Carotid chemoreceptors and respiratory adaptations to dead space loading during incremental exercise

1993 ◽  
Vol 75 (3) ◽  
pp. 1378-1384 ◽  
Author(s):  
N. C. Syabbalo ◽  
T. Zintel ◽  
R. Watts ◽  
C. G. Gallagher

Dead space (VD) loading has been shown to cause an increase in tidal volume and a decrease in respiratory frequency at moderate to high levels of ventilation (VI) during exercise (J. Appl. Physiol. 70: 55–62, 1991). This study examined the role of carotid chemoreceptors (CC) in the breathing pattern response to added VD during maximal incremental exercise; we used hyperoxia to silence the CC. Nine healthy subjects exercised on a bicycle ergometer on 4 different days while inspiring air with VD (AVD) and without VD [air control (AC)] and while inspiring 100% O2 with VD (O2VD) and without VD (O2C). Equipment resistance for VD and control studies was identical, and the exercise tests were done in a randomized order. At a matched level of VI equivalent to 75% VI at the end of the AC experiments (102 l/min), the breathing pattern in the AVD and O2VD tests was significantly deeper and slower (P < 0.05) than that in the AC and O2C tests. The difference in tidal volume between AVD and AC tests (delta = 0.26 +/- 0.16 liter) was not significantly different from that between O2VD and O2C tests (delta = 0.23 +/- 0.23 liter). The breathing pattern was the same in the AC and O2C tests. It is concluded that the altered breathing pattern with VD loading is not mediated by the CC.

1991 ◽  
Vol 70 (1) ◽  
pp. 55-62 ◽  
Author(s):  
C. McParland ◽  
J. Mink ◽  
C. G. Gallagher

We examined the effects of dead space (VD) loading on breathing pattern during maximal incremental exercise in eight normal subjects. Addition of external VD was associated with a significant increase in tidal volume (VT) and decrease in respiratory frequency (f) at moderate and high levels of ventilation (VI); at a VI of 120 l/min, VT and f with added VD were 3.31 +/- 0.33 liters and 36.7 +/- 6.7 breaths/min, respectively, compared with 2.90 +/- 0.29 liters and 41.8 +/- 7.3 breaths/min without added VD. Because breathing pattern does not change with CO2 inhalation during heavy exercise (Gallagher et al. J. Appl. Physiol. 63: 238–244, 1987), the breathing pattern response to added VD is probably a consequence of alteration in the PCO2 time profile, possibly sensed by the carotid body and/or airway-pulmonary chemoreceptors. The increase in VT during heavy exercise with VD loading indicates that the tachypneic breathing pattern of heavy exercise is not due to mechanical limitation of maximum ventilatory capacity at high levels of VT.


A CO 2 rebreathing test was used to determine the breathing pattern and the ventilatory response to CO 2 in 15 Caucasians and 140 New Guineans (coastal and highland men and women, and male highlanders on the coast). The breathing pattern was analysed in terms of the slope and intercept ( M and K ) of the linear regression of ventilation on tidal volume: V e = M ( V t — K ), and of the interpolated tidal volume at a ventilation of 30 1 min-1 (V t,30 ). Each of these parameters bears a common relation to vital capacity throughout the groups studied. The CO 2 response was analysed in terms of the slope and intercept ( S and B ) of the linear regression of ventilation on P CO 2 : V e = S ( P CO 2 — B ). B is lower in women than in men. S is a function of vital capacity, and this relation accounts for the difference in CO 2 sensitivity between men and women, and for part of the difference between the resident highland and coastal groups; part is attributable to altitude-adaptation and disappears on migration. In all these respects, New Guineans resemble Caucasians, and the results demonstrate the importance of the size of the vital capacity in influencing the setting of the respiratory control mechanisms. In addition, there is a residual difference between the ethnic groups, with the New Guineans having the lower CO 2 sensitivities and thus a greater tolerance of CO 2 loads.


CHEST Journal ◽  
1994 ◽  
Vol 106 (1) ◽  
pp. 131-136 ◽  
Author(s):  
Mark I. Zimmerman ◽  
Albert Miller ◽  
Lee K. Brown ◽  
Anand Bhuptani ◽  
Mark F. Sloane ◽  
...  

