Maximum inspiratory muscle endurance capacity during resistive loading in chronic obstructive pulmonary disease

In 10 patients with stable severe chronic obstructive pulmonary disease (COPD) we evaluated the relationship between the degree of airway obstruction and hyperinflation, and the maximum inspiratory muscle endurance capacity during added inspiratory resistive loading. We measured the ratio of forced expiratory volume in 1 s to forced vital capacity (FEV1/FVC) and airway resistance (Raw) as indices of airway obstruction, and the ratio of functional residual capacity to total lung capacity (FRC/TLC) as an index of hyperinflation. The mean resting transdiaphragmatic pressure to its maximum (Pdi/Pdimax), the tension time index of the diaphragm, and the maximum transdiaphragmatic pressure (Pdimax) were also determined. Following 15 min of resting breathing, the patients breathed through added inspiratory resistances which were progressively increased every 3 min until exhaustion. Maximum endurance capacity (ECmax) was defined as the product of the esophageal pressure - time integral and frequency at the maximum load sustainable for 3 min. ECmax correlated significantly with Raw (r = -0.67, p less than 0.04). The addition of FRC/TLC to the analysis resulted in a significant increase in the correlation coefficient (r = 0.86, p less than 0.01). ECmax did not correlate with FEV1/FVC. Both resting Pdi/Pdimax and Pdimax independently influenced ECmax. In addition, Pdimax correlated significantly with FRC/TLC, and resting Pdi/Pdimax with Raw. We conclude that in stable patients with severe COPD, both airway obstruction and hyperinflation affect maximum inspiratory muscle endurance capacity during inspiratory resistive loading.     

Mechanical load and inspiratory muscle action during induced asthma

To examine the relationship between inspiratory mechanical load in asthma and the pattern of respiratory muscle recruitment, we studied lung and chest wall mechanics in 7 asymptomatic asthmatics in whom progressive bronchoconstriction was induced with inhaled aerosolized histamine. A fall in the FEV1 to 49.5 +/- 3.9% of the control value (mean +/- 1 SE) was associated with a 10.7-fold increase in the inspiratory work rate of the inspiratory muscles from 6.7 +/- 1.6 to 71.4 +/- 11.4 Joules/min. Elastic work accounted for 69% of the total work during the control period and 57% at the maximal level of bronchoconstriction studied. The net pressure-time product for the inspiratory muscles, measured over 1 min, rose fivefold from 245 +/- 33 cmH2O.s to a maximum of 1,211 +/- 107 cmH2O.s, indicating a relatively greater increase in the recruitment of the intercostal/accessory muscles of inspiration. The abdominal muscles, which were recruited during bronchoconstriction, relaxed during inspiration, and permitted outward movement of the abdominal wall with progressively smaller net increases in Pga. We concluded that during induced asthma (1) the increase in inspiratory muscle work was largely the result of hyperinflation, (2) the recruitment of the intercostal/accessory muscles exceeded that of the diaphragm, and (3) the combined action of the intercostal/accessory and abdominal muscles favored the diaphragm.     

Metabolic capacity of the diaphragm in patients with COPD

Chronic obstructive pulmonary disease (COPD) is associated with an increased load on the diaphragm. Chronic loading on skeletal muscles results in metabolic changes and fiber-type shifts. Therefore, we investigated whether the load on the human diaphragm imposed by COPD altered oxidative enzyme activity, glycogenolytic enzyme activity and mitochondrial energy generating capacity and efficiency. Biopsies of the diaphragm from COPD patients and control subjects were obtained and activities of L(+)3-hydroxyacylCoA-dehydrogenase (HADH, marker for beta-oxidation capacity) and phosphorylase (marker for glycogenolytic capacity) were measured spectrophotometrically. Mitochondrial energy generating capacity was measured by spectrophotometrical and radiochemical methods. Fiber-type distribution was determined electrophoretically. We found that HADH activity was increased with increasing severity of COPD (P=0.05). No change in glycogenolytic enzyme activity was observed. The activity of the mitochondrial respiratory chain complexes III and IV and oxidation of pyruvate was increased with increasing airflow obstruction. These results suggest that in COPD the diaphragm adapts to a higher workload by increasing the oxidative capacity and mitochondrial function.     

