Short-term modulation of the exercise ventilatory response in young men

2008 ◽  
Vol 104 (1) ◽  
pp. 244-252 ◽  
Author(s):  
Helen E. Wood ◽  
Gordon S. Mitchell ◽  
Tony G. Babb
Keyword(s):  
Dead Space ◽  
Animal Studies ◽  
Ventilatory Response ◽  
Young Men ◽  
Neural Mechanism ◽  
Short Term ◽  
Response Slope ◽  
Ventilatory Drive ◽  
End Tidal ◽  
Exercise In Humans

Arterial isocapnia is a hallmark of moderate exercise in humans and is maintained even when resting arterial Pco2 (PaCO2) is raised or lowered from its normal level, e.g., with chronic acid-base changes or acute increases in respiratory dead space. When resting ventilation and/or PaCO2 are altered, maintenance of isocapnia requires active adjustments of the exercise ventilatory response [slope of the ventilation (V̇e)-CO2 production (V̇co2) relationship, ΔV̇e/ΔV̇co2]. On the basis of animal studies, it has been proposed that a central neural mechanism links the exercise ventilatory response to the resting ventilatory drive without need for changes in chemoreceptor feedback from rest to exercise, a mechanism referred to as short-term modulation (STM). We tested the hypothesis that STM is elicited by increased resting ventilatory drive associated with added external dead space (DS) in humans. Twelve young men were studied in control conditions and with added DS (200, 400, and 600 ml; randomized) at rest and during mild-to-moderate cycle exercise. ΔV̇e/ΔV̇co2 increased progressively as DS volume increased ( P < 0.0001). While resting end-tidal Pco2 (PetCO2) increased with DS, the change in PetCO2 from rest to exercise was not increased, indicating that increased chemoreceptor feedback from rest to exercise cannot account for the greater exercise ventilatory response. We conclude that STM of the exercise ventilatory response is induced in young men when resting ventilatory drive is increased with external DS, confirming the existence of STM in humans.

An assessment of nasal functions in control of breathing

1988 ◽  
Vol 65 (4) ◽  
pp. 1520-1524 ◽  
Author(s):  
Y. Tanaka ◽  
T. Morikawa ◽  
Y. Honda
Keyword(s):  
Steady State ◽  
Dead Space ◽  
Airway Resistance ◽  
Breathing Pattern ◽  
Ventilatory Response ◽  
Control Of Breathing ◽  
Mouth Breathing ◽  
Occlusion Pressure ◽  
Ventilatory Responses ◽  
End Tidal

Breathing pattern and steady-state CO2 ventilatory response during mouth breathing were compared with those during nose breathing in nine healthy adults. In addition, the effect of warming and humidification of the inspired air on the ventilatory response was observed during breathing through a mouthpiece. We found the following. 1) Dead space and airway resistance were significantly greater during nose than during mouth breathing. 2) The slope of CO2 ventilatory responses did not differ appreciably during the two types of breathing, but CO2 occlusion pressure response was significantly enhanced during nose breathing. 3) Inhalation of warm and humid air through a mouthpiece significantly depressed CO2 ventilation and occlusion pressure responses. These results fit our observation that end-tidal PCO2 was significantly higher during nose than during mouth breathing. It is suggested that a loss of nasal functions, such as during nasal obstruction, may result in lowering of CO2, fostering apneic spells during sleep.

Repeated exercise paired with “imperceptible” dead space loading does not alter V˙e of subsequent exercise in humans

2002 ◽  
Vol 92 (3) ◽  
pp. 1159-1168 ◽  
Author(s):  
S. H. Moosavi ◽  
A. Guz ◽  
L. Adams
Keyword(s):  
Associative Learning ◽  
Dead Space ◽  
Breathing Circuit ◽  
Conditioning Session ◽  
Repeated Exercise ◽  
Session Type ◽  
End Tidal ◽  
Response To Exercise ◽  
Exercise In Humans ◽  
Test Control

