Inspiratory Contraction Research Articles

Chest wall dynamics and muscle recruitment during professional flute playing

Respiratory parameters and sound were recorded during professional flute playing in order to assess what physiological processes were associated with the control of sound production that results in 'breath support' which in turn is associated with high quality playing. Four standing young professional flautists played flute excerpts with and without breath support. Recordings included optoelectronic plethysmographic measurements of chest wall volume (V(cw)) and its compartments, surface electromyography of the scalene, lateral abdominal, rectus abdominus, parasternal and sternocleidomastoid muscles, mouth pressure, and sound. Flow was estimated from differentiating V(cw) during playing. Results showed that flute support entails antagonistic contraction of non-diaphragmatic inspiratory muscles that tends to hold the rib cage at higher lung volume. This relieves the expiratory muscles from the task of producing the right mouth pressure, especially at the end of the phrases, so they can contribute more to the finer control of mouth pressure modulations required for high quality playing.

Inspiratory transductance: A potential new measure of the relationship between inspiratory force and the resistance to pulmonary airflow

Most existing lung function tests require a substantial degree of interactive co-operation between patient and clinician. This reduces the clinical usefulness of such tests in patients with cognitive impairment (mainly elderly people), a reduced level of consciousness (for example in patients with a head injury or a severe metabolic disturbance) and children too young to perform the tests. There is a need for measures of airways status that are easier to apply. If the airflow is briefly occluded during inspiration the pressure fall in the airway is proportional to the force of contraction of inspiratory muscles and, because it occurs before flow begins, it is not mechanically altered by airflow resistance. The maximum rate of pressure fall is referred to as dP/dt(max) with the units kPas(-1). After the brief occlusion, the air column accelerates at a rate that is dependent on both dP/dt(max) and the resistance to airflow. The maximum rate of change of airflow is referred to as dV/dt(max), with the units Ls(-1)s(-1). This paper posits an hypothesis that the ratio dV/dt(max)/dP/dt(max) provides an index with the units Ls(-1)kPa(-1) that is a measure of the transformation of inspiratory effort into airflow, and can be referred to as inspiratory transductance. This index is predicted to rise when airflow resistance falls, such as would occur when an attack of asthma responds to bronchodilator drugs. The index is expected to continue to retain directional integrity even when inspiratory muscles become fatigued. Measuring the index would require little co-operation from a conscious patient and none from an unconscious patient.

Gender Differences In The Fatigability Of The Inspiratory Muscles

It is well documented that gender differences exist in human skeletal muscle fatigue; however, a comparison on the fatigability of the inspiratory muscles between females and males has received relatively little attention. PURPOSE To determine if gender differences are present in the fatigability of the inspiratory muscles during intermittent inspiratory muscle contractions. METHODS Inspiratory muscle strength was assessed noninvasively by measuring maximal inspiratory static pressure (PImax) at the mouth near residual volume. Peak pressures reached during the PImax maneuver were recorded and all PImax values are reported as the average of the two highest efforts within 5%.Females (n=11, age=23.5±1.5 yrs; Mean±SEM)) and males (n=11, age=24.1±1.5 yrs) performed resistive breathing on an inspiratory threshold device at 18 breaths/min, set at a target pressure of 65–75%PImax until task failure. Task failure was defined as the inability of the subject to generate sufficient inspiratory pressure to open the threshold valve. For each subject the rate of inspiratory muscle fatigue was calculated as the slope of PImax measured every 2 min during resistive breathing. Recovery of inspiratory muscle force was assessed by measuring PImax in 5 min increments until 45 min post-task failure. RESULTS Resting PImax was lower in females than males (F:-137.0±7.6 cmH2o;M:-172.5±9.8 cmH2o, p < 0.05). No gender difference was present in time to task failure (F:843.1±123.5 s; M:735.8±99.6 s) or in the drop in PImax at task failure (F:14.9±2.5 %; M:16.5±2.3 %). After 2 min of resistive breathing, PImax was lower in females than males (to 89.8±3.8% vs. 94.9±0.1%, respectively), reaching significance for only the females (p < 0.05). During resistive breathing, females were found to have a slower rate of fatigue than males (F:-1.5±0.4 cmH20·min−1; M:-2.9±0.3 cmH20·min−1; p < 0.05). Following task failure, females exhibited prolonged recovery of inspiratory muscle force that was longer than the recovery period found for males (15 min vs. 5 min post-task failure, respectively). CONCLUSION In spite of similar time to task failure, the rate of inspiratory muscle fatigue was slower for females than males. However, recovery of inspiratory muscle strength following task failure was prolonged for females as compared to males.

