Ventilatory Load Research Articles

Ultrasonographic evaluation of diaphragmatic thickness and movement for assessment of diaphragmatic dysfunction in COPD patients

BackgroundsChronic obstructive pulmonary disease (COPD) is often ascribed to the disparity that exists between ventilatory loading and diaphragmatic function. The principal factor contributing to this imbalance is the mechanical difficulties brought about by pulmonary hyperinflation. This causes the fiber lengths of the respiratory muscles to be suboptimal, thereby decreasing the tension generated. The frailty of the respiratory musculature is further exacerbated by hypercapnia, acidosis, nutritional deficiency, and steroid therapy. As the principal respiratory muscle, the diaphragm is responsible for 75% of quiescent lung ventilation. Ultrasonography has exhibited substantial promise in evaluating the effectiveness of the diaphragm. The goal of the research was to assess the diaphragmatic function in COPD patients using ultrasonographic examination and to study its correlation with pulmonary function tests.MethodsThis work was performed on 60 individuals with COPD and 20 healthy volunteers (control group). All the subjects were sequentially examined by chest X-ray and spirometry in one time and then repeated 15–45 min after the first dose of inhalation therapy (salbutamol); then, 6MWT, ABG, and ultrasonography were done for all patients.ResultsIn COPD patients, diaphragmatic thickness and excursion were substantially reduced in comparison to the control group; these parameters were also significantly correlated with pulmonary function tests.ConclusionsA reduction in diaphragmatic thickness and excursion is observed in patients diagnosed with COPD.

Effects of Low-Load/High-Repetition Resistance Training on Exercise Capacity, Health Status, and Limb Muscle Adaptation in Patients With Severe COPD: A Randomized Controlled Trial

Training volume is paramount in the magnitude of physiological adaptations following resistance training. However, patients with severe COPD are limited by dyspnea during traditional two-limb low-load/high-repetition resistance training (LLHR-RT), resulting in suboptimal training volumes. During a single exercise session, single-limb LLHR-RT decreases the ventilatory load and enables higher localized training volumes compared with two-limb LLHR-RT. Does single-limb LLHR-RT lead to more profound effects compared with two-limb LLHR-RT on exercise capacity (6-min walk distance [6MWD]), health status, muscle function, and limb adaptations in patients with severe COPD? Thirty-three patients (mean age 66 ± 7 years; FEV1 39 ± 10%predicted) were randomized to 8weeks of single- or two-limb LLHR-RT. Exercise capacity (6MWD), health status, and muscle function were compared between groups. Quadriceps muscle biopsy specimens were collected to examine physiological responses. Single-limb LLHR-RT did not further enhance 6MWD compared with two-limb LLHR-RT (difference, 14 [-12 to 39 m]. However, 73%in the single-limb group exceeded the known minimal clinically important difference of 30m compared with 25%in the two-limb group (P= .02). Health status and muscle function improved to a similar extent in both groups. During training, single-limb LLHR-RT resulted in a clinically relevant reduction in dyspnea during training compared with two-limb LLHR-RT (-1.75; P= .01), but training volume was not significantly increased (23%; P= .179). Quadriceps muscle citrate synthase activity (19%; P= .03), hydroxyacyl-coenzyme A dehydrogenase protein levels (32%; P< .01), and capillary-to-fiber ratio (41%; P< .01) were increased compared with baseline after pooling muscle biopsy data from all participants. Single-limb LLHR-RT did not further increase mean 6MWD compared with two-limb LLHR-RT, but it reduced exertional dyspnea and enabled more people to reach clinically relevant improvements in 6MWD. Independent of execution strategy, LLHR-RT improved exercise capacity, health status, muscle endurance, and enabled several physiological muscle adaptations, reducing the negative consequences of limb muscle dysfunction in COPD. ClinicalTrials.gov; No.: NCT02283580; URL: www.clinicaltrials.gov.

The hyperpnoea of exercise in health: Respiratory influences on neurovascular control.

