Force length relationship of the normal human diaphragm problems

force length relationship of the normal human diaphragm problems

human diaphragm shape. MANUEL. PAIVA simply as a piston. respiratory mechanics; Laplace law; diaphragmatic tension .. poses problems. Nevertheless, at . Force-length relationships of the normal human diaphragm. J. Appl. Physiol. Force-length relationship of the normal human diaphragm To characterize the in vivo force-length relation of the human diaphragm, we related .. without overt respiratory problems via the Test of Incremental Respiratory Endurance. The length-tension relationship is the observation that the isometric force The passive length-tension relationship reflects the presence of elastic .. Damage to the human quadriceps muscle from eccentric exercise and the Eccentric torque -producing capacity is influenced by muscle length in older healthy adults.

Muscles such as the sternocleidomastoid, scalenes and triangularis sterni that also act on the chest wall are accessory, since they are recruited only with increased inspiratory effort. In fact, activation of these accessory inspiratory muscles is an important clinical sign of inspiratory loading.

In humans, expiration is typically passive requiring no muscle activity, but driven by the elastic recoil of the lung and chest wall. During forced expiration, abdominal muscles are activated to increase intraabdominal pressure, Accordingly, abdominal muscles are classified as accessory respiratory muscles, and their recruitment is also used in the clinical setting as an indicator of respiratory loading. Upper airway muscles Dilator muscles of the pharynx and larynx minimize upper airway resistance during inspiration, thus facilitating airflow into and out of the lungs 87, The pharynx is collapsible and subatmospheric pressures generated in the airway lumen during inspiration can cause airway narrowing and in some cases occlusion e.

Airway patency is maintained during breathing by tightly coordinated co-activation of respiratory pump muscles and muscles of the upper airways. The main airway dilator muscle of the pharynx is the genioglossus.

force length relationship of the normal human diaphragm problems

Contraction of the genioglossus muscle depresses and protrudes the tongue, thereby opposing obstruction of the posterior pharynx during breathing However, contraction of the genioglossus alone is not sufficient to prevent narrowing of the upper airway in humans 87, The position of the hyoid bone strongly influences upper airway resistance.

The hyoid is not connected directly to any other skeletal structure; thus, making it highly mobile If posterior movement of the hyoid is not opposed during inspiration, it can increase airway resistance and limit airflow.

Mechanical Properties of Respiratory Muscles

However, contraction of some of the extrinsic muscles of the neck including the sternothyroid, thyrohyoid, sternohyoid, and geniohyoid results in dilation of the upper airways For example, simultaneous contraction of the sternohyoid and geniohyoid move the hyoid bone in the anterior direction, thus dilating the upper airway, The mylohyoid and digastrics are non-dilator muscleswhile contraction of the omohyoid muscle is likely to constrict the upper airway through posterior displacement of the hyoid bone.

In the larynx, the posterior cricoarytenoid muscle abducts the arytenoid cartilages and separates the vocal cords, thereby increasing glottal diameter and facilitating airflow 1781 Other non-dilator and constrictor muscles play important roles in non-respiratory actions of the upper airways, e. Twitch and tetanic mechanical characteristics have been determined for the geniohyoid, sternohyoid, and genioglossus muscles 70, - Other studies have established the fiber type composition and metabolic characteristics of upper airway dilator muscles in animals and humans 51,, Overall, muscles of the upper airways have faster twitch characteristics than the diaphragm.

During normal breathing, upper airway muscles contract isometrically and maintain patency of the upper airway with approximately the same diameter as in the absence of respiratory drive.

force length relationship of the normal human diaphragm problems

Experimental protocol Procedures were performed as previously described He et al. When returned to relaxing solution, the resting sarcomere length was set to 2. A resting sarcomere length of 2. However, resting tension was not notably elevated in single permeabilized fibres at a sarcomere length of 2. We opted for a resting length of 2. Moreover, during shortening-contractions a standard starting length of 2. We received small diaphragm biopsies too infrequently to quantify directly the specific force—length relationships for each of the fibre-types in both COPD and non-COPD patients.

Fibre length was determined by measuring the distance between the two points of end fixation using the microscope eye-piece graticule. The average fibre cross-sectional area CSA at the resting sarcomere length was determined optically assuming an elliptical cross-section from the mean of three width and depth measurements.

All incubating solutions were pH 7. Whilst incubating solution constituents essentially mirrored those previously described He et al. Following all the incubation steps, the fibre was transferred to the quartz trough, filled with silicone oil.