Inspiratory muscle training in patients with chronic obstructive pulmonary disease: structural adaptation and physiologic outcomes

The present study was aimed at evaluating the effects of a specific inspiratory muscle training protocol on the structure of inspiratory muscles in patients with chronic obstructive pulmonary disease. Fourteen patients (males, FEV1, 24 +/- 7% predicted) were randomized to either inspiratory muscle or sham training groups. Supervised breathing using a threshold inspiratory device was performed 30 minutes per day, five times a week, for 5 consecutive weeks. The inspiratory training group was subjected to inspiratory loading equivalent to 40 to 50% of their maximal inspiratory pressure. Biopsies from external intercostal muscles and vastus lateralis (control muscle) were taken before and after the training period. Muscle samples were processed for morphometric analyses using monoclonal antibodies against myosin heavy chain isoforms I and II. Increases in both the strength and endurance of the inspiratory muscles were observed in the inspiratory training group. This improvement was associated with increases in the proportion of type I fibers (by approximately 38%, p < 0.05) and in the size of type II fibers (by approximately 21%, p < 0.05) in the external intercostal muscles. No changes were observed in the control muscle. The study demonstrates that inspiratory training induces a specific functional improvement of the inspiratory muscles and adaptive changes in the structure of external intercostal muscles.     

Respiratory muscle function

The functional anatomy of the respiratory muscles has been reviewed. The diaphragm has been emphasized, since this is the most important inspiratory muscle, but the view has been presented that the intercostal, scaleni, and other accessory inspiratory muscles become increasingly important as airflow obstruction leads to hyperinflation. As work increases, the demand for energy and hence blood flow to those muscles has to increase. In spite of a large reserve there are situations in which demands may outstrip supply. This leads to local metabolic changes that result in muscle fatigue. We are now capable of detecting this change as alterations in EMG or in the ability to generate pressures. The latter leads to a decrease in the capacity of the respiratory pump to exchange gas, ultimately resulting in hypercapnia and hypoxemia. The true importance of respiratory muscle fatigue and its differentiation from weakness in patients with severe CAO requires more analysis. It is intuitively appropriate to address the overall decrement in the ability to maintain adequate ventilatory work at low energy cost with the different therapeutic modalities thought to be beneficial. A combination of a decrease in the load imposed on the respiratory muscles, an improvement in the contractility of those muscles, and, when there is absolute need, the resting of the fatigued muscles should result in a better chance to lead a meaningful life and perhaps to improve survival in these patients.     

Inspiratory muscle function in patients with severe kyphoscoliosis

In 9 patients with severe kyphoscoliosis we studied inspiratory muscle function by measuring transdiaphragmatic pressure (Pdi) and its components: gastric (Pga) and esophageal (Pes) pressures during quiet breathing. Maximal Pdi and maximal inspiratory mouth pressure (Pimax) were also measured. The results showed that Pimax and Pdimax were significantly lower in patients than in normal subjects. During quiet breathing, all patients had positive swings in Pga, indicating an active contraction of the diaphragm, but Pes was significantly more negative, suggesting the recruitment of intercostal and accessory inspiratory muscles. We did not find significant correlations between Pimax, Pdimax, delta Pga/delta Pes, FVC, PaO2, or PaCO2 and the degree of spinal deformity. The FVC tended to correlate with Pimax (r = 0.63) and with Pdimax (r = 0.53). The Pdi correlated with PaO2 (r = 0.66) and with PaCO2 (r = -0.76; p less than 0.05). A significant correlation was also observed between Pimax and PaO2 (r = 0.785; p less than 0.05) and between Pimax and PaCO2 (r = -0.86; p less than 0.01). We conclude that impairment of inspiratory muscle function is related to the development of ventilatory failure in kyphoscoliosis.     

Sex differences in thoracic adaptation to pulmonary hyperinflation in cystic fibrosis.

