Effect of resistive loads on pattern of respiratory muscle recruitment during exercise

1991 ◽  
Vol 71 (5) ◽  
pp. 1941-1948 ◽  
Author(s):  
M. Ramonatxo ◽  
J. Mercier ◽  
R. Cohendy ◽  
C. Prefaut
Keyword(s):  
Respiratory Muscle ◽  
Minute Ventilation ◽  
Abdominal Muscles ◽  
Resistive Load ◽  
Muscle Recruitment ◽  
O2 Uptake ◽  
Exercise Tests ◽  
Co2 Output ◽  
Resistive Loads ◽  
Mouth Occlusion Pressure

In healthy subjects, we compared the effects of an expiratory (ERL) and an inspiratory (IRL) resistive load (6 cmH2O.l-1.s) with no added resistive load on the pattern of respiratory muscle recruitment during exercise. Fifteen male subjects performed three exercise tests at 40% of maximum O2 uptake: 1) with no-added-resistive load (control), 2) with ERL, and 3) with IRL. In all subjects, we measured breathing pattern and mouth occlusion pressure (P0.1) from the 3rd min of exercise, in 10 subjects O2 uptake (VO2), CO2 output (VCO2), and respiratory exchange ratio (R), and in 5 subjects we measured gastric (Pga), pleural (Ppl), and transdiaphragmatic (Pdi) pressures. Both ERL and IRL induced a high increase of P0.1 and a decrease of minute ventilation. ERL induced a prolongation of expiratory time with a reduction of inspiratory time (TI), mean expiratory flow, and ratio of inspiratory to total time of the respiratory cycle (TI/TT). IRL induced a prolongation of TI with a decrease of mean inspiratory flow and an increase of tidal volume and TI/TT. With ERL, in two subjects, Pga increased and Ppl decreased more during inspiration than during control suggesting that the diaphragm was the most active muscle. In one subject, the increases of Ppl and Pga were weak; thus Pdi increased very little. In the two other subjects, Ppl decreased more during inspiration but Pga also decreased, leading to a decrease of Pdi. This suggests a recruitment of abdominal muscles during expiration and of accessory and intercostal muscles during inspiration. With IRL, in all subjects, Ppl again decreased more, Pga began to decrease until 40% of TI and then increased.(ABSTRACT TRUNCATED AT 250 WORDS)

Influence of prior ventilatory experience on the estimation of breathlessness during exercise

1990 ◽  
Vol 78 (2) ◽  
pp. 149-153 ◽  
Author(s):  
Rachel C. Wilson ◽  
P. W. Jones
Keyword(s):  
Exercise Test ◽  
Prior Experience ◽  
Minute Ventilation ◽  
Normal Subjects ◽  
Resistive Load ◽  
Inspiratory Time ◽  
Borg Scale ◽  
Exercise Tests ◽  
Loaded Breathing ◽  
Inspiratory Load

1. The intensity of breathlessness was measured during exercise in nine normal subjects using a modified Borg scale to examine the effect of prior experience of breathlessness on subsequent estimates of breathlessness. 2. Each subject performed four exercise tests, each of which consisted of two identical runs of workload incrementation (run 1 and run 2). An inspiratory resistive load of 3.8 cmH2O s−1 l−1 was applied during the appropriate run of the exercise test to examine the effect of (a) prior experience of ‘loaded’ breathing on breathlessness estimation during ‘unloaded’ breathing, and (b) prior experience of ‘unloaded’ breathing on breathlessness estimation during ‘loaded’ breathing. Run 1 was the conditioning run; run 2 was the run in which the effect of conditioning was measured. 3. There was a good correlation between breathlessness and minute ventilation during both unloaded’ breathing (median r = 0.93) and ‘loaded’ breathing (median r = 0.95). 4. The slope of the Borg score/minute ventilation relationship was greater during ‘loaded’ breathing than during ‘unloaded’ breathing (P < 0.01). There was no difference in mean Borg score between ‘unloaded’ and ‘loaded’ breathing. 5. After a period of ‘loaded’ breathing during run 1, estimated breathlessness was significantly reduced during ensuing ‘unloaded’ breathing in run 2 (P < 0.01) compared with the exercise test in which ‘unloaded’ breathing was experienced throughout both run 1 and run 2. 6. After a period of ‘unloaded’ breathing in run 1, estimated breathlessness was significantly increased during ensuing ‘loaded’ breathing in run 2 (P < 0.01) compared with the exercise test in which the inspiratory load had already been experienced in run 1. 7. Changes in the pattern of breathing (inspiratory time, expiratory time, total breath duration, inspiration time/total breath duration ratio and tidal volume) were not consistent with the changes in breathlessness. 8. We suggest that perception of breathlessness may be influenced by a subject's immediate prior experience of an altered relationship between breathlessness and ventilation.