Henry Head and his paradoxical reflex.

Henry Head and his paradoxical reflex.

Gas exchange during separate diaphragm and intercostal muscle breathing.

In patients with diaphragm paralysis, ventilation to the basal lung zones is reduced, whereas in patients with paralysis of the rib cage muscles, ventilation to the upper lung zones in reduced. Inspiration produced by either rib cage muscle or diaphragm contraction alone, therefore, may result in mismatching of ventilation and perfusion and in gas-exchange impairment. To test this hypothesis, we assessed gas exchange in 11 anesthetized dogs during ventilation produced by either diaphragm or intercostal muscle contraction alone. Diaphragm activation was achieved by phrenic nerve stimulation. Intercostal muscle activation was accomplished by electrical stimulation by using electrodes positioned epidurally at the T(2) spinal cord level. Stimulation parameters were adjusted to provide a constant tidal volume and inspiratory flow rate. During diaphragm (D) and intercostal muscle breathing (IC), mean arterial Po(2) was 97.1 +/- 2.1 and 88.1 +/- 2.7 Torr, respectively (P < 0.01). Arterial Pco(2) was lower during D than during IC (32.6 +/- 1.4 and 36.6 +/- 1.8 Torr, respectively; P < 0.05). During IC, oxygen consumption was also higher than that during D (0.13 +/- 0.01 and 0.09 +/- 0.01 l/min, respectively; P < 0.05). The alveolar-arterial oxygen difference was 11.3 +/- 1.9 and 7.7 +/- 1.0 Torr (P < 0.01) during IC and D, respectively. These results indicate that diaphragm breathing is significantly more efficient than intercostal muscle breathing. However, despite marked differences in the pattern of inspiratory muscle contraction, the distribution of ventilation remains well matched to pulmonary perfusion resulting in preservation of normal gas exchange.

Factors contributing to thixotropy of inspiratory muscles

Thixotropy is a passive property of the skeletal muscle dependent on the muscle’s immediate history of contraction and length change. Thixotropic properties of inspiratory muscles, introduced by forceful muscle contraction at an inflated lung volume, cause an increased end-expiratory position (EEP) of the rib cage. We searched for factors contributing to the development of inspiratory muscle thixotropy in nine healthy subjects. Using induction plethysmography, we examined aftereffects on EEP of the duration of inspiratory muscle contraction and subsequent muscle relaxation. We also studied effects of inspiratory effort intensity measured by mouth pressure at different lung volumes. EEP elevation was noted subsequent to 5-s contraction followed by 2-s relaxation and was enhanced when conditioned at higher lung volumes with a strong inspiratory effort. Our results suggest four factors that influence inspiratory muscle thixotropy: (1) intensity of muscle contraction, (2) lung volume when contraction occurs, (3) duration of contraction, and (4) muscle relaxation.

Determinants of diaphragm motion in unilateral diaphragmatic paralysis.

Cranial displacement of a hemidiaphragm during sniffs is a cardinal sign of unilateral diaphragmatic paralysis in clinical practice. However, we have recently observed that isolated stimulation of one phrenic nerve in dogs causes the contralateral (inactive) hemidiaphragm to move caudally. In the present study, therefore, we tested the idea that, in unilateral diaphragmatic paralysis, the pattern of inspiratory muscle contraction plays a major role in determining the motion of the inactive hemidiaphragm. We induced a hemidiaphragmatic paralysis in six anesthetized dogs and assessed the contour of the diaphragm during isolated unilateral phrenic nerve stimulation and during spontaneous inspiratory efforts. Whereas the inactive hemidiaphragm moved caudally in the first instance, it moved cranially in the second. The parasternal intercostal muscles were then severed to reduce the contribution of the rib cage muscles to inspiratory efforts and to enhance the force generated by the intact hemidiaphragm. Although the change in pleural pressure (DeltaPpl) was unaltered, the cranial displacement of the paralyzed hemidiaphragm was consistently reduced. A pneumothorax was finally induced to eliminate DeltaPpl during unilateral phrenic nerve stimulation, and this enhanced the caudal displacement of the inactive hemidiaphragm. These observations indicate that, in unilateral diaphragmatic paralysis, the motion of the inactive hemidiaphragm is largely determined by the balance between the force related to DeltaPpl and the force generated by the intact hemidiaphragm.

The activation of muscle spindles enhances the thixotropic behavior of rib cage respiratory muscles.

Rib cage inspiratory muscle contractions at a deep inflated position caused a subsequent increase in rib cage cross-sectional area at the end-expiratory phase. The increase in this area was enhanced by the activation of muscle spindles in the inspiratory muscles by a mechanical vibration combined with muscle contractions.

