Inspiratory Threshold Loading Research Articles

Sustained preinspiratory cortical potentials during prolonged inspiratory threshold loading in humans

Humans can program and control movements, including breathing-related movements. On the electroencephalogram (EEG), this preparation is accompanied by a low-amplitude negativity starting approximately 2.5 s before inspiration that is best known as a Bereitschaftspotential (BP). The presence of BPs has been described during the compensation of mechanical inspiratory loading, thus identifying a cortical involvement in the corresponding ventilatory behavior. The pathophysiological interpretation of this cortical involvement depends on its transient or enduring nature. This study addressed this issue by looking for BPs during sustained inspiratory loading (1 h). Nine healthy male volunteers were studied during unloaded quiet breathing and inspiratory threshold loading (with unloaded expiration). Analyses of EEG signal and ventilatory variables were used to compare beginning and end of sessions. Inspiratory threshold loading caused ventilatory modifications that persisted, unchanged, for an hour. The presence of a BP at the beginning and end of a session was the most frequent occurrence (6 of 9 cases with a 17-cmH2O threshold load; 8 of 9 cases with a 23-cmH2O load). These observations support the hypothesis that the cerebral cortex is involved in the compensation of sustained experimental inspiratory loading. How this translates to respiratory disease involving acute changes in respiratory mechanics remains to be determined.

Acute effects of inspiratory pressure threshold loading upon airway resistance in people with asthma

Large inspiratory pressures may impart stretch to airway smooth muscle and modify the response to deep inspiration (DI) in asthmatics. Respiratory system resistance (Rrs) was assessed in response to 5 inspiratory manoeuvres using the forced oscillation technique: (a) single unloaded DI; (b) single DI at 25 cmH(2)O; (c) single DI at 50% maximum inspiratory mouth pressure [MIP]; (d) 30 DIs at 50% MIP; and (e) 30 DIs at 50% MIP with maintenance of normocapnia. Rrs increased after the unloaded DI and the DI at 25 cmH(2)O but not after a DI at 50% MIP (3.6+/-1.6 hPa Ls(-1) vs. 3.6+/-1.5 hPa Ls(-1); p=0.95), 30 DIs at 50% MIP (3.9+/-1.5 hPa Ls(-1) vs. 4.2+/-2.0 hPa Ls(-1); p=0.16) or 30 DIs at 50% MIP under normocapnic conditions (3.9+/-1.5 hPa Ls(-1) vs. 3.9+/-1.5 hPa Ls(-1); p=0.55). Increases in Rrs in response to DI were attenuated after single and multiple loaded breaths at 50% MIP.

Effects of inspiratory loading on the chaotic dynamics of ventilatory flow in humans

Human ventilation at rest exhibits complexity and chaos. The aim of this study was to determine whether suprapontine interferences with the automatic breathing control could contribute to ventilatory chaos. We conducted a post hoc analysis of a previous study performed in awake volunteers exhibiting cortical pre-motor potentials during inspiratory loading. In eight subjects, flow was recorded at rest, while breathing against inspiratory threshold loads (median 21.5 cm H(2)O) and resistive loads (50 cm H(2)Ol(-1)s(-1)) loads, and while inhaling 7% CO(2)-93% O(2). Chaos was identified through noise titration (noise limit, NL) and the sensitivity to initial conditions was assessed through the largest Lyapunov exponent (LLE). Breath-by-breath variability was evaluated using the coefficient of variation of several ventilatory variables. Chaos was consistently present in ventilatory flow recordings, but mechanical loading did not alter NL, LLE, or variability. In contrast, CO(2) altered chaos and reduced variability. In conclusion, inspiratory loading - and any resultant respiratory-related cortical activity - were not associated with changes in ventilatory chaos in this study, arguing against suprapontine contributions to ventilatory complexity.

