Effect of mild hypoxia on ventilation during exercise

1962 ◽  
Vol 17 (2) ◽  
pp. 239-242 ◽  
Author(s):  
Thomas F. Hornbein ◽  
Albert Roos
Keyword(s):  
Steady State ◽  
Ventilatory Response ◽  
Human Subjects ◽  
Sympathetic Innervation ◽  
Mild Degree ◽  
Flow Through ◽  
Neural Discharge ◽  
Response To Exercise ◽  
Mild Hypoxia ◽  
Rest And Exercise

Hypoxia of mild degree (PaOO2 above 60 mm Hg) produces little or no ventilatory response in resting man during the steady state. To evaluate the possibility that the effectiveness of a hypoxic chemoreceptor drive might be enhanced by exercise, the ventilatory response to mild hypoxia was measured in two human subjects during rest and exercise. Though no significant increase in ventilation occurred at rest above a PaOO2 of 60 mm Hg, a decrease in PaOO2from 100 to 94 mm Hg produced a statistically significant increase in steady state ventilation during moderate exercise. In addition, temporary block of the sympathetic innervation to the carotid and aortic bodies in one subject resulted in a diminution of work hyperpnea. This suggests that increased sympathetic tone during exercise, by reducing blood flow through the chemoreceptors, might result in increased neural discharge and hence increased ventilation even though arterial POO2 is the same as at rest. Thus, activity of the chemoreceptors as modified by sympathetic control of their blood supply may be an important determinant of the ventilatory response to exercise. Since work hyperpnea is enhanced by even mild hypoxia, this ventilatory response may be sufficient to initiate respiratory acclimatization to altitudes so low that resting ventilation on acute exposure is unaffected. Submitted on July 31, 1961

Effect of dopamine on transient ventilatory response to exercise

1986 ◽  
Vol 61 (6) ◽  
pp. 2102-2107 ◽  
Author(s):  
C. L. Boetger ◽  
D. S. Ward
Keyword(s):  
Steady State ◽  
Ventilatory Response ◽  
Work Load ◽  
Exponential Model ◽  
Bicycle Ergometer ◽  
Co2 Production ◽  
Load Testing ◽  
State Response ◽  
Exercise Hyperpnea ◽  
Response To Exercise

The effect of exogenous dopamine on the development of exercise hyperpnea was studied. Using a bicycle ergometer, five subjects performed repetitive square-wave work-load testing from unloaded pedaling to 80% of each subject's estimated anaerobic threshold. The breath-by-breath ventilation (VE), CO2 production (VCO2), and O2 consumption (VO2) responses were analyzed by curve fitting a first-order exponential model. Comparisons were made between control experiments and experiments with a 3-micrograms X kg-1 X min-1 intravenous infusion of dopamine. Steady-state VE, VCO2 and VO2 were unchanged by the dopamine infusion, both during unloaded pedaling and at the heavier work load. The time constants for the increase in VE (tau VE) and VCO2 (tau CO2) were significantly (P less than 0.05) slowed (tau VE = 56.5 +/- 16.4 s for control, and tau VE = 76.4 +/- 26.6 s for dopamine; tau CO2 = 51.5 +/- 10.6 s for control, and tau CO2 = 64.8 +/- 17.4 s for dopamine) (mean +/- SD), but the time constant for VO2 (tau O2) was not significantly affected (tau O2 = 27.5 +/- 11.7 s for control, and tau O2 = 31.0 +/- 10.1 s for dopamine). We conclude that ablation of carotid body chemosensitivity with dopamine slows the transient ventilatory response to exercise while leaving the steady-state response unaffected.

