Chest wall volumes during inspiratory loaded breathing in COPD patients

Chest wall volumes and breathing patterns of 13 male COPD patients were evaluated at rest and during inspiratory loaded breathing (ILB). The sternocleidomastoid (SMM) and abdominal muscle activity was also evaluated. The main compartment responsible for the tidal volume at rest and during ILB was the abdomen. During ILB patients exhibited, in addition to increases in the ratio of inspiratory time to total time of the respiratory cycle and minute ventilation, increases (p < 0.05) in the chest wall tidal volume by an increase in abdomen tidal volume as a result of improvement of end chest wall inspiratory volume without changing on end chest wall expiratory volume. The SMM and abdominal muscle activity increased 63.84% and 1.94% during ILB. Overall, to overcome the load imposed by ILB, COPD patients improve the tidal volume by changing the inspiratory chest wall volume without modifying the predominant mobility of the abdomen at rest and without affecting the end chest wall expiratory volume.     

Compartmental chest wall volume changes during volitional normocapnic hyperpnoea

During increased ventilation, inspiratory rib cage muscles have been suggested to take over part of diaphragmatic work after the diaphragm fatigues. We investigated the extent to which this proposed change in muscle recruitment is associated with changes in the relative contribution of chest wall compartments to tidal volume (V(T)). Thirteen healthy subjects performed 1 h of fatiguing normocapnic hyperpnoea. Chest wall volumes were assessed by optoelectronic plethysmography. While breathing frequency increased (43±3 to 56±5 breaths min(-1), p=0.006) and V(T) decreased during normocapnic hyperpnoea (2.6±0.2 to 1.9±0.1l, p<0.001), the relative contribution of chest wall compartments to V(T) remained unchanged (pulmonary rib cage: 48±9 versus 51±14%; abdominal rib cage: 24±4 versus 23±9%; abdomen: 28±8 versus 26±9%; all p>0.05). In conclusion, fatiguing respiratory work is not associated with a change in compartmental contribution to V(T), even in the presence of a change in breathing pattern.     

Effects of an opioid on respiratory movements and expiratory activity in humans during isoflurane anaesthesia

Opioids increase abdominal muscle activity during anaesthesia. We proposed that opioid activity during anaesthesia would change chest wall size and movement, and contribute to ventilation. Using an optical system to measure chest wall volume, we studied 10 patients during isoflurane anaesthesia, first under the influence of an opioid and then after reversal with naloxone. Measurements were made during quiet breathing and with carbon dioxide stimulation. Airway occlusion pressure was measured to assess inspiratory and expiratory muscle activity. Chest wall volume decreased with the onset of spontaneous breathing, and decreased further when breathing was stimulated by carbon dioxide. Reversal of opioid activity increased chest wall volume. Breathing movements were predominantly abdominal. Opioid action affected the timing and amplitude of breathing but the pattern of abdominal movement was not affected. Since opioids augment abdominal muscle action during expiration, the unchanged pattern of movement can be attributed to both diaphragm and abdominal activity displacing the abdominal wall reciprocally, in the inspiratory and expiratory phases of the respiratory cycle, respectively.     

Influence of diaphragm and rib cage muscle fatigue on breathing during endurance exercise

Inspiratory muscle fatigue (IMF) can develop during exhaustive exercise and cause tachypnea or rapid shallow breathing. We assessed the effects of rib cage muscle (RCM-F) and diaphragm fatigue (DIA-F) on breathing pattern and respiratory mechanics during high-intensity endurance exercise. Twelve healthy subjects performed a constant-load (85% maximal power) cycling test to exhaustion with prior IMF and a cycling test of similar intensity and duration without prior IMF (control). IMF was induced by resistive breathing and assessed by oesophageal and gastric twitch pressure measurements during cervical magnetic stimulation. Both RCM-F and DIA-F increased RCM and abdominal muscle force production during exercise compared to control. With RCM-F, tidal volume decreased while it increased with DIA-F. RCM-F was associated with a smaller increase in end-expiratory oesophageal pressure (i.e. decrease in lung volume) than DIA-F. These results suggest that RCM-F and not DIA-F is associated with rapid shallow breathing and that lowering the operating lung volume with DIA-F may help to preserve diaphragmatic function.     