We employed an associative learning paradigm to test the hypothesis that exercise hyperpnea in humans arises from learned responses forged by prior experience. Twelve subjects undertook a “conditioning” and a “nonconditioning” session on separate days, with order of performance counterbalanced among subjects. In both sessions, subjects performed repeated bouts of 6 min of treadmill exercise, each separated by 5 min of rest. The only difference between sessions was that all the second-to-penultimate runs of the conditioning session were performed with added dead space in the breathing circuit. Cardiorespiratory responses during the first and last runs (the “control” and “test” runs) were compared for each session. Steady-state exercise end-tidal Pco 2 was significantly lower ( P= 0.003) during test than during control runs for both sessions (dropping by 1.8 ± 2 and 1.4 ± 3 Torr during conditioning and nonconditioning sessions, respectively). This and all other test-control run differences tended to be greater during the first session performed regardless of session type. Our data provide no support for the hypothesis implicating associative learning processes in the ventilatory response to exercise in humans.

Peripheral chemoreceptor function after carbonic anhydrase inhibition during moderate-intensity exercise

1999 ◽  
Vol 86 (5) ◽  
pp. 1544-1551 ◽  
Author(s):  
Barry W. Scheuermann ◽  
John M. Kowalchuk ◽  
Donald H. Paterson ◽  
David A. Cunningham
Keyword(s):  
Steady State ◽  
Carbonic Anhydrase ◽  
Ventilatory Threshold ◽  
Ventilatory Response ◽  
Moderate Intensity ◽  
Moderate Intensity Exercise ◽  
Peripheral Chemoreceptor ◽  
Ventilatory Drive ◽  
Carbonic Anhydrase Inhibition ◽  
End Tidal

The effect of carbonic anhydrase inhibition with acetazolamide (Acz, 10 mg/kg) on the ventilatory response to an abrupt switch into hyperoxia (end-tidal [Formula: see text]= 450 Torr) and hypoxia (end-tidal[Formula: see text] = 50 Torr) was examined in five male subjects [30 ± 3 (SE) yr]. Subjects exercised at a work rate chosen to elicit an O2 uptake equivalent to 80% of the ventilatory threshold. Ventilation (V˙e) was measured breath by breath. Arterial oxyhemoglobin saturation (%[Formula: see text]) was determined by ear oximetry. After the switch into hyperoxia, V˙eremained unchanged from the steady-state exercise prehyperoxic value (60.6 ± 6.5 l/min) during Acz. During control studies (Con),V˙e decreased from the prehyperoxic value (52.4 ± 5.5 l/min) by ∼20% (V˙enadir = 42.4 ± 6.3 l/min) within 20 s after the switch into hyperoxia. V˙e increased during Acz and Con after the switch into hypoxia; the hypoxic ventilatory response was significantly lower after Acz compared with Con [Acz, change (Δ) inV˙e/[Formula: see text]= 1.54 ± 0.10 l ⋅ min−1 ⋅ [Formula: see text] −1; Con, ΔV˙e/[Formula: see text]= 2.22 ± 0.28 l ⋅ min−1 ⋅ [Formula: see text] −1]. The peripheral chemoreceptor contribution to the ventilatory drive after acute Acz-induced carbonic anhydrase inhibition is not apparent in the steady state of moderate-intensity exercise. However, Acz administration did not completely attenuate the peripheral chemoreceptor response to hypoxia.

Effects of a 1-yr stay at altitude on ventilation, metabolism, and work capacity

1992 ◽  
Vol 73 (5) ◽  
pp. 1749-1755 ◽  
Author(s):  
T. V. Serebrovskaya ◽  
A. A. Ivashkevich
Keyword(s):  
High Altitude ◽  
Sea Level ◽  
Ventilatory Response ◽  
Second Phase ◽  
Separate Analysis ◽  
Group Iii ◽  
Group I ◽  
Ventilatory Drive ◽  
Group Ii ◽  
End Tidal