Point:Counterpoint: Respiratory sinus arrhythmia is due to a central mechanism vs. respiratory sinus arrhythmia is due to the baroreflex mechanism

Blood pressure and heart periods fluctuate at respiratory frequencies in healthy humans. Some researchers ([8][1], [23][2]) explain this as a cause-and-effect relation: blood pressure changes trigger baroreflex-mediated R-R interval changes. Here I make the case that respiratory sinus arrhythmia is

Inspiratory muscle training in adults with chronic obstructive pulmonary disease: An update of a systematic review

The purpose was to update an original systematic review to determine the effect of inspiratory muscle training (IMT) on inspiratory muscle strength and endurance, exercise capacity, dyspnea and quality of life for adults with chronic obstructive pulmonary disease (COPD). The original MEDLINE and CINAHL search to August 2003 was updated to January 2007 and EMBASE was searched from inception to January 2007. Randomized controlled trials, published in English, with adults with stable COPD, comparing IMT to sham IMT or no intervention, low versus high intensity IMT, and different modes of IMT were included. Nineteen of 274 articles in the original search met the inclusion criteria. The updated search revealed 17 additional articles; 6 met the inclusion criteria, all of which compared targeted, threshold or normocapneic hyperventilation IMT to sham IMT. An update of the sub-group analysis comparing IMT versus sham IMT was performed with 10 studies from original review and 6 from the update. Sixteen meta-analyses are reported. Results demonstrated significant improvements in inspiratory muscle strength (PI(max), PI(max) % predicted, peak inspiratory flow rate), inspiratory muscle endurance (RMET, inspiratory threshold loading, MVV), exercise capacity (Ve(max), Borg Score for Respiratory Effort, 6MWT), Transitional Dyspnea Index (focal score, functional impairment, magnitude of task, magnitude of effort), and the Chronic Respiratory Disease Questionnaire (quality of life). Results suggest that targeted, threshold or normocapneic hyperventilation IMT significantly increases inspiratory muscle strength and endurance, improves outcomes of exercise capacity and one measure of quality of life, and decreases dyspnea for adults with stable COPD.

Initiating oral breathing in response to nasal loading: asthmatics versus healthy subjects

Factors influencing nasal versus oral breathing in asthmatics are not well understood. The current authors hypothesised that asthmatic subjects have enhanced perception of nasal threshold loads, and switch from nasal to oral breathing at a lower load than healthy subjects. In total, 15 mild asthmatic and 20 healthy control subjects breathed nasally via an inspiratory threshold loading device. Nasal loading was progressively increased until subjects switched to oral breathing. Load perception at switching was rated using a Borg scale. Nasal resistance was measured using posterior rhinomanometry. The protocol was repeated before and after nasal decongestant administration in subgroups of 10 healthy control and six asthmatic subjects. Inspiratory nasal resistance was within normal limits for most subjects and was not significantly different between asthmatics and healthy controls. Compared with controls, asthmatics switched to oral breathing at a significantly lower nasal load but rated "difficulty breathing in" at the same level. Decongestant significantly lowered nasal resistance but did not change the nasal load initiating switching in either subgroup. Enhanced perception of nasal loading may trigger increased oral breathing in asthmatics, potentially enhancing exposure to nonconditioned inhaled gas and contributing to the occurrence and/or severity of bronchoconstrictive exacerbations.

Delayed Onset Muscle Soreness Following Inspiratory Threshold Loading In Healthy Men and Women

Delayed Onset Muscle Soreness Following Inspiratory Threshold Loading In Healthy Men and Women

Electroencephalographic evidence for pre‐motor cortex activation during inspiratory loading in humans

Faced with mechanical inspiratory loading, awake animals and anaesthetized humans develop alveolar hypoventilation, whereas awake humans do defend ventilation. This points to a suprapontine compensatory mechanism instead of or in addition to the 'traditional' brainstem respiratory regulation. This study assesses the role of the cortical pre-motor representation of inspiratory muscles in this behaviour. Ten healthy subjects (age 19-34 years, three men) were studied during quiet breathing, CO2-stimulated breathing, inspiratory resistive loading, inspiratory threshold loading, and during self-paced voluntary sniffs. Pre-triggered ensemble averaging of Cz EEG epochs starting 2.5 s before the onset of inspiration was used to look for pre-motor activity. Pre-motor potentials were present during voluntary sniffs in all subjects (average latency (+/-s.d.): 1325 +/- 521 ms), but also during inspiratory threshold loading (1427 +/- 537 ms) and during inspiratory resistive loading (1109 +/- 465 ms). Pre-motor potentials were systematically followed by motor potentials during inspiratory loading. Pre-motor potentials were lacking during quiet breathing (except in one case) and during CO2-stimulated breathing (except in two cases). The same pattern was observed during repeated experiments at an interval of several weeks in a subset of three subjects. The behavioural component of inspiratory loading compensation in awake humans could thus depend on higher cortical motor areas. Demonstrating a similar role of the cerebral cortex in the compensation of disease-related inspiratory loads (e.g. asthma attacks) would have important pathophysiological implications: it could for example contribute to explain why sleep is both altered and deleterious in such situations.