Compartmental chest wall volume changes during volitional hyperpnoea with constant tidal volume in healthy individuals

Prolonged high-intensity ventilation is associated with the development of rapid shallow breathing with decreased end-inspiratory volumes of all chest wall compartments. During respiratory muscle endurance training using normocapnic hyperpnoea, tidal volume (V_T) is normally kept constant. The aim of this study was to investigate possible changes in muscle recruitment during constant-V_T hyperpnoea, to assess potential mechanisms related to rapid shallow breathing. Ten healthy subjects performed 1 h of normocapnic hyperpnoea at 70% of maximal voluntary ventilation. Chest wall volume changes were assessed by optoelectronic plethysmography. End-inspiratory (1.08 ± 0.18 versus 0.96 ± 0.27 l, p = 0.017) and end-expiratory volumes (−0.13 ± 0.15 versus −0.31 ± 0.19 l, p = 0.007) of the pulmonary ribcage decreased significantly and lung function and respiratory muscle strength were reduced (all p < 0.05). Since with forced, constant V_T only the inspiratory rib cage muscles were unable to sustain end-inspiratory volume of their compartment, inspiratory rib cage muscles are the most likely candidate responsible for the development of rapid shallow breathing.     

Sternocleidomastoid muscle deoxygenation in response to incremental inspiratory threshold loading measured by near infrared spectroscopy

This study investigated the pattern of changes in muscle oxygenation, deoxygenation and blood volume in the sternocleidomastoid (SCM) in comparison with the parasternal (PS) and intercostal (IC) muscles during a bout of incremental inspiratory threshold loading (ITL) in healthy subjects using near-infrared spectroscopy. During progressive loading, the PS and IC showed a significant increase in oxygenated hemoglobin (5.9 ± 2.3 and 6.8 ± 2.4 μM, P<0.05) and the SCM showed an increase in deoxygenated hemoglobin (17.3 ± 3.8 μM, P<0.05). Total hemoglobin also steadily increased in the SCM whereas it decreased in the quiescent vastus lateralis muscle (20.7 ± 6.1μM vs. -6.6 ± 2.4 μM, P<0.05), which was used as the control muscle during the ITL. Our data suggests that the SCM is recruited progressively during progressive ITL and is accompanied by an increased blood volume and maintenance of O(2)Hb. Blood redistribution away from the nonactive limb muscles during the ITL may provide one source of maintaining inspiratory muscle blood volume and oxygenation during high respiratory motor output.     

Attenuated inspiratory muscle metaboreflex in endurance-trained individuals

The inspiratory metaboreflex is activated during loaded breathing to task failure and induces sympathetic activation and peripheral vasoconstriction that may limit exercise performance. Inspiratory muscle training appears to attenuate the inspiratory metaboreflex in healthy subjects. Since whole body aerobic exercise training improves breathing endurance and inspiratory muscle strength, we hypothesized that endurance-trained individuals would demonstrate a blunted inspiratory muscle metaboreflex in comparison to sedentary individuals. We studied 9 runners (23±0.7 years; maximal oxygen uptake [VO2 max] = 53 ± 4 ml kg(-1) min(-1)) and 9 sedentary healthy volunteers (24±0.7 years; VO2 max = 37 ±2 ml kg(-1) min(-1)). The inspiratory muscle metaboreflex was induced by breathing against an inspiratory load of 60% of maximal inspiratory pressure (MIP), with prolonged duty cycle. Arterial pressure, popliteal blood flow, and heart rate were measured throughout the protocol. Loaded breathing to task failure increased mean arterial pressure in both sedentary and endurance-trained individuals (96±3 to 100±4 mmHg and 101±3 to 110±5 mmHg). Popliteal blood flow decreased in sedentary but not in trained individuals (0.179±0.01 to 0.141±0.01 cm/s, and 0.211±0.02 to 0.214±0.02 cm/s). Similarly, popliteal vascular resistance increased in sedentary but not in trained individuals (559±35 to 757±56 mmHg s/cm, and 528±69 to 558±64 mmHg s/cm). These data demonstrate that endurance-trained individuals have an attenuated inspiratory muscle metaboreflex.     

