Resistive Breathing Research Articles

Sympathetic vasomotor outflow and blood pressure increase during exercise with expiratory resistance.

The purpose of the present study was to elucidate the effect of increasing expiratory muscle work on sympathetic vasoconstrictor outflow and arterial blood pressure (BP) during dynamic exercise. We hypothesized that expiratory muscle fatigue would elicit increases in sympathetic vasomotor outflow and BP during submaximal exercise. The subjects performed four submaximal exercise tests; two were maximal expiratory pressure (PEmax) tests and two were muscle sympathetic nerve activity (MSNA) tests. In each test, the subjects performed two 10-min exercises at 40% peak oxygen uptake using a cycle ergometer in a semirecumbent position [spontaneous breathing for 5 min and voluntary hyperpnoea with and without expiratory resistive breathing for 5 min (breathing frequency: 60 breaths/min, inspiratory and expiratory times were set at 0.5 sec)]. PEmax was estimated before and immediately after exercises. MSNA was recorded via microneurography of the right median nerve at the elbow. PEmax decreased following exercise with expiratory resistive breathing, while no change was found without resistance. A progressive increase in MSNA burst frequency (BF) appeared during exercise with expiratory resistance (MSNA BF, without resistance: +22 ± 5%, with resistance: +44 ± 8%, P < 0.05), accompanied by an augmentation of BP (mean BP, without resistance: +5 ± 2%, with resistance: +29 ± 5%, P < 0.05). These results suggest that an enhancement of expiratory muscle activity leads to increases in sympathetic vasomotor outflow and BP during dynamic leg exercise.

Expiratory Resistive Loading Increases in Sympathetic Vasomotor Outflow and BP During Dynamic Leg Exercise

High intensity voluntary contraction of the inspiratory muscles against resistive loads augments an increase in muscle sympathetic nerve activity (MSNA) with a corresponding increase in arterial blood pressure (BP) through an inspiratory muscle fatigue-induced metaboreflex. We hypothesized that expiratory muscle fatigue would also elicit increases in MSNA and BP during dynamic leg exercise. PURPOSE: The purpose of this study was to clarify the influence of an enhancement of expiratory muscle activity on sympathetic vasoconstrictor outflow and BP during submaximal exercise. METHODS: The subjects performed two 10-min exercise bouts at 40% peak oxygen uptake using a cycle ergometer in a semirecumbent position [spontaneous breathing for 5 min and with or without expiratory resistive breathing for 5 min (breathing frequency: 60 breaths/min, inspiratory and expiratory times were each constant at 0.5 s)]. MSNA was recorded via microneurography of the right median nerve at the elbow. RESULTS: A large increase in MSNA burst frequency (BF) occurred during exercise with expiratory resistance, accompanied by an augmentation of mean BP (MBP) (with resistance: MSNA BF +39.0%, MBP +42.5%, without resistance: MSNA BF: +12.8%, MBP: +22.9%, from resting values). CONCLUSIONS: These results suggest that an enhancement of expiratory muscle activity leads to large increases in muscle sympathetic vasomotor outflow and BP during dynamic leg exercise.

PP101 - Hydrogen sulphide attenuates lung inflammation caused by resistive breathing

PP101 - Hydrogen sulphide attenuates lung inflammation caused by resistive breathing

Asynchrony of lingual muscle recruitment during sleep in obstructive sleep apnea.

Pharyngeal collapsibility during sleep increases primarily due to decline in dilator muscle activity. However, genioglossus EMG is known to increase during apneas and hypopneas, usually without reversing upper airway obstruction or inspiratory flow limitation. The present study was undertaken to test the hypothesis that intense activation of the genioglossus fails to prevent pharyngeal obstruction during sleep, and to evaluate if sleep-induced changes in tongue muscle coordination may be responsible for this phenomenon. We compared genioglossus and tongue retractors EMG activity in 13 obstructive sleep apnea (OSA) patients during wakefulness, while breathing through inspiratory resistors, to the activity observed at the end of apneas and hypopneas after 25 mg of brotizolam, before arousal, at equal esophageal pressure. During wakefulness, resistive breathing triggered increases in both genioglossus and retractor EMG. Activation of agonist tongue muscles differed considerably from that of the arm, as both genioglossus and retractors were activated similarly during all tongue movements. During sleep, flow limitation triggered increases in genioglossal EMG that could reach more than twofold the level observed while awake. In contrast, EMGs of the retractors reached less than half the wakefulness level. In sleeping OSA patients, genioglossal activity may increase during obstructed breathing to levels that exceed substantially those required to prevent pharyngeal collapse during wakefulness. In contrast, coactivation of retractors is deficient during sleep. These findings suggest that sleep-induced alteration in tongue muscle coordination may be responsible for the failure of high genioglossal EMG activity to alleviate flow limitation.