Effects of expiratory loading on respiration in humans

1980 ◽  
Vol 49 (4) ◽  
pp. 601-608 ◽  
Author(s):  
B. Gothe ◽  
N. S. Cherniack
Keyword(s):  
Muscle Activity ◽  
Healthy Subjects ◽  
Respiratory Muscle ◽  
Resistive Load ◽  
Similar Magnitude ◽  
Occlusion Pressure ◽  
Ventilatory Responses ◽  
Residual Capacity ◽  
Resistive Loads ◽  
The Difference

We examined the effects of expiratory resistive loads of 10 and 18 cmH2O.l-1.s in healthy subjects on ventilation and occlusion pressure responses to CO2, respiratory muscle electromyogram, pattern of breathing, and thoracoabdominal movements. In addition, we compared ventilation and occlusion pressure responses to CO2 breathing elicited by breathing through an inspiratory resistive load of 10 cmH2O.l-1.s to those produced by an expiratory load of similar magnitude. Both inspiratory and expiratory loads decreased ventilatory responses to CO2 and increased the tidal volume achieved at any given level of ventilation. Depression of ventilatory responses to Co2 was greater with the larger than with the smaller expiratory load, but the decrease was in proportion to the difference in the severity of the loads. Occlusion pressure responses were increased significantly by the inspiratory resistive load but not by the smaller expiratory load. However, occlusion pressure responses to CO2 were significantly larger with the greater expiratory load than control. Increase in occlusion pressure observed could not be explained by changes in functional residual capacity or chemical drive. The larger expiratory load also produced significant increases in electrical activity measured during both inspiration and expiration. These results suggest that sufficiently severe impediments to breathing, even when they are exclusively expiratory, can enhance inspiratory muscle activity in conscious humans.

Effect of hyperoxia on substrate utilization during intense submaximal exercise

1986 ◽  
Vol 61 (2) ◽  
pp. 523-529 ◽  
Author(s):  
R. P. Adams ◽  
P. A. Cashman ◽  
J. C. Young
Keyword(s):  
Fatty Acids ◽  
Free Fatty Acids ◽  
Respiratory Exchange Ratio ◽  
Minute Ventilation ◽  
Exercise Bout ◽  
Substrate Utilization ◽  
Submaximal Exercise ◽  
O2 Uptake ◽  
Co2 Output ◽  
Lactate Levels

Six trained males [mean maximal O2 uptake (VO2max) = 66 ml X kg-1 X min-1] performed 30 min of cycling (mean = 76.8% VO2max) during normoxia (21.35 +/- 0.16% O2) and hyperoxia (61.34 +/- 1.0% O2). Values for VO2, CO2 output (VCO2), minute ventilation (VE), respiratory exchange ratio (RER), venous lactate, glycerol, free fatty acids, glucose, and alanine were obtained before, during, and after the exercise bout to investigate the possibility that a substrate shift is responsible for the previously observed enhanced performance and decreased RER during exercise with hyperoxia. VO2, free fatty acids, glucose, and alanine values were not significantly different in hyperoxia compared with normoxia. VCO2, RER, VE, and glycerol and lactate levels were all lower during hyperoxia. These results are interpreted to support the possibility of a substrate shift during hyperoxia.

