Hypoxic ventilatory response and arterial desaturation during heavy work

1989 ◽  
Vol 67 (3) ◽  
pp. 1119-1124 ◽  
Author(s):  
S. R. Hopkins ◽  
D. C. McKenzie
Keyword(s):  
Maximal Exercise ◽  
Ventilatory Response ◽  
Pulmonary Ventilation ◽  
Ideal Gas ◽  
Respiratory Drive ◽  
O2 Uptake ◽  
Arterial Blood ◽  
Arterial Desaturation ◽  
Exercise Ventilation ◽  
Arterial O2 Saturation

Arterial desaturation in athletes during intense exercise has been reported by several authors, yet the etiology of this phenomenon remains obscure. Inadequate pulmonary ventilation, due to a blunted respiratory drive, has been implicated as a factor. To investigate the relationship between the ventilatory response to hypoxia, exercise ventilation, and arterial desaturation, 12 healthy male subjects [age, 23.8 +/- 3.6 yr; height, 181.6 +/- 5.6 cm; weight, 73.7 +/- 6.2 kg; and maximal O2 uptake (VO2max), 63.0 +/- 2.2 ml.kg-1 min-1] performed a 5-min treadmill test at 100% of VO2max, during which arterial blood samples and ventilatory data were collected every 15 s. Alveolar PO2 (PAO2) was determined using the ideal gas equation. On a separate occasion the ventilatory response to isocapnic hypoxia was measured. Arterial PO2 decreased by an average of 29 Torr during the test, associated with arterial desaturation [arterial O2 saturation (SaO2) 92.0%]. PAO2 was maintained; however, alveolar-arterial gas pressure difference increased progressively to greater than 40 Torr. Minimal hypocapnia was observed, despite marked metabolic acidosis. There was no significant correlation observed between hypoxic drives and ventilation-to-O2 uptake ratio or SaO2 (r = 0.1 and 0.06, respectively, P = NS). These data support the conclusions that hypoxic drives are not related to maximal exercise ventilation or to the development of arterial desaturation during maximal exercise.

Effect of endurance exercise training on ventilatory function in older individuals

1985 ◽  
Vol 58 (3) ◽  
pp. 791-794 ◽  
Author(s):  
J. E. Yerg ◽  
D. R. Seals ◽  
J. M. Hagberg ◽  
J. O. Holloszy
Keyword(s):  
Endurance Training ◽  
Maximal Exercise ◽  
Ventilatory Response ◽  
Submaximal Exercise ◽  
Older Individuals ◽  
Ventilatory Function ◽  
O2 Uptake ◽  
Exercise Ventilation ◽  
Ventilatory Equivalent ◽  
Sedentary Subjects

To evaluate the effect of endurance training on ventilatory function in older individuals, 1) 14 master athletes (MA) [age 63 +/- 2 yr (mean +/- SD); maximum O2 uptake (VO2max) 52.1 +/- 7.9 ml . kg-1 . min-1] were compared with 14 healthy male sedentary controls (CON) (age 63 +/- 3 yr; VO2max of 27.6 +/- 3.4 ml . kg-1 . min-1), and 2) 11 sedentary healthy men and women, age 63 +/- 2 yr, were reevaluated after 12 mo of endurance training that increased their VO2max 25%. MA had a significantly lower ventilatory response to submaximal exercise at the same O2 uptake (VE/VO2) and greater maximal voluntary ventilation (MVV), maximal exercise ventilation (VEmax), and ratio of VEmax to MVV than CON. Except for MVV, all of these parameters improved significantly in the previously sedentary subjects in response to training. Hypercapnic ventilatory response (HCVR) at rest and the ventilatory equivalent for CO2 (VE/VCO2) during submaximal exercise were similar for MA and CON and unaffected by training. We conclude that the increase in VE/VO2 during submaximal exercise observed with aging can be reversed by endurance training, and that after training, previously sedentary older individuals breathe at the same percentage of MVV during maximal exercise as highly trained athletes of similar age.

