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PubMed1994

Hyperinflation with intrinsic PEEP and respiratory muscle blood flow.

Increased end-expiratory lung volume and intrinsic positive end-expiratory pressure (PEEP) are common in obstructive lung disease, especially during exacerbations or exercise. This loads the respiratory muscles and may also stress the circulatory system, causing a reduction or redistribution of cardiac output. We measured the blood flow to respiratory muscles and systemic organs using colored microspheres in 10 spontaneously breathing anesthetized tracheotomized dogs. Flows during baseline breathing (BL) were compared with those during hyperinflation (HI) induced by a mechanical analogue of airway closure and with those during an inspiratory resistive load (IR) that produced an equivalent increase in inspiratory work and time-integrated transdiaphragmatic pressure. Cardiac output was unchanged during IR (3.19 +/- 0.27 l/min at BL, 3.09 +/- 0.34 l/min during IR) but was reduced during HI (2.14 +/- 0.29 l/min; P < 0.01). Among the organs studied, flow was unaltered by IR but decreased to the liver and pancreas and increased to the brain during HI. For the respiratory muscles, flow to the diaphragm increased during IR. However, despite a 1.9-fold increase in inspiratory work per minute and a 2.5-fold increase in integrated transdiaphragmatic pressure during HI, blood flow to the diaphragm was unchanged and flow to the scalenes and sternomastoid fell. The only respiratory muscle to which flow increased during HI was the transversus abdominis, an expiratory muscle. We conclude that the circulatory effects of hyperinflation in this model impair inspiratory muscle perfusion and speculate that this may contribute to respiratory muscle dysfunction in hyperinflated states.

Animals↗
PubMed1984

[Changes in the respiratory muscles and their microcirculatory bed during exposure of the body to chronic hypoxia and its aftereffects].

Changes of the respiratory muscles have been studied under the effect of a rarefied atmosphere when the pressure is 560 mm Hg (2,500 m), 405 mm Hg (5,000 m), 286 mm Hg (7,500 m) and during the period of their aftereffect. The experimental group consists of 260 and the control group--of 130 white rats. Adaptation of the respiratory muscles to the effect of the rarefied atmosphere at the pressure of 560 mm Hg takes place mainly at the expense of certain functional changes of the microcirculatory bed and hypertrophy of the muscle fibers. The period of aftereffect is characterized with normalization of these phenomena. Adaptation of the respiratory muscles at the pressure of 405 mm Hg takes place at the expense of hypertrophy of the muscle fibers, small destructive changes and a complex rearrangement of the microcirulatory bed. During the period of aftereffect, by the 40th day no destructive changes are noted in the muscle tissue. The capillary bed undergoes some rearrangements by the 42d -56th day with increasing quantitative indices per area unit. This results in improvement of the muscles nutrition. In the respiratory muscles at the pressure 286 mm Hg, atrophic changes in the muscle fibers take place at certain stages of the experiment. Essential destructive changes are observed, rearrangement of the microcirculatory bed with decreasing convolution of the longitudinal capillaries and a decreasing number of the transversal capillaries are noted by the end of the experiment. During the period of aftereffect, by the 56th day, the external and internal intercostal muscles completely restore their structure, and in the diaphragm the destructive changes remain. By the same time, the microcirculatory bed becomes more rare at the expense of decreasing capillarization of the muscle fibers and a decreasing number of the transversal capillaries.

Animals↗
PubMed1997

Respiratory muscle function and control of breathing in patients with acromegaly.

