Respiratory muscle fitness and exercise endurance in healthy humans

We studied chest wall kinematics and respiratory muscle action in five untrained healthy men walking on a motor-driven treadmill at 2 and 4 miles/h with constant grade (0%). The chest wall volume (Vcw), assessed by using the ELITE system, was modeled as the sum of the volumes of the lung-apposed rib cage (Vrc,p), diaphragm-apposed rib cage (Vrc,a), and abdomen (Vab). Esophageal and gastric pressures were measured simultaneously. Velocity of shortening ( V di) and power [W˙di = diaphragm pressure (Pdi) × V di] of the diaphragm were also calculated. During walking, the progressive increase in end-inspiratory Vcw ( P < 0.05) resulted from an increase in end-inspiratory Vrc,p and Vrc,a ( P < 0.01). The progressive decrease ( P < 0.05) in end-expiratory Vcw was entirely due to the decrease in end-expiratory Vab ( P < 0.01). The increase in Vrc,a was proportionally slightly greater than the increase in Vrc,p, consistent with minimal rib cage distortion (2.5 ± 0.2% at 4 miles/h). The Vcw end-inspiratory increase and end-expiratory decrease were accounted for by inspiratory rib cage (RCM,i) and abdominal (ABM) muscle action, respectively. The pressure developed by RCM,i and ABM and Pdi progressively increased ( P < 0.05) from rest to the highest workload. The increase in V di, more than the increase in the change in Pdi, accounted for the increase inW˙di. In conclusion, we found that, in walking healthy humans, the increase in ventilatory demand was met by the recruitment of the inspiratory and expiratory reserve volume. ABM action accounted for the expiratory reserve volume recruitment. We have also shown that the diaphragm acts mainly as a flow generator. The rib cage distortion, although measurable, is minimized by the coordinated action of respiratory muscles.

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Ventilatory muscle recruitment in exercise with O2 in obstructed patients with mild hypoxemia

Journal of Applied Physiology ◽

10.1152/jappl.1987.63.1.195 ◽

1987 ◽

Vol 63 (1) ◽

pp. 195-200 ◽

Cited By ~ 48

Author(s):

G. J. Criner ◽

B. R. Celli

Keyword(s):

Respiratory Muscle ◽

Airflow Obstruction ◽

Gas Mixture ◽

Muscle Dysfunction ◽

Muscle Recruitment ◽

Transdiaphragmatic Pressure ◽

Leg Cycling ◽

Exercise Endurance ◽

Accessory Muscles

Respiratory muscle dysfunction limits exercise endurance in severe chronic airflow obstruction (CAO). To investigate whether inspiring O2 alters ventilatory muscle recruitment and improves exercise endurance, we recorded pleural (Ppl) and gastric (Pga) pressures while breathing air or 30% O2 during leg cycling in six patients with severe CAO, mild hypoxemia, and minimal arterial O2 desaturation with exercise. At rest, mean (+/- SD) transdiaphragmatic pressure (Pdi) was lower inspiring 30% O2 compared with air (23 +/- 4 vs. 26 +/- 7 cmH2O, P less than 0.05), but the pattern of Ppl and Pga contraction was identical while breathing either gas mixture. Maximal transdiaphragmatic pressure was similar breathing air or 30% O2 (84 +/- 30 vs. 77 +/- 30 cmH2O). During exercise, Pdi increased similarly while breathing air or 30% O2, but the latter was associated with a significant increase in peak inspiratory Pga and decreases in peak inspiratory Ppl and expiratory Pga. In five out of six patients, exercise endurance increased with O2 (671 +/- 365 vs. 362 +/- 227 s, P less than 0.05). We conclude that exercise with O2 alters ventilatory muscle recruitment and increases exercise endurance. During exercise inspiring O2, the diaphragm performs more ventilatory work which may prevent overloading the accessory muscles of respiration.

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Faculty Opinions recommendation of Effect of acute hypoxia on respiratory muscle fatigue in healthy humans.

Faculty Opinions – Post-Publication Peer Review of the Biomedical Literature ◽

10.3410/f.5281956.5223055 ◽

2010 ◽

Author(s):

André Coetzee ◽

Andrew Levin

Keyword(s):

Muscle Fatigue ◽

Respiratory Muscle ◽

Acute Hypoxia ◽

Respiratory Muscle Fatigue ◽

Healthy Humans

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Inspiratory muscle training reduces diaphragm activation and dyspnea during exercise in COPD

Journal of Applied Physiology ◽

10.1152/japplphysiol.01078.2017 ◽

2018 ◽

Vol 125 (2) ◽

pp. 381-392 ◽

Cited By ~ 30

Author(s):

Daniel Langer ◽

Casey Ciavaglia ◽

Azmy Faisal ◽

Katherine A. Webb ◽

J. Alberto Neder ◽

...

