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Exercise training-induced changes in respiratory muscles.

Interest in the adaptive strategies of respiratory muscles in response to exercise training has grown in recent years. Animal studies have clearly demonstrated that regular endurance exercise training results in small but significant increases in oxidative and antioxidant enzyme activities in both inspiratory and expiratory muscles. Further, exercise training has been shown to promote a shift in the fast myosin heavy chain isoforms (e.g. from type IIb to IId) within the costal diaphragm of endurance-trained rodents. Human studies using numerous respiratory muscle training programmes have shown that respiratory muscle training results in an increased work capacity of the ventilatory musculature. However, the issue of whatever respiratory muscle training improves whole body endurance capacity remains controversial. Although some authors have reported that ventilatory muscle training results in improved whole body exercise, many investigators argue that respiratory muscle performance does not limit high intensity exercise tolerance or influence maximum oxygen table uptake (VO2max). The explanation for the divergent findings is unclear but may be due to variance in the exercise tasks used to evaluate exercise endurance. This is an interesting area for future research.

Adaptation, Physiological↗

Respiratory muscle fatigue.

The contribution of respiratory muscle fatigue to the development of ventilatory failure has been the subject of considerable interest and has stimulated much research. Experimental studies in dogs have shown respiratory muscle fatigue to be a cause of ventilatory failure in both cardiogenic and septic shock models. In clinical conditions resulting in acute or chronic hypercapnia, respiratory muscle fatigue is believed to occur; however, the specific role of fatigue has been difficult to prove.

Animals↗

Respiratory muscle training in healthy humans: resolving the controversy.

Specific respiratory muscle training offers the promise of improved exercise tolerance and athletic performance for a wide range of users. However, the literature addressing respiratory muscle training in healthy people remains controversial. Studies into the effect of respiratory muscle training upon whole body exercise performance have used at least one of the following modes of training: voluntary isocapnic hyperpnea, flow resistive loading, and pressure threshold loading. Each of these training modes has the potential to improve specific aspects of respiratory muscle function. Some studies have demonstrated significant improvements in either time to exhaustion or time trial performance, whilst others have demonstrated no effect. We present an overview of the literature that rationalizes its contradictory findings. Retrospective analysis of the literature suggests that methodological factors have played a crucial role in the outcome of respiratory muscle training studies. We conclude that in most well controlled and rigorously designed studies, utilizing appropriate outcome measures, respiratory muscle training has a positive influence upon exercise performance. The mechanisms by which respiratory muscle training improves exercise performance are unclear. Putative mechanisms include a delay of respiratory muscle fatigue, a redistribution of blood flow from respiratory to locomotor muscles, and a decrease in the perceptions of respiratory and limb discomfort.

Adaptation, Physiological↗

Assessment of respiratory muscle function and strength.

Measurement of respiratory muscle strength is useful in order to detect respiratory muscle weakness and to quantify its severity. In patients with severe respiratory muscle weakness, vital capacity is reduced but is a non-specific and relatively insensitive measure. Conventionally, inspiratory and expiratory muscle strength has been assessed by maximal inspiratory and expiratory mouth pressures sustained for 1 s (PImax and PEmax) during maximal static manoeuvre against a closed shutter. However, PImax and PEmax are volitional tests, and are poorly reproducible with an average coefficient of variation of 25%. The sniff manoeuvre is natural and probably easier to perform. Sniff pressure, and sniff transdiaphragmatic pressure are more reproducible and useful measure of diaphragmatic strength. Nevertheless, the sniff manoeuvre is also volition-dependent, and submaximal efforts are most likely to occur in patients who are ill or breathless. Non-volitional tests include measurements of twitch oesophageal, gastric and transdiaphragmatic pressure during bilateral electrical and magnetic phrenic nerve stimulation. Electrical phrenic nerve stimulation is technically difficult and is also uncomfortable and painful. Magnetic phrenic nerve stimulation is less painful and transdiaphragmatic pressure is reproducible in normal subjects. It is a relatively easy test that has the potential to become a widely adopted method for the assessment of diaphragm strength. The development of a technique to measure diaphragmatic sound (phonomyogram) during magnetic phrenic nerve stimulation opens the way for noninvasive assessment of diaphragmatic function.