Increase in lung size has been described in acromegalic patients, but data on respiratory muscle function and control of breathing are relatively scarce. Lung volumes, arterial blood gas tensions, and respiratory muscle strength and activation during chemical stimulation were investigated in a group of 10 patients with acromegaly, and compared with age- and sex-matched normal controls. Inspiratory muscle force was evaluated by measuring pleural (Ppl,sn) and transdiaphragmatic (Pdi,sn) pressures during maximal sniffs. Dynamic pleural pressure swing (Ppl,sw) was expressed both as absolute value and as percentage of Ppl,sn. Expiratory muscle force was assessed in terms of maximal expiratory pressure (MEP). In 8 of the 10 patients, ventilatory and respiratory muscle responses to hyperoxic progressive hypercapnia and to isocapnic progressive hypoxia were also evaluated. Large lungs, defined as total lung capacity (TLC) greater than predicted (above 95% confidence limits), were found in five patients. Inspiratory or expiratory muscle force was below normal limits in all but three patients. During unstimulated tidal breathing, respiratory frequency (fR) and mean inspiratory flow (tidal volume/inspiratory time (VT/tI)) were greater, while inspiratory time (tI) was shorter than in controls. Minute ventilation (V'E) and mean inspiratory flow response slopes to hypercapnia were normal In contrast, four patients had reduced delta(VT/tI)/arterial oxygen saturation (Sa,O2) and three had reduced deltaV'E/Sa,O2. Ppl,sw(%Ppl,sn) response slopes to increasing end-tidal carbon dioxide tension (PET,CO2) and decreasing Sa,O2 did not differ from the responses of the normal subjects, suggesting normal central chemoresponsiveness. At a PET,CO2 of 8 kPa or an Sa,O2 of 80%, patients had greater fR and lower tI compared with controls. Pdi,sn and Ppl,sn related both to deltaV'E/deltaSa,O2 (r=0.729 and r=0.776, respectively) and delta(VT/tI)/deltaSa,O2 (r=0.860 and r=0.90, respectively). Pdi,sn also related both to deltaV'E/deltaPET,CO2 (r=0.8) and delta(VT/tI)/deltaPET,CO2 (r=0.76). In conclusion, the data suggest the relative independence of pneumomegaly and respiratory muscle strength. Peripheral (muscular) factors appear to modulate a normal central motor output to give a more rapid pattern of breathing.

Acromegaly↗
PubMed2002

Effects of prolonged mechanical ventilation on respiratory muscle ultrastructure and mitochondrial respiration in rabbits.

OBJECTIVE: To investigate in rabbits whether prolonged mechanical ventilation (PMV) leads to ultrastructural changes in respiratory muscles and alters diaphragm mitochondrial respiration. DESIGN AND SETTING: Experimental prospective study in a university laboratory. ANIMALS AND INTERVENTIONS: We studied respiratory muscles of seven rabbits after 49+/-1 h of controlled mechanical ventilation. Ten nonventilated rabbits were used as a control group. MEASUREMENTS AND RESULTS: After mechanical ventilation electron-microscopic observations of the diaphragm and the external intercostal muscles revealed disrupted myofibrils, increased number of lipid vacuoles in the sarcoplasm, and smaller mitochondria with focal membrane disruptions. Volumetric and numerical densities of the mitochondria were significantly lower in the PMV group than the control group. Mitochondrial respiration was quantified in isolated diaphragm muscle-cell mitochondria using two respiratory substrates. There was no difference in oxygen consumption values in the three states of mitochondrial respiration between the two groups except for state 2 (basal state) with pyruvate/malate parameter (53.5+/-20 for the ventilated group vs. 33.8+/-10.2 nmol atom O/mg per minute for the control group). There was no significant difference between groups in ADP/O ratio or respiratory control ratio. CONCLUSIONS: PMV leads to respiratory muscle cell degeneration and minor changes in oxidative phosphorylation coupling in diaphragmatic mitochondria. These phenomena may mediate part of damage of respiratory muscles after inactivity related to PMV.

Animals↗
PubMed1993

Respiratory muscle acidosis stimulates endogenous opioids during inspiratory loading.