1987 ◽  
Vol 63 (1) ◽  
pp. 238-244 ◽  
Author(s):  
C. G. Gallagher ◽  
E. Brown ◽  
M. Younes

During progressive exercise ventilation (VI) initially increases through increases in both tidal volume (VT) and respiratory frequency (f) but at high levels of exercise further increases in VI are almost completely due to increases in f and a VT plateau is seen. We wished to determine whether the presence of the VT plateau is due to a tachypneic influence related to very high levels of exercise or whether it represents a stereotypic response of the respiratory system at high levels of VI. We therefore compared breathing pattern in six subjects during maximal incremental exercise (ME) with that in the same subjects when similar levels of VI were obtained by a combination of submaximal exercise and hypercapnia (E/CO2). A VT plateau was seen in all ME and E/CO2 tests. There was no significant difference in the level of the VT plateau between the ME (2.93 +/- 0.17 liters) and E/CO2 (2.97 +/- 0.12 liters) tests. We conclude that the presence and level of the VT plateau during ME is not due to a tachypneic stimulus related to very high levels of exercise but is a function of the level of VI.


2000 ◽  
Vol 88 (5) ◽  
pp. 1859-1869 ◽  
Author(s):  
Denis E. O'Donnell ◽  
Harry H. Hong ◽  
Katherine A. Webb

We mimicked important mechanical and ventilatory aspects of restrictive lung disorders by employing chest wall strapping (CWS) and dead space loading (DS) in normal subjects to gain mechanistic insights into dyspnea causation and exercise limitation. We hypothesized that thoracic restriction with increased ventilatory stimulation would evoke exertional dyspnea that was similar in nature to that experienced in such disorders. Twelve healthy young men [28 ± 2 (SE) yr of age] completed pulmonary function tests and maximal cycle exercise tests under four conditions, in randomized order: 1) control, 2) CWS to 60% of vital capacity, 3) added DS of 600 ml, and 4) CWS + DS. Measurements during exercise included cardiorespiratory parameters, esophageal pressure, and Borg scale ratings of dyspnea. Compared with control, CWS significantly reduced the tidal volume response to exercise, increased dyspnea intensity at any given work rate or ventilation, and thus limited exercise performance. DS stimulated ventilation but had minimal effects on dyspnea and exercise performance. Adding DS to CWS further increased dyspnea by 1.7 ± 0.6 standardized Borg units ( P = 0.012) and decreased exercise performance (total work) by 21 ± 6% ( P = 0.003) over CWS alone. Across conditions, increased dyspnea intensity correlated best with decreased resting inspiratory reserve volume ( r = −0.63, P < 0.0005). Dyspnea during CWS was described primarily as “inspiratory difficulty” and “unsatisfied inspiration,” similar to restrictive disorders. In conclusion, severe dyspnea and exercise intolerance were provoked in healthy normal subjects when tidal volume responses were constrained in the face of increased ventilatory drive during exercise.


1960 ◽  
Vol 15 (3) ◽  
pp. 383-389 ◽  
Author(s):  
J. F. Nunn ◽  
D. W. Hill

Observations were made during both spontaneous and artificial respiration on 12 fit patients anesthetized for routine surgical procedures. Above a tidal volume of 350 ml (BTPS), the anatomical dead space was close to the predicted normal value for the subject. Below 350 ml, it was reduced in proportion to the tidal volume. The physiological dead space (below the carina) approximated to 0.3 times the tidal volume for tidal volumes between 163 and 652 ml (BTPS). Throughout the range the physiological dead space was considerably in excess of the anatomical dead space measured simultaneously. The difference (alveolar dead space) varied from 15 to 231 ml, being roughly proportional to the tidal volume. The mean arterial to end-tidal CO2 tension difference was 4.6 (S.D. ±2.5) mm Hg and not related to tidal volume or arterial CO2 tension. None of the findings appeared to depend on whether the respiration was spontaneous or artificial. Submitted on September 25, 1959


1987 ◽  
Vol 73 (5) ◽  
pp. 519-523 ◽  
Author(s):  
R. Lane ◽  
A. Cockcroft ◽  
A. Guz

1. Nine normal subjects performed 6 min, constant-workload, exercise tests on a bicycle ergometer at either a ‘high workload’ or at a ‘low workload’. During the first ‘high workload’ test their spontaneous breathing pattern was recorded on to magnetic tape. During one subsequent ‘high workload’ test and one ‘low workload’ test they voluntarily copied their recorded breathing pattern. During a second ‘low workload’ test they breathed spontaneously. Isocapnia was maintained by the operator throughout both the copying tests. During the exercise tests ventilation was recorded and subjects indicated the level of their sensation of breathlessness every 30 s. 2. Subjects felt markedly less breathless when a proportion of their ventilation was produced by voluntary effort than when the same total level of ventilation was produced entirely by the stimulus of exercise. Furthermore, voluntary isocapnic hyperventilation during exercise did not increase breathlessness above that normally associated with that level of exercise. 3. These results suggest that it is reflexly driven ventilation, and not simply the level of ventilation itself, which relates to the level of breathlessness during exercise.


