Inspiratory Threshold Loading Research Articles

Effect of external PEEP in patients under controlled mechanical ventilation with an auto-PEEP of 5cmH2O or higher.

BackgroundIn some patients with auto-positive end-expiratory pressure (auto-PEEP), application of PEEP lower than auto-PEEP maintains a constant total PEEP, therefore reducing the inspiratory threshold load without detrimental cardiovascular or respiratory effects. We refer to these patients as “complete PEEP-absorbers.” Conversely, adverse effects of PEEP application could occur in patients with auto-PEEP when the total PEEP rises as a consequence. From a pathophysiological perspective, all subjects with flow limitation are expected to be “complete PEEP-absorbers,” whereas PEEP should increase total PEEP in all other patients. This study aimed to empirically assess the extent to which flow limitation alone explains a “complete PEEP-absorber” behavior (i.e., absence of further hyperinflation with PEEP), and to identify other factors associated with it.MethodsOne hundred patients with auto-PEEP of at least 5 cmH2O at zero end-expiratory pressure (ZEEP) during controlled mechanical ventilation were enrolled. Total PEEP (i.e., end-expiratory plateau pressure) was measured both at ZEEP and after applied PEEP equal to 80 % of auto-PEEP measured at ZEEP. All measurements were repeated three times, and the average value was used for analysis.ResultsForty-seven percent of the patients suffered from chronic pulmonary disease and 52 % from acute pulmonary disease; 61 % showed flow limitation at ZEEP, assessed by manual compression of the abdomen. The mean total PEEP was 7 ± 2 cmH2O at ZEEP and 9 ± 2 cmH2O after the application of PEEP (p < 0.001). Thirty-three percent of the patients were “complete PEEP-absorbers.” Multiple logistic regression was used to predict the behavior of “complete PEEP-absorber.” The best model included a respiratory rate lower than 20 breaths/min and the presence of flow limitation. The predictive ability of the model was excellent, with an overoptimism-corrected area under the receiver operating characteristics curve of 0.89 (95 % CI 0.80–0.97).ConclusionsExpiratory flow limitation was associated with both high and complete “PEEP-absorber” behavior, but setting a relatively high respiratory rate on the ventilator can prevent from observing complete “PEEP-absorption.” Therefore, the effect of PEEP application in patients with auto-PEEP can be accurately predicted at the bedside by measuring the respiratory rate and observing the flow-volume loop during manual compression of the abdomen.

When Breathing Interferes with Cognition: Experimental Inspiratory Loading Alters Timed Up-and-Go Test in Normal Humans.

Human breathing stems from automatic brainstem neural processes. It can also be operated by cortico-subcortical networks, especially when breathing becomes uncomfortable because of external or internal inspiratory loads. How the “irruption of breathing into consciousness” interacts with cognition remains unclear, but a case report in a patient with defective automatic breathing (Ondine's curse syndrome) has shown that there was a cognitive cost of breathing when the respiratory cortical networks were engaged. In a pilot study of putative breathing-cognition interactions, the present study relied on a randomized design to test the hypothesis that experimentally loaded breathing in 28 young healthy subjects would have a negative impact on cognition as tested by “timed up-and-go” test (TUG) and its imagery version (iTUG). Progressive inspiratory threshold loading resulted in slower TUG and iTUG performance. Participants consistently imagined themselves faster than they actually were. However, progressive inspiratory loading slowed iTUG more than TUG, a finding that is unexpected with regard to the known effects of dual tasking on TUG and iTUG (slower TUG but stable iTUG). Insofar as the cortical networks engaged in response to inspiratory loading are also activated during complex locomotor tasks requiring cognitive inputs, we infer that competition for cortical resources may account for the breathing-cognition interference that is evidenced here.

Effect of acute hypoxia on inspiratory muscle oxygenation during incremental inspiratory loading in healthy adults.

