Is low-level respiratory resistive loading during exercise perceived as breathlessness?

1987 ◽  
Vol 73 (6) ◽  
pp. 627-634 ◽  
Author(s):  
R. Lane ◽  
L. Adams ◽  
A. Guz

1. The effect of adding low-level (2.7 cmH2O 1−1 s) external respiratory resistive loads on exercise-induced breathlessness has been examined in naive normal subjects; the intensity of this loading was chosen to simulate that confronting an asthmatic subject during exercise. 2. Each of 18 subjects performed two separate tests in which workload was oscillated while the respiratory loading was changed every minute between no loading, inspiratory loading only, and inspiratory plus expiratory loading. Each loading condition was given three times, and both these changes and those in workload were unpredictable as far as the subject was concerned. 3. The purpose was to ‘confuse’ subjects and obtain subjective estimates of their intensity of breathlessness independent of any expectation associated solely with the readily perceptible changes in external resistances to breathing. The study design was balanced for the group as a whole, both in terms of workload and respiratory loading condition. 4. The addition of these respiratory resistive loads during exercise did not result in a significant increase in the intensity of breathlessness. 5. Estimates of the rate of work of breathing revealed that this increased more with respiratory loading than it did as ventilation rose throughout the test; on the other hand, the intensity of breathlessness increased by a greater extent with continued exercise compared with the changes accompanying the addition of respiratory loads. 6. It is concluded that the intensity of the sensation of breathlessness experienced by normal subjects during exercise is not simply a reflection of an increased rate of work of breathing being performed by the respiratory muscles. 7. It is further suggested that similar studies in which internal resistances are increased experimentally are indicated in order to analyse the factors underlying the breathlessness of asthma.

1983 ◽  
Vol 55 (3) ◽  
pp. 929-934 ◽  
Author(s):  
T. M. Michiels ◽  
R. W. Light ◽  
C. K. Mahutte

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.


1986 ◽  
Vol 61 (1) ◽  
pp. 16-24 ◽  
Author(s):  
P. W. Collett ◽  
L. A. Engel

We examined the relationship between the O2 cost of breathing (VO2 resp) and lung volume at constant load, ventilation, work rate, and pressure-time product in five trained normal subjects breathing through an inspiratory resistance at functional residual capacity (FRC) and when lung volume (VL) was increased to 37 +/- 2% (mean +/- SE) of inspiratory capacity (high VL). High VL was maintained using continuous positive airway pressure of 9 +/- 2 cmH2O and with the subjects coached to relax during expiration to minimize respiratory muscle activity. Six paired runs were performed in each subject at constant tidal volume (0.62 +/- 0.2 liters), frequency (23 +/- 1 breaths/min), inspiratory flow rate (0.45 +/- 0.1 l/s), and inspiratory muscle pressure (45 +/- 2% of maximum static pressure at FRC). VO2 resp increased from 109 +/- 15 ml/min at FRC by 41 +/- 11% at high VL (P less than 0.05). Thus the efficiency of breathing at high VL (3.9 +/- 0.2%) was less than that at FRC (5.2 +/- 0.3%, P less than 0.01). The decrease in inspiratory muscle efficiency at high VL may be due to changes in mechanical coupling, in the pattern of recruitment of the respiratory muscles, or in the intrinsic properties of the inspiratory muscles at shorter length. When the work of breathing at high VL was normalized for the decrease in maximum inspiratory muscle pressure with VL, efficiency at high VL (5.2 +/- 0.3%) did not differ from that at FRC (P less than 0.7), suggesting that the fall in efficiency may have been related to the fall in inspiratory muscle strength. During acute hyperinflation the decreased efficiency contributes to the increased O2 cost of breathing and may contribute to the diminished inspiratory muscle endurance.


1998 ◽  
Vol 85 (1) ◽  
pp. 254-258 ◽  
Author(s):  
Joseph Milic-Emili ◽  
Marcello M. Orzalesi

With the use of the esophageal balloon technique, the working capacity of the respiratory muscles was assessed in four normal subjects by measuring the work per breath (W) and respiratory power (W˙) during maximal voluntary ventilation with imposed respiratory frequencies (f) ranging from 20 to 273 cycles/min. Measurements were made in a body plethysmograph to assess the work wasted as a result of alveolar gas compressibility (Wg′). In line with other types of human voluntary muscle activity, W decreased with increasing f, whereasW˙ exhibited a maximum at f of ∼100 cycles/min. Up to this f value, Wg′ was small relative to W. With further increase in f, the Wg′/W ratio increased progressively, amounting to 8–22% of W˙ at f of 200 cycles/min.