The hypoxic and hypercapnic ventilatory drive, gas exchange, blood lactate and pyruvate concentrations, acid-base balance, and physical working capacity were determined in three groups of healthy males: 17 residents examined at sea level (group I), 24 sea-level natives residing at 1,680-m altitude for 1 yr and examined there (group II), and 17 sea-level natives residing at 3,650-m altitude for 1 yr and examined there (group III). The piecewise linear approximation technique was used to study the ventilatory response curves, which allowed a separate analysis of slopes during the first phase of slow increase in ventilation and the second phase of sharp increase. The hypoxic ventilatory response for both isocapnic and poikilocapnic conditions was greater in group II and even greater in group III. The first signs of consciousness distortion in sea-level residents appeared at an end-tidal O2 pressure level (4.09 +/- 0.56 kPa) higher than that of temporary residents of middle (3.05 +/- 0.12) and high altitude (2.90 +/- 0.07). The hypercapnic response was also increased, although to a lesser degree. Subjects with the highest hypoxic respiratory sensitivity at high altitude demonstrated greater O2 consumption at rest, greater ventilatory response to exercise, higher physical capacity, and a less pronounced anaerobic glycolytic flux but a lower tolerance to extreme hypoxia. That is, end-tidal O2 pressure that caused a distortion of the consciousness was higher in these subjects than in those with lower hypoxic sensitivity. Two extreme types of adaptation strategy can be distinguished: active, with marked reactions of “struggle for oxygen,” and passive, with reduced O2 metabolism, as well as several intermediate types.(ABSTRACT TRUNCATED AT 250 WORDS)

Augmented hypoxic ventilatory response in men at altitude

1992 ◽  
Vol 73 (1) ◽  
pp. 101-107 ◽  
Author(s):  
M. Sato ◽  
J. W. Severinghaus ◽  
F. L. Powell ◽  
F. D. Xu ◽  
M. J. Spellman
Keyword(s):  
Sea Level ◽  
Ventilatory Response ◽  
Hypoxic Ventilatory Response ◽  
Co2 Response ◽  
Altitude Exposure ◽  
Arterial Ph ◽  
Ventilatory Drive ◽  
Normal Males ◽  
End Tidal ◽  
Arterial O2 Saturation

To test the hypothesis that the hypoxic ventilatory response (HVR) of an individual is a constant unaffected by acclimatization, isocapnic 5-min step HVR, as delta VI/delta SaO2 (l.min-1.%-1, where VI is inspired ventilation and SaO2 is arterial O2 saturation), was tested in six normal males at sea level (SL), after 1–5 days at 3,810-m altitude (AL1-3), and three times over 1 wk after altitude exposure (PAL1-3). Equal medullary central ventilatory drive was sought at both altitudes by testing HVR after greater than 15 min of hyperoxia to eliminate possible ambient hypoxic ventilatory depression (HVD), choosing for isocapnia a P′CO2 (end tidal) elevated sufficiently to drive hyperoxic VI to 140 ml.kg-1.min-1. Mean P′CO2 was 45.4 +/- 1.7 Torr at SL and 33.3 +/- 1.8 Torr on AL3, compared with the respective resting control end-tidal PCO2 of 42.3 +/- 2.0 and 30.8 +/- 2.6 Torr. SL HVR of 0.91 +/- 0.38 was unchanged on AL1 (30 +/- 18 h) at 1.04 +/- 0.37 but rose (P less than 0.05) to 1.27 +/- 0.57 on AL2 (3.2 +/- 0.8 days) and 1.46 +/- 0.59 on AL3 (4.8 +/- 0.4 days) and remained high on PAL1 at 1.44 +/- 0.54 and PAL2 at 1.37 +/- 0.78 but not on PAL3 (days 4–7). HVR was independent of test SaO2 (range 60–90%). Hyperoxic HCVR (CO2 response) was increased on AL3 and PAL1. Arterial pH at congruent to 65% SaO2 was 7.378 +/- 0.019 at SL, 7.44 +/- 0.018 on AL2, and 7.412 +/- 0.023 on AL3.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Short-term modulation of the exercise ventilatory response in goats: effects of 8-OH-DPAT and MPPI