To non-invasively examine the effect of acute hypoxia and inspiratory threshold loading (ITL) on inspiratory muscles [sternocleidomastoid (SCM), scalene (SA) and parasternal (PS)] oxygenation in healthy adults using near-infrared spectroscopy (NIRS). Twenty healthy adults (12 M/8 F) were randomly assigned to perform two ITL tests while breathing a normoxic or hypoxic (FIO2 = 15 %) gas mixture. NIRS devices were placed over the SCM, PS, SA, and a control muscle, tibialis anterior (TA), to monitor oxygenated (O2Hb), deoxygenated (HHb), total hemoglobin (tHb) and tissue saturation index (TSI). With the nose occluded, subjects breathed normally for 4 min through a mouthpiece that was connected to a weighted threshold loading device. ITL began by adding a 100-g weight to the ITL device. Then, every 2 min 50-g was added until task failure. Vital signs, ECG and ventilatory measures were monitored throughout the protocol. Participants were 31 ± 12 year and had normal spirometry. At task failure, the maximum load and ventilatory parameters did not differ between the hypoxic and normoxic ITL. At hypoxic ITL task failure, SpO2 was significantly lower, and ∆HHb increased more so in SA, SCM and PS than normoxic values. SCM ∆TSI decreased more so during hypoxic compared to normoxic ITL. ∆tHb in the inspiratory muscles (SCM, PS and SA) increased significantly compared to the decrease in TA during both hypoxic and normoxic ITL. The SCM, an accessory inspiratory muscle was the most vulnerable to deoxygenation during incremental loading and this response was accentuated by acute hypoxia.

Electroencephalographic detection of respiratory-related cortical activity in humans: from event-related approaches to continuous connectivity evaluation.

The presence of a respiratory-related cortical activity during tidal breathing is abnormal and a hallmark of respiratory difficulties, but its detection requires superior discrimination and temporal resolution. The aim of this study was to validate a computational method using EEG covariance (or connectivity) matrices to detect a change in brain activity related to breathing. In 17 healthy subjects, EEG was recorded during resting unloaded breathing (RB), voluntary sniffs, and breathing against an inspiratory threshold load (ITL). EEG were analyzed by the specially developed covariance-based classifier, event-related potentials, and time-frequency (T-F) distributions. Nine subjects repeated the protocol. The classifier could accurately detect ITL and sniffs compared with the reference period of RB. For ITL, EEG-based detection was superior to airflow-based detection (P < 0.05). A coincident improvement in EEG-airflow correlation in ITL compared with RB (P < 0.05) confirmed that EEG detection relates to breathing. Premotor potential incidence was significantly higher before inspiration in sniffs and ITL compared with RB (P < 0.05), but T-F distributions revealed a significant difference between sniffs and RB only (P < 0.05). Intraclass correlation values ranged from poor (-0.2) to excellent (1.0). Thus, as for conventional event-related potential analysis, the covariance-based classifier can accurately predict a change in brain state related to a change in respiratory state, and given its capacity for near "real-time" detection, it is suitable to monitor the respiratory state in respiratory and critically ill patients in the development of a brain-ventilator interface.

EFFECT OF RESPIRATORY MUSCLE TRAINING AS AN ADJUNCT TO CONVENTIONAL THERAPY IN PHASE I CARDIAC REHABILITATION FOR MEDIAN STERNOTOMY PATIENTS

BACKGROUND: Impairment of pulmonary function is a common feature in long standing cardiac diseases. Furthermore, pulmonary impairment is a definite finding after cardiac surgery than after any other major surgical procedures. METHOD: Sixty seven patients of both genders aged between 35-70 years with median sternotomy were divided into two groups by simple random allocation .Group A was given conventional phase I cardiac rehabilitation therapy. Group B was additionally given Inspiratory Muscle Training (IMT) for seven days with inspiratory threshold loading device. The outcome measures pre and post intervention were: the Visual Analogue Scale (VAS) for pain & Maximal Inspiratory pressure (MIP) for inspiratory muscle strength. RESULTS: For parametric data, paired t- test was used for within the group analysis and unpaired t-test for between the group analysis. For non-parametric data, Wilcoxon Sign Rank test was used for within group analysis and Mann Whitney U test for between group analyses. There was significant improvement in VAS and MIP following the use of IMT (p

Repetitive transcranial magnetic stimulation over the supplementary motor area modifies breathing pattern in response to inspiratory loading in normal humans.

