometric investigations, including evaluation of vital capacity (VC), 1 second forced expiratory volume (FEV1) and its percentage index (FEV1%VC), peak expiratory flow and maximal end-expiratory flow (MEF25), were performed directly at the workplace. At the same time mouth inspiratory pressures (MIP) and maximal expiratory pressures (MEP) were evaluated. Chronic bronchitis (according to BMRC questionnaire) was diagnosed in every second worker, and in 11 males and females obstructive impairment of pulmonary function was established; 41% of females and 27% of males were found to have diminished peak expiratory flow. Maximal inspiratory pressures were significantly lower both in the studies males (p < 0.001) and females (p < 0.02) than those in the control groups and amounted to 74.4 +/- 21.5 and 58.1 +/- 24.3 cm H2O, respectively. Maximal expiratory pressures were also significantly lower in the studied males (p < 0.001) and females (p < 0.05) and amounted to 116.6 +/- 28.4 and 74.5 +/- 17.9 cm H2O, respectively. Significant correlation between decreased PEF and the force of expiratory muscles-MEP (In males r = 0.3279, p < 0.05; In females r = 0.7049, p < 0.01) was founded. The investigations performed at the workplace allow the assumption that work at the production of pesticides may result in impairment of pulmonary ventilation, development of chronic bronchitis as well as impaired function of respiratory muscles.

Adult↗

PubMed2000

Effect of digoxin on global respiratory muscle strength after cholecystectomy: a double blind study.

BACKGROUND: Upper abdominal surgery has been shown to impair the function of the respiratory muscles. In addition, controversial results have been reported concerning the effect of digoxin on the diaphragm. The aim of this study was to investigate further the mechanism(s) of respiratory muscle dysfunction after cholecystectomy and the effect of digoxin on the impaired respiratory muscle function. METHODS: Twenty three patients (four men) were studied before and 48 hours after surgery. Eleven received digoxin and 12 placebo. Respiratory muscle strength was assessed 48 hours after surgery by measuring mouth pressure during maximum static inspiratory (PImax) and expiratory (PEmax) efforts before and after 90 minutes of intravenous administration of 0.25 mg digoxin in a double blind, placebo controlled fashion. In addition, spirometric and pain measurements were performed. RESULTS: Postoperatively (+48 h) PImax and PEmax decreased significantly (p<0.01) from their preoperative values in both groups by a similar degree. After administration of digoxin or placebo only the digoxin group showed a significant increase in both PImax (p<0.02) and PEmax (p<0.05) with a mean increase of 15% for PImax and 12.3% for PEmax. The mean difference in PImax (DeltaPImax) and PEmax (DeltaPEmax) between the digoxin and placebo groups was 1.01 (95% CI 0.28 to 2.2) and 1.05 (95% CI 0.04 to 2.4), respectively. Estimates of postoperative pain did not differ between the two groups. Spirometric indices showed a similar restrictive defect postoperatively in both groups but did not change after digoxin or placebo. CONCLUSION: Digoxin improves the impaired global strength of the inspiratory and expiratory muscles after cholecystectomy and this may be clinically relevant. Muscle contractility could play a part in this impairment.

Adult↗

PubMed2006

Exercise performance improves in patients with COPD due to respiratory muscle endurance training.

BACKGROUND: Impaired exercise tolerance is frequently observed in patients with COPD. Respiratory muscle endurance training (RMET) by means of normocapnic hyperpnea can be used to improve respiratory muscle function and probably exercise capacity. RMET is not applied on a large scale because complicated equipment is needed to maintain carbon dioxide homeostasis during hyperpnea, which can also be done by enlarging the dead space of the ventilatory system by breathing through a tube. Therefore, tube breathing might be a new, inexpensive method for home-based RMET. The aim of this study was to assess whether home-based RMET by means of tube breathing improves endurance exercise performance in patients with COPD. METHODS: We randomized 36 patients with moderate-to-severe COPD to RMET by paced tube breathing (n = 18) or sham training (control, n = 18). Both groups trained twice daily for 15 min, 7 days per week, for 5 weeks. RESULTS: Patients receiving RMET showed significant improvements in endurance exercise capacity (constant-load exercise on cycle ergometry; 18 min vs 28 min, p < 0.001), in perception of dyspnea (Borg score; 8.4 vs 5.4, p < 0.001), and respiratory muscle endurance capacity (sustainable inspiratory pressure; 25 cm H(2)O vs 31 cm H(2)O, p = 0.005). Quality of life (chronic respiratory disease questionnaire) also improved (78.7 to 86.6, p = 0.001). The control group showed no significant changes. CONCLUSION: Home-based RMET by means of tube breathing leads to a significant improvement of endurance exercise capacity, a reduction in perception of dyspnea, and an improvement in quality of life in patients with moderate-to-severe COPD.

Aged↗