When It's Hard To Breathe, Maybe Pain Doesn't Matter. Focus on “Dyspnea as a Noxious Sensation: Inspiratory Threshold Loading May Trigger Diffuse Noxious Inhibitory Controls in Humans”

Dyspnea (shortness of breath) and pain are well-evolved warnings of important physiological derangements that may require animals to alter their behavior to survive. Dyspnea and pain are also two of the most common symptoms that bring patients to medical care, another potentially adaptive behavior.

Dyspnea as a Noxious Sensation: Inspiratory Threshold Loading May Trigger Diffuse Noxious Inhibitory Controls in Humans

Dyspnea, a leading respiratory symptom, shares many clinical, physiological, and psychological features with pain. Both activate similar brain areas. The neural mechanisms of dyspnea are less well described than those of pain. The present research tested the hypothesis of common pathways between the two sensations. Six healthy men (age 30-40 yr) were studied. The spinal nociceptive flexion reflex (RIII) was first established in response to electrical sural stimulation. Dyspnea was then induced through inspiratory threshold loading, forcing the subjects to develop 70% of their maximal inspiratory pressure to inhale. This led to progressive inhibition of the RIII reflex that reached 50 +/- 12% during the fifth minute of loading (P < 0.001), was correlated to the intensity of the self-evaluated respiratory discomfort, and had recovered 5 min after removal of the load. The myotatic H-reflex was not inhibited by inspiratory loading, arguing against postsynaptic alpha motoneuron inhibition. Dyspnea, like pain, thus induced counterirritation, possibly indicating a C-fiber stimulation and activation of diffuse noxious inhibitory descending controls known to project onto spinal dorsal horn wide dynamic range neurons. This confirms the noxious nature of certain types of breathlessness, thus opening new physiological and perhaps therapeutic perspectives.

High-intensity inspiratory muscle training in COPD

The aim of the present study was to investigate the effects of an interval-based high-intensity inspiratory muscle training (H-IMT) programme on inspiratory muscle function, exercise capacity, dyspnoea and health-related quality of life (QoL) in subjects with chronic obstructive pulmonary disease. A double-blind randomised controlled trial was performed. Sixteen subjects (11 males, mean forced expiratory volume in one second (FEV(1)) 37.4+/-12.5%) underwent H-IMT performed at the highest tolerable inspiratory threshold load (increasing to 101% of baseline maximum inspiratory pressure). Seventeen subjects (11 males, mean FEV(1 )36.5+/-11.5%) underwent sham inspiratory muscle training (S-IMT) at 10% of maximum inspiratory pressure. Training took place three times a week for 8 weeks and was fully supervised. Pre- and post-training measurements of lung function, maximum inspiratory pressure, maximum threshold pressure, exercise capacity, dyspnoea and QoL (Chronic Respiratory Disease Questionnaire; CRDQ) were obtained. H-IMT increased maximum inspiratory pressure by 29%, maximum threshold pressure by 56%, 6-min walk distance by 27 m, and improved dyspnoea and fatigue (CRDQ) by 1.4 and 0.9 points per item, respectively. These changes were significantly greater than any seen following S-IMT. In conclusion, high-intensity inspiratory muscle training improves inspiratory muscle function in subjects with moderate-to-severe chronic obstructive pulmonary disease, yielding meaningful reductions in dyspnoea and fatigue.

Anaerobic metabolism of inspiratory muscles in COPD

The purpose of this study was to determine if the respiratory muscles of patients with COPD could be made to function anaerobically, as evidenced by an increase in arterial blood lactate concentration ([lactate](a)) during specific loading of the inspiratory muscles and, if so, the effect of a programme of high-intensity inspiratory muscle training on this function. In seven patients with COPD (FEV(1) = 33 +/- 14% of predicted), measurements of [lactate](a) were made each minute during progressive inspiratory threshold loading to voluntary exhaustion. These tests were performed before and after an 8-week programme of specific high-intensity inspiratory muscle training, combined with general whole-body exercise training. During inspiratory muscle loading small increases in [lactate](a) (0.83 +/- 0.32 mM) were observed in two subjects before training, and in five subjects after training (0.69 +/- 0.57 mM). [Lactate](a) only increased when the inspiratory work rate exceeded 6.9 cm H(2)O L/min per kilogram of body weight, and when baseline maximum inspiratory pressure exceeded 65 cm H(2)O. The results of this study demonstrated that it is possible for COPD patients to increase inspiratory muscle work rate to a level requiring a major energy contribution from anaerobic glycolytic metabolism. This was only seen when inspiratory muscle strength and endurance were sufficient to allow it. Some patients who failed to demonstrate an increase in [lactate](a) at baseline did so after a programme of high-intensity inspiratory muscle training.