Keyword(s):

Muscle Strength ◽

Respiratory Muscle ◽

Breathing Pattern ◽

Work Rate ◽

Inspiratory Muscle ◽

Inspiratory Muscle Training ◽

Muscle Training ◽

Lung Volumes ◽

Exercise Endurance ◽

Inspiratory Muscle Strength

Among patients with chronic obstructive pulmonary disease (COPD), those with the lowest maximal inspiratory pressures experience greater breathing discomfort (dyspnea) during exercise. In such individuals, inspiratory muscle training (IMT) may be associated with improvement of dyspnea, but the mechanisms for this are poorly understood. Therefore, we aimed to identify physiological mechanisms of improvement in dyspnea and exercise endurance following inspiratory muscle training (IMT) in patients with COPD and low maximal inspiratory pressure (Pimax). The effects of 8 wk of controlled IMT on respiratory muscle function, dyspnea, respiratory mechanics, and diaphragm electromyography (EMGdi) during constant work rate cycle exercise were evaluated in patients with activity-related dyspnea (baseline dyspnea index <9). Subjects were randomized to either IMT or a sham training control group ( n = 10 each). Twenty subjects (FEV1 = 47 ± 19% predicted; Pimax = −59 ± 14 cmH2O; cycle ergometer peak work rate = 47 ± 21% predicted) completed the study; groups had comparable baseline lung function, respiratory muscle strength, activity-related dyspnea, and exercise capacity. IMT, compared with control, was associated with greater increases in inspiratory muscle strength and endurance, with attendant improvements in exertional dyspnea and exercise endurance time (all P < 0.05). After IMT, EMGdi expressed relative to its maximum (EMGdi/EMGdimax) decreased ( P < 0.05) with no significant change in ventilation, tidal inspiratory pressures, breathing pattern, or operating lung volumes during exercise. In conclusion, IMT improved inspiratory muscle strength and endurance in mechanically compromised patients with COPD and low Pimax. The attendant reduction in EMGdi/EMGdimax helped explain the decrease in perceived respiratory discomfort despite sustained high ventilation and intrinsic mechanical loading over a longer exercise duration. NEW & NOTEWORTHY In patients with COPD and low maximal inspiratory pressures, inspiratory muscle training (IMT) may be associated with improvement of dyspnea, but the mechanisms for this are poorly understood. This study showed that 8 wk of home-based, partially supervised IMT improved respiratory muscle strength and endurance, dyspnea, and exercise endurance. Dyspnea relief occurred in conjunction with a reduced activation of the diaphragm relative to maximum in the absence of significant changes in ventilation, breathing pattern, and operating lung volumes.

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Effects of inspiratory muscle training on respiratory muscle electromyography and dyspnea during exercise in healthy men

Journal of Applied Physiology ◽

10.1152/japplphysiol.00046.2017 ◽

2017 ◽

Vol 122 (5) ◽

pp. 1267-1275 ◽

Cited By ~ 13

Author(s):

Andrew H. Ramsook ◽

Yannick Molgat-Seon ◽

Michele R. Schaeffer ◽

Sabrina S. Wilkie ◽

Pat G. Camp ◽

...

Keyword(s):

Respiratory Muscle ◽

Inspiratory Muscle ◽

Inspiratory Muscle Training ◽

Emg Activity ◽

Respiratory Drive ◽

Muscle Training ◽

Exertional Dyspnea ◽

Healthy Humans ◽

Inspiratory Muscles ◽

Pressure Threshold

Inspiratory muscle training (IMT) has consistently been shown to reduce exertional dyspnea in health and disease; however, the physiological mechanisms remain poorly understood. A growing body of literature suggests that dyspnea intensity can be explained largely by an awareness of increased neural respiratory drive, as measured indirectly using diaphragmatic electromyography (EMGdi). Accordingly, we sought to determine whether improvements in dyspnea following IMT can be explained by decreases in inspiratory muscle electromyography (EMG) activity. Twenty-five young, healthy, recreationally active men completed a detailed familiarization visit followed by two maximal incremental cycle exercise tests separated by 5 wk of randomly assigned pressure threshold IMT or sham control (SC) training. The IMT group ( n = 12) performed 30 inspiratory efforts twice daily against a 30-repetition maximum intensity. The SC group ( n = 13) performed a daily bout of 60 inspiratory efforts against 10% maximal inspiratory pressure (MIP), with no weekly adjustments. Dyspnea intensity was measured throughout exercise using the modified 0–10 Borg scale. Sternocleidomastoid and scalene EMG was measured using surface electrodes, whereas EMGdi was measured using a multipair esophageal electrode catheter. IMT significantly improved MIP (pre: −138 ± 45 vs. post: −160 ± 43 cmH2O, P < 0.01), whereas the SC intervention did not. Dyspnea was significantly reduced at the highest equivalent work rate (pre: 7.6 ± 2.5 vs. post: 6.8 ± 2.9 Borg units, P < 0.05), but not in the SC group, with no between-group interaction effects. There were no significant differences in respiratory muscle EMG during exercise in either group. Improvements in dyspnea intensity ratings following IMT in healthy humans cannot be explained by changes in the electrical activity of the inspiratory muscles. NEW & NOTEWORTHY Exertional dyspnea intensity is thought to reflect an increased awareness of neural respiratory drive, which is measured indirectly using diaphragmatic electromyography (EMGdi). We examined the effects of inspiratory muscle training (IMT) on dyspnea, EMGdi, and EMG of accessory inspiratory muscles. IMT significantly reduced submaximal dyspnea intensity ratings but did not change EMG of any inspiratory muscles. Improvements in exertional dyspnea following IMT may be the result of nonphysiological factors or physiological adaptations unrelated to neural respiratory drive.

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