scholarly journals Ventilatory efficiency in athletes, asthma and obesity

2021 ◽  
Vol 30 (161) ◽  
pp. 200206
Author(s):  
Sophie É. Collins ◽  
Devin B. Phillips ◽  
Andrew R. Brotto ◽  
Zahrah H. Rampuri ◽  
Michael K. Stickland
Keyword(s):  
Minute Ventilation ◽  
Carbon Dioxide Production ◽  
Submaximal Exercise ◽  
Endurance Athletes ◽  
Morbidly Obese ◽  
Arterial Blood Gas ◽  
Ventilatory Efficiency ◽  
Ventilatory Responses ◽  
Arterial Blood ◽  
Exercise Induced

During submaximal exercise, minute ventilation (V′E) increases in proportion to metabolic rate (i.e. carbon dioxide production (V′CO2)) to maintain arterial blood gas homeostasis. The ratio V′E/V′CO2, commonly termed ventilatory efficiency, is a useful tool to evaluate exercise responses in healthy individuals and patients with chronic disease. Emerging research has shown abnormal ventilatory responses to exercise (either elevated or blunted V′E/V′CO2) in some chronic respiratory and cardiovascular conditions. This review will briefly provide an overview of the physiology of ventilatory efficiency, before describing the ventilatory responses to exercise in healthy trained endurance athletes, patients with asthma, and patients with obesity. During submaximal exercise, the V′E/V′CO2 response is generally normal in endurance-trained individuals, patients with asthma and patients with obesity. However, in endurance-trained individuals, asthmatics who demonstrate exercise induced-bronchoconstriction, and morbidly obese individuals, the V′E/V′CO2 can be blunted at maximal exercise, likely because of mechanical ventilatory constraint.

Ventilatory responses of hamsters and rats to hypoxia and hypercapnia

1985 ◽  
Vol 59 (6) ◽  
pp. 1955-1960 ◽  
Author(s):  
B. R. Walker ◽  
E. M. Adams ◽  
N. F. Voelkel
Keyword(s):  
Duty Cycle ◽  
Minute Ventilation ◽  
Natural Habitat ◽  
Blood Gases ◽  
Atmospheric Conditions ◽  
Arterial Blood Gases ◽  
Ventilatory Responses ◽  
Arterial Blood ◽  
Rat Experiments ◽  
Fossorial Species

As a fossorial species the hamster differs in its natural habitat from the rat. Experiments were performed to determine possible differences between the ventilatory responses of awake hamsters and rats to acute exposure to hypoxic and hypercapnic environments. Ventilation was measured with the barometric method while the animals were conscious and unrestrained in a sealed plethysmograph. Tidal volume (VT), respiratory frequency (f), and inspiratory (TI) and expiratory (TE) time measurements were made while the animals breathed normoxic (30% O2), hypercapnic (5% CO2), or hypoxic (10% O2) gases. Arterial blood gases were also measured in both species while exposed to each of these atmospheric conditions. During inhalation of normoxic gas, the VT/100 g was greater and f was lower in the hamster than in the rat. Overall minute ventilation (VE/100 g) in the hamster was less than in the rat, which was reflected in the lower PO2 and higher PCO2 of the hamster arterial blood. When exposed to hypercapnia, the hamster increased VE/100 g solely through VT; however, the VE/100 g increase was significantly less than in the rat. In response to hypoxia, the hamster and rat increased VE/100 g by similar amounts; however, the hamster VE/100 g increase was through f alone, whereas the rat increased both VT/100 g and f. Mean airflow rates (VT/TI) were no different in the hamster or rat in each gas environment; therefore most of the ventilatory responses were the result of changes in TI and TE and respiratory duty cycle (TI/TT).

