Chemical and mechanical adaptations of the respiratory system at rest and during exercise in human pregnancy

2007 ◽  
Vol 32 (6) ◽  
pp. 1239-1250 ◽  
Author(s):  
Dennis Jensen ◽  
Katherine A. Webb ◽  
Denis E. O’Donnell
Keyword(s):  
Respiratory System ◽  
Mechanical Response ◽  
Alternative Hypothesis ◽  
Working Capacity ◽  
Ventilatory Control ◽  
Human Pregnancy ◽  
Female Sex Hormones ◽  
Ventilatory Drive ◽  
Peripheral Chemoreflex ◽  
Aerobic Working Capacity

Human pregnancy is characterized by significant increases in ventilatory drive both at rest and during exercise. The increased ventilation and attendant hypocapnia of pregnancy has been attributed primarily to the stimulatory effects of female sex hormones (progesterone and estrogen) on central and peripheral chemoreflex drives to breathe. However, recent research from our laboratory suggests that hormone-mediated increases in neural (or non-chemoreflex) drives to breathe may contribute importantly to the hyperventilation of pregnancy. This review challenges traditional views of ventilatory control, and outlines an alternative hypothesis of the control of breathing during human pregnancy that is currently being tested in our laboratory. Conventional wisdom suggests that pregnancy-induced increases in central respiratory motor output command in combination with progressive thoraco–abdominal distortion may compromise the normal mechanical response of the respiratory system to exercise, increase the perception of exertional breathlessness, and curtail aerobic exercise performance in otherwise healthy pregnant women. The majority of available evidence suggests, however, that neither pregnancy nor advancing gestation are associated with reduced aerobic working capacity or increased breathlessness at any given work rate or ventilation during exhaustive weight-supported exercise.

Influence of Acute Pain Induced by Activation of Cutaneous Nociceptors on Ventilatory Control 

1997 ◽  
Vol 87 (2) ◽  
pp. 289-296 ◽  
Author(s):  
Elise Sarton ◽  
Albert Dahan ◽  
Luc Teppema ◽  
Aad Berkenbosch ◽  
Maarten van den Elsen ◽  
...  
Keyword(s):  
Carbon Dioxide ◽  
Control System ◽  
Acute Pain ◽  
Moderate Intensity ◽  
Noxious Stimulation ◽  
Ventilatory Control ◽  
Ventilatory Drive ◽  
End Tidal ◽  
Peripheral Chemoreflex ◽  
Sustained Hypoxia

Background Although many studies show that pain increases breathing, they give little information on the mechanism by which pain interacts with ventilatory control. The authors quantified the effect of experimentally induced acute pain from activation of cutaneous nociceptors on the ventilatory control system. Methods In eight volunteers, the influence of pain on various stimuli was assessed: room air breathing, normoxia (end-tidal pressure of carbon dioxide (PET(CO2)) clamped, normoxic and hyperoxic hypercapnia, acute hypoxia, and sustained hypoxia (duration, 15-18 min; end-tidal pressure of oxygen, approximately 53 mmHg). Noxious stimulation was administered in the form of a 1-Hz electric current applied to the skin over the tibial bone. Results While volunteers breathed room air, pain increased ventilation (V(I)) from 10.9 +/- 1.7 to 12.9 +/- 2.5 l/min(-1) (P < 0.05) and reduced PET(CO2) from 38.3 +/- 2.3 to 36.0 +/- 2.3 mmHg (P < 0.05). The increase in V(I) due to pain did not differ among the different stimuli. This resulted in a parallel leftward-shift of the V(I)-carbon dioxide response curve in normoxia and hyperoxia, and in a parallel shift to higher V(I) levels in acute and sustained hypoxia. Conclusions These data indicate that acute cutaneous pain of moderate intensity interacted with the ventilatory control system without modifying the central and peripheral chemoreflex loop and the central modulation of the hypoxia-related output of the peripheral chemoreflex loop. Pain causes a chemoreflex-independent tonic ventilatory drive.

Does the respiratory system limit the aerobic working capacity of humans?

2000 ◽  
Vol 26 (4) ◽  
pp. 481-487 ◽  
Author(s):  
I. S. Breslav ◽  
M. O. Segizbaeva ◽  
G. G. Isaev
Keyword(s):  
Respiratory System ◽  
Working Capacity ◽  
Aerobic Working Capacity

scholarly journals Is the healthy respiratory system built just right, overbuilt, or underbuilt to meet the demands imposed by exercise?

2020 ◽  
Vol 129 (6) ◽  
pp. 1235-1256 ◽  
Author(s):  
Jerome A. Dempsey ◽  
Andre La Gerche ◽  
James H. Hull
Keyword(s):  
Respiratory System ◽  
Exercise Performance ◽  
Respiratory Muscles ◽  
Lung Parenchyma ◽  
Endurance Athletes ◽  
Pulmonary Vasculature ◽  
Blood Gas ◽  
Ventilatory Control ◽  
Response To Exercise ◽  
Homeostatic Response

In the healthy, untrained young adult, a case is made for a respiratory system (airways, pulmonary vasculature, lung parenchyma, respiratory muscles, and neural ventilatory control system) that is near ideally designed to ensure a highly efficient, homeostatic response to exercise of varying intensities and durations. Our aim was then to consider circumstances in which the intra/extrathoracic airways, pulmonary vasculature, respiratory muscles, and/or blood-gas distribution are underbuilt or inadequately regulated relative to the demands imposed by the cardiovascular system. In these instances, the respiratory system presents a significant limitation to O2 transport and contributes to the occurrence of locomotor muscle fatigue, inhibition of central locomotor output, and exercise performance. Most prominent in these examples of an “underbuilt” respiratory system are highly trained endurance athletes, with additional influences of sex, aging, hypoxic environments, and the highly inbred equine. We summarize by evaluating the relative influences of these respiratory system limitations on exercise performance and their impact on pathophysiology and provide recommendations for future investigation.