Sex differences in thoracic adaptation have been reported in patients with cystic fibrosis (CF). The interplay between the pattern of thoracic adaptation and the function of the respiratory muscles in male and female CF patients with pulmonary hyperinflation was investigated. Thoracic dimensions and diaphragm length were measured at residual volume, functional residual capacity and total lung capacity using chest radiography in 23 CF (12 males) and 18 normal (11 males) subjects. Respiratory muscle recruitment during resting breathing was assessed by recording intrathoracic and intra-abdominal pressures. In female CF patients, ribcage expansion was predominant, tending to preserve diaphragm length. In male CF patients, thoracic configuration was normal and diaphragm shortening consequently greater. Ribcage cross-sectional area for a given rib inclination was greater in CF patients, indicating a structural expansion of the ribcage 2.5 times greater in females than males. The contribution of inspiratory ribcage muscles to inspiratory pressure was also greater relative to the diaphragm in the CF group. In conclusion, a structural expansion of the ribcage occurs in cystic fibrosis patients with lung hyperinflation that is greater in females than males. This is associated with an apparent greater contribution of inspiratory ribcage muscles to inspiratory pressure.     

High intensity exercise training-induced metabolic alterations in respiratory muscles.

Limited information exists concerning the effects of high intensity interval exercise training (HIET) on metabolic alterations in both inspiratory and expiratory muscles. To test the hypothesis that HIET will improve the oxidative capacity of the diaphragm and major expiratory muscles, we examined Krebs cycle and beta oxidation enzyme activities in the diaphragm and three groups of expiratory (abdominal) muscles in rats subjected to 12 weeks (5 days.wk-1) of treadmill exercise. Two groups of female Sprague-Dawley rats (age ca 120 days) were studied: (1) HIET group (n = 10; animals performed 6 x ca 5-min running intervals.day-1 at ca 90-95% VO2max); (2) sedentary control group (n = 7). When compared to controls, HIET resulted in significantly elevated (P less than 0.05) activities of 3-hydroxy-acyl-Co-A dehydrogenase (HADH) and citrate synthase (CS) in the costal diaphragm, rectus abdominus, external obliques, and the plantaris muscles. In contrast, training did not increase (P greater than 0.05) the activities of CS or HADH in the crural diaphragm or the internal obliques/transversus abdominus muscles. By comparison, the training-induced increases in oxidative capacity (e.g., CS activity) in the costal diaphragm, rectus abdominus, and external obliques were relatively small (ca 23, 10, 12%, respectively) when contrasted to the exercise-induced increase in CS activity in the plantaris muscle (ca 47%). We conclude that HIET results in small but significant improvements in the oxidative and beta oxidation capacities of the costal diaphragm and at least two abdominal expiratory muscles.     

Air trapping: The major factor limiting diaphragm mobility in chronic obstructive pulmonary disease patients

Background and objective:   Patients with COPD can have impaired diaphragm mechanics. A new method of assessing the mobility of the diaphragm, using ultrasound, has recently been validated. This study evaluated the relationship between pulmonary function and diaphragm mobility, as well as that between respiratory muscle strength and diaphragm mobility, in COPD patients.
Methods:   COPD patients with pulmonary hyperinflation ( n  = 54) and healthy subjects ( n  = 20) were studied. Patients were tested for pulmonary function, maximal respiratory pressures and diaphragm mobility using ultrasound to measure the craniocaudal displacement of the left branch of the portal vein.
Results:   COPD patients had less diaphragm mobility than did healthy individuals (36.5 ± 10.9 mm vs 46.3 ± 9.5 mm, P  = 0.001). In COPD patients, diaphragm mobility correlated strongly with pulmonary function parameters that quantify air trapping (RV: r  = −0.60, P  < 0.001; RV/TLC: r  = −0.76, P  < 0.001), moderately with airway obstruction (FEV₁: r  = 0.55, P  < 0.001; airway resistance: r  = −0.32, P  = 0.02) and weakly with pulmonary hyperinflation (TLC: r  = −0.28, P  = 0.04). No relationship was observed between diaphragm mobility and respiratory muscle strength (maximal inspiratory pressure: r  = −0.11, P  = 0.43; maximal expiratory pressure: r  = 0.03, P  = 0.80).
Conclusion:   The results of this study suggest that the reduction in diaphragm mobility in COPD patients is mainly due to air trapping and is not influenced by respiratory muscle strength or pulmonary hyperinflation.     