Effect of inspiratory threshold loading on ventilatory kinetics during constant-load exercise

Humoral factors play an important role in the control of exercise hyperpnea. The role of neuromechanical ventilatory factors, however, is still being investigated. We tested the hypothesis that the afferents of the thoracopulmonary system, and consequently of the neuromechanical ventilatory loop, have an influence on the kinetics of oxygen consumption (VO2), carbon dioxide output (VCO2), and ventilation (VE) during moderate intensity exercise. We did this by comparing the ventilatory time constants (tau) of exercise with and without an inspiratory load. Fourteen healthy, trained men (age 22.6 +/- 3.2 yr) performed a continuous incremental cycle exercise test to determine maximal oxygen uptake (VO2max = 55.2 +/- 5.8 ml x min(-1) x kg(-1)). On another day, after unloaded warm-up they performed randomized constant-load tests at 40% of their VO2max for 8 min, one with and the other without an inspiratory threshold load of 15 cmH2O. Ventilatory variables were obtained breath by breath. Phase 2 ventilatory kinetics (VO2, VCO2, and VE) could be described in all cases by a monoexponential function. The bootstrap method revealed small coefficients of variation for the model parameters, indicating an accurate determination for all parameters. Paired Student's t-tests showed that the addition of the inspiratory resistance significantly increased the tau during phase 2 of VO2 (43.1 +/- 8.6 vs. 60.9 +/- 14.1 s; P < 0.001), VCO2 (60.3 +/- 17.6 vs. 84.5 +/- 18.1 s; P < 0.001) and VE (59.4 +/- 16.1 vs. 85.9 +/- 17.1 s; P < 0.001). The average rise in tau was 41.3% for VO2, 40.1% for VCO2, and 44.6% for VE. The tau changes indicated that neuromechanical ventilatory factors play a role in the ventilatory response to moderate exercise.

Efficiency of the normal human diaphragm with hyperinflation

We evaluated an index of diaphragm efficiency (Eff(di)), diaphragm power output (Wdi) relative to electrical activation, in five healthy adults during tidal breathing at usual end-expiratory lung volume (EELV) and diaphragm length (L(di ee)) and at shorter L(di ee) during hyperinflation with expiratory positive airway pressure (EPAP). Measurements were repeated with an inspiratory threshold (7.5 cmH(2)O) plus resistive (6.5 cmH(2)O.l(-1).s) load. Wdi was the product of mean inspiratory transdiaphragmatic pressure (DeltaPdi(mean)), diaphragm volume displacement measured fluoroscopically, and 1/inspiratory duration (Ti(-1)). Diaphragm activation, measured with esophageal electrodes, was quantified by computing root-mean-square values (RMS(di)). With EPAP, 1) EELV increased [mean r(2) = 0.91 (SD 0.01)]; 2) in four subjects, L(di ee) decreased [mean r(2) = 0.85 (SD 0.07)] and mean Eff(di) decreased 34% per 10% decrease in L(di ee) (P < 0.001); and 3) in one subject, gastric pressure at EELV increased two- to threefold, L(di ee) was unchanged or increased, and Eff(di) increased at two of four levels of EPAP (P < or = 0.006, ANOVA). Inspiratory loading increased Wdi (P = 0.003) and RMS(di) (P = 0.004) with no change in Eff(di) (P = 0.63) or its relationship with L(di ee). Eff(di) was more accurate in defining changes in L(di ee) [(true positives + true negatives)/total = 0.78 (SD 0.13)] than DeltaPdi(mean).RMS(di)(-1), RMS(di), or DeltaPdi(mean).Ti (all <0.7, P < or = 0.05, without load). Thus Eff(di) was principally a function of L(di ee) independent of inspiratory loading, behavior consistent with muscle force-length-velocity properties. We conclude that Eff(di), measured during tidal breathing and in the absence of expiratory muscle activity at EELV, is a valid and accurate measure of diaphragm contractile function.