2000 ◽  
Vol 279 (5) ◽  
pp. R1880-R1888 ◽  
Author(s):  
Daniel R. Henderson ◽  
Gordon S. Mitchell
Keyword(s):  
Dead Space ◽  
Ventilatory Response ◽  
Short Term ◽  
Measured Variable ◽  
Arterial Blood Gas ◽  
Arterial Blood ◽  
Nonspecific Effects ◽  
Before And After ◽  
Gas Measurements ◽  
Dependent Mechanism

Increased respiratory dead space increases the exercise ventilatory response, a response known as short-term modulation (STM). We hypothesized that STM results from a spinal, serotonin (5-HT)-dependent mechanism. Because 5-HT1A autoreceptors on caudal brain stem raphe neurons inhibit 5-HT release, we hypothesized that 5-HT1A-receptor agonists would inhibit, whereas 5-HT1A-receptor antagonists would enhance, STM. Ventilatory and arterial blood-gas measurements were made at rest and during exercise (4.0–4.5 km/h, 5% grade) in goats with the respiratory mask alone or with increased dead space (0.20–0.25 liter), before and after intravenous administration of the 5-HT1A-receptor agonist 8-hydroxy-2-(di- n-propylamino)tetralin (8-OH-DPAT; 0.1 mg/kg) or the antagonist 4-iodo- N-{2-[4-(methoxyphenyl)-1-piperazinyl]ethyl}- N-2-pyridinylbenzamide (MPPI; 0.08 mg/kg). 8-OH-DPAT increased the slope of the arterial Pco 2 vs. metabolic CO2production relationship and decreased the ventilation vs. metabolic CO2 production relationship during exercise with increased dead space (not with the mask alone), indicating an impairment of STM. In contrast, MPPI had minimal effects on any measured variable. Although nonspecific effects of 8-OH-DPAT cannot be ruled out, impaired STM is consistent with the hypothesis that STM requires active raphe serotonergic neurons and 5-HT release.

Effect of hypercapnia on hypoxic ventilatory drive in carotid body-resected man

1978 ◽  
Vol 45 (6) ◽  
pp. 971-977 ◽  
Author(s):  
George D. Swanson ◽  
Brian J. Whipp ◽  
Robert D. Kaufman ◽  
Kamel A. Aqleh ◽  
Benjamin Winter ◽  
...  
Keyword(s):  
Carotid Body ◽  
Ventilatory Response ◽  
Normal Subjects ◽  
Hypoxic Ventilatory Response ◽  
Small Component ◽  
Ventilatory Drive ◽  
End Tidal ◽  
End Tidal Co2 ◽  
Ventilatory Response To Hypoxia

Steplike end-tidal hypoxic drives (Petcoco2, = 53 Torr) lasting for 5 min were generated in a group of normal subjects and a group of carotid body-resected subjects when end-tidal CO2, was maintained constant under eucapnic (Petcoco2 = 39 Torr) and hypercapnic (Petcoco2 = 49 Torr) conditions. The hypoxic ventilatory response of the normal subjects was prompt and significant in eucapnia and was enhanced in the hypercapnic state, evidencing CO2-O2 interaction. In contrast, the carotid body-resected subjects did not respond to eucapnic hypoxia but did demonstrate a small but significant ventilatory response to hypoxia against the hypercapnic background. This suggests that the aortic bodies in man may contribute a small component of the hypoxic ventilatory drive under hypercapnic conditions, although the possibility of neuromalike ending regeneration cannot be excluded.