Respiration ◽  
1995 ◽  
Vol 62 (4) ◽  
pp. 177-184 ◽  
Author(s):  
Klaus Wassermann ◽  
Anselm Gitt ◽  
Joanna Weyde ◽  
Hans Edmund Eckel

1997 ◽  
Vol 4 (2) ◽  
pp. 101-107 ◽  
Author(s):  
Pere Casan ◽  
Carlos C Villafranca ◽  
Clive Kearon ◽  
Edward JM Campbell ◽  
Kieran J Killian

During exercise, the sustainable activity of large muscle groups is limited by oxygen delivery. The purpose of this study was to see whether the oxygen consumption of the respiratory muscles reaches a similar critical value under maximal resistive loading and hyperventilation. A secondary objective was to see whether dyspnea (estimated discomfort experienced with breathing using the Borg 0-10 scale) and the oxygen consumption of the respiratory muscles are closely related across conditions. This would be expected if intramuscular sensory nerve fibres stimulated as a consequence of metabolic events contributed to this sensation. In six normal subjects the respiratory muscles were progressively activated by the addition of incremental inspiratory resistive loads to a maximum of 300 cm H20×s/L (SD=66.4), and incremental dead space to a maximum of 2638 mL (SD=452), associated with an increase in ventilation to 75.1 L/min (SD=29.79). Each increment was maintained for 5 mins to allow the measurement of oxygen uptake in a steady state. During resistive loading total oxygen consumption increased from 239 mL/min (SD=38.2) to 299 mL/min (SD=52.3) and dyspnea increased to "very severe" (Borg scale 7.5, SD=1.55). During dead space loading total oxygen consumption increased from 270 mL/min (SD=20.2) to 426 mL/min (SD=81.9) and dyspnea increased to "very severe" (7.1, SD=0.66). Oxygen cost of inspiratory muscle power was 25 mL/watt (95% confidence limits 16.7 to 34.3) with dead space loading and 91 mL/watt (95% confidence limits 54 to 128) with resistive loading. Oxygen consumption did not reach a critical common value in the two types of loading, 60 mL/min (SD 22.3) during maximal resistive loading and 156 mL/min (SD 82.4) during maximal dead space loading (P<0.05). Physiological factors limiting the respiratory muscles are not uniquely related to oxygen consumption and appear to be expressed through the activation of sensory structures, perceptually manifested as dyspnea.


1964 ◽  
Vol 19 (1) ◽  
pp. 83-91 ◽  
Author(s):  
M. J. Jaeger ◽  
A. B. Otis

Alveolar gas is compressed and expanded during every breathing cycle. The volume displacement measured at the mouth Vt (tidal volume) is therefore smaller than the volume displacement of the lung V't that may be measured with a body plethysmograph. Experimental data found in normal subjects and in patients with obstructive emphysema confirm the theoretical prediction that the ratio Vt/V't decreases with increasing airway resistance, breathing frequency, and lung volume. The effect was found to be very small in normal subjects breathing at different breathing rates; however, in patients with obstructive emphysema it may be appreciable, presumably because of the high airway resistance and the elevated functional residual capacity. With increasing altitude the effect is expected to be more pronounced. The mechanical work performed in compressing and expanding alveolar gas is not included in the conventional pressure-volume diagram, when intraesophageal pressure is plotted against the volume displacement measured at the mouth. This work may be determined, however, by recording the volume displacement of the lung simultaneously with tidal volume and intraesophageal pressure. Work related to compressibility is insignificant in most circumstances. In patients with obstructive emphysema, however, it becomes appreciable during hyperpnea. The compressibility of alveolar gas was also found to increase the negative work performed by respiratory muscles. volume displacement of the lung (V't); Vt/V't in obstructive emphysema; dynamic pressure-volume diagram; mechanical model - respiratory dynamics; ventilation; negative work of inspiratory muscles; ventilation and breathing work at high altitudes; mechanics of breathing Submitted on June 21, 1963


1985 ◽  
Vol 58 (5) ◽  
pp. 1608-1615 ◽  
Author(s):  
G. L. Jones ◽  
K. J. Killian ◽  
E. Summers ◽  
N. L. Jones