Effects of morphine on ventilatory response to exercise

1979 ◽  
Vol 47 (1) ◽  
pp. 112-118 ◽  
Author(s):  
T. V. Santiago ◽  
J. Johnson ◽  
D. J. Riley ◽  
N. H. Edelman
Keyword(s):  
Steady State ◽  
Metabolic Rate ◽  
Ventilatory Response ◽  
Normal Subjects ◽  
Blood Gas ◽  
Arterial Blood Gas ◽  
Ventilatory Responses ◽  
Arterial Blood ◽  
Response To Exercise ◽  
The Relationship

The effects of analgesic doses of morphine on ventilation, arterial blood gas tensions, chemical control of breathing, and the ventilatory response to exercise were studied in six normal subjects. After administration of 0.2 mg/kg morphine, resting ventilation decreased primarily because of a reduction of tidal volume. Ventilatory responses to carbon dioxide and hypoxia were significantly reduced to one-half and one-third of control, respectively. Ventilatory responses at any given level of exercise were significantly reduced after morphine. However, since oxygen consumption during exercise was similarly reduced after morphine, the relationship between ventilation and metabolic rate during steady-state exercise was not altered by the drug. In addition, morphine prolonged the attainment of steady-state ventilation in four of the six subjects, similar to that reported for chemodenervated subjects. The findings suggest that blunting of chemoreception for hypoxia and hypercapnia has no effect upon the link between metabolic rate and ventilation during steady-state exercise, but the hypoxia chemoreflex may be involved in determining the dynamic characteristics of the response.

Effects of expiratory threshold loading during steady-state exercise

1975 ◽  
Vol 39 (5) ◽  
pp. 697-701 ◽  
Author(s):  
I. Goldstein ◽  
S. Goldstein ◽  
J. A. Urbanetti ◽  
N. R. Anthonisen
Keyword(s):  
Steady State ◽  
Tidal Volume ◽  
Ventilatory Response ◽  
Minute Ventilation ◽  
Bicycle Ergometer ◽  
Inspiratory Capacity ◽  
Mouth Pressure ◽  
Consistent Change ◽  
Residual Capacity ◽  
Response To Exercise

Increases in functional residual capacity (FRC) decrease inspiratory muscle efficiency; the present experiments were designed to determine the effect of FRC change on the ventilatory response to exercise. Six well-trained adults were exposed to expiratory threshold loads (ETL) ranging from 5 to 40 cmH2O during steady-state exercise on a bicycle ergometer at 40–95% VO2max. Inspiratory capacity (IC) was measured and changes of IC interpreted as changes of FRC. ETL did not consistently limit exercise performance. At heavy work (greater than 92% VO2max) minute ventilation decreased with increasing ETL; at moderate work (less than 58% VO2max) it did not. Decreases in ventilation were due to decreases in respiratory frequency with prolongation of the duration of expiration being the most consistent change in breathing pattern. At moderate work levels, FRC increased with ETL; at maximum work it did not. Changes in FRC were dictated by constancy of tidal volume and a fixed maximum end-inspiratory volume of 80–90% of the inspiratory capacity. When tidal volume was such that end-inspiratory volume was less than this value, FRC increased with ETL. Mouth pressure measured during the first 0–1 s of inspiratory effort against an occluded airway (P0-1) was increased by ETL equals 30 cmH2O, in spite of the fact that ventilation was decreased. We concluded that changes in FRC due to ETL had no effect on the ventilatory response to exercise and that changes in P0-1 induced by ETL did not reflect changes of inspiratory drive so much as changes of the pattern of inspiration.

Effects of altered CSF [H+] on ventilatory responses to exercise in the awake goat

1988 ◽  
Vol 65 (2) ◽  
pp. 921-927 ◽  
Author(s):  
C. A. Smith ◽  
L. C. Jameson ◽  
J. A. Dempsey
Keyword(s):  
Steady State ◽  
Carotid Body ◽  
Ventilatory Response ◽  
Fold Increase ◽  
Co2 Production ◽  
Acid Base ◽  
Ventilatory Responses ◽  
Exercise Hyperpnea ◽  
Acid Base Status ◽  
Response To Exercise