In awake humans, breathing depends on automatic brainstem pattern generators. It is also heavily influenced by cortical networks. For example, functional magnetic resonance imaging and electroencephalographic data show that the supplementary motor area becomes active when breathing is made difficult by inspiratory mechanical loads like resistances or threshold valves, which is associated with perceived respiratory discomfort. We hypothesized that manipulating the excitability of the supplementary motor area with repetitive transcranial magnetic stimulation would modify the breathing pattern response to an experimental inspiratory load and possibly respiratory discomfort. Seven subjects (three men, age 25 ± 4) were studied. Breathing pattern and respiratory discomfort during inspiratory loading were described before and after conditioning the supplementary motor area with repetitive stimulation, using an excitatory paradigm (5 Hz stimulation), an inhibitory paradigm, or sham stimulation. No significant change in breathing pattern during loading was observed after sham conditioning. Excitatory conditioning shortened inspiratory time (p = 0.001), decreased tidal volume (p = 0.016), and decreased ventilation (p = 0.003), as corroborated by an increased end-tidal expired carbon dioxide (p = 0.013). Inhibitory conditioning did not affect ventilation, but lengthened expiratory time (p = 0.031). Respiratory discomfort was mild under baseline conditions, and unchanged after conditioning of the supplementary motor area. This is the first study to show that repetitive transcranial magnetic stimulation conditioning of the cerebral cortex can alter breathing pattern. A 5 Hz conditioning protocol, known to enhance corticophrenic excitability, can reduce the amount of hyperventilation induced by inspiratory threshold loading. Further studies are needed to determine whether and under what circumstances rTMS can have an effect on dyspnoea.

Molecular and physiological events in respiratory muscles and blood of rats exposed to inspiratory threshold loading

High-intensity exercise induces oxidative stress and inflammatory events in muscles. Tumor necrosis factor (TNF)-α may alter muscle protein metabolism or promote muscle regeneration. We hypothesized that a program of noninvasive chronic inspiratory loading of different intensities induces a differential pattern of physiological, molecular, and cellular events within rat diaphragms. Antioxidants and TNF-α blockade may influence those events. In the diaphragm, gastrocnemius, and blood of rats exposed to high-intensity inspiratory threshold loads (2hour every 24hours for 14days), with and without treatment with N-acetyl cysteine or infliximab (anti-TNF-α antibody), inflammatory cells and cytokines, superoxide anion production, myogenesis markers, and muscle structure were explored. In all animals, maximum inspiratory pressure (MIP) and body weight were determined. High-intensity inspiratory loading for 2 weeks caused a decline in MIP and body weight, and in the diaphragm induced a reduction in fast-twitch fiber proportions and sizes, whereas inflammatory cells and cytokine levels, including TNF-α immunohistochemical expression, superoxide anion, internal nuclei counts, and markers of myogenesis were increased. Blockade of TNF-α improved respiratory muscle function and structure, and animal weight, and, in the diaphragm, reduced inflammatory cell numbers and superoxide anion production drastically while inducing larger increases in protein and messenger RNA levels and immunohistochemical expression of TNF-α, internal nuclei, and markers of muscle regeneration. Blunting of TNF-α also induced a reduction in blood inflammatory cytokines and superoxide anion production. We conclude that TNF-α synthesized by inflammatory cells or myofibers could have differential effects on muscle structure and function in response to chronic, noninvasive, high-intensity inspiratory threshold loading.

Functional magnetic resonance imaging suggests automatization of the cortical response to inspiratory threshold loading in humans

Inspiratory threshold loading (ITL) induces cortical activation. It is sustained over time and is resistant to distraction, suggesting automaticity. We hypothesized that ITL-induced changes in cerebral activation may differ between single-breath ITL and continuous ITL, with differences resembling those observed after cortical automatization of motor tasks. We analyzed the brain blood oxygen level dependent (BOLD) signal of 11 naive healthy volunteers during 5min of random, single-breath ITL and 5min of continuous ITL. Single-breath ITL increased BOLD in many areas (premotor cortices, bilateral insula, cerebellum, reticular formation of the lateral mesencephalon) and decreased BOLD in regions colocalizing with the default mode network. Continuous ITL induced signal changes in a limited number of areas (supplementary motor area). These differences are comparable to those observed before and after overlearning of motor tasks. We conclude that the respiratory-related cortical activation observed in response to ITL is likely due to automated, attention-independent mechanisms. Also, ITL activates cortical circuits right from the first breath.