Inspiratory resistive breathing induces MMP-9 and MMP-12 expression in the lung

Inspiratory resistive breathing (IRB) is characterized by large negative intrathoracic pressures and was shown to induce pulmonary inflammation in previously healthy rats. Matrix metalloproteinases (MMP)-9 and -12 are induced by inflammation and mechanical stress in the lung. We hypothesized that IRB induces MMP-9 and -12 in the lung. Anesthetized, tracheostomized rats breathed spontaneously through a two-way valve, connected to an inspiratory resistance, with the tidal inspiratory tracheal pressure set at 50% of the maximum. Quietly breathing animals served as controls. After 3 and 6 h of IRB, respiratory mechanics were measured, bronchoalveolar lavage (BAL) was performed, lung injury score was estimated, and lung MMP-9 was estimated by zymography and ELISA. MMP-9 and MMP-12 immunohistochemistry was performed. Isolated normal alveolar macrophages were incubated with BAL from rats that underwent IRB. After 18 h, MMP-9 and -12 levels were measured in supernatants, and immunocytochemistry was performed. Macrophages were treated with IL-1β, IL-6, or TNF-α, and MMP-9 in supernatants was measured. After 6 h of IRB, leukocytes in BAL increased, and IL-1β and IL-6 levels were elevated. Elasticity and injury score were increased after 3 and 6 h of IRB. Lung MMP-9 levels increased after 6 h of IRB. MMP-9 and MMP-12 were detected in alveolar macrophages and epithelial (bronchial/alveolar) cells after 3 and 6 h of IRB. MMP-9 and MMP-12 were found in supernatants after treatment with 6 h of IRB BAL. Cytosolic immunostaining was detected after treatment with 3 and 6 h of IRB BAL. All cytokines induced MMP-9 in culture supernatants. In conclusion, IRB induces MMP-9 and -12 in the lung of previously healthy rats.

Guanylyl cyclase activation reverses resistive breathing-induced lung injury and inflammation.

Inspiratory resistive breathing (RB), encountered in obstructive lung diseases, induces lung injury. The soluble guanylyl cyclase (sGC)/cyclic guanosine monophosphate (cGMP) pathway is down-regulated in chronic and acute animal models of RB, such as asthma, chronic obstructive pulmonary disease, and in endotoxin-induced acute lung injury. Our objectives were to: (1) characterize the effects of increased concurrent inspiratory and expiratory resistance in mice via tracheal banding; and (2) investigate the contribution of the sGC/cGMP pathway in RB-induced lung injury. Anesthetized C57BL/6 mice underwent RB achieved by restricting tracheal surface area to 50% (tracheal banding). RB for 24 hours resulted in increased bronchoalveolar lavage fluid cellularity and protein content, marked leukocyte infiltration in the lungs, and perturbed respiratory mechanics (increased tissue resistance and elasticity, shifted static pressure-volume curve right and downwards, decreased static compliance), consistent with the presence of acute lung injury. RB down-regulated sGC expression in the lung. All manifestations of lung injury caused by RB were exacerbated by the administration of the sGC inhibitor, 1H-[1,2,4]oxodiazolo[4,3-]quinoxalin-l-one, or when RB was performed using sGCα1 knockout mice. Conversely, restoration of sGC signaling by prior administration of the sGC activator BAY 58-2667 (Bayer, Leverkusen, Germany) prevented RB-induced lung injury. Strikingly, direct pharmacological activation of sGC with BAY 58-2667 24 hours after RB reversed, within 6 hours, the established lung injury. These findings raise the possibility that pharmacological targeting of the sGC-cGMP axis could be used to ameliorate lung dysfunction in obstructive lung diseases.

High Thrill and adventure seeking is associated with reduced interoceptive sensitivity: evidence for an altered sex-specific homeostatic processing in high sensation seekers.