Effects of beta-adrenergic blockade on O2 uptake during submaximal and maximal exercise

1983 ◽  
Vol 54 (4) ◽  
pp. 901-905 ◽  
Author(s):  
P. A. Tesch ◽  
P. Kaiser
Keyword(s):  
Heart Rate ◽  
Maximal Exercise ◽  
Pulmonary Ventilation ◽  
Submaximal Exercise ◽  
Beta Blockade ◽  
Adrenergic Blockade ◽  
Maximal Heart Rate ◽  
O2 Consumption ◽  
O2 Uptake ◽  
Beta Adrenergic

Changes in cardiorespiratory variables and perceived rate of exertion (RPE) were studied in 13 trained men performing cycling exercise before and after beta-adrenergic blockade. Propranolol (Inderal, 80 mg) was administered orally 2 h prior to standardized maximal and submaximal exercises. Muscle biopsies were obtained from vastus lateralis at rest for subsequent histochemical analyses of muscle fiber type distribution and capillary supply. During submaximal exercise O2 consumption decreased from 2.76 to 2.59 l . min-1 following blockade (P less than 0.01), whereas heart rate decreased from 157 to 113 beats . min-1 (P less than 0.001). Maximal O2 uptake was lowered from 3.79 to 3.26 l . min-1 (P less than 0.001) and maximal heart rate was reduced from 192 to 142 beats . min-1 (P less than 0.001) as a result of the blockade. Pulmonary ventilation was unaltered in both exercise conditions. “Local” RPE was higher (P less than 0.001) than “central” RPE after beta-blockade in both submaximal and maximal exercise. During normal condition this difference did not appear. Changes in both local and central RPE during submaximal exercise were positively correlated to changes in O2 uptake. Individual variations in the metabolic profile of the exercising muscle had no influence on beta-blockade-induced changes in O2 uptake. It is concluded that blockade of beta-adrenergic receptors reduces O2 consumption during submaximal (approximately 73% maximal O2 uptake) and maximal exercise in habitually trained men.

Bicarbonate attenuates arterial desaturation during maximal exercise in humans

2002 ◽  
Vol 93 (2) ◽  
pp. 724-731 ◽  
Author(s):  
Henning B. Nielsen ◽  
Per P. Bredmose ◽  
Morten Strømstad ◽  
Stefanos Volianitis ◽  
Bjørn Quistorff ◽  
...  
Keyword(s):  
Near Infrared ◽  
Maximal Exercise ◽  
Pulmonary Ventilation ◽  
Constant Infusion ◽  
Blood Temperature ◽  
Arterial Desaturation ◽  
The Difference ◽  
Exercise Induced ◽  
End Tidal ◽  
Exercise In Humans

The contribution of pH to exercise-induced arterial O2 desaturation was evaluated by intravenous infusion of sodium bicarbonate (Bic, 1 M; 200–350 ml) or an equal volume of saline (Sal; 1 M) at a constant infusion rate during a “2,000-m” maximal ergometer row in five male oarsmen. Blood-gas variables were corrected to the increase in blood temperature from 36.5 ± 0.3 to 38.9 ± 0.1°C ( P < 0.05; means ± SE), which was established in a pilot study. During Sal exercise, pH decreased from 7.42 ± 0.01 at rest to 7.07 ± 0.02 but only to 7.34 ± 0.02 ( P < 0.05) during the Bic trial. Arterial Po 2 was reduced from 103.1 ± 0.7 to 88.2 ± 1.3 Torr during exercise with Sal, and this reduction was not significantly affected by Bic. Arterial O2 saturation was 97.5 ± 0.2% at rest and decreased to 89.0 ± 0.7% during Sal exercise but only to 94.1 ± 1% with Bic ( P < 0.05). Arterial Pco 2 was not significantly changed from resting values in the last minute of Sal exercise, but in the Bic trial it increased from 40.5 ± 0.5 to 45.9 ± 2.0 Torr ( P < 0.05). Pulmonary ventilation was lowered during exercise with Bic (155 ± 14 vs. 142 ± 13 l/min; P < 0.05), but the exercise-induced increase in the difference between the end-tidal O2 pressure and arterial Po 2 was similar in the two trials. Also, pulmonary O2 uptake and changes in muscle oxygenation as determined by near-infrared spectrophotometry during exercise were similar. The enlarged blood-buffering capacity after infusion of Bic attenuated acidosis and in turn arterial desaturation during maximal exercise.

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.