Potassium as a respiratory signal in humans

1990 ◽  
Vol 69 (5) ◽  
pp. 1799-1803 ◽  
Author(s):  
C. G. Newstead ◽  
G. C. Donaldson ◽  
J. R. Sneyd
Keyword(s):  
Minute Ventilation ◽  
Blood Chemistry ◽  
Carbon Dioxide Production ◽  
Renal Transplant Recipients ◽  
Transplant Recipients ◽  
Arterial Blood ◽  
Respiratory Signal ◽  
Carbon Dioxide Production Rate ◽  
The Relationship ◽  
Resting Muscle

Six renal transplant recipients underwent a series of incremental exercise experiments. Minute ventilation (VE), carbon dioxide production rate (VCO2), and arterial blood chemistry were measured at rest and while subjects exercised on a stationary bicycle. Four of the subjects performed a similar experiment while exercising on a static rowing machine. Within each subject, arterial potassium concentration ([K+]a) was linearly related to VCO2 and VE during exercise. The slope of the relationship between [K+]a and VCO2 was similar in the cycling and rowing experiments. This implies that the absorption of potassium by resting muscle does not significantly limit the arterial hyperkalemia seen during exercise. When VE, VCO2, and [K+]a were measured 1 and 5 min after the end of cycling there was no correlation, whereas VE continued to be closely correlated with VCO2. The relationship demonstrated between change in [K+]a and VCO2 in these experiments is compatible with change of [K+]a acting as a respiratory signal during exercise but not during recovery from exercise in humans.

Ventilatory response to moderate and severe hypoxia in adult dogs: role of endorphins

1988 ◽  
Vol 65 (3) ◽  
pp. 1383-1388 ◽  
Author(s):  
J. I. Schaeffer ◽  
G. G. Haddad
Keyword(s):  
Ventilatory Response ◽  
Minute Ventilation ◽  
Severe Hypoxia ◽  
Moderate Hypoxia ◽  
Arterial Blood Gas ◽  
Arterial Blood ◽  
Before And After ◽  
The Relationship ◽  
Arterial Po2

To determine the role of opioids in modulating the ventilatory response to moderate or severe hypoxia, we studied ventilation in six chronically instrumented awake adult dogs during hypoxia before and after naloxone administration. Parenteral naloxone (200 micrograms/kg) significantly increased instantaneous minute ventilation (VT/TT) during severe hypoxia, (inspired O2 fraction = 0.07, arterial PO2 = 28-35 Torr); however, consistent effects during moderate hypoxia (inspired O2 fraction = 0.12, arterial PO2 = 40-47 Torr) could not be demonstrated. Parenteral naloxone increased O2 consumption (VO2) in severe hypoxia as well. Despite significant increases in ventilation post-naloxone during severe hypoxia, arterial blood gas tensions remained the same. Control studies revealed that neither saline nor naloxone produced a respiratory effect during normoxia; also the preservative vehicle of naloxone induced no change in ventilation during severe hypoxia. These data suggest that, in adult dogs, endorphins are released and act to restrain ventilation during severe hypoxia; the relationship between endorphin release and moderate hypoxia is less consistent. The observed increase in ventilation post-naloxone during severe hypoxia is accompanied by an increase in metabolic rate, explaining the isocapnic response.

Exercise-induced hypoxemia in older athletes

1994 ◽  
Vol 76 (1) ◽  
pp. 120-126 ◽  
Author(s):  
C. Prefaut ◽  
F. Anselme ◽  
C. Caillaud ◽  
J. Masse-Biron
Keyword(s):  
Blood Gases ◽  
Blood Gas Analysis ◽  
Gas Analysis ◽  
Lung Water ◽  
Arterial Blood Gas ◽  
Arterial Blood ◽  
Older Athletes ◽  
Level Of Training ◽  
Exercise Induced ◽  
Arterial Po2

To determine whether exercise induces hypoxemia in highly trained older “master” athletes (MA), as it does in certain elite endurance-trained young athletes (YA), 10 MA (65.3 +/- 2.6 yr), 10 control subjects (CS; 68.3 +/- 2.2 yr), and 10 endurance-trained YA (23.3 +/- 1.1 yr) performed an incremental exercise test. During testing, blood samples for arterial blood gas analysis were drawn during the last 20 s of each load. Lung exchanges were measured using a breath-by-breath automated exercise device. Exercise-induced hypoxemia (EIH) appeared in all MA and 8 of 10 YA, whereas there were no changes in the blood gases of CS. In MA, arterial PO2 decreased significantly from 40% of maximal O2 uptake onward and was associated with a significant increase in the ideal alveolar-arterial O2 difference from 60% onward. The MA also showed a lower ventilation for a given absolute load compared with CS. In all subjects arterial PCO2 rose slightly but significantly during the work, but this increase was most marked in MA. The EIH differed between MA and YA in the following ways: 1) all MA showed a drop in arterial PO2 during exercise, 2) this drop appeared earlier and was significantly greater for a given load in MA, and 3) EIH appeared at a lower level of training regimen in MA. This hypoxemia was at first isolated, probably at least partially due to relative hypoventilation, and then was associated with a widened ideal alveolar-arterial O2 difference, which may have been due to an increase in extravascular lung water.(ABSTRACT TRUNCATED AT 250 WORDS)

