Ventilatory response of spinal cord-lesioned subjects to electrically induced exercise

1990 ◽  
Vol 68 (6) ◽  
pp. 2312-2321 ◽  
Author(s):  
D. R. Brown ◽  
H. V. Forster ◽  
L. G. Pan ◽  
A. G. Brice ◽  
C. L. Murphy ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Partial Pressure ◽  
Venous Return ◽  
Ventilatory Response ◽  
Co2 Partial Pressure ◽  
Human Spinal Cord ◽  
Co2 Output ◽  
Hamstring Muscles ◽  
Exercise Hyperpnea ◽  
End Tidal

Seven human spinal cord-lesioned subjects (SPL) underwent electrically induced muscle contractions (EMC) of the quadriceps and hamstring muscles for 10 min: 5 min control, 2 min with venous return from the legs occluded, and 3 min postocclusion. Group mean changes in CO2 output compared with rest were +107 +/- 30.6, +21 +/- 25.7, and +192 +/- 37.0 (SE) ml/min during preocclusion, occlusion, and postocclusion EMC, respectively. Mean arterial CO2 partial pressure (PaCO2) obtained from catheterized radial arteries at 15- to 30-s intervals showed a significant (P less than 0.05) hypocapnia (36.2 Torr) during occlusion and a significant (P less than 0.05) hypercapnia (38.1 Torr) postocclusion relative to a group mean preocclusion EMC PaCO2 of 37.5 Torr. Relative to preocclusion EMC, expired ventilation (VE) decreased during occlusion and increased after release of occlusion. However, changes in VE always occurred after changes in end-tidal PCO2 (mean 41 s after occlusion and 10 s after release of occlusion). In the two subjects investigated during hyperoxia, the VE and PaCO2 responses to occlusion and release did not differ from normoxia. We conclude that the data do not support mediation of the EMC hyperpnea in SPL by humoral mechanisms that others have proposed for mediation of the exercise hyperpnea in spinal cord-intact humans.

Control of breathing at the start of exercise as influenced by posture

1983 ◽  
Vol 55 (5) ◽  
pp. 1460-1466 ◽  
Author(s):  
D. Weiler-Ravell ◽  
D. M. Cooper ◽  
B. J. Whipp ◽  
K. Wasserman
Keyword(s):  
Stroke Volume ◽  
Phase I ◽  
Ventilatory Response ◽  
Normal Subjects ◽  
Initial Increase ◽  
Base Line ◽  
Co2 Output ◽  
End Tidal ◽  
Response To Exercise ◽  
Initial Change

It has been suggested that the initial phase of the ventilatory response to exercise is governed by a mechanism which responds to the increase in pulmonary blood flow (Q)--cardiodynamic hyperpnea. Because the initial change in stroke volume and Q is less in the supine (S) than in the upright (U) position at the start of exercise, we hypothesized that the increase in ventilation would also be less in the first 20 s (phase I) of S exercise. Ten normal subjects performed cycle ergometry in the U and S positions. Inspired ventilation (VI), O2 uptake (VO2), CO2 output (VCO2), corrected for changes in lung gas stores, and end-tidal O2 and CO2 tensions were measured breath by breath. Heart rate (HR) was determined beat by beat. The phase I ventilatory response was markedly different in the two positions. In the U position, VI increased abruptly by 81 +/- 8% (mean +/- SE) above base line. In the S position, the phase I response was significantly attenuated (P less than 0.001), the increase in VI being 50 +/- 6%. Similarly, the phase I VO2 and VO2/HR responses reflecting the initial increase in Q and stroke volume, were attenuated (P less than 0.001) in the S posture, compared with that for U; VO2 increased 49 +/- 5.3 and 113 +/- 14.7% in S and U, respectively, and VO2/HR increased 16 +/- 3.0 and 76 +/- 7.1% in the S and U, respectively. The increase in VI correlated well with the increase in VO2, (r = 0.80, P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Diaphragm electrical activity during negative lower torso pressure in quadriplegic men

1981 ◽  
Vol 51 (3) ◽  
pp. 654-659 ◽  
Author(s):  
R. B. Banzett ◽  
G. F. Inbar ◽  
R. Brown ◽  
M. Goldman ◽  
A. Rossier ◽  
...  
Keyword(s):  
Partial Pressure ◽  
Tidal Volume ◽  
Respiratory System ◽  
Afferent Pathways ◽  
Co2 Partial Pressure ◽  
Inspiratory Muscles ◽  
Spinal Lesions ◽  
Diaphragm Electrical Activity ◽  
End Tidal ◽  
End Tidal Co2

We recorded the diaphragm electromyogram (EMG) of quadriplegic men before and during exposure of the lower torso to continuous negative pressure, which caused shortening of the inspiratory muscles by expanding the respiratory system by one tidal volume. The moving-time-averaged diaphragm EMG was larger during expansion of the respiratory system. When we repeated the experiment with subjects who breathed through a mouthpiece, we found qualitatively similar EMG changes and little or no change in tidal volume or end-tidal CO2 partial pressure. When the pressure was applied or removed rapidly, changes in EMG occurred within one or two breaths. Because end-tidal CO2 partial pressure did not increase, and because the response was rapid, we suggest that the response results from proprioceptive, rather than chemoreceptive, reflexes. As most of these men had complete spinal lesions at C6 or C7 the afferent pathways are likely to be vagal or phrenic.

