Myoelectric activity in individual lumbar erector spinae muscles in sitting. A study with surface and wire electrodes.
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The quantitative distribution of drugs in seven cases of intoxication has been investigated especially in different muscles distinguished by their functions. The analyses have been verified in two respiratory muscles (m. intercostalis and diaphragma) and two skeletal muscles, being inactive during unconsciousness (m. psoas major and m. quadriceps). In all cases, higher concentrations of drugs have been found in the respiratory muscles than in the skeletal muscles. During the acute phase of intoxication an enhanced quantity of drugs is stored in the active respiratory muscles. The skeletal muscle shows reduced metabolism activities with lowered storage of drugs.
We examined the effects of expiratory resistive loads of 10 and 18 cmH2O.l-1.s in healthy subjects on ventilation and occlusion pressure responses to CO2, respiratory muscle electromyogram, pattern of breathing, and thoracoabdominal movements. In addition, we compared ventilation and occlusion pressure responses to CO2 breathing elicited by breathing through an inspiratory resistive load of 10 cmH2O.l-1.s to those produced by an expiratory load of similar magnitude. Both inspiratory and expiratory loads decreased ventilatory responses to CO2 and increased the tidal volume achieved at any given level of ventilation. Depression of ventilatory responses to Co2 was greater with the larger than with the smaller expiratory load, but the decrease was in proportion to the difference in the severity of the loads. Occlusion pressure responses were increased significantly by the inspiratory resistive load but not by the smaller expiratory load. However, occlusion pressure responses to CO2 were significantly larger with the greater expiratory load than control. Increase in occlusion pressure observed could not be explained by changes in functional residual capacity or chemical drive. The larger expiratory load also produced significant increases in electrical activity measured during both inspiration and expiration. These results suggest that sufficiently severe impediments to breathing, even when they are exclusively expiratory, can enhance inspiratory muscle activity in conscious humans.
Our aim was to determine whether inspiratory muscle fatigue changes breathing pattern and whether any changes seen occur before mechanical fatigue develops. Nine normal subjects breathed through a variable inspiratory resistance with a predetermined mouth pressure (Pm) during inspiration and a fixed ratio of inspiratory time to total breath duration. Breathing pattern after resistive breathing (recovery breathing pattern) was compared with breathing pattern at rest and during CO2 rebreathing (control breathing pattern) for each subject. Relative rapid shallow breathing was seen after mechanical fatigue and also in experiments with electromyogram evidence of diaphragmatic fatigue where Pm was maintained at the predetermined level during the period of resistive breathing. In contrast there was no significant difference between recovery and control breathing patterns when neither mechanical nor electromyogram fatigue was seen. It is suggested that breathing pattern after inspiratory muscle fatigue changes in order to minimize respiratory sensation.
A syndrome consisting of a rigid spine and myopathy predominantly affecting proximal limb muscles has been previously described in children, and as with most neuromuscular disorders, the respiratory muscles appear to be affected only at an advanced stage in the disease. We describe an adult male with this syndrome who presented with ventilatory failure caused by severe respiratory muscle weakness and who demonstrated profound nocturnal arterial oxygen desaturation, particularly during rapid eye movement sleep. Treatment with negative pressure ventilation initially resulted in only modest improvements in symptoms, blood gas tensions, and nocturnal desaturation. The cause of this only partial improvement was upper airway obstruction provoked by the mode of ventilatory support used. After tracheostomy there was a dramatic and sustained improvement in symptoms and blood gas tensions and complete abolition of nocturnal arterial oxygen desaturation. This is the first report of an adult with the rigid spine syndrome presenting with ventilatory failure and cor pulmonale due to severe respiratory muscle weakness.
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Fast and slow twitch muscle fibers have distinct contractile properties. Here we determined that membrane excitability also varies with fiber type. Na+ currents (INa) were studied with the loose-patch voltage clamp technique on 29 histochemically classified human intercostal skeletal muscle fibers at the endplate border and > 200 microns from the endplate (extrajunctional). Fast and slow twitch fibers showed slow inactivation of endplate border and extrajunctional INa and had increased INa at the endplate border compared to extrajunctional membrane. The voltage dependencies of INa were similar on the endplate border and extrajunctional membrane, which suggests that both regions have physiologically similar channels. Fast twitch fibers had larger INa on the endplate border and extrajunctional membrane and manifest fast and slow inactivation of INa at more negative potentials than slow twitch fibers. For normal muscle, the differences between INa on fast and slow twitch fibers might: (1) enable fast twitch fibers to operate at high firing frequencies for brief periods; and (2) enable slow twitch fibers to operate at low firing frequencies for prolonged times. Disorders of skeletal membrane excitability, such as the periodic paralyses and myotonias, may impact fast and slow twitch fibers differently due to the distinctive Na+ channel properties of each fiber type.