Serum skeletal troponin I following inspiratory threshold loading in healthy young and middle-aged men

The purpose of this study was to determine if serum levels of skeletal troponin I (sTnI, fast and slow isoforms) could provide a sensitive marker of respiratory muscle damage in healthy humans subjected to inspiratory loads. To accomplish this, we studied healthy, young (27?±?2?years, Mean?±?SEM, n?=?5) and middle-aged (55?±?5, n?=?5) men to (1) determine the magnitude, pattern, and time course of the presence of sTnI in the serum after a single 60?min bout of inspiratory threshold loading [ITL, ~70% of maximal inspiratory pressure (MIP)], (2) determine the distribution and magnitude of DOMS after loading, and (3) compare fast and slow sTnI levels, and their relationship to other markers/indices of muscle injury including delayed onset muscle soreness (DOMS), serum creatine kinase (CK) levels, and force generating capacity of the respiratory muscles [MIP and maximal expiratory pressure (MEP)]. There was a 24?±?4 and 27?±?3% increase in fast sTnI 1?hour (p?相似文献   

Impaired exercise ventilatory mechanics with the self-contained breathing apparatus are improved with heliox

The effect of the self-contained breathing apparatus (SCBA) with compressed air (BA-A) on ventilatory mechanics, work of breathing (WOB), pulmonary function, and respiratory muscle fatigue, was compared with that of a low resistance breathing valve (LRV). Further, the effect of unloading the respiratory muscles with heliox with the SCBA (BA-H) was compared with BA-A and LRV. Twelve men completed three randomized exercise trials on separate days, each consisting of three 10 min bouts of stepping exercise (Bouts 1, 2, and 3) separated by a 5 min recovery. Subjects wore firefighter protective equipment including the SCBA. At rest, FEV₁ and peak expiratory flow rates were lower with BA-A than with LRV, but were higher with BA-H than either with BA-A or LRV. After Bout 3, expiratory reserve volume, expiratory resistive WOB, and inspiratory elastic WOB were increased in BA-A compared to LRV but these were lower with BA-H compared to BA-A. After Bout 3, maximal inspiratory and expiratory pressures were reduced with BA-A, but not with LRV or BA-H. In summary, we found that the SCBA reduced resting pulmonary function, and increased expiratory reserve volume, work of breathing, and respiratory muscle fatigue during stepping exercise, and these changes can be reduced with the use of heliox.     

Respiratory and leg muscles perceived exertion during exercise at altitude

We compared the rate of perceived exertion for respiratory (RPE,resp) and leg (RPE,legs) muscles, using a 10-point Borg scale, to their specific power outputs in 10 healthy male subjects during incremental cycle exercise at sea level (SL) and high altitude (HA, 4559 m). Respiratory power output was calculated from breath-by-breath esophageal pressure and chest wall volume changes. At HA ventilation was increased at any leg power output by ～ 54%. However, for any given ventilation, breathing pattern was unchanged in terms of tidal volume, respiratory rate and operational volumes of the different chest wall compartments. RPE,resp scaled uniquely with total respiratory power output, irrespectively of SL or HA, while RPE,legs for any leg power output was exacerbated at HA. With increasing respective power outputs, the rate of change of RPE,resp exponentially decreased, while that of RPE,legs increased. We conclude that RPE,resp uniquely relates to respiratory power output, while RPE,legs varies depending on muscle metabolic conditions.     

Nocturnal non-invasive positive pressure ventilation: physiological effects on spontaneous breathing