Measurement and analysis of gas exchange during exercise using a programmable calculator

1980 ◽  
Vol 49 (3) ◽  
pp. 456-461 ◽  
Author(s):  
D. Y. Sue ◽  
J. E. Hansen ◽  
M. Blais ◽  
K. Wasserman
Keyword(s):  
Gas Exchange ◽  
Respiratory Exchange Ratio ◽  
Minute Ventilation ◽  
Co2 Production ◽  
O2 Consumption ◽  
Exercise Tests ◽  
Programmable Calculator ◽  
Arterial Blood Gas ◽  
Arterial Blood ◽  
End Tidal

Although exercise testing is useful in the diagnosis and management of cardiovascular and pulmonary diseases, a rapid comprehensive method for measurement of ventilation and gas exchange has been limited to expensive complex computer-based systems. We devised a relatively inexpensive, technically simple, and clinically oriented exercise system built around a desktop calculator. This system automatically collects and analyzes data on a breath-by-breath basis. Our calculator system overcomes the potential inaccuracies of gas exchange measurement due to water vapor dilution and mismatching of expired flow and gas concentrations. We found no difference between the calculator-derived minute ventilation, CO2 production, O2 consumption, and respiratory exchange ratio and the values determined from simultaneous mixed expired gas collections in 30 constant-work-rate exercise studies. Both tabular and graphic displays of minute ventilation, CO2 production, O2 consumption, respiratory exchange ratio, heart rate, end-tidal O2 tension, end-tidal CO2 tension, and arterial blood gas value are included for aid in the interpretation of clinical exercise tests.

Effect of metabolic rate on ventilatory roll-off during hypoxia

1994 ◽  
Vol 76 (6) ◽  
pp. 2310-2314 ◽  
Author(s):  
W. M. Gershan ◽  
H. V. Forster ◽  
T. F. Lowry ◽  
M. J. Korducki ◽  
A. L. Forster ◽  
...  
Keyword(s):  
Metabolic Rate ◽  
Minute Ventilation ◽  
Face Mask ◽  
Co2 Production ◽  
O2 Consumption ◽  
Arterial Blood Gas ◽  
Arterial Blood ◽  
Series Of Experiments ◽  
Carotid Arterial ◽  
Arterial Po2

This study was done to determine 1) whether goats demonstrate the roll-off phenomenon, i.e., a secondary decrease in minute ventilation (VE), after an initial hyperventilation during various levels of hypoxia and, if so, 2) whether roll-off could be due to changes in metabolic rate. We hypothesized that roll-off occurs in the goat during hypoxia but is not due to hypometabolism. To answer question 1, eight unanesthetized adult goats were exposed to 15–20 min of hypoxia at 0.15, 0.12, and 0.09 inspired O2 fraction (FIO2), resulting in 60, 40, and 30 Torr arterial PO2, respectively. Goats were fitted with a face mask connected to a spirometer to measure VE, and arterial blood gas samples were obtained via carotid arterial catheters. Roll-off was seen with 0.15 and 0.12 FIO2, whereas VE steadily increased with 0.09 FIO2. During hypoxia, arterial PCO2 fell 2, 3, and 7 Torr at 0.15, 0.12, and 0.09 FIO2, respectively. In the second series of experiments, nine different goats were exposed to 30 min of 0.12 FIO2. O2 consumption and CO2 production were measured five times during baseline and hypoxia. VE increased to 32% above baseline values after 2 min of hypoxia and then gradually decreased by 18%. Changes in breathing frequency and tidal volume contributed to the roll-off. O2 consumption decreased (P = 0.0029, analysis of variance) and CO2 production increased (P = 0.0027) during hypoxia, although both changes were small (< 7%) compared with the eventual 18% decrease in VE. We conclude that the adult goat demonstrates the roll-off phenomenon during moderate levels of hypoxia. (ABSTRACT TRUNCATED AT 250 WORDS)