The epifluorescence head of the microscope was lowered so that the objective made contact with the silicone fluid and the shutter for the fluorescence excitation light was opened. Laser photolysis resulted in the release of 1. At a predetermined time after photolysis, the fibre was shortened at a predetermined velocity. The lower ribs have a prominent lateral as well as ventral movement during inspiration, the so-called "bucket-handle" motion.

In the relaxed adult human, the ribs are angled down Caudad so that during inspiration, the lower and intermediate ribs move outward, away from the spine, providing an effective ventral and lateral expansion of the rib cage48, It is now well established by a variety of studies that intercostal muscles move the rib cage. Patients who have undergone destruction of intercostal nerves on one side of the thorax for treatment of pulmonary tuberculosis, show less respiratory movement of the ribs on the effected side50; in hemiplegic patients, outward displacement of the rib is reduced on the paralysed side In supine subjects with complete diaphragmatic paralysis, rib cage displacements are exaggerated and abdominal wall displacements are paradoxical when the abdominal muscles remain relaxed10,52, The function of the intercostal muscles has been a subject of controversy throughout medical history It is now commonly considered that external intercostal muscles and the interchondral part of the internal intercostal muscles the parasternal muscles are inspiratory and serve to raise the ribs, whereas the interosseous part of the internal intercostals are expiratory and act to lower the ribs.

Mechanical action of the abdominal muscles The abdominal muscles have a number of functions: As respiratory muscles have expiratory functions as well as inspiratory ones. As expiratory muscles act in two ways: Because the abdominal contents are incompressible, this causes the diaphragm to move cranially into the thoracic activity.

This contraction results in an increase in pleural pressure and a decrease in lung volume. Therefore the abdominal muscles are considered to be powerful expiratory muscles assisting in such activities as forced expiration and coughing.

The other function of the abdominal muscles in relation to breathing is to displace the rib cage, acting to pull the lower ribs down and inward, again an expiratory action They assist inspiration in two ways: Their activity is tonic, unrelated to phases of respiration and it is greatest in the dependent regions of the abdomen25,55,56 and b through a second mechanism by which the abdominal muscles can assist inspiration is by contracting in phase with expiration.

Length tension relationship – Strength & Conditioning Research

By contracting during expiration and forcing the diaphragm cranially into the thoracic cavity, these muscles can reduce lung volume below the neutral position of the respiratory system. Hence, when they relax at end-expiration, they promote passive descent of the diaphragm, therefore lung volume can increase before the onset of inspiratory muscle contraction. Mechanical action of the accessory muscles Many of theses muscles have prominently non-respiratory functions and many are relatively small or inaccessible.

As a result, they have not been extensively studied by respiratory physiologists. Scalene muscles The importance of the scaleni as muscles of inspiration is disputed but it is now believed that they are true muscles of inspiration and should probably not be called "accessory"59, Studies using needle electrodes show that the scalenes are active during quiet breathing in upright and supine postures. Others classify them with the sternomastoid as accessory muscles. By their origins and insertions, these muscles must elevate the first two ribs, and therefore, they may be inspiratory but their exact mode of action is not well known, because these muscles rarely if ever act individually.

Sternocleidomastoid muscles It has been suggested that the human sternocleidomastoid muscles have a predominantly "pump-handle" action on the rib cage, elevating the first rib and sternum and allowing the resultant decrease in transthoracic pressure to cause inward displacement of the lateral rib cage and abdomen The sternomastoids are probably the most important accessory muscles of inspiration and their participation in breathing with dyspnoea is a well known clinical observation.

The triangularis sterni Most normal subjects when breathing at rest in the supine posture do not activate this muscle unlike cats and dogs It always contracts during vigorous expiratory efforts such as coughing, laughing and during expiration below FRC61, During such manoeuvres, the triangularis sterni acts to lower the ribs and increase pleural pressures. Other muscles There are other muscles whose origins and insertions suggest that they may have a respiratory function under the right conditions.

In particular the trapezii and the platysma as well as some laryngeal muscles contract during inspiration. Despite that they have been considered unimportant to the breathing in normal man8, Despite their central role in ventilation their physiology has been relatively neglected, perhaps partly because of the complexity of their function, and the difficulties of studying them Statics and dynamics of contraction of these muscles are difficult to study in VIVO because force, initial length, velocity of shortening and magnitude of the neural drive of individual muscles are not measurable without invasive methods Understanding of the function of the respiratory muscles depends on the relationships of frequency-force, length-tension, force-velocity and fatigability-frequency.