Effect of ethanol and naloxone on control of ventilation and load perception

1983 ◽  
Vol 55 (3) ◽  
pp. 929-934 ◽  
Author(s):  
T. M. Michiels ◽  
R. W. Light ◽  
C. K. Mahutte
Keyword(s):  
Normal Subjects ◽  
Ethanol Ingestion ◽  
Resistive Load ◽  
Load Compensation ◽  
Ventilatory Responses ◽  
Resistive Loading ◽  
Resistive Loads ◽  
Mouth Occlusion Pressure ◽  
Load Perception ◽  
Respiratory Depressant

The respiratory depressant effects of ethanol and their potential reversibility by naloxone were studied in 10 normal subjects. Ventilatory and mouth occlusion pressure (P0.1) responses to hypercapnia and hypoxia without and with an inspiratory resistive load (13 cmH2O X 1(-1) X S) were measured. The resistive load detected with 50% probability (delta R50) and the exponent (n) in Stevens' psychophysical law for magnitude estimation of resistive loads were studied using standard psychophysical techniques. Each of these studies was performed before ethanol ingestion, after ethanol ingestion (1.5 ml/kg, by mouth), and then again after naloxone (0.8 mg iv). Ethanol increased delta R50 (P less than 0.05) and decreased n (P less than 0.05). Naloxone caused no further change in these parameters. The load compensation (Lc), defined as the ratio of loaded to unloaded response slopes, was not significantly changed after ethanol and naloxone. No correlation was found between the Lc and delta R50 or n. The ventilatory and P0.1 responses to hypercapnia and hypoxia with and without inspiratory resistive loading decreased after ethanol (P less than 0.05, hypercapnia; NS, hypoxia). After naloxone the hypercapnic ventilatory responses increased (P less than 0.05). This suggests that the respiratory depressant effects of ethanol may be mediated via endorphins.

Effects of chest wall vibration on breathlessness during hypercapnic ventilatory response

1998 ◽  
Vol 84 (5) ◽  
pp. 1487-1491 ◽  
Author(s):  
Hidenori Edo ◽  
Hiroshi Kimura ◽  
Mafumi Niijima ◽  
Hideo Sakabe ◽  
Masato Shibuya ◽  
...  
Keyword(s):  
Chest Wall ◽  
Visual Analog Scale ◽  
Ventilatory Response ◽  
Minute Ventilation ◽  
Resistive Load ◽  
Vibratory Stimulation ◽  
Analog Scale ◽  
Hypercapnic Ventilatory Response ◽  
Mouth Occlusion Pressure ◽  
Inspiratory Load

Vibratory stimulation applied to the chest wall during inspiration reduces the intensity of breathlessness, whereas the same stimulation during expiration has no effect or may increase breathlessness. The purpose of the present study was to determine whether vibration reduced the intensity of breathlessness during progressive hypercapnia with and without the addition of an external resistive load. A second objective was to see whether the mouth occlusion pressure at 0.2 s (P0.2) was reduced by the vibratory stimulation. Hypercapnic ventilatory response was conducted in 10 healthy male volunteers with simultaneous measurement of visual analog scale, P0.2, and minute ventilation. Hypercapnic ventilatory response was performed and randomly combined with or without vibratory stimulation (100 Hz) as well as with or without inspiratory load. With inspiratory load, in-phase vibration did not cause any significant changes in the slopes of P0.2 and minute ventilation to CO2, whereas the slope of visual analog scale to CO2 significantly decreased from 0.47 ± 0.15 to 0.34 ± 0.11 (SE) cm/Torr ( P < 0.05). We conclude that in-phase vibration could decrease the slope of breathlessness elicited by inspiratory load combined with hypercapnia without changing motor output.