The personality trait of sensation seeking (SS) has been traditionally linked to the construct of exteroception, i.e. sensing of the outside world. Little is known about the relationship between SS and interoception, i.e. sensing originating in the body. Interoceptive sensations have strong affective and motivational components that may influence behaviors such as risk-taking in SS. This investigation examined whether interoceptive differences contribute to different behavioral characteristics in SS. Using an inspiratory resistive load breathing task, the response to an aversive interoceptive stimulus as a basic homeostatic process was studied in 112 subjects (n=74 females, 38 males). A linear-mixed model approach was used to examine the influence of thrill and adventure seeking (TAS) on the interoceptive response across three levels of breathing resistances (10, 20, 40 cmH2O/L/sec). High relative to low TAS individuals were less responsive in evaluating intensities of perceived choking with increasing inspiratory resistive loads. This effect was driven by male, but not female high TAS individuals and was particularly associated with reduced interoceptive sensitivity in males. The conceptualization of SS as primarily driven by exteroceptive stimuli can be expanded to a view of an altered homeostasis in SS, specifically in males.

English

Abstract Introduction Weaning from mechanical ventilation is usually accomplished with spontaneous breathing trials. The discontinuation of mechanical ventilation and the resumption of spontaneous breathing may increase oxygen demands, and patients, mainly those with limited cardiorespiratory reserve, are subjected to pulmonary and cardiovascular stress. In addition, emotional distress due to agitation after interruption of sedative drugs, anxiety and other sources of discomfort potentially contributes to pulmonary and cardiovascular stress. There is evidence of metabolic and endocrine stress response expressed as an increase in oxygen consumption and plasma concentration of catecholamines and other hormones involved in the stress system activation, in patients during the weaning process from mechanical ventilation, especially during failing weaning attempts. Furthermore, extrapolating from both physical exercise and inspiratory resistive breathing data, there is evidence of immune response expressed as an increase of proinflammatory cytokine blood levels. The purpose of this review is to summarise the published information about neurormonal and inflammatory stress response during weaning from mechanical ventilation. Neurormonal and inflammatory responses during weaning trials from mechanical ventilation

Soluble guanylyl cyclase as a therapeutic target in chronic obstructive pulmonary disease (COPD)

Background Resistive breathing (RB) due to airflow limitation is the pathophysiologic hallmark of chronic obstructive pulmonary disease (COPD). Nitric oxide (NO) is a physiological regulator of smooth muscle tone that acts through activation of soluble guanylyl cyclase (sGC). We hypothesized that increased smooth muscle tone limiting airflow in COPD could result from reduced sGC. Herein, we investigated the expression and downstream signalling of sGC in RB.

Expiratory muscle fatigue does not regulate operating lung volumes during high-intensity exercise in healthy humans

To determine whether expiratory muscle fatigue (EMF) is involved in regulating operating lung volumes during exercise, nine recreationally active subjects cycled at 90% of peak work rate to the limit of tolerance with prior induction of EMF (EMF-ex) and for a time equal to that achieved in EMF-ex without prior induction of EMF (ISO-ex). EMF was assessed by measuring changes in magnetically evoked gastric twitch pressure. Changes in end-expiratory and end-inspiratory lung volume (EELV and EILV) and the degree of expiratory flow limitation (EFL) were quantified using maximal expiratory flow-volume curves and inspiratory capacity maneuvers. Resistive breathing reduced gastric twitch pressure (-24 ± 14%, P = 0.004). During EMF-ex, EELV decreased from rest to the 3rd min of exercise [39 ± 8 vs. 27 ± 7% of forced vital capacity (FVC), P = 0.001] before increasing toward baseline (34 ± 8% of FVC end exercise, P = 0.073 vs. rest). EILV increased from rest to the 3rd min of exercise (54 ± 8 vs. 84 ± 9% of FVC, P = 0.006) and remained elevated to end exercise (88 ± 9% of FVC). Neither EELV (P = 0.18) nor EILV (P = 0.26) was different at any time point during EMF-ex vs. ISO-ex. Four subjects became expiratory flow limited during the final minute of EMF-ex and ISO-ex; the degree of EFL was not different between trials (37 ± 18 vs. 35 ± 16% of tidal volume, P = 0.38). At end exercise in both trials, EELV was greater in subjects without vs. subjects with EFL. These findings suggest that 1) contractile fatigue of the expiratory muscles in healthy humans does not regulate operating lung volumes during high-intensity sustained cycle exercise; and 2) factors other than "frank" EFL cause the terminal increase in EELV.

