Running exercise with end-expiratory breath holding up to the breaking point induces large and early fall in muscle oxygenation

Author(s):  
Xavier Woorons ◽  
François Billaut ◽  
Christine Lamberto
1967 ◽  
Vol 17 (1) ◽  
pp. 43-56 ◽  
Author(s):  
Syôiti KOBAYASI ◽  
Chieko SASAKI

1962 ◽  
Vol 17 (2) ◽  
pp. 225-227 ◽  
Author(s):  
Albert B. Craig ◽  
Lauro S. Halstead ◽  
Gerhard H. Schmidt ◽  
Brian R. Schnier

The PaCOCO2 at the breaking point was found to be higher during exercise than during rest in four subjects. The breaking-point curve during exercise was elevated over the entire range of various oxygen concentrations studied, indicating that whatever the changes produced they are related to the contribution of CO2 to the urge to breathe and are independent of O2. At least part of the elevated PaCOCO2 may be accounted for by an overshoot of PaCOCO2 related to the rate of rise of Pco2. This was shown by increasing the rate of accumulation of CO2 by inhaling different O2-CO2 gas mixtures to simulate the increased CO2 production during exercise. However, certain calculations indicate that this is not the only difference between voluntary apnea during exercise as compared with that during rest. Submitted on June 30, 1961


1959 ◽  
Vol 14 (5) ◽  
pp. 689-693 ◽  
Author(s):  
F. J. Klocke ◽  
H. Rahn

Following normal breathing of O2 seven untrained subjects held their breath beginning with a maximal inspiration. Breath-holding times ranged from 3.1 to 8.5 minutes and ‘breaking-point’ alveolar CO2 tensions from 51 to 91 mm Hg. Under these conditions, the maximum breath-holding time in minutes ( x) can be related to the rise in alveolar CO2 tension in mm Hg ( y), according to the equation x = 0.13 y + 1.4. After hyperventilation on O2, the breath-holding times were noticeably extended ranging from 6 to 14 minutes, but the breaking-point alveolar CO2 tensions did not exceed those noted above. In all cases, the measured changes in lung volume can be explained by the uptake of oxygen alone since the amount of CO2 is essentially unaltered during apnea. The decreases in lung volume observed are related to the total breath-holding time, about 13 minutes being required for a change in lung volume equal to the vital capacity. Three subjects were able to absorb their entire vital capacity volume during breath holding since no volume could be expired at the breaking point. Submitted on April 8, 1959


1961 ◽  
Vol 16 (4) ◽  
pp. 583-586 ◽  
Author(s):  
B. Albert ◽  
JR. Craig

Several incidents of losing consciousness while swimming underwater are known to the author. Experiments were designed to find out how this could happen. Four types of breath holding were executed: a) at rest, b) after hyperventilation, c) during mild exercise, and d) after hyperventilation and during exercise. At the breaking point the subject made a maximal expiration, and the end tidal air was analyzed for O2 and CO2. It was found that when the breaking point was reached, the Pco2 was higher and the Po2 lower during exercise than at rest. The lowest Po2 was observed after the subject had exercised following hyperventilation: the Po2 was 34 mm or below in 4 of the 12 subjects, a degree of hypoxia often associated with unconsciousness. Other experiments including underwater swimming support the conclusion that loss of consciousness after hyperventilation and during exercise is possible and is probably due to hypoxia. Submitted on December 30, 1960


1962 ◽  
Vol 17 (2) ◽  
pp. 221-224 ◽  
Author(s):  
E. G. Cummings

Men stood astride a moving treadmill belt and at a verbal signal held their breath, jumped on the treadmill belt, and walked or ran at a series of speeds up to 9 mph until the breaking point was reached. Breath-holding time decreased sharply with increasing exercise rates, but began to level off at approximately 30 sec between 6 and 9 mph. Breaking-point alveolar Po2 decreased and Pco2 increased with increasing treadmill speeds. When these two factors were applied in the Otis, Fenn, and Rahn ventilation equation to describe ventilation at the breaking point, the ventilation ratio increased, and it was observed that the men withstood a stronger stimulus to breathe as the work rate increased, even though the breath-holding time remained fairly constant at higher work levels. Apparently at the beginning of work the stimulus to breathe is the combination of a relatively weak neurogenic stimulus and an accumulating chemical stimulus. It is postulated that the constancy of beginning breath-holding times at high work rates may reflect a transport time for the chemical stimulus to reach the receptor area from working muscles via the circulation. Submitted on September 25, 1961


1977 ◽  
Vol 42 (5) ◽  
pp. 717-721 ◽  
Author(s):  
D. Bartlett

Breath holding to the breaking point was studied at FRC in six healthy subjects in the sitting position. Breath-holding time increased with successive trials within experimental sessions in all subjects. To study the influence of Valsalva and Mueller maneuvers on breath-holding performance, sustained inspiratory or expiratory effort against an occluded mouthpiece was initiated 5 s before the anticipated breaking point, determined in previous trials. The subject tried to maintain a target mouth pressure of +20 or -20 cmH2O, displayed on an oscilloscope, for the remainder of the breath hold. Both types of maneuver consistently prolonged breath-holding time in all subjects. However, a control maneuver, in which the subjects squeezed rubber bulbs with their hands, was equally effective in prolonging breath-holding time. The results demonstrate the important influence of psychological factors on breath-holding performance and emphasize the need for caution in the interpretation of effects of “relieving maneuvers” on breath-holding time.