What is the topic of this review? Elevated demand is placed on the respiratory muscles during whole-body exercise-induced hyperpnoea. What is the role of elevated demand in neural modulation of cardiovascular control in respiratory and locomotor skeletal muscle, and what are the mechanisms involved? What advances does it highlight? There is a sympathetic restraint of blood flow to locomotor muscles during near-maximal exercise, which might function to maintain blood pressure. During submaximal exercise, respiratory muscle blood flow might be also be reduced if ventilatory load is sufficiently high. Methodological advances (near-infrared spectroscopy with indocyanine green) confirm that blood flow is diverted away from respiratory muscles when the work of breathing is alleviated. It is known that the respiratory muscles have a significant increasing oxygen demand in line with hyperpnoea during whole-body endurance exercise and are susceptible to fatigue, in much the same way as locomotor muscles. The act of ventilation can itself be considered a form of exercise. The manipulation of respiratory load at near-maximal exercise alters leg blood flow significantly, demonstrating a competitive relationship between different skeletal muscle vascular beds to perfuse both sets of muscles adequately with a finite cardiac output. In recent years, the question has moved towards whether this effect exists during submaximal exercise, and the use of more direct measurements of respiratory muscle blood flow itself to confirm assumptions that uphold the concept. Evidence thus far has shown that there is a reciprocal effect on blood flow redistribution during ventilatory load manipulation observed at the respiratory muscles themselves and that the effect is observable during submaximal exercise, where active limb blood flow was reduced in conditions that simulated a high work of breathing. This has clinical applications for populations with respiratory disease and heart failure, where the work of breathing is remarkably high, even during submaximal efforts.

Practical Clinical Application of an Extracorporeal Carbon Dioxide Removal System in Acute Respiratory Distress Syndrome and Acute on Chronic Respiratory Failure.

We retrospectively reviewed the medical records of 11 patients supported with a veno-venous low-flow extracorporeal carbon dioxide (CO2) removal (ECCO2R) device featuring a large gas exchange surface membrane lung (ML) (i.e., 1.8 m). Seven patients suffered from exacerbation of a chronic pulmonary disease, while four subjects were affected by acute respiratory distress syndrome (ARDS). Twenty-four hours of ECCO2R treatment reduced arterial PCO2 from 63 ± 12 to 54 ± 11 mm Hg (p < 0.01), increased arterial pH from 7.29 ± 0.07 to 7.39 ± 0.06 (p < 0.01), and decreased respiratory rate from 32 ± 10 to 21 ± 8 bpm (p < 0.05). Extracorporeal blood flow and CO2 removal were 333 ± 37 and 94 ± 18 ml/min, respectively. The median duration of ECCO2R treatment was 7 days (6.5-9.5). All four ARDS patients were invasively ventilated at the time of treatment start, no one was extubated and they all died. Among the seven patients with exacerbation of chronic pulmonary diseases, four were managed with noninvasive ventilation at ECCO2R institution, while three were extubated after starting the extracorporeal treatment. No one of these seven patients was intubated or re-intubated after ECCO2R institution and five (71%) survived to hospital discharge. A low-flow ECCO2R device with a large surface ML removes a relevant amount of CO2 resulting in a decreased arterial PCO2, an increased arterial pH, and in a reduced ventilatory load.

Reductions in dead space ventilation with nasal high flow depend on physiological dead space volume: metabolic hood measurements during sleep in patients with COPD and controls.

Nasal high flow (NHF) reduces minute ventilation and ventilatory loads during sleep but the mechanisms are not clear. We hypothesised NHF reduces ventilation in proportion to physiological but not anatomical dead space.11 subjects (five controls and six chronic obstructive pulmonary disease (COPD) patients) underwent polysomnography with transcutaneous carbon dioxide (CO2) monitoring under a metabolic hood. During stable non-rapid eye movement stage 2 sleep, subjects received NHF (20 L·min-1) intermittently for periods of 5-10 min. We measured CO2 production and calculated dead space ventilation.Controls and COPD patients responded similarly to NHF. NHF reduced minute ventilation (from 5.6±0.4 to 4.8±0.4 L·min-1; p<0.05) and tidal volume (from 0.34±0.03 to 0.3±0.03 L; p<0.05) without a change in energy expenditure, transcutaneous CO2 or alveolar ventilation. There was a significant decrease in dead space ventilation (from 2.5±0.4 to 1.6±0.4 L·min-1; p<0.05), but not in respiratory rate. The reduction in dead space ventilation correlated with baseline physiological dead space fraction (r2=0.36; p<0.05), but not with respiratory rate or anatomical dead space volume.During sleep, NHF decreases minute ventilation due to an overall reduction in dead space ventilation in proportion to the extent of baseline physiological dead space fraction.