Neural respiratory drive measured during inspiratory threshold loading and acute hypercapnia in healthy individuals

Understanding the effects of respiratory load on neural respiratory drive and respiratory pattern are key to understanding the regulation of load compensation in respiratory disease. The aim of the study was to examine and compare the recruitment pattern of the diaphragm and parasternal intercostal muscles when the respiratory system was loaded using two methods. Twelve subjects performed incremental inspiratory threshold loading up to 50% of their maximal inspiratory pressure, and 10 subjects underwent incremental, steady-state hypercapnia to a maximal inspired CO2 of 5%. The diaphragmatic electromyogram (EMGdi) was measured using a multipair oesophageal catheter, and the parasternal intercostal muscle EMG (sEMGpara) was recorded from bipolar surface electrodes positioned in the second intercostal space. The EMGdi and sEMGpara were analysed over the last minute of each increment of both protocols, normalized using the peak EMG recorded during maximal respiratory manoeuvres and expressed as EMG%max. The EMGdi%max and sEMGpara%max increased in parallel during the two loading methods, although EMGdi%max was consistently greater than sEMGpara%max in both conditions, inspiratory threshold loading [bias (SD) 9 (3)%, 95% limits of agreement 4-15%] and hypercapnia [bias (SD) 6 (3)%, 95% limits of agreement -0.05 to 12%]. Inspiratory threshold loading resulted in more pronounced increases in mean (SD) EMGdi%max [10 (7)-45 (28)%] and sEMGpara%max [5.3 (3.1)-40 (28)%] from baseline compared with EMGdi%max [7 (4)-21 (8)%] and sEMGpara%max [4.7 (2.3)-10 (4)%] during hypercapnia, despite comparable levels of ventilation. These data support the use of sEMGpara%max, as a non-invasive alternative to EMGdi%max recorded with an invasive oesophageal electrode catheter, for the quantification of neural respiratory drive. This technique should make evaluation of respiratory muscle function easier to undertake and therefore more readily acceptable in patients with respiratory disease, in whom transduction of neural respiratory drive to pressure generation can be compromised.

A Safe Inspiratory Threshold Load in Chronic Obstructive Pulmonary Disease Patients

Objective: To determine a safe threshold resistive load that induce minimal respiratory muscle damage in clinical measures like maximal inspiratory pressure, delayed onset muscle soreness and plasma creatine kinase following a bout of inspiratory loading exercise in COPD patients. Material and Method: 30 patients with GOLD stages II and III were selected with random sampling and were divided into Group A, B & C and received inspiratory threshold loading (ITL) at intensities of 70, 50 and 30% maximal inspiratory pressure (MIP) respectively for 30 minutes. Pre and post ITL readings of delayed onset muscle soreness at 0, 4, 24 and 48 hours and maximal inspiratory pressure and plasma creatine kinase at 0, 24 and 48 hours were conducted. Results: There was a significant difference in VAS and Body chart diagram of delayed onset muscle soreness, MIP and plasma creatine in Group A than C (p 0.05). Conclusion: Inspiratory threshold loading performed at low intensity loads (

Inspiratory Muscle Training Reduces Sympathetic Nervous Activity and Improves Inspiratory Muscle Weakness and Quality of Life in Patients With Chronic Heart Failure

To evaluate the effect of inspiratory muscle training (IMT) on cardiac autonomic modulation and on peripheral nerve sympathetic activity in patients with chronic heart failure (CHF). Functional capacity, low-frequency (LF) and high-frequency (HF) components of heart rate variability, muscle sympathetic nerve activity inferred by microneurography, and quality of life were determined in 27 patients with CHF who had been sequentially allocated to 1 of 2 groups: (1) control group (with no intervention) and (2) IMT group. Inspiratory muscle training consisted of respiratory exercises, with inspiratory threshold loading of seven 30-minute sessions per week for a period of 12 weeks, with a monthly increase of 30% in maximal inspiratory pressure (PI(max)) at rest. Multivariate analysis was applied to detect differences between baseline and followup period. Inspiratory muscle training significantly increased PI(max) (59.2 ± 4.9 vs 87.5 ± 6.5 cmH(2)O, P = .001) and peak oxygen uptake (14.4 ± 0.7 vs 18.9 ± 0.8 mL·kg(-1)·min(-1), P = .002); decreased the peak ventilation (VE)/carbon dioxide production (VCO(2)) ratio (35.8 ± 0.8 vs 32.5 ± 0.4, P = .001) and the VE/VCO(2) slope (37.3 ± 1.1 vs 31.3 ± 1.1, P = .004); increased the HF component (49.3 ± 4.1 vs 58.4 ± 4.2 normalized units, P = .004) and decreased the LF component (50.7 ± 4.1 vs 41.6 ± 4.2 normalized units, P = .001) of heart rate variability; decreased muscle sympathetic nerve activity (37.1 ± 3 vs 29.5 ± 2.3 bursts per minute, P = .001); and improved quality of life. No significant changes were observed in the control group. Home-based IMT represents an important strategy to improve cardiac and peripheral autonomic controls, functional capacity, and quality of life in patients with CHF.

