Propranolol and Inspiratory Muscle Performance in Normal Subjects

1988 ◽  
Vol 28 (7) ◽  
pp. 625-633 ◽  
Author(s):  
Nick Mucciardi ◽  
James Muspratt ◽  
Michael J. Miller
Brain ◽  
1994 ◽  
Vol 117 (4) ◽  
pp. 661-670 ◽  
Author(s):  
G. M. Allen ◽  
S. C. Gandevia ◽  
I. R. Neering ◽  
I. Hickie ◽  
R. Jones ◽  
...  

1999 ◽  
Vol 86 (3) ◽  
pp. 845-851 ◽  
Author(s):  
Julie R. Wright ◽  
D. I. McCloskey ◽  
Richard C. Fitzpatrick

The effects of changes in arterial perfusion across the physiological range on the fatigue of a working human hand muscle were studied in seven normal subjects. With the hand above heart level, subjects made repeated isometric contractions of the adductor pollicis muscle at 50% of maximal voluntary contraction in a 6-s on, 4-s off cycle. To assess fatigue, a maximal isometric twitch was elicited in each “off” period by electrical stimulation of the ulnar nerve. The experiment was repeated at least 2 days later with the hand at heart level. Five subjects showed faster fatigue with the arm elevated, and two subjects showed little difference in fatigue for the two conditions. Central blood pressure rose in proportion to fatigue for the subjects overall and returned quickly to its initial level afterwards. We conclude that human muscle fatigue can be increased by physiological reductions in perfusion pressure. Central blood pressure increases as the muscle fatigues, a response that may partially offset declining muscle performance.


2016 ◽  
Vol 228 ◽  
pp. 61-68 ◽  
Author(s):  
Mehdi Chlif ◽  
David Keochkerian ◽  
Abdou Temfemo ◽  
Dominique Choquet ◽  
Said Ahmaidi

1986 ◽  
Vol 60 (1) ◽  
pp. 299-303 ◽  
Author(s):  
F. D. McCool ◽  
D. R. McCann ◽  
D. E. Leith ◽  
F. G. Hoppin

We examined the effects of varying inspiratory pressures and flows on inspiratory muscle endurance. Four normal subjects performed voluntary forced breathing with various assigned inspiratory tasks. Duty cycle, tidal volume, and mean lung volume were the same in all tasks. Mean esophageal pressure, analogous to a pressure-time integral (PTes), was varied over a wide range. In each task the subject maintained an assigned PTes while breathing on one of a range of inspiratory resistors, and this gave a range of inspiratory flows at any given PTes. Inspiratory muscle endurance for each task was assessed by the length of time the task could be maintained (Tlim). For a given resistor, Tlim increased as PTes decreased. At a given PTes, Tlim increased as the external resistance increased and therefore as mean inspiratory flow rate (VI) decreased. Furthermore, for a given Tlim, PTes and VI were linearly related with a negative slope. We conclude that inspiratory flow, probably because of its relationship to the velocity of muscle shortening, is an independent variable importantly influencing endurance of the inspiratory muscles.


2017 ◽  
Vol 63 (1) ◽  
pp. 86-91 ◽  
Author(s):  
Magno F Formiga ◽  
Michael A Campos ◽  
Lawrence P Cahalin

1993 ◽  
Vol 85 (5) ◽  
pp. 637-642 ◽  
Author(s):  
J. E. Clague ◽  
J. Carter ◽  
M. G. Pearson ◽  
P. M. A. Calverley

1. The physiological basis of inspiratory effort sensation remains uncertain. Previous studies have suggested that pleural pressure, rather than inspiratory muscle fatigue, is the principal determinant of inspiratory effort sensation. However, only a limited range of inspiratory flows and breathing patterns have been examined. We suspected that inspiratory effort sensation was related to the inspiratory muscle tension-time index developed whatever the breathing pattern or load, and that this might explain the additional rise in sensation seen with hypercapnia. 2. To investigate this we measured hypercapnic re-breathing responses in seven normal subjects (six males, age range 21–38 years) with and without an inspiratory resistive load of 10 cm H2O. Pleural and transdiaphragmatic pressures, mouth occlusion pressure and breathing pattern were measured. Diaphragmatic and ribcage tension-time indices were calculated from these data. Inspiratory effort sensation was recorded using a Borg scale at 30s intervals during each rebreathing run. 3. Breathing pattern and inspiratory pressure partitioning were unrelated to changes in inspiratory effort sensation during hypercapnia. Tension-time indices reached pre-fatiguing levels during both free breathing and inspiratory resistive loading. 4. Stepwise multiple regression analysis using pooled mechanical, chemical and breathing pattern variables showed that pleural pressure was more closely related to inspiratory effort sensation than was transdiaphragmatic pressure. When converted to tension-time indices, ribcage tension-time index was the major determinant of inspiratory effort sensation during loaded rebreathing, but partial pressure of CO2 was an important independent variable, whereas during unloaded rebreathing partial pressure of CO2 was the most important determinant of inspiratory effort sensation. 5. These results suggest that the pattern of inspiratory pressure partitioning and inspiratory flow rate have little influence on inspiratory effort sensation during CO2 stimulated breathing. The close association between inspiratory effort sensation and ribcage tension-time index, an index of inspiratory muscle work, suggests that inspiratory effort sensation may forewarn of potential inspiratory muscle fatigue. Changes in PaCO2 have a small independent effect on respiratory perception.


1987 ◽  
Vol 135 (4) ◽  
pp. 919-923 ◽  
Author(s):  
J. B. Martyn ◽  
R. H. Moreno ◽  
P. D. Paré ◽  
R. L. Pardy

1987 ◽  
Vol 62 (3) ◽  
pp. 1299-1306 ◽  
Author(s):  
R. L. Begle ◽  
J. B. Skatrud ◽  
J. A. Dempsey

The role of conscious factors in the ventilatory compensation for shortened inspiratory muscle length and the potency of this compensatory response were studied in five normal subjects during non-rapid-eye-movement sleep. To shorten inspiratory muscles, functional residual capacity (FRC) was increased and maintained for 2–3 min at a constant level (range of increase 160–1,880 ml) by creating negative pressure within a tank respirator in which the subjects slept. Minute ventilation was maintained in all subjects over the entire range of increased FRC (mean change +/- SE = -3 +/- 1%) through preservation of tidal volume (-2 +/- 2%) despite slightly decreased breathing frequency (-6 +/- 2%). The decrease in frequency (-13 +/- 2%) was due to a prolongation in expiratory time. Inspiratory time shortened (-10 +/- 1%). Mean inspiratory flow increased 15 +/- 3% coincident with an increase in the slope of the moving time average of the integrated surface diaphragmatic electromyogram (67 +/- 21%). End-tidal CO2 did not rise. In two subjects, control tidal volume was increased 35–50% with CO2 breathing. This augmented tidal volume was still preserved when FRC was increased. We concluded that the compensatory response to inspiratory muscle shortening did not require factors associated with the conscious state. In addition, the potency of this response was demonstrated by preservation of tidal volume despite extreme shortening of the inspiratory muscles and increase in control tidal volumes caused by CO2 breathing. Finally, the timing changes we observed may be due to reflexes following shortening of inspiratory muscle length, increase in abdominal muscle length, or cardiovascular changes.


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