Inspiratory Resistive (R) Load Endurance Testing in Normal Healthy Adults: Load compensation, effort sensation and affective perception.

Increased respiratory load is a key feature in various respiratory diseases, accompanied by ventilatory compensation, cognitive awareness and affective perception. Loaded breathing can occur from minutes to days requiring the individual to modulate their breathing pattern to maintain alveolar ventilation, minimize work of breathing and minimize aversive load sensations. Increased inspiratory load is associated with cognitive sensation of the load magnitude and affective escape behavior to reduce the aversive perception of loaded breathing. During exacerbations of lung diseases, an individual often must compensate for increased loads that exceed their ability to sustain alveolar ventilation. Yet it is difficult to assess the capacity of an individual to adapt to an increased respiratory load. The aim of this study was to determine the ventilatory and perceptual endurance response to a high magnitude inspiratory R load applied for 10 minutes. It was hypothesized that some individuals would be able to complete the task and other individuals would terminate the task early. It was further hypothesized that early termination of the task would be due to increased aversive affective awareness. Healthy participants were tested while breathing through a non‐rebreathing circuit with an inspiratory load R=50 cmH20/L/s. The individual respired with no‐load for 1 minute, then the load was applied for 10 minutes, followed by 1 minute of no‐load breathing. The subject was instructed that they could terminate the task at any time by removing the mouthpiece. Subjects estimated their perceived load intensity (MEInt) and unpleasantness (MEUn) every minute. Fear (MEF) was estimated before and after the load trial. Two of six subjects terminated the trial early. The ventilatory load pattern for all subjects was a load dependent increased maximum inspiratory pressure, decreased airflow, increased inspiratory duration and unchanged expiratory duration, increased total breath time, increased inspiratory volume, unchanged minute ventilation, PCO2 and PO2. The MEInt increased with the onset of the load, was constant throughout the task and was the same for individuals that completed and stopped the task. MEUn increased with the load onset with greater MEUn for subjects that stopped early. The individuals that stopped early had equal MEF at task onset but much greater MEF when the task stopped. The results suggest that inspiratory R50 endurance capacity is decreased in individuals with greater negative affective responses to high magnitude loaded breathing.This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

Influence of Upper-Body Exercise on the Fatigability of Human Respiratory Muscles.

ABSTRACTPurposeDiaphragm and abdominal muscles are susceptible to contractile fatigue in response to high-intensity, whole-body exercise. This study assessed whether the ventilatory and mechanical loads imposed by high-intensity, upper-body exercise would be sufficient to elicit respiratory muscle fatigue.MethodsSeven healthy men (mean ± SD; age = 24 ± 4 yr, peak O2 uptake [V˙O2peak] = 31.9 ± 5.3 mL·kg−1·min−1) performed asynchronous arm-crank exercise to exhaustion at work rates equivalent to 30% (heavy) and 60% (severe) of the difference between gas exchange threshold and V˙O2peak. Contractile fatigue of the diaphragm and abdominal muscles was assessed by measuring pre- to postexercise changes in potentiated transdiaphragmatic and gastric twitch pressures (Pdi,tw and Pga,tw) evoked by supramaximal magnetic stimulation of the cervical and thoracic nerves, respectively.ResultsExercise time was 24.5 ± 5.8 min for heavy exercise and 9.8 ± 1.8 min for severe exercise. Ventilation over the final minute of heavy exercise was 73 ± 20 L·min−1 (39% ± 11% maximum voluntary ventilation) and 99 ± 19 L·min−1 (53% ± 11% maximum voluntary ventilation) for severe exercise. Mean Pdi,tw did not differ pre- to postexercise at either intensity (P > 0.05). Immediately (5–15 min) after severe exercise, mean Pga,tw was significantly lower than pre-exercise values (41 ± 13 vs 53 ± 15 cm H2O, P < 0.05), with the difference no longer significant after 25–35 min. Abdominal muscle fatigue (defined as ≥15% reduction in Pga,tw) occurred in 1/7 subjects after heavy exercise and 5/7 subjects after severe exercise.ConclusionsHigh-intensity, upper-body exercise elicits significant abdominal, but not diaphragm, muscle fatigue in healthy men. The increased magnitude and prevalence of fatigue during severe-intensity exercise is likely due to additional (nonrespiratory) loading of the thorax.