Effects of Expiratory Positive Airway Pressure on Dynamic Hyperinflation During Exercise in Patients With COPD

Expiratory positive airway pressure (EPAP) is a form of noninvasive positive-pressure ventilatory support that, in spite of not unloading respiratory muscles during inspiration, may reduce the inspiratory threshold load and attenuate expiratory dynamic airway compression, contributing to reduced expiratory air-flow limitation in patients with COPD. We sought to determine the effects of EPAP on operational lung volumes during exercise in COPD patients. This was a nonrandomized, experimental comparison of 2 exercise conditions (with and without EPAP); subjects completed a treadmill exercise test and performed, before and immediately after exercise, lung volume measurements. Those who overtly developed dynamic hyperinflation (DH), as defined by at least a 15% reduction from pre-exercise inspiratory capacity (IC), were invited for an additional research visit to repeat the same exercise protocol while receiving EPAP through a spring loaded resistor face mask. The primary outcome was IC variance (pre-post exercise) comparison under the 2 exercise conditions. Forty-six subjects (32 males), a mean 65.0 ± 8.2 years of age, and with moderate to severe COPD (FEV(1) = 38 ± 16% predicted) were initially enrolled. From this initial sample, 17 (37%) presented overt DH, as previously defined. No significant difference was found between these subjects and the rest of the initial sample. Comparing before and after exercise, there was significantly less reduction in IC observed when EPAP was used (-0.18 ± 0.35 L vs -0.57 ± 0.45 L, P = .02), allowing greater IC final values (1.45 ± 0.50 L vs 1.13 ± 0.52 L, P = .02). The application of EPAP reduced DH, as shown by lower operational lung volumes after submaximal exercise in COPD patients who previously manifested exercise DH.

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 < 0.01) and 3 days (p < 0.01) after ITL. Slow sTnI was elevated by 24 ± 10% (p < 0.05) 4 days postITL. Other indices of respiratory muscle injury such as CK, MIP and MEP did not show a difference in mean data following ITL; DOMS was slightly but significantly increased following ITL. Our results suggest that sTnI has superior sensitivity compared to other biomarkers/indices of skeletal muscle injury. Future studies examining the impact of respiratory muscle injury with ventilator weaning should consider using sTnI as a sensitive marker of skeletal muscle injury.

Dyspnea-pain counterirritation induced by inspiratory threshold loading: a laser-evoked potentials study

experimentally induced dyspnea of the work/effort type inhibits, in a top-down manner, the spinal transmission of nociceptive inputs (dyspnea-pain counterirritation). Previous studies have demonstrated that this inhibition can be assessed by measuring the nociceptive flexion reflex (RIII). However, its clinical application is limited because of the strong discomfort associated with the electrical stimuli required to elicit the RIII reflex. we examined whether the dyspnea-pain counterirritation phenomenon can be evaluated by measuring the effect of work/effort type dyspnea on the magnitude of laser-evoked brain potentials (LEPs). 10 normal male volunteers were studied (age: 19-30 years). LEPs were elicited using a CO(2) laser stimulator delivering 10- to 15-ms stimuli of 6 ± 0.7 W over a 12.5 mm(2) area. The EEG was recorded using nine scalp channels. Non-nociceptive somatosensory-evoked potentials (SEPs) served as control. LEPs and SEPs were recorded before, during, and after 10 min of experimentally induced dyspnea [inspiratory threshold loading (ITL)]. pain caused by the nociceptive laser stimulus was mild. ITL consistently induced dyspnea, mostly of the "excessive effort" type. Amplitude of the N2-P2 wave of LEPs decreased by 37.6 ± 13.8% during ITL and was significantly correlated with the intensity of dyspnea [r = 0.66, CI 95% (0.08-0.92, P = 0.0319)]. In contrast, ITL had no effect on the magnitude of non-nociceptive SEPs. experimentally induced dyspnea of the work/effort type reduces the magnitude of LEPs. This reduction correlates with the intensity of dyspnea. The recording of LEPs could constitute a clinically applicable approach to assess the dyspnea-pain counterirritation phenomenon in patients.