The dynamic process of how non-invasive positive pressure ventilation (NPPV) improves spontaneous ventilation is unclear. Therefore, daytime trends of blood gases and breathing pattern were assessed by measurements 0, 0.5, 1, 3, 7, 11 and 15 h after cessation of nocturnal controlled NPPV in patients with chronic hypercapnic respiratory failure. Twelve patients (six COPD/six restrictive) who were established on NPPV and 12 controls (six COPD/six restrictive) completed. PaCO2 decreased during controlled NPPV (P < 0.02). PaCO2 additionally decreased step by step during the first 3 h of spontaneous breathing after switching from NPPV to spontaneous breathing (P < 0.05), but remained unchanged in controls. The PaCO2 decrease was due to a stepwise increase in tidal volume (P < 0.05) at an unchanged breathing frequency. Accordingly, minute ventilation also stepwise increased (P < 0.03). There were no significant changes in controls. Improvements of PaCO2 and tidal volume occurred even after 5.7 +/- 3.1 days following first NPPV trials, but became more evident after 2 months. Maximal inspiratory mouth pressures increased in chronic obstructive pulmonary disease (COPD) patients (P < 0.05), and respiratory drive increased in restrictive patients (P < 0.05) following 2 months of NPPV. Lung function parameters and inspiratory impedance remained unchanged. Improvements in health-related quality of life were evident and were correlated to the decline of elevated bicarbonate levels (r = 0.72, P < 0.01). In conclusion, there is a stepwise adaptation process lasting 3h when switching from nocturnal controlled NPPV to daytime spontaneous breathing in which tidal volume increases and PaCO2 drops after an initial PaCO2 decrease while on NPPV.     

Inspiratory muscles do not limit maximal incremental exercise performance in healthy subjects

We investigated whether the inspiratory muscles affect maximal incremental exercise performance using a placebo-controlled, crossover design. Six cyclists each performed six incremental exercise tests. For three trials, subjects exercised with proportional assist ventilation (PAV). For the remaining three trials, subjects underwent sham respiratory muscle unloading (placebo). Inspiratory muscle pressure (P(mus)) was reduced with PAV (-35.9+/-2.3% versus placebo; P<0.05). Furthermore, V(O2) and perceptions of dyspnea and limb discomfort at submaximal exercise intensities were significantly reduced with PAV. Peak power output, however, was not different between placebo and PAV (324+/-4W versus 326+/-4W; P>0.05). Diaphragm fatigue (bilateral phrenic nerve stimulation) did not occur in placebo. In conclusion, substantially unloading the inspiratory muscles did not affect maximal incremental exercise performance. Therefore, our data do not support a role for either inspiratory muscle work or fatigue per se in the limitation of maximal incremental exercise.     

Acute and chronic responses of the upper airway to inspiratory loading in healthy awake humans: an MRI study

We assessed upper airway responses to acute and chronic inspiratory loading. In Experiment I, 11 healthy subjects underwent T(2)-weighted magnetic resonance imaging (MRI) of upper airway dilator muscles (genioglossus and geniohyoid) before and up to 10 min after a single bout of pressure threshold inspiratory muscle training (IMT) at 60% maximal inspiratory mouth pressure (MIP). T(2) values for genioglossus and geniohyoid were increased versus control (p<0.001), suggesting that these airway dilator muscles are activated in response to acute IMT. In Experiment II, nine subjects underwent 2D-Flash sequence MRI of the upper airway during quiet breathing and while performing single inspirations against resistive loads (10%, 30% and 50% MIP); this procedure was repeated after 6 weeks of IMT. Lateral narrowing of the upper airway occurred at all loads, whilst anteroposterior narrowing occurred at the level of the laryngopharynx at loads > or =30% MIP. Changes in upper airway morphology and narrowing after IMT were undetectable using MRI.     

Task failure from inspiratory resistive loaded breathing: a role for inspiratory muscle fatigue?

The use of non-invasive resistive breathing to task failure to assess inspiratory muscle performance remains a matter of debate. CO₂ retention rather than diaphragmatic fatigue was suggested to limit endurance during inspiratory resistive breathing. Cervical magnetic stimulation (CMS) allows discrimination between diaphragmatic and rib cage muscle fatigue. We tested a new protocol with respect to the extent and the partitioning of inspiratory muscle fatigue at task failure. Nine healthy subjects performed two runs of inspiratory resistive breathing at 67 (12)% of their maximal inspiratory mouth pressure, respiratory rate ( f_R), paced at 18 min^–1, with a 15-min pause between runs. Diaphragm and rib cage muscle contractility were assessed from CMS-induced esophageal (P_es,tw), gastric (P_ga,tw), and transdiaphragmatic (P_di,tw) twitch pressures. Average endurance times of the first and second runs were similar [9.1 (6.7) and 8.4 (3.5) min]. P_di,tw significantly decreased from 33.1 to 25.9 cmH₂O in the first run, partially recovered (27.6 cmH₂O), and decreased further in the second run (23.4 cmH₂O). P_es,tw also decreased significantly (–5.1 and –2.4 cmH₂O), while P_ga,tw did not change significantly (–2.0 and –1.9 cmH₂O), indicating more pronounced rib cage rather than diaphragmatic fatigue. End-tidal partial pressure of CO₂ (P_ETCO₂) rose from 37.2 to 44.0 and 45.3 mmHg, and arterial oxygen saturation (S_aO₂) decreased in both runs from 98% to 94%. Thus, task failure in mouth-pressure-targeted, inspiratory resistive breathing is associated with both diaphragmatic and rib cage muscle fatigue. Similar endurance times despite different degrees of muscle fatigue at the start of the runs indicate that other factors, e.g. increases in P_ETCO₂, and/or decreases in S_aO₂, probably contributed to task-failure.     