Electric Stimulation↗

Influence of central chemoreceptor afferent inputs on respiratory muscle activity.

Respiratory activity can be substantially affected by perturbations confined to the superficial areas of the ventrolateral surface of the medulla, the putative site of central chemoreceptors. In this study we compared the effect of thermal and pharmacological interventions that are known to alter respiration on the electrical activity of the rib cage muscles, diaphragm, and abdominal muscles. With cooling of the intermediate areas to 20 degrees C, tidal volume decreased 50%. The electrical activity of the diaphragm decreased less than the other muscles (diaphragm less than inspiratory intercostal less than expiratory intercostal). Abdominal muscle activity was depressed as much as expiratory intercostal activity but reappeared with further cooling to 10 degrees C if cooling was prolonged and the vagi were intact. gamma-Aminobutyric acid (GABA) and its agonist muscimol, like cooling, reduced expiratory and inspiratory intercostal activity more than diaphragm activity. Nicotine, a respiratory stimulant, applied to the intermediate areas increased inspiratory intercostal activity more than the diaphragm. The results suggest that under the conditions of the experiments the rib cage musculature, and probably the abdominal muscles as well, are more responsive than the diaphragm to depression or excitation of chemosensitive elements in the superficial regions of the medulla.

Animals↗

Changes in histochemical profile of rat respiratory muscles in hypo- and hyperthyroidism.

Rat respiratory muscles underwent considerable changes in histochemical fibre type profile in response to hypo- and hyperthyroidism. Hypothyroidism increased the proportion of type 1 slow oxidative fibres in diaphragm and to a lesser extent in intercostal muscles. Hyperthyroidism resulted in a decreased proportion of type 1 fibres in both diaphragm and intercostals. These changes were broadly comparable to those reported previously in rat limb muscles. In normal rat respiratory muscles, the type 1 fibres were characterized by very high levels of beta-hydroxybutyrate dehydrogenase which was thought to contribute to the fatigue-resistance of these muscles. The type 2B fast glycolytic fibres, and to a lesser extent type 2A fast oxidative fibres, contained high levels of mitochondrial alpha-glycerophosphate dehydrogenase, an enzyme known to be specifically affected in dysthyroid states. The implications of the observed changes in fibre type profile with respect to the oxidative metabolism of rat respiratory muscles are discussed.

Animals↗

Respiratory muscle function in patients with neuromuscular disorders and cardiopulmonary diseases.

Respiratory muscle dysfunction frequently occurs in patients with neuromuscular disorders, cardiopulmonary diseases and in patients in intensive care units. Respiratory muscle weakness and/or fatigue is responsible for dyspnoea, reduced exercise tolerance, nocturnal desaturation, and prolonged weaning from mechanical ventilation. Chronic respiratory muscle weakness may also be associated with poor quality of life and increased mortality. Patients with severe respiratory muscle weakness are at increased risk of respiratory failure due to respiratory infections, electrolyte imbalance, sedation or uncontrolled inspired oxygen therapy. Although respiratory muscle weakness is often seen in clinical practice, the consequences and the precise point at which respiratory muscle fatigue occurs remain elusive. This article reviews the pathophysiology of respiratory muscle weakness and fatigue, and therapeutic interventions for enhancing respiratory muscle function in patients with neuromuscular and cardiopulmonary diseases.

Female↗

Influence of excessive weight loss after gastroplasty for morbid obesity on respiratory muscle performance.