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.

Acute Cardiorespiratory Responses to Inspiratory Pressure Threshold Loading

We tested the acute responses to differing pressure threshold inspiratory loading intensities in well-trained rowers. The purpose of this study was to evaluate 1) how the magnitude of inspiratory pressure threshold loading influences repetition maximum (RM), tidal volume (VT), and external work undertaken by the inspiratory muscle; and 2) whether the inspiratory muscle metaboreflex is activated during acute inspiratory pressure threshold loading. Eight males participated in seven trials. Baseline measurements of maximal inspiratory pressure (PImax), resting tidal volume (VT), and forced vital capacity (FVC) were made. During the remaining sessions, participants undertook a series of resistive inspiratory breathing tasks at loads corresponding to 50%, 60%, 70%, 80%, and 90% of PImax using a pressure threshold inspiratory muscle trainer. The number of repetitions completed at each load, VT, heart rate (fc), and measures of arterial blood pressure was assessed continuously during each trial. A standardized cutoff of 10% FVC was used to define the RM, which decreased as loading intensity increased (P < 0.05). This response was nonlinear, with an abrupt decrease in RM occurring at loads > or =70% of PImax. The most commonly used inspiratory muscle training regimen of 30RM corresponded to 62.5% +/- 4.6% of PImax and also resulted in the highest external work output. Tidal volume (VT) decreased significantly over time at 60%, 70%, and 80% of PImax (P < 0.05), as did the amount of external work completed (P<0.05). Although all loads elicited a sustained increase in fc, only the 60% load elicited a sustained rise in mean arterial blood pressure (P = 0.016), diastolic blood pressure (P = 0.015), and systolic blood pressure (P = 0.002), providing evidence for a metaboreflex response at this load.

Loading of Trained Inspiratory Muscles Speeds Lactate Recovery Kinetics

The purpose of this study was to investigate the effects of inspiratory threshold loading (ITL) and inspiratory muscle training (IMT) on blood lactate concentration ([lac(-)]B) and acid-base balance after maximal incremental cycling. Eighteen subjects were divided into a control (n = 9) or an IMT group (n = 9). Before and after a 6-wk intervention, subjects completed two maximal incremental cycling tests followed by 20 min of recovery with (ITL) or without (passive recovery (PR)) a constant inspiratory resistance (15 cm H2O). The IMT group performed 6 wk of pressure threshold IMT at 50% maximal inspiratory mouth pressure. Throughout recovery, acid-base balance was quantified using the physicochemical approach by measuring the strong ion difference ([SID] = [Na+] + [K+] - [Cl-] + [lac-]), the total concentration of weak acids ([Atot-]), and the partial pressure of carbon dioxide (PCO2). After the intervention, maximal inspiratory mouth pressure increased in the IMT group only (+34%). No differences in lactate clearance were observed between PR and ITL before the intervention in both groups and after the intervention in the control group. After IMT, relative to PR, [lac-]B was reduced throughout ITL (minutes 2-20) by 0.66 +/- 1.28 mmol x L(-1) (P < 0.05), and both the fast (lactate exchange) and the slow (lactate clearance) velocity constants of the lactate recovery kinetics were increased (P < 0.05). Relative to pre-IMT, ITL reduced plasma [H], which was accounted for by an IMT-mediated increase in [SID] due almost exclusively to a 1.7-mmol x L(-1) reduction in [lac-]B. After maximal exercise, ITL affected lactate recovery kinetics only after IMT. Our data support the notion that the inspiratory muscles are capable of lactate clearance that increases [SID] and reduces [H+]. These effects may facilitate subsequent bouts of high-intensity exercise.