2021 ◽  
Vol 12 ◽  
Author(s):  
Paul F. McCulloch ◽  
B. W. Gebhart ◽  
J. A. Schroer

During breath holding after face immersion there develops an urge to breathe. The point that would initiate the termination of the breath hold, the “physiological breaking point,” is thought to be primarily due to changes in blood gases. However, we theorized that other factors, such as lung volume, also contributes significantly to terminating breath holds during face immersion. Accordingly, nine naïve subjects (controls) and seven underwater hockey players (divers) voluntarily initiated face immersions in room temperature water at Total Lung Capacity (TLC) and Functional Residual Capacity (FRC) after pre-breathing air, 100% O2, 15% O2 / 85% N2, or 5% CO2 / 95% O2. Heart rate (HR), arterial blood pressure (BP), end-tidal CO2 (etCO2), and breath hold durations (BHD) were monitored during all face immersions. The decrease in HR and increase in BP were not significantly different at the two lung volumes, although the increase in BP was usually greater at FRC. BHD was significantly longer at TLC (54 ± 2 s) than at FRC (30 ± 2 s). Also, with each pre-breathed gas BHD was always longer at TLC. We found no consistent etCO2 at which the breath holding terminated. BDHs were significantly longer in divers than in controls. We suggest that during breath holding with face immersion high lung volume acts directly within the brainstem to actively delay the attainment of the physiological breaking point, rather than acting indirectly as a sink to produce a slower build-up of PCO2.


1974 ◽  
Vol 47 (3) ◽  
pp. 193-199 ◽  
Author(s):  
J. R. A. Rigg ◽  
A. S. Rebuck ◽  
E. J. M. Campbell

1. Two series of experiments were performed in an attempt to elucidate the mechanism of relief of the discomfort of breath-holding. 2. In the first the effect of varying the size of a single breath at the breaking point of breath-holding on the time of a second breath-hold (BHT2) was observed in three normal subjects. The effect of two different non-ventilatory chest-wall manœuvres, performed at the breaking point, on the duration of a second breath-hold in two additional subjects was then studied. 3. The volume of an unrestricted relieving breath was always greater than 70% of vital capacity. When the size of the breath was restricted to as little as 20% of the free relieving volume, BHT2 was unchanged. 4. An inspiratory effort against an occluded airway or an isovolume movement of the rib cage and abdomen performed at the breaking point of breath-holding were as effective as a control relieving breath in allowing resumption of apnoea. 5. There seem to be two possible mechanisms of relief. First, afferent information may be generated by some consequence of diaphragmatic contraction. Secondly, changes of local pressure-volume relationships within the lung may alter the pattern of vagal afferent activity, independent of an overall change in lung volume.


1964 ◽  
Vol 19 (3) ◽  
pp. 408-412 ◽  
Author(s):  
E. Agostoni ◽  
G. Sant'Ambrogio ◽  
P. Mognoni

The effect of d-methylamphetamine, caffeine, and analeptics on the alveolar Pco2 during spontaneous breathing and at the onset of diaphragm activity during breath holding has been studied. After d-methylamphetamine the value of alveolar Pco2 at the onset of diaphragm activity, as well as at the breaking point, is significantly increased, while the ventilation-alveolar Pco2 relationship is not changed. After caffeine the value of the alveolar Pco2 at the onset of diaphragm activity, as well as at the breaking point, is significantly decreased and the ventilation-alveolar Pco2 relationship is significantly shifted to a lower Pco2. The value of alveolar Pco2 at onset of diaphragm activity is significantly decreased by prethcamide, increased by pentylenetetrazol, and not affected by dimefline. The ventilation-alveolar Pco2 relationship was not changed by such analeptics. These data, together with those previously obtained on hypoxia, suggest that factors changing the ventilation-alveolar Pco2 relationship also affect the onset of diaphragm activity, while the onset of diaphragm activity can be changed without affecting the ventilatory response to CO2. effect of analeptics on breath holding and on CO2 response curve; breaking point of breath holding; effect of caffeine on breath holding and on CO2 response curve; effect of d-methylamphetamine on breath holding and on CO2 response curve; ventilation-alveolar Pco2 relationship Submitted on July 5, 1963


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