Characteristics of diaphragmatic fatigue during exhaustive exercise until task failure

The diaphragm was postulated to fatigue relatively early during exhaustive whole body exercise without further loss in contractility as exercise proceeds towards task failure. Diaphragmatic contractility was investigated prior/during/after exhaustive whole body exercise until task failure by using lung volume corrected twitch transdiaphragmatic pressure (TwPdi(c)) during magnetic phrenic nerve stimulation (every 45s). Eleven cyclists exercised to exhaustion (workloads ≥85% maximal oxygen uptake; 20.7±9.8min). Individual post hoc calculation of TwPdi(c) was conducted (diaphragmatic contractility versus lung volume). Diaphragmatic fatigue (i.e. TwPdi reduction baseline/recovery ≥10%) occurred in 9/11 subjects (82% "fatiguers"; baseline/recovery TwPdi(c) -16±13%, p<0.01). Fatiguers TwPdi(c) was: baseline: 2.99±0.40kPa, exercise-onset: 2.98±0.41kPa, initial third: 2.80±0.67kPa, second third: 2.54±0.55kPa, final third-task failure: 2.51±0.44kPa, recovery: 2.50±0.52kPa. Diaphragmatic contractility and lung volume (rest) were strongly related (r(2)=0.98, mean TwPdi(c) gradient 0.78kPa/l). To conclude, diaphragmatic contractility (lung volume corrected) decreases relatively early (initial two thirds) during exhaustive exercise and remains preserved towards task failure. This confirms previous assumptions postulating that respiratory performance is sustained without further fatigue of the primary inspiratory muscle.     

Mouth pressure twitches induced by cervical magnetic stimulation to assess inspiratory muscle fatigue

This study aimed at determining whether twitch mouth pressure (TwPmo) induced by cervical magnetic stimulation (CMS) was sensitive to inspiratory muscle fatigue produced by whole body exercise (WBE) in normal subjects. Twenty subjects performed one or two of the following protocols: (i). cycling at 85% V(O(2),max) until exhaustion; (ii). inspiratory resistive load (IRL) breathing at 62% of maximal inspiratory pressure until task failure. In eight subjects, oesophageal (TwPoes), gastric (TwPga) and transdiaphragmatic (TwPdi) pressures were recorded. The TwPmo was significantly reduced (P<0.05) 20 min after both WBE and IRL, from 17.5+/-4.4 to 15.9+/-3.9 cmH(2)O and from 19.4+/-4.9 to 17.7+/-4.5 cmH(2)O, respectively. Subsequently to IRL, the TwPdi decrease was associated with a reduction in TwPoes/TwPga ratio; not after WBE. Independently of the mode of ventilatory loading, inspiratory muscle fatigue was detected. Thus, inspiratory muscle fatigue after WBE can be assessed in normal subjects with a noninvasive technique.     