The Ventilatory Response to Hypoxia Below the Carbon Dioxide Threshold

1997 ◽  
Vol 22 (1) ◽  
pp. 23-36 ◽  
Author(s):  
Theodore Rapanos ◽  
James Duffin
Keyword(s):  
Carbon Dioxide ◽  
Partial Pressure ◽  
Ventilatory Response ◽  
Pressure Threshold ◽  
Partial Pressures ◽  
Progressive Hypoxia ◽  
End Tidal ◽  
Peripheral Chemoreflex ◽  
Ventilatory Response To Hypoxia ◽  
Lower Carbon

The ventilatory response to acute progressive hypoxia below the carbon dioxide threshold using rebreathing was investigated. Nine subjects rebreathed after 5 min of hyperventilation to lower carbon dioxide stores. The rebreathing bag initially contained enough carbon dioxide to equilibrate alveolar and arterial partial pressures of carbon dioxide to the lowered mixed venous partial pressure (≈ 30 mmHg), and enough oxygen to establish a chosen end-tidal partial pressure (50-70 mmHg), within one circulation time. During rebreathing, end-tidal partial pressure of carbon dioxide increased while end-tidal partial pressure of oxygen fell. Ventilation increased linearly with end-tidal carbon dioxide above a mean end-tidal partial pressure threshold of 39 ± 2.7 mmHg. Below this peripheral-chemoreflex threshold, ventilation did not increase, despite a progressive fall in end-tidal oxygen partial pressure to a mean of 37 ± 4.1 mmHg. In Conclusion, hypoxia does not stimulate ventilation when carbon dioxide is below its peripheral-chemoreflex threshold. Key words: peripheral chemoreflex, rebreathing technique, hyperventilation

METABOREFLEX CHANGES RELATIONSHIP BETWEEN END-TIDAL CO2 PARTIAL PRESSURE AND VENTILATION

2003 ◽  
Vol 35 (Supplement 1) ◽  
pp. S229
Author(s):  
N Hayashi ◽  
T Miyamoto ◽  
Y Fukuba ◽  
T Yoshida
Keyword(s):  
Partial Pressure ◽  
Co2 Partial Pressure ◽  
End Tidal ◽  
End Tidal Co2

Ventilatory and PaCO2 responses to voluntary and electrically induced leg exercise

1988 ◽  
Vol 64 (1) ◽  
pp. 218-225 ◽  
Author(s):  
A. G. Brice ◽  
H. V. Forster ◽  
L. G. Pan ◽  
A. Funahashi ◽  
T. F. Lowry ◽  
...  
Keyword(s):  
Ventilatory Response ◽  
Human Subjects ◽  
Muscle Contractions ◽  
Co2 Production ◽  
Central Command ◽  
Co2 Partial Pressure ◽  
Leg Extension ◽  
Hamstring Muscles ◽  
Leg Exercise ◽  
Command Signals

We studied the role of central command mediation of exercise hyperpnea by comparing the ventilatory and arterial CO2 partial pressure (PaCO2) responses to voluntary (ExV) and electrically induced (ExE) muscle contractions in normal, awake human subjects. We hypothesized that if central command signals are critical to a normal ventilatory response, then ExE should cause a slower ventilatory response resulting in hypercapnia at the onset of exercise. ExE was induced through surface electrodes placed over the quadriceps and hamstring muscles. ExE and ExV produced leg extension (40/min) against a spring load that increased CO2 production (VCO2) 100-1,000 ml/min above resting level. PaCO2 and arterial pH during work transitions and in the steady state did not differ significantly from rest (P greater than 0.05) or between ExE and ExV. The temporal pattern of ventilation, tidal volume, breathing frequency, and inspired and expired times, and the ventilation-VCO2 relationship were similar between ExE and ExV. We conclude that since central command was reduced and/or eliminated by ExE, central command is not requisite for the precise matching of alveolar ventilation to increases in VCO2 during low-intensity muscle contractions.

Ventilatory responses to static handgrip exercise

1983 ◽  
Vol 54 (6) ◽  
pp. 1457-1462 ◽  
Author(s):  
S. R. Muza ◽  
L. Y. Lee ◽  
R. L. Wiley ◽  
S. McDonald ◽  
F. W. Zechman
Keyword(s):  
Time Course ◽  
Ventilatory Response ◽  
Maximum Voluntary Contraction ◽  
Muscle Afferents ◽  
Voluntary Contraction ◽  
Static Exercise ◽  
Handgrip Exercise ◽  
Co2 Partial Pressure ◽  
Ventilatory Responses ◽  
End Tidal