Human Inspiratory Muscle Fatigue during Strenuous Resistive Loads under Normoxic and Hypoxic Conditions

A study involving nine healthy males was conducted to determine the developmental rate of inspiratory muscle fatigue during resistive loads under normoxic and hypoxic conditions. The subjects aged 19 to 38 years performed a bicycle exercise test of increasing power during an exhaustive inspiratory–expiratory resistive load of 40 cm water column/l s–1 inhaling air or oxygen. The volumetric and temporal respiratory parameters, the partial CO2 pressure in the alveolar gas, the total force of inspiratory muscle contractions, the electrical activity of parasternal muscles (EMG), and the initial inspiratory activity were recorded. The degree of inspiratory muscle fatigue was assessed by the “tension–time” index Pm /Pm maxTI /TT as well as by the ratio of the mean amplitudes of the EMG-signal spectrum in the high-frequency (H) range to the mean spectrum amplitudes in the low-frequency (L) range (H/L). It was established that human working capacity during increasing muscular loads against the background of highly resistive breathing was not a function of the oxygen content in the inhalation mixtures within 21 to 100%; i.e., the maximal power of the work done did not significantly differ. It was shown that pulmonary ventilation, the force generated by inspiratory muscles, the breathing effort values, the initial inspiratory activity value, and the “tension–time” index increased in parallel with the intensity of the exercise when both air and oxygen were inhaled. The Pm /Pm maxTI /TT values in the last minutes of the muscular load significantly exceeded the fatigue zone range, attaining 0.25 to 0.45 in different subjects. By the moment of refusal to continue the work, the H/L ratio had decreased by an average of 36% when air and oxygen were inhaled. The limitation of the physical working capacity of a healthy individual during an exhaustive resistive load is considered to be linked to inspiratory muscle fatigue developing at an equal rate under both normoxic and hyperoxic conditions. An impairment of the arterial blood supply to inspiratory muscles due to occlusion of the intramuscular vessels during intense muscular contractions and a considerable shortening of the time of the relaxation of the respiratory muscles in the expiratory phase is supposed to occur in forced respiration with an additional gas flow obstruction. The fact of the alternation of the electrical activity between the parasternal and other inspiratory muscles within individual inspiratory phases combined with resistive and physical loads is established, which may serve as one of the signs of inspiratory muscle fatigue.

Flow triggering added to pressure support ventilation improves comfort and reduces work of breathing in mechanically ventilated patients

Purpose: The purpose of this study was to measure the effect of flow triggering (FT), added to pressure support ventilation (PSV), during spontaneous breathing in intubated patients. Materials and Methods: A prospective observational study was conducted at a Comprehensive Cancer Center, University Hospital. Fourteen consecutive critically ill, mechanically ventilated patients on PSV with positive end-expiratory pressure were studied. Flow triggering was added to PSV in spontaneously breathing ventilated patients. Results: Respiratory rate ( f), minute ventilation (Vε), patient work of breathing (WOB p), respiratory drive (P 0.1), rapid shallow breathing index ( f/V t), tidal volume (V t) and a visual analog scale of breathing effort and comfort all improved. There was a large decrease in WOB p, and P 0.1, when flow triggering was added to PSV ( P < .001). There was a moderate decrease in f/V t during the same procedure ( P < .01). Twelve patients felt subjectively better with the intervention. Conclusions: Flow triggering offers an excellent complement to PSV because it improves patient comfort and reduces the magnitude of the inspiratory effort as well as the delay time between inspiratory muscle contraction and gas flow. It augments gas exchange at no metabolic cost to the patient while reducing the work of breathing.

Experimental reinnervation of a strap muscle with a few roots of the phrenic nerve in rabbits.

In order to compare application of the roots of the phrenic nerve to the ansa hypoglossi for laryngeal muscle neurotization, 1 or more roots from the phrenic nerve were implanted into the right sternothyroid (RST) muscle of rabbits (n = 36). Controls were intact animals (in which RST innervation is provided by the ansa; n = 6) and denervated ones (n = 6). At 66 +/- 2 days (mean +/- SE) after neurotization, during quiet breathing, inspiratory electromyographic activity and isometric contraction force were observed in all reinnervated RST muscles (n = 24). During maximal inspiratory effort, electromyographic activity and force increased. In animals reinnervated by the C4 root alone, forces (46.22 +/- 7.8 g) were significantly higher than in intact animals (10.83 +/- 5.0 g). Retrograde labeling proved the phrenic origin of the neurotization. Electromyography of the diaphragm was recorded. We conclude that in rabbits, neurotization of a strap muscle by 1 or 2 roots of the phrenic nerve allows inspiratory contraction, even during quiet breathing. Such inspiratory activity is not observed in sternothyroid muscles of intact animals innervated by the ansa hypoglossi.