Costal and crural diaphragm, and intercostal and genioglossal electromyogram activities during spontaneous augmented breaths (sighs) in kittens

Spontaneously occurring augmented breaths (sighs) are common in infants. The pattern of electrical activity of the inspiratory muscles of the thorax and upper airway during augmented breaths, however, has not been fully characterized in this less than fully mature age group. We therefore examined costal and crural diaphragm and external intercostal and genioglossal EMG activities during spontaneous augmented breaths (n = 46) in 10 anesthetized (1.35% halothane) 1-month-old kittens breathing room air. EMG responses were assessed by comparing the spontaneous augmented breaths (AB) to the five immediately preceding breaths (control). The peak moving time average EMG activity observed during the AB was 240 +/- 32% (mean +/- SD) of control for the costal diaphragm, 279 +/- 66% of control for the crural diaphragm, and 274 +/- 68% of control for the external intercostal muscle. The mean increase in EMG activity during the AB was not significantly different among these three muscle groups (P greater than 0.25). Genioglossal EMG activity during AB was observed in only 1 of 10 study animals. These results document that during AB in anesthetized kittens, activity of the thoracic inspiratory muscles (costal/crural diaphragm and external intercostal muscles) increase in parallel, suggesting that they are modulated in a uniform manner. The infrequent observance of genioglossal activity during AB suggests that either 1) halothane anesthesia depresses genioglossal activity more than diaphragmatic and intercostal activity during AB or 2) that genioglossal recruitment is not necessary to maintain upper airway patency during this period of heightened respiratory drive.     

Activation of the inspiratory intercostal muscles by electrical stimulation of the spinal cord

Electrical stimulation of the spinal cord was evaluated as a method of activating the inspiratory intercostal muscles. Studies were performed in anesthetized dogs after hyperventilation-induced apnea. A stainless steel electrode, rubberized along its entire length except for 2 to 3 mm at the distal tip, was introduced epidurally onto the dorsal surface of the thoracic spinal cord. Stimulating electrodes were also placed in each hemidiaphragm. Intercostal electromyograms, inspired volume, and thoracoabdominal movements were monitored. The inspiratory capacity was determined in each animal as the volume required to achieve an airway pressure of +25 cm H2O during passive lung inflation. Spinal cord stimulation at the T2-T3 spinal level resulted in maximal inspired volume generation and electrical activation of the parasternal, external, and internal intercostal muscles of the upper and midrib cage regions as determined by electromyograms. Intrathoracic pressure swings increased progressively with increasing stimulus amplitude and frequency until plateaus were reached at 6 mA and 40 Hz, respectively. Postphrenicotomy spinal cord stimulation resulted in expansion of the rib cage and reduction in circumference of the abdominal compartment. Inspired volumes during spinal cord stimulation were 537 +/- 49 ml (prephrenicotomy, prone), 347 +/- 19.6 ml (postphrenicotomy, prone), and 303 +/- 30.6 ml (postphrenicotomy, supine). Bilateral diaphragm activation alone resulted in inspired volumes of 404 +/- 39 ml. Combined diaphragm and postphrenicotomy spinal cord stimulation (supine) resulted in an inspired volume of 712 +/- 72 ml, which approximated the inspiratory capacity (803 +/- 35 ml). Our results suggest that spinal cord stimulation may be a useful physiologic and clinical tool to produce coordinated contraction of the inspiratory intercostal muscles.     

Does inhaled albuterol improve diaphragmatic contractility in patients with chronic obstructive pulmonary disease?

We tested the hypothesis that the decrease in dyspnea in patients with COPD with inhaled albuterol is in part due to increased diaphragmatic contractility. Eleven patients with COPD inhaled albuterol or placebo in a double-blind randomized manner. Subsequently, dyspnea was measured while patients breathed through inspiratory resistors, and diaphragmatic contractility was quantified during maximal inspiratory efforts and after twitch stimulation of the phrenic nerves. Albuterol produced a decrease in dyspnea (5 +/- 2 to 4 +/- 2 [SD] Borg units, p < 0.01), and increases in maximal transdiaphragmatic pressure (92.4 +/- 37.2 to 102.8 +/- 37.2 cm H(2)O, p < 0.03) and potentiated twitch transdiaphragmatic pressures (21.6 +/- 7.1 to 25.2 +/- 7.6 cm H(2)O, p < 0.02). The decrease in dyspnea correlated with the increases in maximal and twitch transdiaphragmatic pressures: r = -0.64 (p = 0. 04) and r = -0.65 (p = 0.04), respectively. Compared with placebo, albuterol produced an increase in inspiratory capacity (1.87 +/- 0. 71 to 2.26 +/- 0.74 L, p = 0.002), which accounted for the increases in maximal and twitch transdiaphragmatic pressures. The decrease in dyspnea correlated with the increase in inspiratory capacity (r = -0. 62, p = 0.04), but not with the increase in FEV(1) (r = -0.13, p = 0. 72). In conclusion, albuterol relieves dyspnea and enhances respiratory muscle output in patients with COPD primarily by improving the length-tension relationship of the diaphragm rather than by improving its contractility.     