Previous research indicates that fatiguing static exercise causes hyperventilation and a decrease of end-tidal CO2 partial pressure PETCO2. The objectives of this study were 1) to examine the changes in pattern of breathing during static exercise, and 2) to define the isocapnic ventilatory response. Six healthy males were studied once a week at one of three levels of static handgrip exercise: 15, 25, or 30% maximum voluntary contraction (MVC) was sustained for 5 min while holding PETCO2 constant or allowing it to run free. During 25 and 30% MVC, we observed 1) progressive increases in mean tidal volume (VT), inspiratory ventilation (VI), VT/TI, heart rate (HR), and arterial BP, 2) increased breath-to-breath variability of VT, 3) no significant changes in respiratory frequency (f), and 4) progressive decreases in PETCO2. Keeping PETCO2 constant at preexercise levels did not change the pattern or magnitude of the ventilatory response to exercise. The time course and magnitude of the subjects' perceived effort resembled the time course and magnitude of the ventilatory response. The variability of VT during the response to static exercise suggests an element of control instability. The identical ventilatory responses during hypocapnic and isocapnic conditions may result from the slow response of the central chemoreceptors; an overriding influence of muscle afferents; and/or increased central command arising with fatigue.

Effect of quiet sleep on resting and CO2-stimulated breathing in humans

1981 ◽  
Vol 50 (4) ◽  
pp. 724-730 ◽  
Author(s):  
B. Gothe ◽  
M. D. Altose ◽  
M. D. Goldman ◽  
N. S. Cherniack
Keyword(s):  
Partial Pressure ◽  
Tidal Volume ◽  
Quiet Sleep ◽  
Rib Cage ◽  
Co2 Partial Pressure ◽  
Ventilatory Responses ◽  
Quantitative Measurements ◽  
End Tidal ◽  
End Tidal Co2 ◽  
Different Levels

We examined the effects of different levels of inspired CO2 on ventilation and the pattern of breathing in healthy adults during the awake and the stage II quiet-sleep states. During both states, subjects were studied supine with their heads enclosed in a canopy. Tidal volume (VT) was determined from quantitative measurements of abdominal and rib cage excursions with magnetometers. Inspired CO2 was raised by blending CO2-enriched gas into the airflow, which continuously flushed the canopy. During sleep, while room air was breathed, VT decreased significantly from 410 to 360 ml, and respiratory rate also fell from 17 to 16 breaths/min. As a consequence, ventilation was significantly reduced from 6.5 to 5.8 l/min, and end-tidal CO2 partial pressure (PCO2) rose from 39.1 to 42.5 Torr. Ventilatory responses to CO2 were reduced, on the average, during sleep to 79% of waking levels. The change in average inspiratory flow produced by CO2 was also less during sleep. Waking and sleeping ventilatory responses to CO2 correlated inversely with the rise in end-tidal PCO2 when room air was breathed during sleep. At all levels of VT, the rib cage contribution to VT was greater during quiet sleep than during wakefulness. These findings suggest that quiet sleep, in addition to depressing ventilation and the response to CO2 alters the manner in which VT is attained by rib cage and abdominal displacements.

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.

Cardiopulmonary control during exercise in the duck

1983 ◽  
Vol 55 (5) ◽  
pp. 1574-1581 ◽  
Author(s):  
J. P. Kiley ◽  
M. R. Fedde
Keyword(s):  
Partial Pressure ◽  
Flow Rate ◽  
Minute Ventilation ◽  
Minor Component ◽  
Blood Gases ◽  
Exercise Heart Rate ◽  
Co2 Partial Pressure ◽  
Co2 Sensitivity ◽  
Arterial Blood ◽  
Exercise Hyperpnea

To determine the importance of nonhumoral drives to exercise hyperpnea in birds, we exercised adult White Pekin ducks on a treadmill (3 degrees incline) at 1.44 km X h-1 for 15 min during unidirectional artificial ventilation. Intrapulmonary gas concentrations and arterial blood gases could be regulated with this ventilation procedure while allowing ventilatory effort to be measured during both rest and exercise. Ducks were ventilated with gases containing either 4.0 or 5.0% CO2 in 19% O2 (balance N2) at a flow rate of 12 l X min-1. At that flow rate, arterial CO2 partial pressure (PaCO2) could be maintained within +/- 2 Torr of resting values throughout exercise. Arterial O2 partial pressure did not change significantly with exercise. Heart rate, mean arterial blood pressure, and mean right ventricular pressure increased significantly during exercise. On the average, minute ventilation (used as an indicator of the output from the central nervous system) increased approximately 400% over resting levels because of an increase in both tidal volume and respiratory frequency. CO2-sensitivity curves were obtained for each bird during rest. If the CO2 sensitivity remained unchanged during exercise, then the observed 1.5 Torr increase in PaCO2 during exercise would account for only about 6% of the total increase in ventilation over resting levels. During exercise, arterial [H+] increased approximately 4 nmol X l-1; this increase could account for about 18% of the total rise in ventilation. We conclude that only a minor component of the exercise hyperpnea in birds can be accounted for by a humoral mechanism; other factors, possibly from muscle afferents, appear responsible for most of the hyperpnea observed in the running duck.

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