Inspiratory muscle training in adults with chronic obstructive pulmonary disease: A systematic review

The purpose of this study was to conduct a systematic review to determine the effect of inspiratory muscle training (IMT) on inspiratory muscle strength and endurance, exercise capacity, dyspnea and quality of life for adults with chronic obstructive pulmonary disease (COPD). A systematic review of the literature was conducted according the Cochrane Collaboration protocol using Medline and CINAHL. Nineteen of 274 extracted articles met the inclusion criteria and addressed comparisons of interest which included: IMT versus sham; IMT versus no intervention; low- versus high-intensity IMT; and two different modes of IMT. Thirteen meta-analyses were reported. Results indicate that targeted resistive or threshold IMT was associated with significant improvements in some outcomes of inspiratory muscle strength (PI(max) (cm H2O)) and endurance (Inspiratory Threshold Loading (kPa)), exercise capacity (Borg Scale for Respiratory Effort (modified Borg scale), Work Rate maximum (Watts)), and dyspnea (Transition Dyspnea Index), whereas IMT without a target or not using threshold training did not show improvement in these variables. There was no conclusive evidence regarding quality of life measures. IMT is effective for adults with COPD when using threshold or targeted devices that control or provide a target for training intensity.

Respiratory and Skeletal Muscles in Hypogonadal Men with Chronic Obstructive Pulmonary Disease

Hypogonadism, found in about one-third of patients with chronic obstructive pulmonary disease (COPD), has potential for decreasing muscle mass and muscle performance. Compared with eugonadal patients, we hypothesized that hypogonadal patients with COPD have decreased respiratory and skeletal muscle performance. Nineteen hypogonadal and 20 eugonadal men with COPD (FEV(1) 1.14 +/- 0.08 and 1.17 +/- 0.11 L [standard error], respectively) were studied. Diaphragmatic contractility, assessed as transdiaphragmatic twitch pressure generated by phrenic nerve stimulation, was similar in hypogonadal and eugonadal patients: 20.6 +/- 2.2 and 19.8 +/- 2.5 cm H(2)O, respectively. During progressive inspiratory threshold loading, hypogonadal and eugonadal patients had similar respiratory muscle endurance times (302 +/- 29 and 313 +/- 48 seconds, respectively) and airway pressure sustained during the last minute of loading (38.2 +/- 3.0 and 40.5 +/- 4.7 cm H(2)O, respectively) (similar to predicted values in healthy subjects). Hypogonadal and eugonadal patients had equivalent limb muscle strength and endurance. During cycle exercise to exhaustion, exercise performance, gas exchange, and respiratory muscle recruitment (estimated by esophageal and gastric pressure swings during tidal breathing) were similar in both groups. In conclusion, hypogonadism does not decrease respiratory or limb muscle performance and exercise capacity in men with moderate-to-severe COPD who, for the most part, are not underweight.

Oxygen consumption and PEEPe in ventilated COPD patients

The intrinsic positive-end-expiratory pressure (PEEPi) increases the inspiratory load, the cost of breathing and thus oxygen consumption (V(O2)). It has been shown that applying an extrinsic positive-end-expiratory pressure (PEEPe) reduces the inspiratory threshold load but the optimal PEEPe level is still in debate. We hypothesize that the best level of PEEPe could induce a decrease in V(O2) by reducing the V(O2) demands from PEEPi. Nine mechanically ventilated COPD patients were included. The level of PEEPe was determined in accordance with the static PEEPi. V(O2) was measured using an automatic gas analyser during synchronized intermittent mandatory ventilation (SIMV): without PEEPe, with a PEEPe equal to 50% of static PEEPi and with a PEEPe equal to 100% of static PEEPi. Static PEEPi appeared to be significantly correlated with the degree of airflow obstruction (FEV1) (P<0.05). Applying a PEEPe equal to static PEEPi resulted in a significant decrease in V(O2) (P<0.05) whereas the change in V(O2) proved to be unpredictable for a PEEPe level of 50% of static PEEPi. In conclusion, V(O2) decreases progressively when increasing PEEPe up to a level equal to 100% of static PEEPi. Thus, in mechanically ventilated COPD patients with a FEV1 < or = 1000 ml, applying a PEEPe of 5 cmH2O should be recommended.