Frequency-pressure relationship The force developed by a skeletal muscle is a function of the frequency of stimulation figure 6. The frequency-force relationships result from the summation of twitch tension during repeated stimulation.

This relationship is useful in assessing force development by different muscles and for the evaluation of high and low frequency fatigue by the same muscle.

Since respiratory muscles are inaccessible for the measurement of force directly in vivo, their force is measured indirectly as measurement of the pressures generated by them.

The frequency-force pressure curve for the respiratory muscles is similar to those of other human skeletal muscles. Using the technique of percutaneous stimulation over the motor point of the sternomastoid muscle, it is possible to describe the function of the sternomastoid in the same terms as those used to describe the function of limb skeletal muscles in humans.

Similar frequency-force curves were recorded from a strain gauge applied to the mastoid process using a force transducer The recording of Pdi in response to electrical stimulation of the right phrenic nerve allows a similar myogram to be obtained from the diaphragm When the diaphragm becomes fatigued, its frequency-pressure curve is depressed at all stimulation frequencies.

Force-length relationship The force-length relationship indicates that when a muscle is stimulated at its optimal resting length, it produces its maximum contractile force figure 7. When the muscle is either stretched beyond the optimal resting length or alternatively is foreshortened prior to contraction, supramaximal stimulation of the muscle produces submaximal force.

In the case of the diaphragm, there is little or no evidence for compromise of its contractile force by over stretching, but at lung volumes above normal FRC, the diaphragm and other inspiratory muscles are foreshortened and their contractile force is curtailed.

In contrast, expiratory muscle contraction force is curtailed at low lung volumes39, Force-velocity relationships For any muscle length, the maximum contractile force is greatest when the muscle is prevented from shortening figure 8. If the muscle is allowed to shorten during its contraction, its contractile force declines hyperbolically as a function of the velocity with which the muscle shortens.

This is termed the "force-velocity relationship" When both the tension and velocity are normalised to the maximum value, slow muscles show greater curvature than fast muscles.

Length tension relationship

The force-velocity relationship of the diaphragm muscle is intermediate between those of slow type I and those fast type II skeletal muscles Effect of respiratory muscle weakness on lung volumes Weakness of these muscles reduces the capacity to generate the negative intrathoracic pressure to expand the lungs with a reduction in total lung capacity TLC and a parallel fall in vital capacity VC. Weakness of the muscles of expiration, principally the abdominal musculature and the internal intercostals, reduces the capacity to generate positive intrathoracic pressures.

This weakness reduces expiratory reserve volume or high, increases residual volume, and further reduces vital capacity. Gas transfer corrected for the reduced lung volume KCO is normal or high, and a low KCO implies that muscle weakness is unlikely to be the sole explanation of a respiratory problem Effects of respiratory muscle weakness on lung mechanics Moderate weakness of the inspiratory muscles prevents lung recoil pressure Pst, L from being developed at full inflation and therefore truncates the upper part of the static pressure-volume PV curve of the lung.

However in patients with long-standing and severe respiratory muscle weakness pulmonary compliance is reduced also, indicating that in these patients the elastic properties of the lung are altered. The cause of this reduced lung distensibility is not clear. Three factors can theoretically affect lung compliance: Chest wall mechanics in respiratory muscle weakness Several pathogenic mechanisms are involved in malfunction of the chest wall in patients with neuromuscular disorders.

As noted before, FRC is frequently decreased in these patients. It has been suggested that the fall in FRC in these conditions is caused primarily by a decrease in the outward pull of the chest wall. Several studies have shown that chest wall compliance is decreased to about two-thirds of normal values in patients with long-standing neuromuscular disorders.

These measurements apply to the entire chest wall, but it seems reasonable to speculate that these changes are primarily due to altered stiffness of the rib cage85, Further contributing factors can be the development of scoliosis, particularly, in patients with muscular dystrophy, and fibrotic changes and spasticity in the rib cage muscles, as it occurs in patients with tetraplegia.

In conclusion, the alterations in lung volumes seen in patients with chronic neuromuscular disorders are attributable to a combination of muscle weakness and alterations of the mechanical propertles of the lungs and chest wall Cough impairment-airway function The effectiveness of cough is reduced in expiratory muscle weakness because the cough induces dynamic compression, affecting the linear velocity of airflow through the large intrathoracic airways.