We investigated the effects of selective large changes in the acid-base environment of medullary chemoreceptors on the control of exercise hyperpnea in unanesthetized goats. Four intact and two carotid body-denervated goats underwent cisternal perfusion with mock cerebrospinal fluid (CSF) of markedly varying [HCO-3] (CSF [H+] = 21-95 neq/l; pH 7.68-7.02) until a new steady state of alveolar hypo- or hyperventilation was reached [arterial PCO2 (PaCO2) = 31-54 Torr]. Perfusion continued as the goats completed two levels of steady-state treadmill walking [2 to 4-fold increase in CO2 production (VCO2)]. With normal acid-base status in CSF, goats usually hyperventilated slightly from rest through exercise (-3 Torr PaCO2, rest to VCO2 = 1.1 l/min). Changing CSF perfusate [H+] changed the level of resting PaCO2 (+6 and -4 Torr), but with few exceptions, the regulation of PaCO2 during exercise (delta PaCO2/delta VCO2) remained similar regardless of the new ventilatory steady state imposed by changing CSF [H+]. Thus the gain (slope) of the ventilatory response to exercise (ratio of change in alveolar ventilation to change in VCO2) must have increased approximately 15% with decreased resting PaCO2 (acidic CSF) and decreased approximately 9% with increased resting PaCO2 (alkaline CSF). A similar effect of CSF [H+] on resting PaCO2 and on delta PaCO2/VCO2 during exercise also occurred in two carotid body-denervated goats. Our results show that alteration of the gain of the ventilatory response to exercise occurs on acute alterations in resting PaCO2 set point (via changing CSF [H+]) and that the primary stimuli to exercise hyperpnea can operate independently of central or peripheral chemoreception.

Transient responses to CO2 breathing of human subjects awake and asleep

1963 ◽  
Vol 18 (2) ◽  
pp. 289-294 ◽  
Author(s):  
F. J. D. Fuleihan ◽  
T. Nakada ◽  
J. T. Suero ◽  
E. S. Merrifield ◽  
R. E. Dutton ◽  
...  
Keyword(s):  
Steady State ◽  
Ventilatory Response ◽  
Human Subjects ◽  
Control Period ◽  
Sodium Pentobarbital ◽  
Transient Responses ◽  
Control Value ◽  
Oxygen Breathing ◽  
Significant Difference ◽  
End Tidal

Ventilation and end-tidal Pco2 were studied in six subjects awake and asleep (following the ingestion of 200–300 mg sodium pentobarbital) during oxygen breathing and the administration and withdrawal of 4% CO2 in oxygen. During the control period as well as steady-state CO2 breathing, ventilation was significantly lower in asleep than in awake subjects. There was no significant difference between sleep and wakefulness in end-tidal Pco2 or in the slope of the ventilatory response to 4% CO2. The transient responses of ventilation and end-tidal Pco2 of the group as a whole were similar in sleep and wakefulness. Ventilation changed more slowly than did end-tidal Pco2. End-tidal Pco2 overshot beyond the steady-state CO2 breathing value at the onset of CO2 breathing; and undershot below the control value during recovery. The magnitudes of both the overshoot and undershoot of end-tidal Pco2 were correlated significantly to the slope of the ventilatory response to 4% CO2, in the whole group awake and asleep. Submitted on October 4, 1962

Response to hypercapnia and exercise hyperpnea in graded anesthesia

1984 ◽  
Vol 57 (6) ◽  
pp. 1796-1802 ◽  
Author(s):  
T. Chonan ◽  
Y. Kikuchi ◽  
W. Hida ◽  
C. Shindoh ◽  
H. Inoue ◽  
...  
Keyword(s):  
Steady State ◽  
Ventilatory Response ◽  
Minute Ventilation ◽  
Exercise Hyperpnea ◽  
Sciatic Nerves ◽  
End Tidal ◽  
Response To Exercise ◽  
The Relationship ◽  
End Tidal Co2 ◽  
Rebreathing Method