Dyspnoea at rest and at the end of different exercises in patients with near-fatal asthma.

Blunted perception of dyspnoea under resistive loading has been observed in patients with a history of near-fatal asthma (NFA). The perception of dyspnoea at rest and at the end point of various exercises was assessed in such patients. Respiratory function and exercise capacity (6-min walking distance, incremental cycloergometry and inspiratory threshold loading) were assessed in seven NFA and eight non-NFA patients. Dyspnoea (Borg scale) was measured at rest and at the end point of the various exercises. Dyspnoea at rest was significantly lower in NFA patients. Although exercise tolerance was similarly reduced in both the NFA and non-NFA groups, dyspnoea at peak cycle exercise was significantly lower in the former (2.6+/-2 versus 6.1+/-3.8 (Borg scale; mean+/-SD)), who mainly (86%) stopped because of leg discomfort. A similar trend was observed in the 6-min walking distance and inspiratory threshold loading tests. Dyspnoea at peak exercise was the best indicator of the NFA condition, with a sensitivity of 100% and specificity of 63% for a Borg scale score of < or = 6. Perception of dyspnoea is blunted in near-fatal asthma patients at both rest and the end point of various forms of exercise. Dyspnoea at peak exercise is the best indicator of the near-fatal asthma condition.

The effect of learning on ventilatory responses to inspiratory threshold loading in COPD

Background: Progressive threshold loading (PTL) is a common test of respiratory muscle endurance. Healthy naı̈ve subjects improve endurance with successive exposures to PTL by altering their breathing responses, thus necessitating a familiarization period before reproducible measures can be obtained. This study sought to determine whether a similar “learning effect” is evident in patients with COPD, and what the mechanism of any such effect may be. Methods: Ten subjects with COPD (FEV 1 34±13% predicted) underwent PTL on four occasions (>24 h apart). During PTL measurements were obtained of breathing pattern and maximum threshold pressure ( P thmax) achieved. Maximum inspiratory pressure ( P Imax) was measured on each occasion. Results: Over the four tests P Imax improved by 21±16% ( sd) ( P<0.05) and P thmax by 32±21% ( P<0.05) with a plateau in these measures achieved by test three. P thmax/ P Imax was unchanged, being 61±11% at test one and 67±12% at test four. In contrast to healthy subjects, PTL was not associated with increased expiratory time or decreased end-expiratory lung volume. Conclusions: In contrast to P Imax and P thmax, which changed with successive tests, a single measure of the ratio P thmax/ P Imax may present a useful guide to the endurance capacity of the respiratory muscles in patients with COPD.

Feasibility of High-Intensity, Interval-Based Respiratory Muscle Training in COPD

Specific respiratory muscle training can improve respiratory muscle function in patients with COPD, but the magnitude of improvement appears dependent on the magnitude of the training load. High training loads are difficult to achieve using conventional, constant loading techniques, but may be possible using interval-based training techniques. To assess the feasibility of high-intensity respiratory muscle training, nine subjects with moderate-to-severe COPD (FEV(1) 34 +/- 12% predicted [mean +/- SD]) completed 8 weeks of interval-based respiratory muscle training combined with a general exercise program. This involved three 20-min sessions per week, each session comprising seven 2-min bouts of breathing against a constant inspiratory threshold load, each bout separated by 1 min of unloaded recovery. Inspiratory load was progressively incremented. Respiratory muscle strength (maximum inspiratory pressure generated against an occluded airway [PImax]) and endurance (maximum pressure generated against a progressively increasing inspiratory threshold load [Pthmax]) were measured before and immediately after the 8-week training period. By the third training session (week 1), subjects breathed against a threshold that required generation of pressures equivalent to 68 +/- 5% of the pretraining PImax. By week 8, this had increased to 95 +/- 12% of the pretraining PImax. On completion of training, PImax had increased by 32 +/- 27% (p < 0.05), Pthmax had increased by 56 +/- 33% (p < 0.05), and Pthmax/PImax had increased by 20 +/- 20% (p < 0.05). This study has demonstrated that high-intensity, interval-based respiratory muscle training is feasible in patients with moderate-to-severe COPD, resulting in significant improvements in respiratory muscle strength and endurance when performed three times a week for 8 weeks.