Optimization of Frequency-Controlled Asynchronous Electric Drive for Ventilatory Loading

The analysis of losses of power in the adjustable asynchronous electric drive and optimization of the frequency and adjustable asynchronous electric drive with ventilator loading is carried out, and also it is developed management system of the energy saving electric drive with ventilator loading. The system of the electric drive minimizing losses of engine capacity is experimentally probed.

Short-term modulation of the ventilatory response to exercise is preserved in obstructive sleep apnea

BackgroundThe ventilatory response to exercise can be transiently adjusted in response to environmentally (e.g., breathing apparatus) or physiologically altered conditions (e.g., respiratory disease), maintaining constant relative arterial PCO2 regulation from rest to exercise (Mitchell and Babb, 2006); this augmentation is called short-term modulation (STM) of the exercise ventilatory response. Obesity and/or obstructive sleep apnea could affect the exercise ventilatory response and the capacity for STM due to chronically increased mechanical and/or ventilatory loads on the respiratory system, and/or recurrent (chronic) intermittent hypoxia experienced during sleep. We hypothesized that: (1) the exercise ventilatory response is augmented in obese OSA patients compared with obese non-OSA adults, and (2) the capacity for STM with added dead space is diminished in obese OSA patients. MethodsNine obese adults with OSA (age: 39±6 yr, BMI: 40±5kg/m2, AHI: 25±24 events/h [range 6–73], mean±SD) and 8 obese adults without OSA (age: 38±10 yr, BMI: 37±6kg/m2, AHI: 1±2) completed three, 20-min bouts of constant-load submaximal cycling exercise (8min rest, 6min at 10 and 30W) with or without added external dead space (200 or 400mL; 20min rest between bouts). Steady-state measurements were made of ventilation (V˙E), oxygen consumption V˙O2), carbon dioxide production (V˙CO2), and end-tidal PCO2 (PETCO2). The exercise ventilatory response was defined as the slope of the V˙E-V˙CO2 relationship (ΔV˙E/ΔV˙CO2). ResultsIn control (i.e. no added dead space), the exercise ventilatory response was not significantly different between non-OSA and OSA groups (ΔV˙E/ΔV˙CO2 slope: 30.5±4.2 vs 30.5±3.8, p>0.05); PETCO2 regulation from rest to exercise did not differ between groups (p>0.05). In trials with added external dead space, ΔV˙E/ΔV˙CO2 increased with increased dead space (p < 0.05) and the PETCO2 change from rest to exercise remained small (<2mmHg) in both groups, demonstrating STM. There were no significant differences between groups. ConclusionsContrary to our hypotheses: (1) the exercise ventilatory response is not increased in obese OSA patients compared with obese non-OSA adults, and (2) the capacity for STM with added dead space is preserved in obese OSA and non-OSA adults.

S123 Does Exercising With Domiciliary Non-invasive Ventilation (niv) Improve Quality Of Life (qol) In Patients With Severe Chronic Obstructive Pulmonary Disease (copd)?

Introduction and objectives Patients with severe COPD experience breathlessness leading to exercise limitation impacting on QoL. Pulmonary rehabilitation (PR) can improve QoL, but those with the severest disease are frequently hospitalised and cannot readily access PR. Previous studies have trialled positive pressure as a means of relieving ventilatory load, allowing more severe COPD patients to exercise.1 Studies have assessed mixed pathology or stable COPD patients.2,3 In this study, we have assessed patients with severe COPD admitted to hospital with Type 2 respiratory failure and acidosis treated with acute NIV. Methods 18 patients (11 female), recruited during admission were randomised into 3 groups. Group 1 received standard hospital physiotherapy care; Group 2 exercised on NIV (Trilogy 100, Philips-Respironics) with a mean pressure support of 10 cmH2O twice weekly during admission; Group 3 exercised on NIV twice weekly during hospital admission and continued this at home for 3 months post-discharge. Exercising included weights, pedal cycling and walking. QoL was assessed using the St Georges Respiratory Questionnaire (SGRQ) and the London Chest Activities of Daily Living Questionnaire (LCADL). Mean changes in total scores for SGRQ and LCADL were compared between baseline and at 3 months (M3). Data are mean±SD or mean (range). Results The group (n = 18) age was 66.5 years [46–97], FEV1: 25% predicted [9–51%] and MRC score 3 [1–4]). 3/18 patients died during the study. The results are presented in [Table 1][1]. Conclusion Patients exercising with NIV, in hospital and at home twice weekly (Group 3) showed the greatest improvement in QoL, compared to the other two groups. The use of NIV during exercise at home may assist patients unable to access pulmonary rehabilitation.