Hypoxic effects on sympathetic vasomotor outflow and blood pressure during exercise with inspiratory resistance

The purpose of the present study was to clarify the influence of inspiratory resistive breathing during exercise under hypoxic conditions on muscle sympathetic nerve activity (MSNA) and blood pressure (BP). Six healthy males completed this study. The subjects performed a submaximal exercise test using a cycle ergometer in a semirecumbent position under normoxic [inspired oxygen fraction (FiO2) = 0.21] and hypoxic (FiO2 = 0.12-0.13) conditions. The subjects carried out two 10-min exercises at 40% peak oxygen uptake [spontaneous breathing for 5 min and voluntary breathing with inspiratory resistance for 5 min (breathing frequency: 60 breaths/min, inspiratory and expiratory times were set at 0.5 s each)]. MSNA was recorded via microneurography of the right median nerve at the elbow. A progressive increase in MSNA burst frequency (BF) during leg-cycling exercise with inspiratory resistance in normoxia and hypoxia were accompanied by an augmentation of BP. The increased MSNA BF and mean arterial BP (MBP) during exercise with inspiratory resistive breathing in hypoxia (MSNA BF, 55.7 ± 1.4 bursts/min, MBP, 134.3 ± 6.6 mmHg) were higher than those in normoxia (MSNA BF, 39.2 ± 1.8 bursts/min, MBP, 123.6 ± 4.5 mmHg). These results suggest that an enhancement of inspiratory muscle activity under hypoxic condition leads to large increases in muscle sympathetic vasomotor outflow and BP during dynamic leg exercise.

Cardiovascular and Respiratory Effect of Yogic Slow Breathing in the Yoga Beginner: What Is the Best Approach?

Slow breathing increases cardiac-vagal baroreflex sensitivity (BRS), improves oxygen saturation, lowers blood pressure, and reduces anxiety. Within the yoga tradition slow breathing is often paired with a contraction of the glottis muscles. This resistance breath “ujjayi” is performed at various rates and ratios of inspiration/expiration. To test whether ujjayi had additional positive effects to slow breathing, we compared BRS and ventilatory control under different breathing patterns (equal/unequal inspiration/expiration at 6 breath/min, with/without ujjayi), in 17 yoga-naive young healthy participants. BRS increased with slow breathing techniques with or without expiratory ujjayi (P < 0.05 or higher) except with inspiratory + expiratory ujjayi. The maximal increase in BRS and decrease in blood pressure were found in slow breathing with equal inspiration and expiration. This corresponded with a significant improvement in oxygen saturation without increase in heart rate and ventilation. Ujjayi showed similar increase in oxygen saturation but slightly lesser improvement in baroreflex sensitivity with no change in blood pressure. The slow breathing with equal inspiration and expiration seems the best technique for improving baroreflex sensitivity in yoga-naive subjects. The effects of ujjayi seems dependent on increased intrathoracic pressure that requires greater effort than normal slow breathing.

Pneumothorax Caused by Aggressive Use of an Incentive Spirometer in a Patient With Emphysema

A 68-year-old man presented to the emergency department with a small pneumothorax following aggressive use of an incentive spirometer. The patient had a baseline chest radiograph consistent with emphysema. He was initially treated with oxygen in the emergency department, with resolution of his symptoms. The pneumothorax resolved spontaneously over a period of 3 days. The development of the pneumothorax was likely due to the patient's repeated forceful inspiratory maneuvers in the setting of emphysema and lung hyperinflation. Inspiratory resistive breathing can cause large negative swings in intrathoracic pressure, which may result in mechanical stress of lung tissue. This is the first report of a secondary pneumothorax associated with use of an incentive spirometer. Patients with bullous emphysema should be counseled to avoid frequent high intensity maneuvers with an incentive spirometer if the potential benefits of the procedure are marginal.

Effect of Resistive Load on the Inspiratory Work and Power of Breathing during Exertion

The resistive work of breathing against an external load during inspiration (WRI) was measured at the mouth, during sub-maximal exercise in healthy participants. This measure (which excludes the elastic work component) allows the relationship between resistive work and power, ventilation and exercise modality to be explored. A total of 45 adult participants with healthy lung function took part in a series of exercise protocols, in which the relationship between WRI, power of breathing, PRI and minute ventilation, were assessed during rest, while treadmill walking or ergometer cycling, over a range of exercise intensities (up to 150 Watts) and ventilation rates (up to 48 L min−1) with applied constant resistive loads of 0.75 and 1.5 kPa.L.sec−1. Resting WRI was 0.12 JL−1 and PRI was 0.9 W. At each resistive load, independent of the breathing pattern or exercise mode, the WRI increased in a linear fashion at 20 mJ per litre of , while PRI increased exponentially. With increasing resistive load the work and power at any given increased exponentially. Calculation of the power to work ratio during loaded breathing suggests that loads above 1.5 kPa.L.sec−1 make the work of resistive breathing become inhibitive at even a moderate (>30 L sec−1). The relationship between work done and power generated while breathing against resistive loads is independent of the exercise mode (cycling or walking) and that ventilation is limited by the work required to breathe, rather than an inability to maintain or generate power.