Delayed Onset Muscle Soreness After Inspiratory Threshold Loading in Healthy Adults

Skeletal muscle damage occurs following high-intensity or unaccustomed exercise; however, it is difficult to monitor damage to the respiratory muscles, particularly in humans. The aim of this study was to use clinical measures to investigate the presence of skeletal muscle damage in the inspiratory muscles. Ten healthy subjects underwent 60 minutes of voluntary inspiratory threshold loading (ITL) at 70% of maximal inspiratory pressure. Maximal inspiratory and expiratory mouth pressures, delayed onset muscle soreness on a visual analogue scale and plasma creatine kinase were measured prior to ITL, and at repeated time points after ITL (4, 24 and 48 hours post-ITL). Delayed onset muscle soreness was present in all subjects 24 hours following ITL (intensity = 22 +/- 6 mm; significantly higher than baseline p = 0.02). Muscle soreness was reported primarily in the anterior neck region, and was correlated to the amount of work done by the inspiratory muscles during ITL (r = 0.72, p = 0.02). However, no significant change was observed in maximal inspiratory or expiratory pressures or creatine kinase. These findings suggest that an intense bout of ITL results in muscle soreness primarily in the accessory muscles of inspiration, however, may be insufficient to cause significant muscle damage in healthy adults.

Estimation of respiratory muscle endurance using an inspiratory threshold loading device in patients with chronic pulmonary emphysema and in elderly subjects

We studied respiratory muscle endurance with an inspiratory threshold loading (ITL) device using Martyn's method (2-min incremental loading test) in 9 patients with chronic pulmonary emphysema (CPE patients) and in 9 elderly subjects with no lung disease (NE subjects), and their endurance was compared with that of 9 normal young subjects (NY subjects). In 11 cases (8 CPE patients and 3 NE subjects) a treadmill exercise test was performed and cardiopulmonary parameters obtained from the ITL and treadmill tests were compared. The maximum weight tolerated for 2 minutes (Wmax) and the mean peak inspiratory mouth pressure/maximum inspiratory mouth pressure ratio at the maximum load (Ppk/MIP at Max Load) were used as indices of respiratory muscle endurance. CPE patients had significantly decreased Wmax compared with those of NE and NY subjects. Wmax in all cases positively correlated with Ppk/MIP at Max Load, and endurance time of both the ITL and treadmill tests. During both tests, SaO2 significantly decreased, and heart rate and mean blood pressure significantly increased. There was less change in SaO2 and heart rate during the ITL test than during the treadmill test, and neither arrhythmias nor ST changes on ECG were observed during the ITL test. These results indicate that the ITL test can be easily and safely employed in CPE patients and elderly subjects to estimate respiratory muscle endurance.

Postoperative Noninvasive Ventilation

Thesemodificationsoftherespiratoryfunctionoccur early after surgery and are more often transient andcould lead to ARF. The clinical result (severity of theARF) is the product of perioperative-related ventilatoryimpairment and severity of the preoperative pulmonarycondition. Maintenance of adequate oxygenation in thepostoperative period is of major importance, especiallywhen pulmonary complications such as ARF occur. Al-though invasive endotracheal mechanical ventilation hasremained the cornerstone of ventilatory strategy for manyyearsforsevereARF,severalstudieshaveshownthatmor-tality associated with pulmonary disease is largely relatedto complications of postoperative reintubation and me-chanicalventilation.Therefore,majorobjectivesforanes-thesiologists are first to prevent the occurrence of postop-erative complications and second to ensure oxygenadministration and carbon dioxide removal while avoid-ing intubation if ARF occurs. Noninvasive ventilation(NIV) does not require an artificial airway (endotrachealtube or tracheotomy), and its use is well established toprevent ARF occurrence (prophylactic treatment) or totreat ARF to avoid reintubation (curative treatment) (fig.1). Studies show that patient-related risk factors, such aschronic obstructive pulmonary disease, age older than 60yr, American Society of Anesthesiologists class of II orhigher, obesity, functional dependence, and congestiveheart failure, increase the risk for postoperative pulmo-nary complications.