Locomotor and diaphragm muscle fatigue in endurance athletes performing time-trials of different durations.

Fatigue in leg muscles might differ between running and cycling due to inherent differences in muscle activation patterns. Moreover, postural demand placed upon the diaphragm during running could augment the development of diaphragm fatigue. We investigated quadriceps and diaphragm fatigue in 11 runners and 11 cyclists (age: 29 ± 5 years; [Formula: see text]O2,peak: 66.9 ± 5.5 ml min(-1) kg(-1)) by assessing quadriceps twitch force (Q tw) and transdiaphragmatic twitch pressure (P di,tw) before and after 15- and 30-min time-trials (15TT, 30TT). Inspiratory muscle fatigue was also obtained after volitional normocapnic hyperpnoea (NH) where postural demand is negligible. We hypothesized that running and cycling would induce different patterns of fatigue and that runners would develop less respiratory muscle fatigue when performing NH. The reduction in Q tw was greater in cyclists (32 ± 6 %) compared to runners (13 ± 8 %, p < 0.01), but not different for 15TTs (23 ± 13 %) and 30TTs (21 ± 11 %, p = 0.34). Overall P di,tw was more reduced after 15TTs (24 ± 8 %) than after 30TTs (20 ± 9 %, p = 0.04) while being similar for runners and cyclists (p = 0.78). Meanwhile, breathing duration in NH and the magnitude of inspiratory muscle fatigue were also not different (both p > 0.05). Different levels of leg muscle fatigue in runners and cyclists could in part be related to the specific muscle activation patterns including concentric contractions in both modalities but eccentric contractions in runners only. Diaphragm fatigue likely resulted from the large ventilatory load which is characteristic for both exercise modalities and which was higher in 15TTs than in 30TTs (+27 %, p < 0.01) while postural demand appears to be of less importance.

Chronic hypoventilation and its management

While obstructive sleep apnoea syndrome dominates discussion of the prevalence of sleep disordered breathing, nocturnal hypoventilation remains extremely prevalent in those with chronic ventilatory disorders and in the natural history of these conditions pre-dates the development of daytime ventilatory failure. In this review the clinical management of chronic hypoventilation in neuromuscular disease will be considered and then compared with that in obesity hypoventilation syndrome. In simple terms these conditions illustrate the polar opposite ends of the spectrum, as in neuromuscular disease the reduced capacity of the respiratory system is unable to withstand a normal respiratory load, and in obesity hypoventilation syndrome the normal capacity of the respiratory system is unable to tolerate a substantially increased ventilatory load.

Respiratory muscle training extends exercise tolerance without concomitant change to peak oxygen uptake: Physiological, performance and perceptual responses derived from the same incremental exercise test

There is conjecture over the efficacy of respiratory muscle training (RMT). The aim of this study was to establish whether or not exercise tolerance, physical performance and effort perceptions are influenced by RMT. Thirty-six healthy males (age 24 ± 4) agreed to participate (experimental group (EXP) n = 18, control (CON) n = 18). RMT was performed using an inspiratory pressure-threshold training device at either 55% (EXP) or 10% (CON) of maximal inspiratory effort. Measurements of spirometry and maximal static inspiratory mouth pressure were taken before and after 4 weeks of RMT in addition to an incremental test to volitional exhaustion for the determination of: (i) V˙O(2) peak; (ii) maximal velocity at volitional exhaustion (vV˙O(2) peak)); (iii) time to volitional exhaustion; and (iv) effort perceptions. There were no differences in spirometry, but mean maximal static inspiratory mouth pressure increased significantly in EXP (P < 0.01). V˙O(2) peak was unchanged following the 4-week intervention for both EXP and CON, although the proportion of EXP attaining the criteria for a V˙O(2) plateau significantly increased (P < 0.05). Both time to volitional exhaustion (P < 0.05) and vV˙O(2) peak were significantly improved for EXP (P < 0.05), while effort perceptions were reduced (P < 0.05). EXP tolerated higher running velocities during incremental exercise and demonstrated a significant flattening (plateau) of V˙O(2) after training. This suggests that RMT may promote an improved performance outcome vV˙O(2) peak probably as a result of blunted afferent sensations reducing the perceived discomfort of exercise at high ventilatory loads.