Oxidative stress, respiratory muscle dysfunction, and potential therapeutics in chronic obstructive pulmonary disease

Chronic obstructive pulmonary disease (COPD) is a highly relevant disorder that induces respiratory muscle dysfunction. One prevalent symptom of COPD is resistive breathing which causes respiratory muscle to significantly increase the magnitude of contractions, resulting in reactive oxygen species (ROS) formation and oxidative stress. Through cellular signaling cascades, ROS activate molecules such as mitogen-activated protein kinases and nuclear factor-κB. These signaling molecules stimulate the release of cytokines which in turn cause damage to the diaphragm, involving sarcomeric disruptions. In response to COPD induced fatigue, the diaphragm undergoes a beneficial fibertype shift to type I muscle fibers, which are more resistant to hypoxia than type II fibers. The lung hyperinflation that occurs in COPD also causes intercostal muscle dysfunction, thereby exacerbating COPD symptoms. In addition, COPD is known to have a connection with heart failure, diabetes, and aging, further decreasing respiratory function. Currently, there is no cure for this disorder. Nevertheless, various potential therapeutic strategies focusing on respiratory muscle have been identified including respiratory muscle training, β2-agonist therapy, and lung volume reduction surgery. In this review, we will outline the role of COPD, oxidative stress, and related complications in respiratory muscle dysfunction.

Nitric oxide regulates cytokine induction in the diaphragm in response to inspiratory resistive breathing

Resistive breathing (encountered in chronic obstructive pulmonary disease and asthma) results in cytokine upregulation and decreased nitric oxide (NO) levels in the strenuously contracting diaphragm. NO can regulate gene expression. We hypothesized that endogenously produced NO downregulates cytokine production triggered by strenuous diaphragmatic contraction. Wistar rats treated with vehicle, the nonselective NO synthase inhibitor NG-nitro-l-arginine-methylester (l-NAME), or the NO donor diethylenetriamine-NONOate (DETA) were subjected to inspiratory resistive breathing (IRB; 50% of maximal inspiratory pressure) for 6 h or sham operation. Additional groups of rats were subjected to IRB for 6 h with concurrent administration of l-NAME and inhibitors of NF-κB (BAY-11-7082), ERK1/2 (PD98059), or P38 (SB203580). Inhibition of NO production (with l-NAME) resulted in upregulation of IRB-induced diaphragmatic IL-6, IL-10, IL-2, TNF-α, and IL-1β levels by 50%, 53%, 60%, 47%, and 45%, respectively. In contrast, the NO donor (DETA) attenuated the IRB-induced cytokine upregulation to levels characteristic of quietly breathing animals. l-NAME augmented IRB-induced activation of MAPKs (P38 and ERK1/2) and NF-κB, whereas DETA triggered the opposite effect. NF-κB and ERK1/2 inhibition in l-NAME-treated animals blunted the l-NAME-induced cytokine upregulation except IL-6, whereas P38 inhibition blunted all (including IL-6) cytokine upregulation. NO downregulates IRB-induced cytokine production in the strenuously contracting diaphragm through its action on MAPKs and NF-κB.

Tolerance to a hemorrhagic challenge during heat stress is improved with inspiratory resistance breathing

The mechanism(s) by which heat stress alters blood pressure control and tolerance to a simulated hemorrhagic challenge is multifaceted; however, heat‐induced reductions in central blood volume play a key role. Inspiratory resistance breathing improves blood pressure control and tolerance during simulated hemorrhage in normothermic individuals. It is unknown if similar improvements occur with this maneuver in heat stress conditions. This study tested the hypothesis that inspiratory resistance breathing improves tolerance to simulated hemorrhage in individuals with elevated internal temperatures. On 2 separate days, 8 subjects performed a simulated hemorrhage challenge (lower body negative pressure, LBNP) to pre‐syncope following an increase in internal temperature of 1.5 °C. During one trial subjects breathed through an inspiratory impedance device set at 0 cmH20 of resistance (Sham) while on the other day the device was set at −7 cmH20 of resistance (Experimental). Tolerance was quantified as cumulative stress index (CSI). Subjects were more tolerant to the LBNP challenge during the Experimental protocol as indexed by a larger CSI (Sham: 520±306 mmHg × min; Experimental: 682±324 mmHg × min, P&lt;0.01). These data indicate that inspiratory resistance breathing modestly improves tolerance to a simulated hemorrhagic challenge during heat stress.Support NIH‐HL61388 &amp; HL84072