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In 19 pentobarbital sodium-anesthetized kittens aged 5-34 days, inspired O2 was reduced from 21 to 6-12%. Respiratory frequency (f) and tidal volume (VT) increased within 30 s. Over 5 min f fell to about 60% below control; VT usually fell but remained above control. Arterial pressure fell in 80% of trials, sometimes before f fell. Arterial CO2 was below control, but raising inspired CO2 to keep expired CO2 at control did not prevent the fall in f and VT. The relation between VT and esophageal pressure or diaphragm electromyogram (EMG) did not change consistently, nor was the ratio of high to low frequencies in the diaphragm EMG altered. Carotid chemoreceptor discharge increased within 15 s, and at 5 min it was much above control. We conclude that the change in the breathing pattern in hypoxia is probably due to the activation of a central mechanism.
The psychophysical technique of magnitude scaling was used to assess the sensation of respiratory muscle force in patients with low cervical spinal cord transection. The exponents of the power function relationship between load magnitude and sensation intensity during graded elastic and resistive ventilatory loading in the quadriplegic patients were 0.51 and 0.54, respectively. These values were significantly lower than those in normal subjects (P less than 0.05). This impairment in load sensation could not be attributed to differences in either the duration or magnitude of the forces generated by muscles of inspiration during loading, since the power function relationships between airway pressure and sensation intensity corrected for inspiratory duration were also significantly lower in the quadriplegic patients compared with the normal subjects. In contrast the perception of respiratory force during inspiratory maneuvers against a closed airway, as determined by both magnitude estimation and production tests, was the same in normal subjects and quadriplegics. These results suggest that afferent signals from rib cage receptors are important in shaping the intensity of the sensation during submaximal ventilatory loading. During maximal loading, i.e., airway occlusion, when respiratory muscle tension changes proportionally with the motor command, centrally generated efferent command signals may be employed to subserve the sensation of respiratory muscle force when inputs from rib cage muscle receptors are not available.
Breathlessness is a common complaint in patients with hyperthyroidism, and respiratory failure requiring artificial ventilation, although rare, can occur. While a proximal myopathy is frequently recognized, diaphragm muscle function has not hitherto been studied in detail in thyrotoxicosis. The strength of the quadriceps femoris and respiratory muscles was therefore assessed in seven consecutive thyrotoxic patients, on presentation and during medical treatment, when euthyroid. Prior to therapy, reduced quadriceps muscle strength, vital capacity, and global expiratory and inspiratory muscle strength were found. Diaphragmatic weakness was present in one of four patients studied by measuring transdiaphragmatic pressures during maximal sniffs and during bilateral phrenic nerve stimulation at 1 Hz (twitch). After treatment, significant improvement occurred in quadriceps muscle strength, vital capacity, and global respiratory muscle strength. Sniff and twitch transdiaphragmatic pressures also increased significantly. These results indicate that respiratory muscle weakness occurs in hyperthyroidism and that such weakness is reversible with medical treatment. It is important to realize that respiratory muscles may be directly affected when assessing thyrotoxic patients with breathlessness, as severe involvement of the respiratory muscles may cause respiratory failure.
According to myogenic models that relate abnormal EMG patterns to the experience of pain, lumbar paravertebral muscle activity has been considered to play an important role in chronic low back pain. In the present study, 40 chronic low back pain patients and 40 matched non-patient controls were compared on lumbar paravertebral EMG during mechanically stabilized static and dynamic postures. Differences between groups in lumbar curvature and spinal range of motion were determined using a dual goniometer technique. Although the two groups did not differ on absolute levels of EMG during quiet standing, significant differences were found for EMG patterns during dynamic postures. In addition, most patients did not show the flexion-relaxation response or the expected pattern of EMG responses during trunk rotation, most likely because of restricted range of motion and/or compensatory posturing. These findings provide support for the biomechanical model of chronic pain and indicate the need for further research pertaining to pain behavior and movement-related lumbar muscle activity.
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The diseases which are commonly complicated by hypercapnic respiratory failure also compromise the respiratory muscles in several ways. Increased work of breathing, mechanical disadvantage, neuromuscular disease, impaired nutritional status, shock, hypoxemia, acidosis, and deficiency of potassium, magnesium, and inorganic phosphorus are the major non-neurologic factors which contribute to respiratory muscle fatigue and failure. Respiratory muscle fatigue has two components. High frequency fatigue occurs rapidly with intense contractile efforts but is usually not severe. It also recovers rapidly with rest. Low frequency fatigue develops more slowly but is severe and requires hours for recovery. Since the spontaneous rate of neural stimulation is predominantly in the low frequency range, this component of fatigue is of particular clinical importance. Fatigue of the inspiratory muscles leads to acute respiratory acidosis, but before carbon dioxide retention occurs, it can be recognized from characteristic symptoms and signs. These include dyspnea which responds to mechanical ventilation, rapid shallow breathing, and asynchronous movements of the chest and abdomen. Inspiratory muscle fatigue must be treated by putting these muscles to rest, by mechanically supporting ventilation. In addition, underlying metabolic nutritional and circulatory abnormalities must be corrected and infection treated. Aminophylline and isoproterenol can restore inspiratory muscle contractility, but controlled clinical trials remain to be done regarding their application in acute and chronic respiratory failure. Inspiratory muscle training improves strength and endurance in patients with obstructive lung disease, cystic fibrosis, and spinal cord injury, but does not always improve physical exercise performance. Again, more work is needed to develop the indications for inspiratory muscle training and to determine the optimum type and duration of the training regimen.