The ability of the respiratory muscles to sustain ventilation against increasing inspiratory resistive loads was measured in 10 normal subjects. All subjects reached a maximum rating of perceived respiratory effort and at maximum resistance showed signs of respiratory failure (CO2 retention, O2 desaturation, and rib cage and abdominal paradox). The maximum resistance achieved varied widely (range 73–660 cmH2O X l-1 X s). The increase in O2 uptake (delta Vo2) associated with loading was linearly related to the integrated mouth pressure (IMP): delta Vo2 = 0.028 X IMP + 19 ml/min (r = 0.88, P less than 0.001). Maximum delta Vo2 was 142 ml/min +/- SD 68 ml/min. There were significant (P less than 0.05) relationships between the maximum voluntary inspiratory pressure against an occluded airway (MIP) and both maximum IMP (r = 0.80) and maximum delta Vo2 (r = 0.76). In five subjects, three imposed breathing patterns were used to examine the effect of different patterns of respiratory muscle force deployment. Increasing inspiratory duration (TI) from 1.5 to 3.0 and 6.0 s, at the same frequency of breathing (5.5 breaths/min) reduced peak inspiratory pressure and increased the maximum resistance tolerated (190, 269, and 366 cmH2O X l-1 X s, respectively) and maximum IMP (2043, 2473, and 2913 cmH2O X s X min-1, but the effect on maximum delta Vo2 was less consistent (166, 237, and 180 ml/min). The ventilatory endurance capacity and the maximum O2 uptake of the respiratory muscles are related to the strength of the inspiratory muscles, but are also modified through the pattern of force deployment.


1986 ◽  
Vol 27 (4) ◽  
pp. 443-460 ◽  
Author(s):  
Mitsuhiro YOKOTA ◽  
Shoji NODA ◽  
Masafumi KOIDE ◽  
Naoki KAWAI ◽  
Reiki YOSHIDA ◽  
...  

Author(s):  
Margarita Khomyakova

The author analyzes definitions of the concepts of determinants of crime given by various scientists and offers her definition. In this study, determinants of crime are understood as a set of its causes, the circumstances that contribute committing them, as well as the dynamics of crime. It is noted that the Russian legislator in Article 244 of the Criminal Code defines the object of this criminal assault as public morality. Despite the use of evaluative concepts both in the disposition of this norm and in determining the specific object of a given crime, the position of criminologists is unequivocal: crimes of this kind are immoral and are in irreconcilable conflict with generally accepted moral and legal norms. In the paper, some views are considered with regard to making value judgments which could hardly apply to legal norms. According to the author, the reasons for abuse of the bodies of the dead include economic problems of the subject of a crime, a low level of culture and legal awareness; this list is not exhaustive. The main circumstances that contribute committing abuse of the bodies of the dead and their burial places are the following: low income and unemployment, low level of criminological prevention, poor maintenance and protection of medical institutions and cemeteries due to underperformance of state and municipal bodies. The list of circumstances is also open-ended. Due to some factors, including a high level of latency, it is not possible to reflect the dynamics of such crimes objectively. At the same time, identification of the determinants of abuse of the bodies of the dead will reduce the number of such crimes.


1990 ◽  
Vol 68 (5) ◽  
pp. 2177-2181 ◽  
Author(s):  
M. Manohar

Regional distribution of diaphragmatic blood flow (Q; 15-microns-diam radionuclide-labeled microspheres) was studied in normal (n = 7) and laryngeal hemiplegic (LH; n = 7) ponies to determine whether the added stress of inspiratory resistive breathing during maximal exercise may cause 1) redistribution of diaphragmatic Q and 2) crural diaphragmatic Q to exceed that in maximally exercising normal ponies. LH-induced augmentation of already high exertional work of breathing resulted in diminished locomotor exercise capacity so that maximal exercise in LH ponies occurred at 25 km/h compared with 32 km/h for normal ponies. The costal and crural regions received similar Q in both groups at rest. However, exercise-induced increments in perfusion were significantly greater in the costal region of the diaphragm. At 25 km/h, costal diaphragmatic perfusion was 154 and 143% of the crural diaphragmatic Q in normal and LH ponies. At 32 km/h, Q in costal diaphragm of normal ponies was 136% of that in the crural region. Costal and crural diaphragmatic Q in LH ponies exercised at 25 km/h exceeded that for normal ponies but was similar to the latter during exercise at 32 km/h. Perfusion pressure for the three conditions was also similar. It is concluded that diaphragmatic perfusion heterogeneity in exercising ponies was preserved during the added stress of inspiratory resistive breathing. It was also demonstrated that vascular resistance in the crural and costal regions of the diaphragm in maximally exercised LH ponies remained similar to that in maximally exercising normal ponies.


Sign in / Sign up

Export Citation Format

Share Document