Der schwer entwöhnbare Patient

Approximately 10% of patients with mechanical ventilation experience prolonged weaning and also have an increased morbidity and mortality. Once spontaneous breathing trials have failed the organ systems responsible should be identified. This can be accomplished during the spontaneous breathing trial using clinical examination, measurement of blood gases, echocardiography and imaging techniques. Specific patterns allow the diagnosis of pathological respiratory mechanisms, weak ventilatory muscles, heart failure, myocardial ischemia and psychiatric problems. Respiratory and cardiac limitations of weaning can be overcome by reducing the ventilatory load, training of the ventilatory muscles and reducing cardiac workload. A cooperative sedation strategy as well as an early start of weaning and rehabilitation can prevent prolonged weaning in critically ill patients.

Continuous Transcutaneous Submental Electrical Stimulation in Obstructive Sleep Apnea: A Feasibility Study

The therapeutic value of transcutaneous electrical stimulation of the genioglossus muscle in patients with obstructive sleep apnea (OSA) to reduce sleep-disordered breathing is unclear. Contraction of the genioglossus muscles during transcutaneous stimulation was investigated using ultrasonography in 11 healthy subjects (seven men, mean [SD] age 30 [6] years; BMI, 24.2 [3.5] kg/m(2)). Esophageal and gastric pressures were measured with balloon catheters, and transesophageal diaphragm electromyogram (EMGdi) was recorded during polysomnography in 11 patients with OSA (eight men, aged 51 [16] years; BMI, 42.0 [9.7] kg/m(2)) while transcutaneous electrical stimulation of the genioglossus was applied in non-rapid eye movement sleep (stage N2). Ultrasonography measurements showed a significant increase in tongue diameter during stimulation (sagittal: 10.0% [2.8%]; coronal: 9.4 % [3.7%]). The measurements were reproducible and repeatable. In patients with OSA, snoring decreased during stimulation (P < .001) and oxygenation improved (P = .001); the respiratory disturbance index (RDI) fell from 28.1 (26.3) to 10.2 (10.2) events per hour during stimulation (P = .002), returning to 26.6 (26.0) events per hour after stimulation was stopped. Transdiaphragmatic pressure swing decreased from 24.1 (13.5) cm H(2)O to 19.7 (7.1) cm H(2)O (P = .022), increasing to 24.2 (10.8) cm H(2)O afterward, and EMGdi fell from 23.8% max (12.6% max) to 15.7% max (6.4% max) (P < .001), rising to 22.6% max (10.4% max) post stimulation. Continuous transcutaneous electrical stimulation of the genioglossus contracts the genioglossus muscle and reduces ventilatory load and neural respiratory drive in patients with OSA.

Effects of Aerobic Fitness and Pulmonary Function on Mechanical Ventilatory Constraints During Exercise in Healthy Women