Inspiratory muscle training improves lung function and exercise capacity in adults with cystic fibrosis

STUDY OBJECTIVES: To investigate the effects of high-intensity inspiratory muscle training (IMT) on inspiratory muscle function (IMF), diaphragm thickness, lung function, physical work capacity (PWC), and psychosocial status in patients with cystic fibrosis (CF). DESIGN: Twenty-nine adult patients with CF were randomly assigned to three groups. Two groups were required to complete an 8-week program of IMT in which the training intensity was set at either 80% of maximal effort (group 1; 9 patients) or 20% of maximal effort (group 2; 10 patients). A third group of patients did not participate in any form of training and acted as a control group (group 3; 10 patients). INTERVENTIONS: In all patients, baseline and postintervention measures of IMF were determined by maximal inspiratory pressure (Pimax), and sustained Pimax (SPimax); pulmonary function, body composition, and physical activity status were also determined. In addition, diaphragm thickness was measured at functional residual capacity (FRC) and total lung capacity (TLC) [TDIcont], and the diaphragm thickening ratio (TR) was calculated (TR = thickness during Pimax at FRC/mean thickness at FRC). Subjects also completed an incremental cycle ergometer test to exhaustion and two symptom-related questionnaires, prior to and following training. RESULTS: Following training, significant increases in Pimax and SPimax (p < 0.05), TDIcont (p < 0.05), TR (p < 0.05), vital capacity (p < 0.05), TLC (p < 0.05), and PWC (p < 0.05) were identified, and decreases in anxiety scores (p < 0.05) and depression scores (p < 0.01) were noted in group 1 patients compared to group 3 patients. Group 2 patients significantly improved Pimax and SPimax (both p < 0.05) only with respect to group 3 patients. No significant differences were observed in group 3 patients. CONCLUSION: An 8-week program of high-intensity IMT resulted in significant benefits for CF patients, which included increased IMF and thickness of the diaphragm (during contraction), improved lung volumes, increased PWC, and improved psychosocial status.     

Inspiratory muscle unloading by neurally adjusted ventilatory assist during maximal inspiratory efforts in healthy subjects

BACKGROUND: Neurally adjusted ventilatory assist (NAVA) is a mode of mechanical ventilation in which the ventilator is controlled by the electrical activity of the diaphragm (EAdi). During maximal inspirations, the pressure delivered can theoretically reach extreme levels that may cause harm to the lungs. The aims of this study were to evaluate whether NAVA could efficiently unload the respiratory muscles during maximal inspiratory efforts, and if a high level of NAVA would suppress EAdi without increasing lung-distending pressures. METHOD: In awake healthy subjects (n = 9), NAVA was applied at increasing levels in a stepwise fashion during quiet breathing and maximal inspirations. EAdi and airway pressure (Paw), esophageal pressure (Pes), and gastric pressure, flow, and volume were measured. RESULTS: During maximal inspirations with a high NAVA level, peak Paw was 37.1 +/- 11.0 cm H(2)O (mean +/- SD). This reduced Pes deflections from - 14.2 +/- 2.7 to 2.3 +/- 2.3 cm H(2)O (p < 0.001) and EAdi to 43 +/- 7% (p < 0.001), compared to maximal inspirations with no assist. At high NAVA levels, inspiratory capacity showed a modest increase of 11 +/- 11% (p = 0.024). CONCLUSION: In healthy subjects, NAVA can safely and efficiently unload the respiratory muscles during maximal inspiratory maneuvers, without failing to cycle-off ventilatory assist and without causing excessive lung distention. Despite maximal unloading of the diaphragm at high levels of NAVA, EAdi is still present and able to control the ventilator.     

Subcellular adaptation of the human diaphragm in chronic obstructive pulmonary disease.