Inspiratory muscle fatigue increases sympathetic vasomotor outflow and blood pressure during submaximal exercise

The purpose of this study was to elucidate the influence of inspiratory muscle fatigue on muscle sympathetic nerve activity (MSNA) and blood pressure (BP) response during submaximal exercise. We hypothesized that inspiratory muscle fatigue would elicit increases in sympathetic vasoconstrictor outflow and BP during dynamic leg exercise. The subjects carried out four submaximal exercise tests: two were maximal inspiratory pressure (PI(max)) tests and two were MSNA tests. In the PI(max) tests, the subjects performed two 10-min exercises at 40% peak oxygen uptake using a cycle ergometer in a semirecumbent position [spontaneous breathing for 5 min and with or without inspiratory resistive breathing for 5 min (breathing frequency: 60 breaths/min, inspiratory and expiratory times were each set at 0.5 s)]. Before and immediately after exercise, PI(max) was estimated. In MSNA tests, the subjects performed two 15-min exercises (spontaneous breathing for 5 min, with or without inspiratory resistive breathing for 5 min, and spontaneous breathing for 5 min). MSNA was recorded via microneurography of the right median nerve at the elbow. PI(max) decreased following exercise with resistive breathing, whereas no change was found without resistance. The time-dependent increase in MSNA burst frequency (BF) appeared during exercise with inspiratory resistive breathing, accompanied by an augmentation of diastolic BP (DBP) (with resistance: MSNA, BF +83.4%; DBP, +23.8%; without resistance: MSNA BF, +19.2%; DBP, -0.4%, from spontaneous breathing during exercise). These results suggest that inspiratory muscle fatigue induces increases in muscle sympathetic vasomotor outflow and BP during dynamic leg exercise at mild intensity.

Cytokines and resistive breathing

This review summarizes and analyzes the results of the present experimental studies indicating immune system involvement in control of breathing. The hypothesis about the role of cytokines in the mechanisms of respiratory muscle fatigue and reduced ventilatory sensitivity to hypercapnia during respiration with the added resistive loading is justified. The possible ways of implementing of respiratory cytokine effects are discussed.

Effects of inspiratory muscle training on dynamic hyperinflation in patients with COPD

Dynamic hyperinflation has important clinical consequences in patients with chronic obstructive pulmonary disease (COPD). Given that most of these patients have respiratory and peripheral muscle weakness, dyspnea and functional exercise capacity may improve as a result of inspiratory muscle training (IMT). The aim of the study was to analyze the effects of IMT on exercise capacity, dyspnea, and inspiratory fraction (IF) during exercise in patients with COPD. Daily inspiratory muscle strength and endurance training was performed for 8 weeks in 10 patients with COPD GOLD II and III. Ten patients with COPD II and III served as a control group. Maximal inspiratory pressure (Pimax) and endurance time during resistive breathing maneuvers (tlim) served as parameter for inspiratory muscle capacity. Before and after training, the patients performed an incremental symptom limited exercise test to maximum and a constant load test on a cycle ergometer at 75% of the peak work rate obtained in the pretraining incremental test. ET was defined as the duration of loaded pedaling. Following IMT, there was a statistically significant increase in inspiratory muscle performance of the Pimax from 7.75 ± 0.47 to 9.15 ± 0.73 kPa (P < 0.01) and of tlim from 348 ± 54 to 467 ± 58 seconds (P < 0.01). A significant increase in IF, indicating decreased dynamic hyperinflation, was observed during both exercise tests. Further, the ratio of breathing frequency to minute ventilation (bf/V′E) decreased significantly, indicating an improved breathing pattern. A significant decrease in perception of dyspnea was also measured. Peak work rate during the incremental cycle ergometer test remained constant, while ET during the constant load test increased significantly from 597.1 ± 80.8 seconds at baseline to 733.6 ± 74.3 seconds (P < 0.01). No significant changes during either exercise tests were measured in the control group. The present study found that in patients with COPD, IMT results in improvement in performance, exercise capacity, sensation of dyspnea, and improvement in the IF prognostic factor.