Activation of endogenous opioid pathways during intense inspiratory flow-resistive loading (IRL) results in greater inhibition of EMG activity in the external oblique (EMGeo) relative to the diaphragm (EMGdi). Dichloroacetate (DCA) abolishes opioid-mediated inhibitory influences upon these muscles, suggesting a causal relationship between respiratory muscle lactic acidosis and activation of endogenous opioid pathways, during IRL. We tested the hypothesis that a more intense acidosis of the external oblique relative to the diaphragm may be the signal that determines the differential inhibitory opioid-mediated effect upon the respiratory muscles during IRL. Unanesthetized goats were exposed to IRL (50 cm H2O/1/s) for 120 min, before and after intravenous pretreatment with DCA (50 mg/kg) or saline. We measured peak phasic EMGdi and EMGeo, and respective muscle interstitial pH (pHdi, pHeo) using flexible pH probes. After 120 min IRL with saline, pHdi, and pHeo declined by -0.12 +/- 0.03 (mean +/- SEM) and -0.20 +/- 0.04 units, respectively (p < 0.05, pHdi versus pHeo). Naloxone (NLX), 0.3 mg/kg given intravenously at this time, increased EMGdi by 26.5 +/- 6.1%, but EMGeo by 81.9 +/- 13.3% (p < 0.05, EMGdi versus EMGeo). DCA blunted both the change in pHdi and pHeo during IRL (to -0.01 +/- 0.01 and -0.08 +/- 0.03 units, respectively) (p < 0.05, DCA versus saline) and the increase in EMGdi and EMGeo with NLX (to -1.0 +/- 2.6% and 5.7 +/- 5.8%, respectively) (p < 0.05, DCA versus saline).(ABSTRACT TRUNCATED AT 250 WORDS)

Acidosis, Lactic↗
PubMed1996

Adaptive strategies of respiratory muscles in response to endurance exercise.

The purpose of this review is to discuss the adaptive strategies of mammalian respiratory muscles in response to whole-body endurance exercise training. It is now clear that endurance training results in small (i.e., 20-30%) but significant increases in mitochondrial enzyme activity and the activities of key antioxidant enzymes (i.e., superoxide dismutase and glutathione peroxidase) within the rodent diaphragm. Interestingly, the magnitude of this training-induced increase in costal diaphragmatic oxidative and antioxidant enzyme activity is relatively independent of the exercise duration and intensity. Although the crural diaphragm of rodents is also capable of increasing its oxidative and antioxidant capacity in response to endurance training, high-to moderate-intensity exercise of long duration is required to promote these changes. Endurance training also increases the oxidative capacity of other key rodent inspiratory muscles, such as the parasternal intercostals and external intercostals. Furthermore, endurance training results in small (approximately 10%) increased in the oxidative capacity of key abdominal (expiratory) muscles. Whether the improvement in oxidative capacity of respiratory muscles is of significant magnitude to result in improvement in respiratory muscle performance remains an unanswered question.

Adaptation, Physiological↗
PubMedDate not supplied

Respiratory muscle function in patients with chronic obstructive pulmonary disease.

Respiratory muscle (RM) dysfunction is a progressive process, including both RM weakness and fatigue, that may advance to the point of respiratory failure. It occurs as a result of increased RM workloads, altered length-tension relationship of respiratory muscles, malnourished states, and altered cellular environment in chronic obstructive pulmonary disease (COPD). Consideration of multiple patient factors is necessary when identifying patient risk for RM dysfunction and designing plans of care. This article discusses the RM pump, including its measurement, in patients with COPD.

Electromyography↗
PubMed1984

Respiratory muscle oxygen consumption estimated by the diaphragm pressure-time index.

The O2 consumption of the respiratory muscles (VO2resp), work of breathing, and the time integral of the transdiaphragmatic pressure (TTdi) were measured in four normal subjects breathing against inspiratory resistance. A total of 39 runs were performed at mean tidal transdiaphragmatic pressures (Pdi) ranging from 15 to 53 cmH2O, respiratory frequencies from 3.5 to 22 breaths/min, and inspiratory time durations (TI) from 32 to 76% of the total breath duration. Each run was maintained from 8 to 17 min and the above parameters were kept constant by the subject via visual feedback of Pdi and TI with an oscilloscope. Most of the runs (36 of 39) were performed at TTdi values below those known to produce respiratory muscle fatigue. We found a strong linear correlation between the VO2resp and the TTdi (r = 0.74, P less than 0.001) and a weaker correlation between VO2resp and W (r = 0.31, P less than 0.05). These data suggest that TTdi is a good estimator of VO2resp over a wide range of respiratory patterns during inspiratory resistance breathing. The high variability seen in respiratory muscle efficiency during resistive breathing may be due to W not being a good indicator of the energy consumed by the respiratory muscles.

Adult↗
PubMed1999

Respiratory muscle training for tetraplegic patients: A literature review.