Effect of inspiratory resistive loading on control of ventilation during progressive exercise

1987 ◽  
Vol 62 (1) ◽  
pp. 134-140 ◽  
Author(s):  
A. D. D'Urzo ◽  
K. R. Chapman ◽  
A. S. Rebuck
Keyword(s):  
Ventilatory Response ◽  
Minute Ventilation ◽  
Work Load ◽  
Cycle Ergometer ◽  
Resistive Load ◽  
Co2 Output ◽  
Exercise Ventilation ◽  
Resistive Loading ◽  
End Tidal ◽  
Arterial O2 Saturation

Eight healthy volunteers performed gradational tests to exhaustion on a mechanically braked cycle ergometer, with and without the addition of an inspiratory resistive load. Mean slopes for linear ventilatory responses during loaded and unloaded exercise [change in minute ventilation per change in CO2 output (delta VE/delta VCO2)] measured below the anaerobic threshold were 24.1 +/- 1.3 (SE) = l/l of CO2 and 26.2 +/- 1.0 l/l of CO2, respectively (P greater than 0.10). During loaded exercise, decrements in VE, tidal volume, respiratory frequency, arterial O2 saturation, and increases in end-tidal CO2 tension were observed only when work loads exceeded 65% of the unloaded maximum. There was a significant correlation between the resting ventilatory response to hypercapnia delta VE/delta PCO2 and the ventilatory response to VCO2 during exercise (delta VE/delta VCO2; r = 0.88; P less than 0.05). The maximal inspiratory pressure generated during loading correlated with CO2 sensitivity at rest (r = 0.91; P less than 0.05) and with exercise ventilation (delta VE/delta VCO2; r = 0.83; P less than 0.05). Although resistive loading did not alter O2 uptake (VO2) or heart rate (HR) as a function of work load, maximal VO2, HR, and exercise tolerance were decreased to 90% of control values. We conclude that a modest inspiratory resistive load reduces maximum exercise capacity and that CO2 responsiveness may play a role in the control of breathing during exercise when airway resistance is artificially increased.

Airway resistance and respiratory muscle function in snorers during NREM sleep

1985 ◽  
Vol 59 (2) ◽  
pp. 328-335 ◽  
Author(s):  
J. B. Skatrud ◽  
J. A. Dempsey
Keyword(s):  
Tidal Volume ◽  
Muscle Function ◽  
Respiratory Muscle ◽  
Dynamic Compression ◽  
Nrem Sleep ◽  
Abdominal Muscles ◽  
Resistive Load ◽  
Rib Cage ◽  
Inspiratory Muscles ◽  
Respiratory Muscle Function

The effect of non-rapid-eye-movement (NREM) sleep on total pulmonary resistance (RL) and respiratory muscle function was determined in four snorers and four nonsnorers. RL at peak flow increased progressively from wakefulness through the stages of NREM sleep in all snorers (3.7 +/- 0.4 vs. 13.0 +/- 4.0 cmH2O X 0.1(-1) X s) and nonsnorers (4.8 +/- 0.4 vs. 7.5 +/- 1.1 cmH2O X 1(-1) X s). Snorers developed inspiratory flow limitation and progressive increase in RL within a breath. The increased RL placed an increased resistive load on the inspiratory muscles, increasing the pressure-time product for the diaphragm between wakefulness and NREM sleep. Tidal volume and minute ventilation decreased in all subjects. The three snorers who showed the greatest increase in within-breath RL demonstrated an increase in the contribution of the lateral rib cage to tidal volume, a contraction of the abdominal muscles during a substantial part of expiration, and an abrupt relaxation of abdominal muscles at the onset of inspiration. We concluded that the magnitude of increase in RL leads to dynamic compression of the upper airway during inspiration, marked distortion of the rib cage, recruitment of the intercostal muscles, and an increased contribution of expiratory muscles to inspiration. This increased RL acts as an internal resistive load that probably contributes to hypoventilation and CO2 retention in NREM sleep.