Ventilatory responses to increased blood flow and decreased lung volume in awake dogs

1988 ◽  
Vol 65 (2) ◽  
pp. 714-720
Author(s):  
E. Chow ◽  
E. J. Cha ◽  
S. M. Yamashiro
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Lung Volume ◽  
Negative Pressure ◽  
Minute Ventilation ◽  
Ventilatory Responses ◽  
Arterial Blood ◽  
Teflon Membrane ◽  
Negative Pressure Breathing ◽  
Significant Change

The effect of decreased lung volume on ventilatory responses to arteriovenous fistula-induced increased cardiac output was studied in four chronic awake dogs. Lung volume decreases were imposed by application of continuous negative-pressure breathing of -10 cmH2O to the trachea. The animals were surgically prepared with chronic tracheostomy, indwelling carotid artery catheter, and bilateral arteriovenous femoral shunts. Control arteriovenous blood flow was 0.5 l/min, and test flow level was 2.0 l/min. Arterial blood CO2 tension (PaCO2) was continuously monitored using an indwelling Teflon membrane mass spectrometer catheter, and inhaled CO2 was given to maintain isocapnia throughout. Increased fistula flow alone led to a mean 52% increase in cardiac output (CO), whereas mean systemic arterial blood pressure (Psa) fell 4% (P less than 0.01). Negative-pressure breathing alone raised Psa by 3% (P less than 0.005) without a significant change in CO. Expired minute ventilation (VE) increased by 27% (P less than 0.005) from control in both of these conditions separately. Combined increased flow and negative pressure led to a 50% increase in CO and 56% increase in VE (P less than 0.0025) without any significant change in Psa. Effects of decreased lung volume and increased CO appeared to be additive with respect to ventilation and to occur under conditions of constant PaCO2 and Psa. Because both decreased lung volume and increased CO occur during normal exercise, these results suggest that mechanisms other than chemical regulation may play an important role in the control of breathing and contribute new insights into the isocapnic exercise hyperpnea phenomenon.

Depression of ventilatory responses after daily, cyclic hypercapnic hypoxia in piglets

2001 ◽  
Vol 90 (3) ◽  
pp. 1065-1073 ◽  
Author(s):  
Karen A. Waters ◽  
Kellie D. Tinworth
Keyword(s):  
Minute Ventilation ◽  
Stimulus Presentation ◽  
Face Mask ◽  
Respiratory Pattern ◽  
Treatment Groups ◽  
Time To Peak ◽  
Ventilatory Responses ◽  
Arterial Blood ◽  
Hypercapnic Hypoxia ◽  
And Control

Ventilatory responses (VRs) were measured via a sealed face mask and pneumotachograph in 30 unsedated, mixed-breed miniature piglets at 12.6 ± 2.3 days of age ( day 1) and then repeated after seven daily 24-min exposures to 10% O2-6% CO2 [hypercapnic hypoxia (HH)]. Arterial blood was sampled at baseline, after 10 min of exposure, and after 10 min of recovery. VRs included hypoxia (10% O2 in N2), hypercapnia (6% CO2 in air), and HH (10% O2-6% CO2-balance N2). Treatment groups ( n = 10 each) were exposed to 24 min of HH from day 2 to 8 as sustained HH (24 min of HH and then 24 min of air) or cyclic HH (4 min of HH alternating with 4 min of air). Day 1 and 9data were compared in treatment and control groups. After cyclic HH, respiratory responses to CO2 were reduced during hypercapnia and during HH ( P < 0.001 vs. control for minute ventilation in both). In both treatment groups, time to peak minute ventilation was delayed in hypoxia ( P = 0.02, ANOVA), and response amplitude was increased ( P < 0.001 and P = 0.003, sustained and cyclic HH, respectively, vs. control). Respiratory pattern was also altered during the VRs and among treatment groups. Stimulus presentation characteristics exert effects on VRs that are independent of those elicited by daily HH.