Pulmonary hyperinflation impairs the function of the diaphragm in patients with chronic obstructive pulmonary disease (COPD). However, it has been recently demonstrated that the muscle can counterbalance this deleterious effect, remodelling its structure (i.e. changing the proportion of different types of fibres). The aim of this study was to investigate whether the functional impairment present in COPD patients can be associated with structural subcellular changes of the diaphragm. Twenty individuals (60+/-9 yrs, 11 COPD patients and 9 subjects with normal spirometry) undergoing thoracotomy were included. Nutritional status and respiratory function were evaluated prior to surgery. Then, small samples of the costal diaphragm were obtained and processed for electron microscopy analysis. COPD patients showed a mean forced expiratory volume in one second (FEV1) of 60+/-9% predicted, a higher concentration of mitochondria (n(mit)) in their diaphragm than controls (0.62+/-0.16 versus 0.46+/-0.16 mitochondrial transections (mt) x microm(-2), p<0.05). On the other hand, subjects with air trapping (residual volume (RV)/total lung capacity (TLC) >37%) disclosed not only a higher n(mit) (0.63+/-0.17 versus 0.43+/-0.07 mt x microm(-2), p<0.05) but shorter sarcomeres (L(sar)) than subjects without this functional abnormality (2.08+/-0.16 to 2.27+/-0.15 microm, p<0.05). Glycogen stores were similar in COPD and controls. The severity of airways obstruction (i.e. FEV1) was associated with n(mit) (r=-0.555, p=0.01), while the amount of air trapping (i.e. RV/TLC) was found to correlate with both n(mit) (r=0.631, p=0.005) and L(sar) (r=-0.526, p<0.05). Finally, maximal inspiratory pressure (PI,max) inversely correlated with n(mit) (r=-0.547, p=0.01). In conclusion, impairment in lung function occurring in patients with chronic obstructive pulmonary disease is associated with subcellular changes in their diaphragm, namely a shortening in the length of sarcomeres and an increase in the concentration of mitochondria. These changes form a part of muscle remodelling, probably contributing to a better functional muscle behaviour.     

Mitochondrial function in diaphragm of emphysematous hamsters after treatment with nandrolone

Respiratory failure in patients with COPD may be caused by insufficient force production or insufficient endurance capacity of the respiratory muscles. Anabolic steroids may improve respiratory muscle function in COPD. The effect of anabolic steroids on mitochondrial function in the diaphragm in emphysema is unknown. In an emphysematous male hamster model, we investigated whether administration of the anabolic steroid nandrolone decanoate (ND) altered the activity of mitochondrial respiratory chain complexes in the diaphragm. The bodyweight of hamsters treated with ND was decreased after treatment compared with initial values, and serum testosterone levels were significantly lower in hamsters treated with ND than in control hamsters. No difference in the activity of mitochondrial respiratory chain complexes in the diaphragm between normal and emphysematous hamsters was observed. Treatment with ND did not change the activity of mitochondrial respiratory chain complexes in the diaphragm of both normal and emphysematous hamsters. In emphysematous hamsters, administration of ND decreased the activity of succinate:cytochrome c oxidoreductase compared with ND treatment in normal hamsters. We conclude that anabolic steroids have negative effects on the activity of succinate:cytochrome c oxidoreductase and anabolic status in this emphysematous hamster model.     

External intercostal muscle activity during acute hypoxia in the kitten

The effects of acute hypoxia on the recruitment of external intercostal muscle activity were determined in 12 kittens, aged 14 to 36 days. The animals were anesthetized with 1.23 +/- 0.23% halothane and bipolar electrodes were placed in the costal and crural diaphragm and in dorsal external intercostal muscles. Acute hypoxia was induced by the animals breathing 13% oxygen; arterial gases were sampled during baseline conditions and at 1 and 5 min after induction of hypoxia. Peak-moving average (PA) and minute electromyogram (EMG) activity (PA x f) were recorded during baseline conditions and at 1 and 5 min after onset of acute hypoxia. At 1 min of acute hypoxia, PA and PA x f of the costal diaphragm, crural diaphragm, and external intercostal muscles were significantly increased above baseline values (P less than 0.01). After 5 min of acute hypoxia, PA of all three muscles remained elevated above baseline values (P less than 0.05) but PA x f returned toward baseline levels. Respiratory frequency remained unchanged during the hypoxic stimulus. These data document that the newborn is capable of increasing inspiratory external intercostal muscle EMG activity during acute hypoxia. We speculate that this phasic recruitment could be of physiologic benefit to the newborn by stabilizing the complaint chest wall and by increasing the contribution of rib cage expansion to tidal breathing.     