Ventilatory response to inspired CO2 in normal and carotid body-denervated ponies

1982 ◽  
Vol 52 (6) ◽  
pp. 1614-1622 ◽  
Author(s):  
J. P. Klein ◽  
H. V. Forster ◽  
G. E. Bisgard ◽  
R. P. Kaminski ◽  
L. G. Pan ◽  
...  
Keyword(s):  
Partial Pressure ◽  
Carotid Body ◽  
Ventilatory Response ◽  
Pulmonary Ventilation ◽  
Control Period ◽  
Experimental Period ◽  
Co2 Partial Pressure ◽  
Arterial Blood ◽  
Arterial Ph ◽  
Insight Into

The purpose of these studies was to gain insight into mechanisms regulating pulmonary ventilation (VE), arterial CO2 partial pressure (PaCO2), and arterial pH (pHa) in ponies when inspired CO2 partial pressure (PICO2) is above normal. Ponies were studied four times daily each weekday for 2 wk in an environmental chamber. Each study consisted of a 15-min control period (PICO2 = 0.7 Torr) followed by a 15- to 30-min experimental period during which PICO2 in the chamber was 0.7, 7, 14, 21, 28, or 42 Torr (PIO2 = 147 Torr throughout). Between 11 and 15 min of each period, four 3-ml samples of arterial blood were drawn, each over 45 s. In 12 normal ponies, elevation of PICO2 to 7 Torr caused PaCO2 to increase approximately 0.4 Torr (P less than 0.01) and pHa to decrease approximately 0.003 (P less than 0.02) relative to control. The hypercapnia and acidosis increased progressively as PICO2 was increased in 7- to 14-Torr increments to 42 Torr (P less than 0.02). Accordingly, the hyperpnea in these ponies during CO2 inhalation could have been mediated by carotid and intracranial chemoreceptors. One month after carotid body denervation (CBD) in nine ponies, PaCO2 during control conditions was 6 Torr above normal, but during CO2 inhalation, PaCO2 changed less from control than during CO2 inhalation before CBD (P less than 0.01). The delta VE/ delta PaCO2 near eupneic PaCO2 appeared to be above normal 1 mo after CBD (P less than 0.01). The mechanism of this increase was not discernible from our data. Finally, our data indicated that the magnitude of the hypercapnia and acidosis during CO2 inhalation was inversely related to PaCO2 and breathing frequency during control conditions.

Increased arterial desaturation in trained cyclists during maximal exercise at 580 m altitude

1996 ◽  
Vol 80 (6) ◽  
pp. 2204-2210 ◽  
Author(s):  
C. J. Gore ◽  
A. G. Hahn ◽  
G. C. Scroop ◽  
D. B. Watson ◽  
K. I. Norton ◽  
...  
Keyword(s):  
Sea Level ◽  
Maximal Exercise ◽  
O2 Consumption ◽  
Arterial Desaturation ◽  
Hypobaric Chamber ◽  
Group Data ◽  
Arterial O2 Saturation ◽  
Arterial Po2 ◽  
Similar Decrease

This study utilized a hypobaric chamber to compare the effects of mild hypobaria (MH; 50 mmHg, approximately 580 m altitude) on blood O2 status and maximal O2 consumption (VO2max) in 9 untrained and 11 trained (T) cyclists with VO2max values of 51 +/- 3 and 77 +/- 1 ml.kg-1.min-1, respectively. In both groups, arterial O2 saturation (SaO2) decreased significantly during maximal exercise, and this effect was enhanced with MH. Both these responses were significantly greater in the T cyclists in whom the final SaO2 during MH was 86.5 +/- 0.9%. When the group data were combined, approximately 65% of the variance in SaO2 could be attributed to a widened alveolar-arterial Po2 difference. The arterial PO2 during maximal exercise at sea level in the T group was on the steeper portion of the hemoglobin-O2-loading curve (T, 68.3 +/- 1.3 Torr; untrained, 89.0 +/- 2.9 Torr) such that a similar decrease in arterial PO2 in the two groups in response to MH resulted in a significantly greater fall in both SaO2 and calculated O2 content in the T group. As a consequence, the VO2max fell significantly only in the T group (mean change, -6.8 +/- 1.5%; range, + 1.2 to - 12.3%), with approximately 70% of this decrease being due to a fall in O2 content. This is the lowest altitude reported to decrease VO2max, suggesting that T athletes are more susceptible to a fall in inspired PO2.