BACKGROUND: Morbidly obese subjects are known to have impaired respiratory function and inefficient respiratory muscles. A study was undertaken to investigate the influence of excessive weight loss on pulmonary and respiratory muscle function in morbidly obese individuals who underwent gastroplasty to induce weight loss. METHODS: Twenty one obese individuals with mean (SE) body mass index (BMI) 41.5 (4.5) kg/m2 without overt obstructive airways disease (FEV1/FVC ratio > 80%) were studied before and six months after vertical banded gastroplasty. Only patients who had lost at least 20% of baseline BMI were included in the study. Standard pulmonary function tests and respiratory muscle strength and endurance were measured. RESULTS: Before operation the predominant abnormalities in respiratory function were significant reductions in lung volumes and respiratory muscle endurance and, to a lesser degree, reductions in respiratory muscle strength. All parameters increased towards normal values after weight loss with significant increases in functional residual capacity (FRC) from 84.0 (2.2) to 91.3 (2.5)% of predicted normal values (mean difference 7.3, 95% confidence interval of difference (CI) 4.2 to 10.5), total lung capacity (TLC) from 85.6 (3.0) to 93.5 (3.7)% of predicted normal values (mean difference 7.9, 95% CI 4.5 to 11.5), residual volume (RV) from 86.7 (3.1) to 96.4 (3.0) of predicted normal values (mean difference 9.7, 95% CI 5.2 to 14.1), expiratory reserve volume (ERV) from 76.6 (3.0) to 89.0 (3.4)% of predicted normal values (mean difference 12.4, 95%, CI 6.3 to 18.9), respiratory muscle strength: PImax from 92 (4.4) to 113 (4.6) cm H2O (mean difference 21, 95% CI 12.2 to 31.6), PEmax from 144 (5.6) to 166 (4.3) cm H2O (mean difference 22, 95% CI 12.9 to 32.0), and endurance: PmPeak/PImax from 56 (1.4) to 69 (2.0)% (mean difference 13, 95% CI 9.7 to 16.9). The strongest correlation was between weight loss and the improvement in respiratory muscle endurance. CONCLUSIONS: Lung volumes and respiratory muscle performance are decreased in obese individuals. Weight loss following gastroplasty is associated with improvement in lung volumes and respiratory muscle function.

Adult↗

Comparison of twitch depression of the adductor pollicis and the respiratory muscles. Pharmacodynamic modeling without plasma concentrations.

BACKGROUND: Although the respiratory muscles (the diaphragm and the laryngeal adductors) recover from paralysis more rapidly than does the adductor pollicis, patients can develop complete paralysis of the respiratory muscles, but not of the adductor pollicis, after bolus administration of vecuronium. The authors used a pharmacodynamic model not requiring muscle relaxant plasma concentrations to reconcile these findings. METHODS: The pharmacodynamic model is based on the traditional model, in which: (1) vecuronium concentration at the neuromuscular junction (C(effect)) is a function of the plasma concentration versus time curve and a rate constant for equilibration between plasma and the neuromuscular junction (k(eo)); and (2) effect is a function of C(effect), the steady-state plasma concentration that produces 50% effect (C50), and a factor to explain the sigmoid relationship between concentration and effect. In the absence of vecuronium plasma concentrations, an empiric model (rather than the usual effect compartment model) can be used to mimic the time delay (proportional, but not identical, to 1/k(eo)) between dose and effect. The model can be used to estimate the steady-state infusion rate that produces 50% effect (IR50), equal to the product of C50 and vecuronium plasma clearance; IR50 for different muscle groups then can be compared to assess relative sensitivity. The authors applied this model to published effect data for subjects given 40-70 micrograms/kg vecuronium in whom paralysis of three muscle groups was measured during opioid/propofol anesthesia. RESULTS: For IR50, the ratio of values for the larynx:diaphragm:adductor pollicis was 1.4:1.2:1; for the equilibration constant (inversely proportional to the time delay), the ratio for the respiratory muscles to the adductor pollicis was 2.5:1. CONCLUSIONS: Vecuronium concentrations peak earlier at the respiratory muscles than at the adductor pollicis, possibly the result of greater perfusion to these organs, leading to earlier onset of paralysis. The observation that bolus injection of vecuronium produces greater paralysis of the respiratory muscles than of the adductor pollicis, despite greater resistance of the respiratory muscles, can be explained by differential rates of equilibration between plasma and various muscles.

Humans↗

Respiratory muscle training.

The application of skeletal muscle training principles to the respiratory muscles is a relatively new field. Strength and endurance training of the respiratory muscles can be achieved in normal humans and in patients with neuromuscular and chronic obstructive pulmonary diseases. Careful monitoring is required throughout a training program to ensure that the respiratory muscles are, in fact, being trained. This is a promising area, although further research is necessary to determine the indications for respiratory muscle training. Furthermore, it is still necessary to determine the optimal mode of training.

Breathing Exercises↗

[Physiopathology of respiratory muscles in malnutrition].