Inspiratory augmentation during asphyxic hyperpnoea and gasping: proprioceptive influences

The relative inspiratory augmentations of sternomastoid, scalene, external intercostal, interchondral and diaphragmatic electromyographic activities were examined during the progressive asphyxia induced by rebreathing in pentobarbitone/urethane anaesthetized rabbits. Diaphragmatic activity augmented significantly less than that of the scalene, intercostal and interchondral muscles in response to the asphyxic increase in inspiratory drive (hyperpnoea). Cervical vagotomy significantly increased the levels of inspiratory activity during the asphyxic hyperpnoea but did not abolish these relations. Dorsal rhizotomy at levels appropriate for the respective recording sites significantly limited the intercostal and interchondral augmentations, and depressed diaphragmatic activity to a less pronounced extent, but did not affect scalene activity. The asphyxic apnoea succeeding the hyperpnoea was terminated by gasping respiration. Excepting the interchondrals each muscle exhibited significantly greater electromyographic amplitudes during gasping than during the terminal hyperpnoeic efforts. Only during gasping were the sternomastoid muscles recruited. The intercostal and scalene gasps were significantly greater than those exhibited by either the interchondrals or the diaphragm. Such disproportionate responses were not affected by vagotomy or dorsal rhizotomy. The disparate inspiratory contributions during progressive asphyxia can therefore only be partially accounted for by differences in proprioceptive control.     

Human respiratory muscles: fibre morphology and capillary supply

In man the diaphragm (DIA) and abdominal muscles comprise approximately 50% slow-twitch (ST) fibres, whereas a higher proportion (60%) is found in intercostal muscles and the scalenes. All respiratory muscles show an equal distribution of fast-twitch (FTa and b) fibres with the exception of the expiratory intercostal muscles which have few FTb fibres. The inspiratory muscles have a uniformly small fibre size, in contrast to the expiratory intercostal muscle fibres which are large. The fibre size of the inspiratory muscles is maintained with ageing, whereas that of the expiratory intercostal muscles appears to be reduced after the age of 50 yrs. Capillary supply is most abundant in the expiratory muscles followed by DIA and the inspiratory intercostal muscles. In patients with chronic obstructive pulmonary disease (COPD) it is unknown whether a reduction in fibre size of the thoracic respiratory muscles is caused by extreme use due to increased ventilatory work, or by disuse due to an increased involvement of the extrathoracic respiratory muscles. Histochemical characteristics suggest that, in normal humans, the load on the inspiratory muscles is relatively small during contractions, whereas the expiratory intercostal muscles are exposed to severe continuous activity with a heavy load.     

Mechanical properties of respiratory muscles in primates.

We examined the in-vitro mechanical characteristics of the diaphragm and parasternal intercostal muscles in adult baboons. At optimal length (Lo) the parasternal intercostal muscles were consistently faster than the diaphragm as judged by a shorter time-to-peak tension and a reduced twitch-to-tetanus ratio. However, maximal absolute force at Lo, corrected for cross-sectional area, revealed that the inherent strengths of both inspiratory muscles were identical (31.5 +/- 3.2 N/cm2 for diaphragm vs 29.5 +/- 1.1 N/cm2 for parasternal intercostals). Moreover, at submaximal stimulation rates, the parasternal intercostals produced significantly less tension at Lo than the diaphragm. At lengths less than Lo, however, the parasternal intercostal muscles generated significantly less tetanic tension than the diaphragm. These differences are similar to previously reported values in dogs (Farkas et al. (1985) J. Appl. Physiol. 59: 528-535). Thus, based on our findings, it appears that within a given species, the parasternal intercostals are quite different in mechanical terms from the diaphragm. Since both muscles are recruited at all levels of ventilation, including quiet breathing, these differences do not appear to be related to the activation levels. Moreover, since the present results were similar to those in dogs, the differences between both muscles do not appear to be affected or altered by body habitus.