This paper reviews the evidence concerning the effectiveness of respiratory muscle training for tetraplegic patients. While respiratory muscle strength/endurance and/or pulmonary function have been shown to improve after inspiratory muscle training, a lack of controlled studies means it is not possible to exclude spontaneous recovery from being responsible for the improvements seen. It is not known if inspiratory muscle training improves quality of life or decreases morbidity. There are limited data which suggest that, for ventilator dependent tetraplegics, strengthening the muscles of the neck and upper thorax may improve vital capacity and allow limited ventilator-free time. The effectiveness of other techniques such as glossopharyngeal breathing, expiratory muscle training and exercise as methods of improving respiratory muscle strength/endurance is unknown.

Journal Article↗
PubMed1988

Respiratory muscle rest therapy.

This article discusses the role of respiratory muscle rest therapy in hypercapnic ventilatory failure and/or inspiratory muscle fatigue associated with primary lung disease, diseases of the chest wall, and neuromuscular diseases. Some animal data on the role of ventilatory muscle rest therapy in states characterized by a low cardiac output and arterial hypotension are also reviewed. Additionally, a method for quantitating the degree of respiratory muscle rest elicited by negative pressure ventilation devices is presented.

Cardiac Output, Low↗
PubMed1993

Respiratory muscle stiffness is age- and muscle-specific.

We investigated the possible contribution of respiratory muscles to the well documented increase in chest wall stiffness with age. Diaphragm and internal intercostal muscle strips were dissected from male Fischer 344 rats of 3, 6, 12, and 24 months of age. Muscles were subjected, in vitro, to stress-strain and yield point tests. Passive tension data from these tests were normalized to a reference length (Lr), which was defined in terms of absolute stress, 700 Pascals. In general, Lr of diaphragm was found to be 90% of the length (Lo) required for maximal tetanic tension. Within a range of stretch between Lr and 130% Lr, diaphragm muscles from adult rats (6-12 month) were more compliant than those of either young (3 month) or old (24 month) animals. In contrast, intercostal muscles from old rats were stiffer than those of young or adult rats. Yield strength of both muscles was constant with age, but diaphragm muscles were found to have a higher yield strength than intercostal muscles from any age. Thus, only some passive mechanical properties of respiratory muscles vary with age, and this variation in muscle-specific. A surprising finding of this study was that diaphragm muscles of adult animals were more compliant than those of either young or old rats.

Aging↗
PubMed1999

Respiratory muscle training in neuromuscular disease: long-term effects on strength and load perception.

PURPOSE: Deterioration of respiratory muscle function in patients with neuromuscular disorders is primarily responsible for the high morbidity and mortality associated with these diseases. METHODS: The potential benefit of respiratory muscle training (RMT) on preservation of respiratory muscle strength and respiratory load perception (RLP) was examined in 21 children (mean age: 12.2 +/- 1.8 yr [SD], 16 male) with Duchenne's muscular dystrophy or spinal muscular atrophy type III, and in 20 age-, weight-, and sex-matched controls. Subjects were randomly allocated to undergo incremental RMT with resistive inspiratory and expiratory loads for a period of 6 months (trained group, TR) or to perform similar exercises with no load (NT). Maximal static inspiratory (Pi(max)) and expiratory (Pe(max)) pressures and RLP (modified Borg visual analog scale 0-10) were assessed on two separate occasions before beginning of the training protocol, monthly throughout RMT duration, and every 3-6 months upon cessation of RMT for 1 yr. RESULTS: In controls, no significant changes in maximal static pressures or load perception occurred during RMT or thereafter. Training in neuromuscular disorder (NMD) patients was associated with improvements in Pi(max) (mean delta max: +19.8 +/- 3.8 cmH2O in TR vs +4.2 +/- 3.6 cmH2O in NT; P < 0.02) and in Pe(max) (mean delta max: +27.1 +/- 4.9 cmH2O in TR vs -1.8 +/- 3.4 cmH2O in NT; P < 0.004). Similarly, RLP significantly decreased during the RMT period in TR (mean delta: 1.9 +/- 0.3; P < 0.01) but did not change in NT (-0.2 +/- 0.2). In addition, with cessation of RMT, static pressures returned to pretraining values in TR within approximately 3 months. However, RLP was still improved after 12 months. CONCLUSIONS: We conclude that in children with NMD, although RMT-induced increases in expiratory muscle strength are rapidly reversible, long-lasting improvements in RLP occur and could be associated with decreased respiratory symptoms.