Inspiratory flow dynamics during phrenic nerve stimulation in awake normals during nasal breathing.

The loss of upper airway (UA) dilators preactivation before inspiratory muscle contraction is an important determinant of the pathophysiology of obstructive sleep apnea. We hypothetized that phrenic nerve stimulation could provide a practical way to explore the effects of the dissociation between UA dilators and inspiratory muscles, and possibly to determine UA critical closing pressure during wakefulness. The pattern of inspiratory airflow was therefore studied in normal awake subjects during diaphragm twitches induced by either electrical phrenic stimulation (ES) or cervical magnetic stimulation (CMS) (n = 9) and with and without a nasal stent during ES (n = 7). End-expiratory stimulations applied during exclusive nasal breathing induced 200 to 300 ms twitch inspiratory flow. The average maximal twitch flow of flow-limited twitches was higher during CMS than ES (1.18 +/- 0.29 L.

Breathing responses to small inspiratory threshold loads in humans.

To investiage the effect of inspiratory threshold load (ITL) on breathing, all previous work studied loads that were much greater than would be encountered under pathophysiological conditions. We hypothesized that mild ITL from 2.5 to 20 cmH2O is sufficient to modify control and sensation of breathing. The study was performed in healthy subjects. The results demonstrated that with mild ITL 1) inspiratory difficulty sensation could be perceived at an ITL of 2.5 cmH2O; 2) tidal volume increased without change in breathing frequency, resulting in hyperpnea; and 3) although additional time was required for inspiratory pressure to attain the threshold before inspiratory flow was initiated, the total inspiratory muscle contraction time remained constant. This resulted in shortening of the available time for inspiratory flow, so that the tidal volume was maintained or increased by significant increase in mean inspiratory flow. On the basis of computer simulation, we conclude that the mild ITL is sufficient to increase breathing sensation and alter breathing control, presumably aiming at maintaining a certain level of ventilation but minimizing the energy consumption of the inspiratory muscles.

Physiological basis and pharmacology of motion sickness: an update

Motion sickness can occur when sensory inputs regarding body position in space are contradictory or are different from those predicted from experience. Signals from the vestibular system are essential for triggering motion sickness. The evolutionary significance of this malady is unclear, although it may simply represent the aberrant activation of vestibuloautonomic pathways that typically subserve homeostasis. The neural pathways that produce nausea and vomiting during motion sickness are presumed to be similar to those that generate illness after ingestion of toxins. The neural substrate of nausea is unknown but may include neurons in the hypothalamus and inferior frontal gyrus of the cerebral cortex. The principal motor act of vomiting is accomplished through the simultaneous contractions of inspiratory and expiratory respiratory muscles and is mediated by neurons in the lateral medullary reticular formation and perhaps by cells near the medullary midline. Cocontraction of the diaphragm and abdominal muscles increases pressure on the stomach, which causes gastric contents to be ejected through the mouth. Effective drugs for combating motion sickness include antihistamines, antimuscarinics, 5-HT 1A (serotonergic) receptor agonists and neurokinin type 1 receptor antagonists. However, considerable information concerning the physiological basis and pharmacology of motion sickness is unknown; future research using animal models will be required to understand this condition.

Abdominal muscle recruitment and PEEPi during bronchoconstriction in chronic obstructive pulmonary disease.

BACKGROUND: It has been recently shown that, when breathing at rest, many patients with severe chronic obstructive pulmonary disease (COPD) contract abdominal muscles during expiration, and that this contraction is...

Respiratory muscle length and strength in patients with chronic abdominal distension.

Starling's law (the energy of muscle contraction is proportional to the initial fiber length) has been applied to contraction of inspiratory muscles. Its application to the expiratory muscles is difficult because both maximal length and maximal pressure development occur at total lung capacity (TLC). We hypothesize that decrease of both inspiratory (Pimax) and expiratory (Pemax) muscle strength in chronic ascites (CA) will reflect generalized muscle weakness and stretching of both the diaphragm and abdominal wall as well. To test this hypothesis, we evaluated Pimax and diaphragm length (at functional residual capacity) in 22 patients. Pemax, external oblique and transversus abdominus muscle lengths, and anterior abdominal wall muscle thickness were measured at TLC. We found Pimax (78 +/- 19% predicted), Pemax (61 +/- 17%), and--as an index of general muscle strength--handgrip strength (75 +/- 22%) all to be minimally reduced. Respiratory muscle strength did not correlate with any measurement of inspiratory/expiratory muscle length or thickness. With fluid removal, abdominal muscles shortened; diaphragmatic curvature decreased although diaphragm length was unchanged. Nevertheless, neither Pimax nor Pemax increased. Respiratory muscle strength depends upon generalized muscle strength more so than upon muscle length in CA patients.