Females with a higher maximal aerobic capacity (Vo2max) have higher ventilatory requirements during exercise relative to their untrained counterparts. The higher ventilatory loads in trained females might make them more susceptible to developing expiratory flow limitation (EFL) during exercise. However, the interrelationship between aerobic fitness, pulmonary function and EFL has not been well characterized in women. PURPOSE: To determine the effect of Vo2max and maximal expiratory flow-volume (MEFV) curve characteristics on EFL in healthy women. METHODS: A progressive stepwise cycle test to exhaustion was completed by 22 healthy females (age=28±5; Vo2max=49±8, range 31-62 ml·kg-1·min-1). A MEFV curve was generated by having subjects perform several expirations from total lung capacity to residual volume at different efforts before and after exercise. Tidal breaths at each exercise stage were superimposed within the MEFV curve by having subjects perform inspiratory capacity maneuvers. The magnitude of EFL was calculated as the percent of the tidal breath that met or exceeded the outer boundary of the MEFV curve. Subjects were partitioned into those with EFL (n=10) and those with no EFL (NEFL; n=12). RESULTS: There was no difference in Vo2max between the EFL group and the NEFL group (47±5 vs. 51±10 ml·kg-1·min-1, respectively, P >0.05). There was no relationship between the degree of EFL and Vo2max (r=0.18, P>0.05). Absolute values were different between the EFL and NEFL groups for: peak expiratory flow (PEF) (6.9±0.9 vs. 8.5±1.0 l·sec-1, P < 0.05), and for forced expiratory flows at 75% of vital capacity (FEF75%) (6.0±0.6 vs. 7.6±0.9 l·sec-1, P<0.05), 50% of vital capacity (FEF50%) (3.5±0.4 vs. 5.6±1.0 l·sec-1, P<0.05) and 25% of vital capacity (FEF25%) (1.8±0.2 vs. 3.0±0.9 l·sec-1, P<0.05). The forced vital capacity was significantly larger in the NEFL group compared to the EFL group (4.4±0.5 vs. 3.8±0.4 l, P<0.05). When expressed as a percentage of PEF, FEF75% was not different between groups (87±7 vs. 90±6%, P>0.05) while FEF50% (52± 8 vs. 66±6%, P<0.05) and FEF25% (26±6 vs. 35±7.39%, P<0.05) were different. CONCLUSION: The degree of EFL experienced by women appears to be more associated with lung size and the characteristics of their MEFV curve rather than aerobic fitness. Funding: BC Lung Association and NSERC

In Memoriam: Neil S. Cherniack, M.D. (1931–2009)

neil s. cherniack, m.d., a long-time member of the American Physiological Society (APS), former Editor-In-Chief of the Journal of Applied Physiology ( JAP ), and a pioneering respiratory physiologist, died on October 21, 2009, at the age of 78. A renowned scientist, educator, and clinician, Dr.

Breathlessness, fatigue and the respiratory muscles

Breathlessness is a common symptom in respiratory, cardiovascular and malignant disease. It reduces exercise tolerance and mobility, and is an important determinant of quality of life. The multifactorial nature of the symptom often presents difficulties in understanding why individual patients are breathless, and how breathlessness should best be palliated, especially in advanced disease. However, insights into the neurophysiological factors underlying the symptom can be gained by considering the balance between the load on, and capacity of, the respiratory muscles and increased neural respiratory drive, reflecting increased respiratory effort. Mismatch between efferent neural respiratory drive and afferent feedback, reflecting the degree of neuromechanical dissociation, is also important. This paper describes mechanisms by which ventilatory load, capacity and drive may be affected by disease, and how these can be measured physiologically. The schema presented also provides a framework for understanding the mechanisms by which interventions that relieve breathlessness may have their effect.

A physiological model of patient-reported breathlessness during daily activities in COPD

Breathlessness during daily activities has a significant impact on quality of life in chronic obstructive pulmonary disease. Herein, we present a physiological model of patient-reported breathlessness based on the relationship between ventilatory load, respiratory muscle capacity, neural respiratory drive and neuromechanical dissociation during daily activities. This model should facilitate an understanding of the mechanisms driving increased intensity of breathlessness during daily activities and the relief of breathlessness following medical or surgical interventions. The model should also provide a structure on which to base the development of patient-reported outcome instruments to measure the severity of breathlessness during daily activities in chronic obstructive pulmonary disease.

Development of Central Sleep Apnea After Maxillofacial Surgery for Obstructive Sleep Apnea

Central sleep apnea is a rarely reported complication of surgery for obstructive sleep apnea (OSA). We report the case of a 38-year-old male who developed marked central sleep apnea 3 months after a maxillomandibular advancement for moderate OSA, which spontaneously resolved on his 6-month postoperative polysomnogram. Five prior cases of this postoperative complication have been reported in nonobese individuals after tracheostomy for OSA. Additionally, a recent study demonstrated that patients with atmospheric pharyngeal closing pressures are susceptible to unstable ventilation. We hypothesize that latent high loop gain from chronic OSA, coupled with atmospheric pharyngeal closing pressures, predisposed our patient to develop unstable ventilation after an abrupt postoperative change in his ventilatory load. Our case supports delaying postoperative polysomnography > or = 6 months in individuals at high risk for this complication.