As a result, cough and clearance of secretions is defective in these patients, contributing to the high prevalence of bronchopulmonary infections. Respiratory muscle weakness would be expected to have larger effects on maximum inspiratory rates for two reasons: Very few studies have been done on maximum inspiratory flow-rates in respiratory weakness88, Similarly, it might be expected that maximum voluntary ventilation MVV measured over 15 sec would be reduced disproportionally to changes in FEV1 in respiratory muscle weakness, but only a small trend in this direction has been found in myasthenia gravis90 and in myotonic dystrophy Ventilatory drive Patients with respiratory muscle weakness breath faster and with a smaller tidal volume than healthy subjects82,92, This tachypnoea may be related to the diffuse microatelectasis, reduction of lung compliance or different signals from the weakened muscles themselves Alterations in the central control mechanisms of respiration have been repeatedly suggested in a number of patients with neuromuscular disorders However reductions in the ventilatory responses can be accepted as evidence of damaged medullary respiratory centres only if there are no accompanying abnormalities of lower motor neuron respiratory muscles or lung mechanics.

Ventilation and blood gases The main change in blood gases in patients with respiratory muscle weakness is usually a fall in arterial PO Hypoxaemia without an elevated PaCO2 has been reported in patients with acute poliomyelitis during respiratory treatment and in a number of patients with other neuromuscular disorders82, In these cases decreased PaO2 coexists with an increase in alveolar-to-arterial tension difference for oxygen A-a PO2.

Initially the tachypnea causes an increase in alveolar ventilation, resulting in alveolar and arterial hypocapnia99, Persistent hypercapnia may be a late and dramatic event and may occur only at a terminal stage of the disease, as in Duchenne's muscular dystrophy. However, hypercapnia may occasionally appear relatively early in the course of some chronic neuromuscular disorders, such as in limb-girdle dystrophy or in myotonic dystrophy.

Physiological classification of fatigue Muscle fatigue can be defined as the inability to sustain the required or expected force with continued contractions. When exercise ceases or it's intensity is reduced, the muscle will recover. Recovery from some forms of peripheral muscle fatigue is complete within seconds, but may be gradual with full recovery taking hours The command chain for voluntary muscular activity involves many steps and force failure i.

As a simple practical analysis it is worth separating central from peripheral fatigue In the history of human muscle fatigue it was popular in the early years to attribute fatigue to failure of central neural processes.

Comparisons between forces generated by maximum stimulated contractions and forces by maximum voluntary contraction at different stages of the experiment allowed central fatigue to be assessed The importance of peripheral fatigue was first clearly demonstrated by Merton Causes of peripheral muscle fatique Several experimental models have been used to study fatigue: There are many possible sites and mechanisms with which fatigue may occur in a peripheral muscle.

Changes in membrane electrical characteristics from efflux of potassium ions, or increased cellular water content during exercise, may effect propagation of the action potential along the muscle membrane and the T-tubule, leading to a reduction in activation and therefore force generation.

The excitation-contraction coupling process may be impaired by changes in the amount of calcium stored in or released from the sarcoplasmic reticulum Cossbridge formation can be affected and it may reduce force generation in several ways i.

It is often thought that decreased intracellular pH is the cause of muscle fatigue but such relation is not clear. Patients suffering from McArdle's syndrome myophorylase deficiency can fatigue with no lactic acid production Other metabolic changes i.

Furthermore as pH falls the concentrations of phosphocreatinine Pcr falls, adenosine diphosphate ADPadenosine monophosphate AMP and inorganic phosphate Pi in diprotonated form increase, the latter has been found to be directly related to force changes It has recently been proposed that the metabolic determinants of fatigue as well as the recovery from it are related to the nature of exercise used to induce it25, When work is sustained for h, the point of exhaustion is related with the depletion of the glycogen stores of the working muscle During heavy exercise, large amounts of energy are converted to heat and the subsequent rise in body temperature and fluid loss may impair performance and enhance central fatigue.

Eccentric contractions where the muscle is forcibly extended during activation produce more profound and longlasting fatigue despite having low metabolic cost, Respiratory muscle fatigue By analogy with limb muscles, fatigue could develop in the respiratory muscles and contribute to hypercapnic ventilatory failure Patients with severe lung disease and hyperinflation have reduced force-generating capacity of the respiratory muscles.

In contrast their ventilatory requirements are increased. These muscles, particularly the inspiratory are subject to large loads with every breath for prolonged periods with little opportunity to rest

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