Impact of breathing pattern on work of breathing in healthy subjects and patients with COPD

The impact of the respiratory pattern on respiratory muscle workload represents an unresolved controversy and is important for the treatment of patients with respiratory disorders and respiratory muscle failure. We designed this study to investigate the relationship of respiratory pattern and inspiratory workload. We measured esophageal pressure and inspiratory flow and calculated work of breathing, tidal volume and respiratory rate. Ten healthy subjects and 10 COPD patients participated and performed five different breathing patterns starting from respiratory rate 12 and tidal volume 1l or quiet breathing, respectively. They were instructed to increase respiratory rate by 50 and 100% as well as tidal volume by 50 and 100% while maintaining constant minute-ventilation. In healthy subjects Delta VT was the single best parameter to predict Delta WOB (R=0.958, R(2)=0.918, p<0.0001). The relationships of changes in tidal volume, respiratory rate and rapid shallow breathing index to changes in WOB were linear. In the COPD Delta VT was also the single best parameter to predict changes in work of breathing (R=0.777, R(2)=0.604, p<0.0001), however the relation of respiratory rate and rapid shallow breathing index to work of breathing was exponential (e-function) with lower indices generating higher workload. We conclude that rapid shallow breathing might be a strategy to compensate for burdensome respiratory mechanics. In COPD patients however we observed a critical threshold where any further increases in rapid shallow breathing index will be of no further benefit.     

Respiratory muscle training improves swimming endurance in divers

Respiratory muscles can fatigue during prolonged and maximal exercise, thus reducing performance. The respiratory system is challenged during underwater exercise due to increased hydrostatic pressure and breathing resistance. The purpose of this study was to determine if two different respiratory muscle training protocols enhance respiratory function and swimming performance in divers. Thirty male subjects (23.4 ± 4.3 years) participated. They were randomized to a placebo (PRMT), endurance (ERMT), or resistance respiratory muscle training (RRMT) protocol. Training sessions were 30 min/day, 5 days/week, for 4 weeks. PRMT consisted of 10-s breath-holds once/minute, ERMT consisted of isocapnic hyperpnea, and RRMT consisted of a vital capacity maneuver against 50 cm H₂O resistance every 30 s. The PRMT group had no significant changes in any measured variable. Underwater and surface endurance swim time to exhaustion significantly increased after RRMT (66%, P < 0.001; 33%, P = 0.003) and ERMT (26%, P = 0.038; 38%, P < 0.001). Breathing frequency (f _b) during the underwater endurance swim decreased in RRMT (23%, P = 0.034) and tidal volume (V _T) increased in both the RRMT (12%, P = 0.004) and ERMT (7%, P = 0.027) groups. Respiratory endurance increased in ERMT (216.7%) and RRMT (30.7%). Maximal inspiratory and expiratory pressures increased following RRMT (12%, P = 0.015, and 15%, P = 0.011, respectively). Results from this study indicate that respiratory muscle fatigue is a limiting factor for underwater swimming performance, and that targeted respiratory muscle training (RRMT > ERMT) improves respiratory muscle and underwater swimming performance.     

Chest wall kinematics, respiratory muscle action and dyspnoea during arm vs. leg exercise in humans

Aim: We hypothesize that different patterns of chest wall (CW) kinematics and respiratory muscle coordination contribute to sensation of dyspnoea during unsupported arm exercise (UAE) and leg exercise (LE). Methods: In six volunteer healthy subjects, we evaluated the volumes of chest wall (V_cw) and its compartments, the pulmonary apposed rib cage (V_rc,p), the diaphragm‐abdomen apposed rib cage (V_rc,a) and the abdomen (V_ab), by optoelectronic plethysmography. Oesophageal, gastric and trans‐diaphragmatic pressures were simultaneously measured. Chest wall relaxation line allowed the measure of peak rib cage inspiratory muscle, expiratory muscle and abdominal muscle pressures. The loop V_rc,p/V_rc,a allowed the calculation of rib cage distortion. Dyspnoea was assessed by a modified Borg scale. Results: There were some differences and similarities between UAE and LE. Unlike LE with UAE: (i) V_cw and V_rc,p at end inspiration did not increase, whereas a decrease in V_rc,p contributed to decreasing CW end expiratory volume; (ii) pressure production of inspiratory rib cage muscles did not significantly increase from quiet breathing. Not unlike LE, the diaphragm limited its inspiratory contribution to ventilation with UAE with no consistent difference in rib cage distortion between UAE and LE. Finally, changes in abdominal muscle pressure, and inspiratory rib cage muscle pressure predicted 62% and 41.4% of the variability in Borg score with UAE and LE, respectively (P < 0.01). Conclusion: Leg exercise and UAE are associated with different patterns of CW kinematics, respiratory muscle coordination, and production of dyspnoea.