The effect of chest wall transcutaneous electrical nerve stimulation on dyspnoea

We studied the effects of transcutaneous electrical nerve stimulation (TENS) over the chest wall on breathlessness in normal subjects during exercise. Eleven male subjects performed a progressive incremental exercise test to break point on four consecutive days. TENS (continuous form, frequency 100 Hz, pulse width 200 μs) was applied during three of these tests — over the second intercostal spaces during inspiration (‘in phase’ with the underlying inspiratory muscle contraction) or expiration (‘out of phase’ with contraction) or over the deltoid muscles during inspiration (control), and not on the fourth occasion in random order. Breathlessness (Borg scale), heart rate, respiratory frequency, tidal volume, minute ventilation and minute oxygen uptake were measured. No significant differences were found for any of the measured variables between the four study days. We conclude that TENS under these circumstances has no effect on the sensation of breathlessness or on the measured physiological variables in normal subjects during exercise.

Neck muscle activity in patients with severe chronic obstructive pulmonary disease.

The present studies were designed to assess the pattern of activity and the frequency of activation of the neck muscles in patients with chronic obstructive pulmonary disease (COPD). Using concentric needle electrodes, we thus recorded the electromyograms of the scalene, sternocleidomastoid, and trapezius muscles during resting breathing in 40 stable patients with severe chronic airflow obstruction (FEV1 = 0.69 +/- 0.18 L) and hyperinflation (FRC = 228 +/- 40% of predicted); 17 patients were hypercapnic at rest. When breathing in the seated posture, all patients (100%) had strong inspiratory contraction of the scalenes. In contrast, no patient showed inspiratory activity in the trapezius, and only four patients (10%) showed definite, invariable inspiratory activity in the sternocleidomastoid. These two muscles were silent in the supine posture as well, even though the adoption of this posture was associated with an increase in dyspnea in most patients. We conclude, therefore, that in contrast to conventional thinking, most stable patients with severe COPD do not use the sternocleidomastoids or the trapezii when breathing at rest. Additional measurements indicated that the sternocleidomastoid inspiratory activity previously recorded in such patients was in general caused by a cross-contamination from surrounding muscles.

What do fully paralyzed awake humans feel when they attempt to move?

Subjects are able to judge the strength of muscle contraction. In theory, the force of muscular exertion could be perceived either from mechanoreceptor afferents or from knowledge of central motor command (corollary discharge). Sensations of great effort or exerted force have been described by subjects when their limbs were weakened by fatigue or partial paralysis. This has been taken as evidence that effort sensations arise from central motor commands rather than from mechanoreceptor afferent signals produced by muscle contraction. To differentiate between these possibilities, we used neuromuscular block to completely paralyze four waking subjects and required them to attempt maximal contraction of inspiratory muscles and of hand muscles. They were questioned after recovery about what their sensations were when attempting these contractions. None described the sensations of exerted force, great effort, or heaviness, which would have been expected if motor commands alone were the source of these sensations. The contradiction between our findings and those previously reported suggests that the specific neural mechanisms for effort sensations must be reexamined.

Inspiratory muscle performance relative to the ventilatory threshold in healthy subjects

Inspiratory muscle performance, ventilation, and gas exchange were studied during exercise in healthy subjects to look for typical changes of pattern of contraction at the ventilatory threshold (VT). The steepening of the slope of carbon dioxide output (VCO2) vs oxygen uptake (VO2) at the VT was accompanied by a nonlinear increase of the mean rate of esophageal pressure development (Pes/TI) vs the esophageal pressure time index (PTIes) reflecting both the relative force (Pbreath/Pesmax) and duration (TI/TTOT) required for inspiration. The esophageal pressure time integral within one breath (Pbreath.dTI) was one of the best single predictors of the ventilatory equivalent for oxygen (VE/VO2) at the VT. Moreover, we presented inspiratory muscle load indices as a mirror image of breathing pattern, with the obvious advantage that the ventilation component can be compared with better established methods of presenting ventilatory output. Inspiratory muscle performance during exercise should link the increased metabolic rate to ventilatory output. We conclude that 1) there exists an inspiratory muscle threshold that is well correlated to commonly used gas exchange thresholds, and 2) the efficiency of ventilation and gas exchange during exercise could be linked to pressure and timing of inspiratory muscle contraction.