Dynamic response of peripheral chemoreflex loop to changes in end-tidal CO2

1988 ◽  
Vol 64 (5) ◽  
pp. 1779-1785 ◽  
Author(s):  
A. Berkenbosch ◽  
J. DeGoede ◽  
D. S. Ward ◽  
C. N. Olievier ◽  
J. VanHartevelt
Keyword(s):  
Time Delay ◽  
Ventilatory Response ◽  
Neural Mechanism ◽  
Artificial Brain ◽  
End Tidal ◽  
Alpha Chloralose ◽  
Peripheral Chemoreflex ◽  
Mean Time ◽  
Arterial Po2 ◽  
End Tidal Co2

The dynamic ventilatory response of the peripheral chemoreflex loop after isoxic step changes in end-tidal PCO2 (PETCO2) (range 5–30 Torr) was studied in 12 alpha-chloralose-urethan-anesthetized cats. The technique of artificial brain stem perfusion allowed the response to be observed in isolation from the central chemoreflex loop. The data were fitted by an exponential with time delay. During normoxia the mean time constant and time delay (with SD) were 8.6 +/- 7.3 and 3.3 +/- 0.9 s, respectively (9 cats, 56 runs). During hypoxia [arterial PO2 (PaO2) approximately 60 Torr] these values were 6.0 +/- 4.5 and 2.9 +/- 0.9 s (6 cats, 38 runs). In 17 of the 94 runs an augmented breath occurred in the first three breaths after the stepwise increase in PETCO2. For these augmented breaths, tidal volume, inspiratory time, and expiratory time were not different from the next augmented breath occurring in the same run in the steady state. Neither a rate-sensitive component nor a central neural mechanism (central afterdischarge), with the property of maintaining an increased but slowly declining respiratory activity for some minutes after cessation of the PETCO2 challenge, was found. We conclude that the description of the ventilatory response of the peripheral chemoreflex loop to step changes in PETCO2 with a single exponential and time delay is adequate.

scholarly journals Ventilatory response to exercise in cardiopulmonary disease: the role of chemosensitivity and dead space

2018 ◽  
Vol 51 (2) ◽  
pp. 1700860 ◽  
Author(s):  
Jason Weatherald ◽  
Caroline Sattler ◽  
Gilles Garcia ◽  
Pierantonio Laveneziana
Keyword(s):  
Gas Exchange ◽  
Partial Pressure ◽  
Dead Space ◽  
Ventilatory Response ◽  
Heart Function ◽  
Cardiopulmonary Exercise Testing ◽  
Cardiopulmonary Disease ◽  
The Difference ◽  
End Tidal ◽  
Response To Exercise

The lungs and heart are irrevocably linked in their oxygen (O2) and carbon dioxide (CO2) transport functions. Functional impairment of the lungs often affects heart function andvice versa. The steepness with which ventilation (V′E) rises with respect to CO2production (V′CO2) (i.e.theV′E/V′CO2slope) is a measure of ventilatory efficiency and can be used to identify an abnormal ventilatory response to exercise. TheV′E/V′CO2slope is a prognostic marker in several chronic cardiopulmonary diseases independent of other exercise-related variables such as peak O2uptake (V′O2). TheV′E/V′CO2slope is determined by two factors: 1) the arterial CO2partial pressure (PaCO2) during exercise and 2) the fraction of the tidal volume (VT) that goes to dead space (VD) (i.e.the physiological dead space ratio (VD/VT)). An alteredPaCO2set-point and chemosensitivity are present in many cardiopulmonary diseases, which influenceV′E/V′CO2by affectingPaCO2. Increased ventilation–perfusion heterogeneity, causing inefficient gas exchange, also contributes to the abnormalV′E/V′CO2observed in cardiopulmonary diseases by increasingVD/VT. During cardiopulmonary exercise testing, thePaCO2during exercise is often not measured andVD/VTis only estimated by taking into account the end-tidal CO2partial pressure (PETCO2); however,PaCO2is not accurately estimated fromPETCO2in patients with cardiopulmonary disease. Measuring arterial gases (PaO2andPaCO2) before and during exercise provides information on the real (and not “estimated”)VD/VTcoupled with a true measure of gas exchange efficiency such as the difference between alveolar and arterial O2partial pressure and the difference between arterial and end-tidal CO2partial pressure during exercise.

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