2008 ◽  
Vol 105 (3) ◽  
pp. 854-858 ◽  
Author(s):  
Yandong Jiang ◽  
Yafen Liang ◽  
Robert M. Kacmarek

Upper airway unidirectional breathing, nose in and mouth out, is used by panting dogs to facilitate heat removal via water evaporation from the respiratory system. Why some humans instinctively employ the same breathing pattern during respiratory distress is still open to question. We hypothesized that 1) humans unconsciously perform unidirectional breathing because it improves breathing efficiency, 2) such an improvement is achieved by bypassing upper airway dead space, and 3) the magnitude of the improvement is inversely proportional to the tidal volume. Four breathing patterns were performed in random order in 10 healthy volunteers first with normal breathing effort, then with variable tidal volumes: mouth in and mouth out (MMB); nose in and nose out (NNB); nose in and mouth out (NMB); and mouth in and nose out (MNB). We found that unidirectional breathing bypasses anatomical dead space and improves breathing efficiency. At tidal volumes of ∼380 ml, the functional anatomical dead space during NMB (81 ± 31 ml) or MNB (101 ± 20 ml) was significantly lower than that during MMB (148 ± 15 ml) or NNB (130 ± 13 ml) (all P < 0.001), and the breathing efficiency obtained with NMB (78 ± 9%) or MNB (73 ± 6%) was significantly higher than that with MMB (61 ± 6%) or NNB (66 ± 3%) (all P < 0.001). The improvement in breathing efficiency increased as tidal volume decreased. Unidirectional breathing results in a significant reduction in functional anatomical dead space and improvement in breathing efficiency. We suggest this may be the reason that such a breathing pattern is preferred during respiratory distress.


1992 ◽  
Vol 73 (2) ◽  
pp. 591-595 ◽  
Author(s):  
C. S. Poon

We examined the effects of different modes of airway CO2 load on the ventilation-CO2 output (VE-VCO2) relationship during mild to moderate exercise. Four young and three older male subjects underwent incremental steady-state treadmill exercise while breathing a mixture of CO2 in O2 (CO2 loading) or 100% O2 with and without a large external dead space [DS loading and control (C), respectively]. During DS loading, the elevated arterial PCO2 (PaCO2) remained constant from rest to mild exercise and began to increase only at higher work rates. To achieve similar chemical drive, the same PaCO2 levels were established during CO2 loading by external PCO2 forcing. In the young group, CO2 loading resulted in a steepening of the VE-VCO2 relationship compared with C, whereas in the older group the reverse pattern was found. DS loading resulted in a consistent increase in the VE-VCO2 slope compared with C and CO2 loading [39.1 +/- 5.6 (mean +/- SD) vs. 24.9 +/- 5.0 and 26.7 +/- 4.4, respectively] in all subjects. The difference in potentiation of VE-VCO2 by CO2 and DS loading was not due to differences in mean chemical drive or changes in breathing pattern. Thus changes in the profile of airway CO2 influx may have an independent influence on ventilatory CO2-exercise interaction. Peripheral chemoreceptors mediation, although important, is not obligatory for this behavior.


1959 ◽  
Vol 14 (3) ◽  
pp. 339-344 ◽  
Author(s):  
R. L. Riley ◽  
S. Permutt ◽  
S. Said ◽  
M. Godfrey ◽  
T. O. Cheng ◽  
...  

Physiologic dead space was determined in the supine and upright postures by simultaneous sampling and subsequent analysis of arterial blood and expired gas for Pco2. In seven normal men there was invariably a higher dead space in the upright than in the supine position. The difference averaged 83 ml and was statistically significant (S.E. 25 ml and P < 0.01). The ratio of dead space to tidal volume also invariably increased on assuming the upright posture. Evidence is presented for believing that most of the change in physiologic dead space resulted from a change in alveolar dead space. Estimated changes in the ratio of alveolar dead space to alveolar tidal volume suggest that approximately one seventh of the total number of alveoli became nonperfused on changing from the supine to the erect posture. These findings are consistent with bronchospirometric and hemodynamic evidence that the apex of the lung is virtually nonperfused in the resting human subject in the upright posture. Submitted on November 12, 1958


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