OBJECTIVES: a) To present the pathophysiological concepts behind undernutrition-related effects on respiratory muscle composition and function; b) to review the existing literature on the possible role of undernutrition-related effects on respiratory muscles as pathogenetic factors of ventilatory failure. DATA SOURCES: Selected recent references and pertinent literature in the english language dealing with the effects of undernutrition on respiratory muscle composition and function in the experimental and clinical settings. DATA EXTRACTION: Peer-reviewed clinical or basic research journals. DATA SYNTHESIS: Derangements of respiratory muscle function (fatigue and weakness) play a role in the pathogenesis of respiratory failure, as they are able to determine respiratory muscle pump failure and ventilatory insufficiency. Undernutrition negatively influences respiratory muscle function both through a direct effect of loss of contractile elements, and also indirectly, by worsening or inducing muscle composition derangements. Respiratory muscles are not spared by the process of wasting associated to undernutrition, and both experimental and clinical data are consistent with a decrease in respiratory muscle mass due to fiber size reduction. As respiratory muscle weakness in course of undernutrition is more than proportional to muscle mass decrease, the presence of alterations in the remaining muscle cell is likely. Derangements in both respiratory and skeletal muscle composition with particular regard to high energy phosphate compound depletion (low cell ATP and phosphocreatine content) and to cationic depletion (low muscle magnesium and potassium content), have been reported in patients with respiratory failure due to acute ot chronic lung disease; undernourished patients had the more severe derangements of muscle composition. CONCLUSIONS: Undernutrition is associated with important alterations in respiratory muscle structure and function. Undernutrition-related effects on respiratory muscles, by inducing respiratory muscle weakness through derangements in muscle energy production, transport and utilization, could represent important "metabolic" factors in the pathogenesis of ventilatory failure.

Humans↗

Clinical assessment of the respiratory muscles.

This review examines approaches to evaluation of the respiratory muscles and describes new techniques that may be more quantitative, less effort dependent, and less invasive than conventional methods. To evaluate strength of the respiratory muscles, maximum inspiratory and expiratory pressures remain useful measures. Potential methodologic errors, however, necessitate careful technique. Evaluation of the twitch response to direct phrenic nerve stimulation may ultimately prove more quantitative and less effort dependent than measurements of maximum pressure. Many techniques are also available to measure endurance of respiratory muscles, but most are less than satisfactory outside the research environment because of poor reproducibility and other procedural difficulties. The maximum incremental resistive loading test, however, has proven to be practical and well tolerated. There is little substitute for careful clinical observation of respiratory muscle coordination and movement, particularly in the patient with suspected respiratory muscle weakness or chest wall distortion. In conclusion, though the respiratory muscles are difficult to evaluate, techniques are available that can be quite helpful for assessment, particularly in response to interventions such as rehabilitation.

Diaphragm↗

Long-term follow-up of symptoms, pulmonary function, respiratory muscle strength, and exercise performance after botulism.

Respiratory muscle weakness occurs commonly at presentation in patients with botulism. Although clinical improvement occurs over several months, symptoms such as fatigue and dyspnea persist in many patients in the long term. To determine whether continued respiratory muscle weakness might contribute to these symptoms, we compared lung function tests, respiratory muscle strength, and exercise performance in 13 patients 2 years after type B botulism. We found that residual symptoms including dyspnea and fatigue were common in botulism patients at 2 years postintoxication. Lung function tests had returned to normal in all patients. Maximal inspiratory and expiratory pressures were similar between botulism patients and control subjects. Evaluation of individual results showed evidence of inspiratory muscle weakness in four of 13 patients with botulism (Plmax less than 65% predicted). Maximal oxygen consumption and maximal workload during exercise were reduced in botulism patients in comparison to control subjects. During exercise, botulism patients had a more rapid and shallow breathing pattern and a higher dyspnea score at a given minute ventilation in comparison to control subjects. Reasons for premature exercise termination in botulism patients were multifactorial. Although respiratory muscle weakness may have been contributory in some patients, most appeared to be limited by reduced cardiovascular fitness, leg fatigue, or reduced motivation.

Adult↗

[The EOL trainer for respiratory muscles].