Airway Resistance↗
PubMed1994

Respiratory muscle function and exercise capacity in multiple sclerosis.

Patients with multiple sclerosis (MS) show a poor exercise tolerance. A reduction in respiratory muscle strength has also been reported. The purpose of this study was to evaluate whether reduction in exercise tolerance was related to respiratory muscle dysfunction. Twenty four multiple sclerosis patients (mean +/- SD age: 48 +/- 9 yrs, duration of illness 12.2 +/- 6 yrs, severity of illness as assessed by Expanded Disability Scale Score (EDSS) 5.3 +/- 2), underwent detailed evaluation of lung function tests, arterial blood gas analysis, respiratory muscle strength and endurance, and exercise test on an arm ergometer. Sixteen of the 24 patients were able to perform the exercise test (Group I), whilst the other eight were not (group II). Arterial blood gases and lung function tests were normal for both groups. Respiratory muscle strength as assessed both by maximal inspiratory pressure (MIP) and maximal expiratory pressure (MEP) was significantly reduced (MIP 18-76 cmH2O; MEP 16-82 cmH2O) compared to predicted values. Inspiratory muscle endurance time was significantly reduced in Group II in comparison to Group I (247 +/- 148 vs 397 +/- 154 s, respectively). Both MIP and MEP were significantly related to inspiratory muscle endurance time. Endurance time, MIP and MEP were inversely significantly related to duration of illness, whilst only endurance time was significantly related to Expanded Disability Scale Score.(ABSTRACT TRUNCATED AT 250 WORDS)

Blood Gas Analysis↗
PubMed1989

Respiratory muscle fatigue research: implications for clinical practice.

Research into respiratory muscle fatigue and failure has centered around three issues: the factors that place individuals at risk for fatigue; the physiologic manifestations of fatigue development; and the various treatment alternatives available to prevent and respond to respiratory muscle failure. Selected studies in this field of investigation are discussed, and applications to clinical practice are proposed.

Aged↗
PubMed1986

Effect of respiratory muscle training in patients with neuromuscular diseases and in normals.

In order to evaluate the possible effects of respiratory muscle training in patients with neuromuscular disease, we trained a group of 12 patients and 6 normal subjects for 8 weeks with 4 weeks of strength training and 4 weeks of endurance training of the respiratory muscles. We measured static and dynamic lung volumes and maximal expiratory flows in a whole-body plethysmograph and endurance in an original set-up. The main finding was a significant rise in vital capacity and respiratory muscle endurance in the patient group; therefore, daily specific training of the respiratory muscles can improve strength and endurance in patients with neuromuscular diseases as well as in normal subjects.

Adult↗
PubMed1997

Respiratory muscle weakness and normal ventilatory drive in dilative cardiomyopathy.

BACKGROUND: In dilative cardiomyopathy several factors influence dyspnoea. Patients with chronic heart failure may demonstrate impairment of breathing pattern, ventilatory drive and respiratory muscle strength, as well as reduction of ventilatory efficiency. The purpose of this study was to evaluate whether dilative cardiomyopathy is accompanied by changes in breathing pattern, respiratory muscle weakness and ventilatory neural drive. METHODS: We investigated 47 patients (36 men, mean age = 47.8 +/- 11.2 years) with chronic heart failure due to dilative cardiomyopathy, and 30 healthy subjects (10 men, mean age = 35.4 +/- 11.7 years) served as controls. Patients and controls underwent evaluation of left ventricular ejection fraction by 2D echocardiography, spirometry, body plethysmography, mouth occlusion pressure and respiratory muscle strength, as well as by submaximal treadmill exercise testing with gas exchange measurements. The patients' results were compared to controls and predicted standard normal values, and evaluated for differences according to the degree of severity of functional impairment. RESULTS: Patients with dilative cardiomyopathy demonstrated a slight reduction in lung volumes (15% of the patients with obstructive and 15% with restrictive lung function pattern) and diffusion capacity (20.4 +/- 6.8 vs 15.4 +/- 6.7 ml.min-1.kPa-1; P < 0.01). In neural drive, as assessed by mouth occlusion pressure, there was no significant difference between patients and controls. There was a slight but significant reduction in respiratory muscle strength, as assessed by measuring maximal inspiratory pressure in patients with dilative cardiomyopathy (6.7 +/- 2.4 kPa vs 8.6 +/- 3.5 kPa; P < 0.01). The observed changes were more pronounced in the severe chronic heart failure patients (with a reduction in ventilatory efficiency) whereas no relationship among indices of cardiac or respiratory function was found. CONCLUSIONS: Patients with chronic heart failure due to dilative cardiomyopathy develop respiratory muscle weakness without changes in neural ventilatory drive, and slight changes in breathing pattern related to the severity of the disease.