Pulmonary mechanisms and work of breathing at maximal ventilation and raised air pressure

1981 ◽  
Vol 50 (4) ◽  
pp. 747-753 ◽  
Author(s):  
C. M. Hesser ◽  
D. Linnarsson ◽  
L. Fagraeus
Keyword(s):  
Maximal Exercise ◽  
Work Of Breathing ◽  
Pulmonary Ventilation ◽  
Transpulmonary Pressure ◽  
Air Pressure ◽  
Lung Volumes ◽  
Gas Density ◽  
Peak Flows ◽  
Inspiratory Muscles ◽  
Exercise Ventilation

Pulmonary ventilation (V) and the interrelationships of airflow, transpulmonary pressure, and lung volume during inspiration and expiration were studied in eight healthy subjects who performed maximal exercise (MEx; 140% VO2 max), 15-s maximal voluntary ventilation (MVV), and forced inspiratory and expiratory vital capacity (FVC) maneuvers at 1, 3, and 6 ATA. Maximal exercise ventilation and MVV amounted to 149 +/- 7 (mean +/- SE) and 193 +/- 9 l . min-1, respectively, at 1 ATA and were both reduced by approximately 37% at 3 ATA and by 50% at 6 ATA. Expiratory peak flows during MEx and MVV were equal to the maximal flows obtained during FVC at comparable lung volumes, whereas inspiratory peak flows during MEx were 20% less than the FVC flows. Despite a sixfold increase in gas density, the rate of mechanical work of breathing decreased when the pressure was raised to 6 ATA, during MEx from 8 +/- 1 to 6 +/- 1 W, and during MVV from 28 +/- 5 to 18 +/- 3 W. With increasing gas density there was a shift of lung volumes in the inspiratory direction with consequent reductions of inspiratory-to-expiratory flow ratios. We conclude that depletion of energy stores in the inspiratory muscles contributed to limiting V during MEx at raised air pressure.

Ventilatory Response to Exercise and to Co2 Rebreathing in Normal Subjects

1972 ◽  
Vol 43 (6) ◽  
pp. 861-867 ◽  
Author(s):  
A. S. Rebuck ◽  
N. L. Jones ◽  
E. J. M. Campbell
Keyword(s):  
Carbon Dioxide ◽  
Ventilatory Response ◽  
Normal Subjects ◽  
O2 Uptake ◽  
Co2 Output ◽  
Exercise Ventilation ◽  
Progressive Exercise ◽  
Response To Exercise ◽  
Rebreathing Method ◽  
Ventilatory Response To Co2

1. Changes in ventilation during progressive exercise were measured in eleven normal subjects. Ventilatory response to carbon dioxide at rest was measured in the same subjects using a rebreathing method. 2. The range of ventilatory response to exercise was 16·6–32·0 litres min−1 (litres CO2 min−1)−1 (mean 22·7; SD 5·35); response to O2 uptake was 17·0–43·9 litres min−1 (litres O2 min−1)−1 (mean 29·02; SD 9·07). Ventilatory response to CO2 (Sco2) ranged from 0·81 to 3·22 litre min−1 mmHg−1 (mean 1·87; SD 0·62). 3. There was a highly significant (P < 0·001) correlation between the changes in response to increasing CO2 output or O2 uptake, and Sco2. 4. The results are compatible with the suggestion that ventilation during exercise in normal subjects is directly related to their chemosensitivity to CO2, those having the highest sensitivity showing the greatest exercise ventilation.

Ventilatory effects of hypoxia and adenosine infusion in patients after bilateral carotid endarterectomy

1990 ◽  
Vol 78 (1) ◽  
pp. 25-31 ◽  
Author(s):  
T. L. Griffiths ◽  
S. J. Warren ◽  
A. D. B. Chant ◽  
S. T. Holgate
Keyword(s):  
Carotid Endarterectomy ◽  
Ventilatory Response ◽  
Adenosine Infusion ◽  
Respiratory Drive ◽  
Stimulant Effect ◽  
Carotid Bodies ◽  
Ventilatory Drive ◽  
Bilateral Carotid ◽  
Respiratory Stimulant ◽  
Ventilatory Effects

1. We have studied the carotid body contribution to hypoxic respiratory drive, using a hypoxic/hyperoxic switching technique, and the ventilatory response to intravenous infusion of adenosine, a recently described respiratory stimulant, in five patients with bilateral carotid endarterectomy. 2. The contribution made by the carotid bodies to total ventilatory drive during hypoxia varied from 2.5% to 45.9%. 3. The ventilatory response to adenosine infusion varied from a 7% decrease to a 25% increase in ventilation. 4. Those patients with intact hypoxic ventilatory drive showed respiratory stimulation, whereas of the two patients with attenuated chemoreflexes, one showed no stimulation and the other depression of ventilation in response to adenosine infusion. 5. We conclude that adenosine exerts its respiratory stimulant effect via an action on the peripheral chemoreceptors. This may coexist with a centrally mediated respiratory depression that is masked when the carotid bodies are intact.

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