A training equipment for respiratory muscles is suggested. It may create peak load at the initial phase of inspiration and expiration, thereby ensuring less fatiguability of respiratory muscles. The efficacy of the training equipment was estimated by clinical and instrumental methods in a group of 43 patients suffering from chronic bronchitis and compared to that of the throttle type trainer in 36 control patients. External respiratory function, acid-base balance and myocardial contractility were found to be significantly improved in the experimental group as compared to the controls.

Bronchitis↗

Respiratory muscle energetics during endotoxic shock in dogs.

Respiratory muscle O2 consumption, lactate production, and endogenous substrate utilization during endotoxic shock were assessed in two groups of anesthetized spontaneously breathing dogs. In the endotoxin group (Escherichia coli endotoxin 10 mg/kg iv) and the sham group (saline iv), we sampled diaphragm, external intercostal, and gastrocnemius muscle tissue for glycogen and lactate concentrations before and after 3 h of the experimental period. Only in the endotoxin group did blood pressure and cardiac output decline significantly. Arterial O2 content did not change significantly during shock, whereas mixed venous, phrenic venous, and femoral venous O2 contents dropped to 8.0 +/- 1.1, 5.8 +/- 0.8, and 3.6 +/- 0.6 ml/dl at 60 min of shock, respectively, with little change thereafter. At 30 min of shock, femoral venous lactate rose higher than arterial values, whereas at 90 min of shock, onward, phrenic venous lactate was significantly higher than arterial concentrations. All muscle tissues showed significant lactate production and glycogen depletion after shock. In a second set of experiments we measured respiratory muscle blood flow during shock with radioactive microspheres. At 60 min of shock, diaphragmatic and intercostal blood flow rose by six- and twofold, respectively, whereas gastrocnemius blood flow declined significantly. We conclude that during endotoxin shock 1) the increased demands of the respiratory muscles are met by increasing blood flow and O2 extraction; 2) anaerobic metabolism and respiratory muscle substrate depletion, or both, may contribute to the observed fatigue.

Animals↗

Dyspnoea in health and obstructive pulmonary disease : the role of respiratory muscle function and training.

A consistent finding of recent research on respiratory muscle training (RMT) in healthy humans has been an attenuation of respiratory discomfort (dyspnoea) during exercise. We argue that the neurophysiology of dyspnoea can be explained in terms of Cambell's paradigm of length-tension inappropriateness. In the context of this paradigm, changes in the contractile properties of the respiratory muscles modify the intensity of dyspnoea predominantly by changing the required level of motor outflow to these respiratory muscles. Thus, factors that impair the contractile properties of the respiratory muscles (e.g. the pattern of tension development, functional weakening and fatigue) have the potential to increase the intensity of dyspnoea, while factors that improve the contractile properties of these respiratory muscles (e.g. RMT) have the potential to reduce the intensity of dyspnoea. In patients with obstructive pulmonary disease, functional weakening of the inspiratory muscles in response to dynamic lung hyperinflation appears to be a central component of dyspnoea. A decrease in the intensity of respiratory effort sensation (during exercise and loaded breathing) has been observed in both healthy individuals and patients with obstructive pulmonary disease after RMT. We conclude that RMT has the potential to reduce the severity of dyspnoea in healthy individuals and in patients with obstructive pulmonary disease, and that this probably occurs via a reduction in the level of motor outflow. Further work is required to clarify the role of RMT in the management of other disease conditions in which the function of the respiratory muscles is impaired, or the loads that they must overcome are elevated (e.g. cardiorespiratory and neuromuscular disorders).

Asthma↗

Effects of surgery on the function of the respiratory muscles.

The function of the respiratory muscles (RM) is affected positively or negatively by a variety of surgical procedures. Cardiac, thoracic and upper abdominal surgery impair the RM function and lead to postoperative complications such as hypoxia, atelectasis, aspiration and infections. Preoperative assessment of RM function is cardinal to avoid or attenuate these complications. Three types of surgical procedures, lung transplantation, lung volume reduction surgery and surgery for obesity have been shown to improve RM function. A mechanism by which these types of operation have shown beneficial effects on RM function is multifactorial, depending on geometrical factors, from the reduction of hyperinflation and those depending on changes on the control of breathing. Physicians dealing with postoperative care of patients should be aware of the pathophysiological mechanisms that impair or improve respiratory muscle function as a result of a surgery as well as of the therapeutic modalities.

Abdomen↗