Resistive Load Detection during Passive Ventilation

1980 ◽  
Vol 59 (6) ◽  
pp. 493-495 ◽  
Author(s):  
K. J. Killian ◽  
C. K. Mahutte ◽  
E. J. M. Campbell
Keyword(s):  
Muscle Contraction ◽  
Spontaneous Breathing ◽  
Respiratory Muscle ◽  
Essential Role ◽  
Normal Subjects ◽  
Assisted Ventilation ◽  
Resistive Load ◽  
Load Detection ◽  
Resistive Loads

1. By using standard psychophysical techniques resistive load detection was estimated in five normal subjects during spontaneous breathing and during passive ventilation in a Drinker respirator. 2. During assisted ventilation a gross deterioration in resistive load detection occurred. 3. The findings imply that active respiratory muscle contraction plays an essential role in the detection of added resistive loads.

Effect of beta-adrenergic blockade on response to exercise in sedentary and active subjects

1989 ◽  
Vol 67 (1) ◽  
pp. 103-109 ◽  
Author(s):  
V. Brusasco ◽  
B. Violante ◽  
G. Buccheri
Keyword(s):  
Minute Ventilation ◽  
Respiratory Control ◽  
Work Capacity ◽  
Constant Load ◽  
Adrenergic Blockade ◽  
O2 Uptake ◽  
Physically Active ◽  
Co2 Output ◽  
Group A ◽  
Type Of Exercise

The response to incremental work after placebo and propranolol (80 mg, orally) was studied in 11 sedentary (S) and 11 physically active (PA) healthy subjects. O2 uptake, CO2 output, and minute ventilation were significantly reduced at all or most work rates after propranolol in S subjects, whereas in PA subjects only O2 uptake was occasionally significantly reduced. Maximum work capacity during the propranolol trial was significantly increased by 17% in the S group but was unaltered in the PA group. A subanaerobic threshold constant work test in five sedentary subjects demonstrated that propranolol had no effect on the respiratory response both early and late in exercise. In addition, propranolol did not impair the ability of the respiratory control system to maintain alveolar PCO2 at new set points when external dead space was added during constant load work. We conclude that alterations of gas exchange during incremental work after propranolol administration are related to both physical fitness and type of exercise.

Effect of respiratory muscle weakness on P0.1 induced by partial curarization

1984 ◽  
Vol 57 (4) ◽  
pp. 1150-1157 ◽  
Author(s):  
R. H. Holle ◽  
R. B. Schoene ◽  
E. J. Pavlin
Keyword(s):  
Muscle Weakness ◽  
Respiratory Muscle ◽  
Minute Ventilation ◽  
Normal Subjects ◽  
Base Line ◽  
Respiratory Drive ◽  
Respiratory Muscle Weakness ◽  
Residual Capacity ◽  
Mouth Occlusion Pressure ◽  
Line Slope

Mouth occlusion pressure 0.1 s after onset of inspiration (P0.1) reflects central respiratory drive (CRD), but its dependence on respiratory muscle strength is unknown. To clarify this relationship, we produced progressive levels of respiratory muscle weakness by infusion of d-tubocurarine in eight supine spontaneously breathing normal subjects. Hypercapnic ventilatory response (HCVR) was measured before curarization and at mild (mean inspiratory effort 62 +/- 3% of control), moderate (42 +/- 3%), and severe (23 +/- 1%) weakness. At the severe level of weakness 1) supine functional residual capacity was not significantly changed from base line, 2) the percent of base-line slope of delta P0.1/delta PCO2 (122 +/- 27%) was significantly greater (P less than 0.01) than that for change in expired minute ventilation (delta VE)/delta PCO2 (39 +/- 10%), 3) the percent of base-line delta P0.1/delta VE (381 +/- 46%) during HCVR was significantly increased (P less than 0.01), 4) the P0.1 response was significantly increased from base line at two out of three specific levels of PCO2 while the VE was unchanged or significantly decreased, and 5) peak inspiratory resistance did not significantly change. Thus P0.1, unlike VE, did not decrease with even severe respiratory muscle weakness. Indeed, P0.1 increased at two out of three levels of PCO2 under circumstances when higher CRD is expected. One potential explanation for the results is that P0.1 may at least qualitatively reflect CRD up to the level of severe respiratory muscle weakness attained in this study.

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