Adult↗
PubMed2006

Bench-to-bedside review: weaning failure--should we rest the respiratory muscles with controlled mechanical ventilation?

The use of controlled mechanical ventilation (CMV) in patients who experience weaning failure after a spontaneous breathing trial or after extubation is a strategy based on the premise that respiratory muscle fatigue (requiring rest to recover) is the cause of weaning failure. Recent evidence, however, does not support the existence of low frequency fatigue (the type of fatigue that is long-lasting) in patients who fail to wean despite the excessive respiratory muscle load. This is because physicians have adopted criteria for the definition of spontaneous breathing trial failure and thus termination of unassisted breathing, which lead them to put patients back on the ventilator before the development of low frequency respiratory muscle fatigue. Thus, no reason exists to completely unload the respiratory muscles with CMV for low frequency fatigue reversal if weaning is terminated based on widely accepted predefined criteria. This is important, since experimental evidence suggests that CMV can induce dysfunction of the diaphragm, resulting in decreased diaphragmatic force generating capacity, which has been called ventilator-induced diaphragmatic dysfunction (VIDD). The mechanisms of VIDD are not fully elucidated, but include muscle atrophy, oxidative stress and structural injury. Partial modes of ventilatory support should be used whenever possible, since these modes attenuate the deleterious effects of mechanical ventilation on respiratory muscles. When CMV is used, concurrent administration of antioxidants (which decrease oxidative stress and thus attenuate VIDD) seems justified, since antioxidants may be beneficial (and are certainly not harmful) in critical care patients.

Animals↗
PubMed2001

[Selective training of respiratory muscles in patients with chronic heart failure].

BACKGROUND: Patients with chronic heart failure have a lower inspiratory muscle strength and fatigue endurance. AIM: To assess the effects of selective training of respiratory muscles in patients with heart failure. PATIENTS AND METHODS: Twenty patients with stable chronic heart failure, aged 58.3 +/- 3 years with an ejection fraction of 28 +/- 9%, were subjected to respiratory muscle training with threshold valves. The load was fixed in 30% of maximal inspiratory pressure (PImax) in 11 and in 10% of PImax in nine. Two sessions of 15 minutes, 6 days per week, during 6 weeks were done. Degree of dyspnea (Mahler score), maximal oxygen uptake, distance walked in 6 minutes, respiratory muscle function and left ventricular ejection fraction were measured before and after training. RESULTS: Both training loads were associated to an improvement in dyspnea (+2.7 +/- 1.8 and +2.8 +/- 1.8 score points with 30% PImax and 10% PImax respectively), maximal oxygen uptake (from 19 +/- 3 to 21.6 +/- 5 and from 16 +/- 5 to 18.6 +/- 7 ml/kg/min with 30% PImax and 10% PImax respectively, p < 0.05), PImax (from 78 +/- 22 to 99 +/- 22 and from 72 +/- 34 to 82.3 cm H20 with 30% PImax and 10% PImax respectively), sustained PImax (from 63 +/- 18 to 90 +/- 22 and from 58 +/- 3 to 69 +/- 3 cm H20 with 30% PImax and 10% PImax respectively), and maximal sustained load (from 120 +/- 67 to 195 +/- 47 and from 139 +/- 120 to 192 +/- 154 g with 30% PImax and 10% PImax respectively). The distance walked in 6 min only increased in subjects trained at 30% PImax (from 451 +/- 78 to 486 +/- 68 m). CONCLUSIONS: Selective training of respiratory muscles results in a functional improvement of patients with chronic heart failure.

Breathing Exercises↗