We examined the relationship between response to hypercapnia and ventilatory response to exercise under graded anesthesia in eight dogs. The response to hypercapnia was measured by the CO2 rebreathing method under three grades of chloralose-urethan anesthesia. The degrees of response to hypercapnia (delta VE/delta PETCO2, 1 X min-1 X Torr-1) in light (L), moderate (M), and deep (D) anesthesia were 0.40 +/- 0.05 (mean +/- SE), 0.24 +/- 0.03, and 0.10 +/- 0.02, respectively, and were significantly different from each other. Under each grade of anesthesia, exercise was performed by electrically stimulating the bilateral femoral and sciatic nerves for 4 min. The time to reach 63% of full response of the increase in ventilation (tauVE) after beginning of exercise was 28.3 +/- 1.5, 38.1 +/- 5.2, and 56.0 +/- 6.1 s in L, M, and D, respectively. During steady-state exercise, minute ventilation (VE) in L, M, and D significantly increased to 6.17 +/- 0.39, 5.14 +/- 0.30, and 3.41 +/- 0.16 1 X min-1, from resting values of 3.93 +/- 0.34, 2.97 +/- 0.17, and 1.69 +/- 0.14 1 X min-1, respectively, while end-tidal CO2 tension (PETCO2) in L decreased significantly to 34.8 +/- 0.9 from 35.7 +/- 0.9, did not change in M (38.9 +/- 1.1 from 38.9 +/- 0.8), and increased significantly in D to 47.3 +/- 1.9 from 45.1 +/- 1.7 Torr.(ABSTRACT TRUNCATED AT 250 WORDS)

Transient effect of sudden mild hypoxia on respiration

1961 ◽  
Vol 16 (1) ◽  
pp. 11-14 ◽  
Author(s):  
Thomas F. Hornbein ◽  
Albert Roos ◽  
Zora J. Griffo
Keyword(s):  
Steady State ◽  
Sea Level ◽  
Carotid Body ◽  
Ventilatory Response ◽  
Transient Increase ◽  
Transient Responses ◽  
Transient Effect ◽  
The Difference ◽  
Mild Hypoxia

Recent studies of carotid body chemoreceptor activity in cats show that the activity of these organs increases markedly over a range of alveolar pO2 considerably higher than the alveolar pO2 of 50–60 mm Hg known to produce an increase in ventilation in the steady state. In an attempt to explain this discrepancy between chemoreceptor activity and ventilation, the transient ventilatory response to two breaths of a low O2 mixture was observed and correlated with the alveolar pO2 during this brief hypoxic stimulus. A transient increase in ventilation could be detected at an alveolar pO2 of 93 mm Hg, that is, considerably higher than the highest pO2 known to increase ventilation during the steady state. These findings are interpreted as evidence of an increased chemoreceptor drive when alveolar O2 tension is lowered only slightly below that existing at sea level. Possible reasons for the difference between the steady state and transient responses are discussed. Submitted on June 6, 1960

Ventilatory response to CO2 and O2 near eupnea in awake dogs

1988 ◽  
Vol 65 (2) ◽  
pp. 788-796 ◽  
Author(s):  
W. W. Hwang ◽  
S. M. Yamashiro ◽  
D. Sedlock ◽  
F. S. Grodins
Keyword(s):  
Steady State ◽  
High Frequency ◽  
Ventilatory Response ◽  
Nonlinear Behavior ◽  
High Frequency Ventilation ◽  
Frequency Ventilation ◽  
Extracorporeal Circuits ◽  
The Subject ◽  
Ventilatory Response To Co2 ◽  
Mild Hypoxia

The problem faced in determining the ventilatory response to CO2 near eupnea has been the difficulty of unloading metabolically produced CO2 from the subject in the steady state. Previous methods using extracorporeal circuits to unload CO2 are technically difficult and provide a limited number of experimental states per experiment. Using the method of high-frequency ventilation to unload CO2, we were able to obtain a large number of determinations in the same subject under conditions of hypoxia, normoxia, and hyperoxia. Data collected in five awake dogs show that the ventilatory response to CO2 is linear down to apnea during normoxic conditions but exhibits nonlinear behavior dependent on the level of arterial O2 tension. During hyperoxic conditions, the response was concave curvilinear, with a statistically significant decrease in slope near apnea. In contrast, mild hypoxia led to a convex curvilinear response with an increased slope near apnea.

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