Changes in arterial blood gas tensions during unsteady-state exercise

1978 ◽  
Vol 44 (1) ◽  
pp. 93-96 ◽  
Author(s):  
I. H. Young ◽  
A. J. Woolcock
Keyword(s):  
Minute Ventilation ◽  
Normal Subjects ◽  
Stair Climbing ◽  
Arterial Oxygen ◽  
Arterial Blood Gas ◽  
Laboratory Exercise ◽  
Arterial Blood ◽  
Rapid Fall ◽  
Subsequent Rise ◽  
Vertical Height

Arterial oxygen (Pao2) and carbon dioxide (Paco2) tensions and inspired minute ventilation were measured during the first 2 min of stair-climbing exercise in nine normal subjects. The subjects climbed a staircase at a rate of approximately 9 m vertical height every minute and arterial blood was drawn from an indwelling cannula at 15-s intervals. Large falls in Pao2 from a resting value of 92 +/- 2.0 (mean +/- SE) Torr to a lowest value of 65 +/- 3.4 Torr were recorded in the first 50 s of exercise while Paco2 oscillated around the resting value. Most subjects demonstrated an initial plateau of Pao2 for at least 7 s followed by a rapid fall and subsequent rise toward the resting level after 1 min. The falls in Pao2 measured were larger than those reported for laboratory exercise. The possible reasons for this discrepancy are discussed.

scholarly journals Effect of positive end-expiratory pressure on additional passive ventilation generated by CPR compressions in a porcine model

2021 ◽  
Vol 9 (1) ◽  
Author(s):  
Yosef Levenbrown ◽  
Md Jobayer Hossain ◽  
James P. Keith ◽  
Katlyn Burr ◽  
Anne Hesek ◽  
...  
Keyword(s):  
Carbon Dioxide ◽  
Cardiopulmonary Resuscitation ◽  
Minute Ventilation ◽  
Positive End Expiratory Pressure ◽  
Arterial Blood Gas ◽  
Volumetric Capnography ◽  
Arterial Blood ◽  
Yorkshire Pigs ◽  
The Mean ◽  
Clinically Significant

Abstract Background Compressions given during cardiopulmonary resuscitation generate small, ineffective passive ventilations through oscillating waves. Positive end-expiratory pressure increases the volume of these passive ventilations; however, its effect on passive ventilation is unknown. Our objective was to determine if increasing positive end-expiratory pressure during cardiopulmonary resuscitation increases passive ventilation generated by compressions to a clinically significant point. This study was conducted on 13 Landrace-Yorkshire pigs. After inducing cardiac arrest with bupivacaine, cardiopulmonary resuscitation was performed with a LUCAS 3.1. During cardiopulmonary resuscitation, pigs were ventilated at a positive end-expiratory pressure of 0, 5, 10, 15, 20 cmH2O (randomly determined) for 9 min. Using the NM3 respiratory monitoring device, expired minute ventilation and volumetric capnography were measured. Arterial blood gas was obtained for each positive end-expiratory pressure level to compare the effects of positive end-expiratory pressure on carbon dioxide. Results Increasing positive end-expiratory pressure from 0 to 20 cmH2O increased the mean (SEM) expired minute ventilation from 6.33 (0.04) to 7.33 (0.04) mL/min. With the 5-cmH2O incremental increases in positive end-expiratory pressure from 0 to 20 cmH2O, volumetric capnography increased from a mean (SEM) of 94.19 (0.78) to 115.18 (0.8) mL/min, except for 15 cmH2O, which showed greater carbon dioxide exhalation with volumetric capnography compared with 20 cmH2O. PCO2 declined significantly as positive end-expiratory pressure was increased from 0 to 20 cmH2O. Conclusions When increasing positive end-expiratory pressure from 0 to 20, the contribution to overall ventilation from gas oscillations generated by the compressions became more significant, and may even lead to hypocapnia, especially when using positive end-expiratory pressures between 15 and 20.

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