Skeletal muscle chemoreflex and pHi in exercise ventilatory control

1998 ◽  
Vol 84 (2) ◽  
pp. 676-682 ◽  
Author(s):  
David A. Oelberg ◽  
Allison B. Evans ◽  
Mirko I. Hrovat ◽  
Paul P. Pappagianopoulos ◽  
Samuel Patz ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Minute Ventilation ◽  
Venous Blood ◽  
Hydrogen Ion ◽  
Positive Pressure ◽  
Resonance Spectroscopy ◽  
Ventilatory Control ◽  
Ventilatory Drive ◽  
Repetition Time ◽  
Muscle Chemoreflex

Oelberg, David A., Allison B. Evans, Mirko I. Hrovat, Paul P. Pappagianopoulos, Samuel Patz, and David M. Systrom. Skeletal muscle chemoreflex and pHi in exercise ventilatory control. J. Appl. Physiol. 84(2): 676–682, 1998.—To determine whether skeletal muscle hydrogen ion mediates ventilatory drive in humans during exercise, 12 healthy subjects performed three bouts of isotonic submaximal quadriceps exercise on each of 2 days in a 1.5-T magnet for 31P-magnetic resonance spectroscopy (31P-MRS). Bilateral lower extremity positive pressure cuffs were inflated to 45 Torr during exercise (BLPPex) or recovery (BLPPrec) in a randomized order to accentuate a muscle chemoreflex. Simultaneous measurements were made of breath-by-breath expired gases and minute ventilation, arterialized venous blood, and by 31P-MRS of the vastus medialis, acquired from the average of 12 radio-frequency pulses at a repetition time of 2.5 s. With BLPPex, end-exercise minute ventilation was higher (53.3 ± 3.8 vs. 37.3 ± 2.2 l/min; P < 0.0001), arterialized[Formula: see text] lower (33 ± 1 vs. 36 ± 1 Torr; P = 0.0009), and quadriceps intracellular pH (pHi) more acid (6.44 ± 0.07 vs. 6.62 ± 0.07; P = 0.004), compared with BLPPrec. Blood lactate was modestly increased with BLPPex but without a change in arterialized pH. For each subject, pHi was linearly related to minute ventilation during exercise but not to arterialized pH. These data suggest that skeletal muscle hydrogen ion contributes to the exercise ventilatory response.

Influences of Subanesthetic Isoflurane on Ventilatory Control in Humans

1995 ◽  
Vol 83 (3) ◽  
pp. 478-490. ◽  
Author(s):  
Maarten van den Elsen ◽  
Albert Dahan ◽  
Jacob DeGoede ◽  
Aad Berkenbosch ◽  
Jack van Kleef
Keyword(s):  
Carbon Dioxide ◽  
Healthy Volunteers ◽  
Ventilatory Response ◽  
Carbon Dioxide Tension ◽  
Central Component ◽  
Ventilatory Control ◽  
Ventilatory Responses ◽  
End Tidal ◽  
Peripheral Chemoreflex ◽  
Ventilatory Response To Hypoxia

Background The purpose of this study was to quantify in humans the effects of subanesthetic isoflurane on the ventilatory control system, in particular on the peripheral chemoreflex loop. Therefore we studied the dynamic ventilatory response to carbon dioxide, the effect of isoflurane wash-in upon sustained hypoxic steady-state ventilation, and the ventilatory response at the onset of 20 min of isocapnic hypoxia. Methods Study 1: Square-wave changes in end-tidal carbon dioxide tension (7.5-11.5 mmHg) were performed in eight healthy volunteers at 0 and 0.1 minimum alveolar concentration (MAC) isoflurane. Each hypercapnic response was separated into a fast, peripheral component and a slow, central component, characterized by a time constant, carbon dioxide sensitivity, time delay, and off-set (apneic threshold). Study 2: The ventilatory changes due to the wash-in of 0.1 MAC isoflurane, 15 min after the induction of isocapnic hypoxia, were studied in 11 healthy volunteers. Study 3: The ventilatory responses to a step decrease in end-tidal oxygen (end-tidal oxygen tension from 110 to 44 mmHg within 3-4 breaths; duration of hypoxia 20 min) were assessed in eight healthy volunteers at 0, 0.1, and 0.2 MAC isoflurane. Results Values are reported as means +/- SF. Study 1: The peripheral carbon dioxide sensitivities averaged 0.50 +/- 0.08 (control) and 0.28 +/- 0.05 l.min-1.mmHg-1 (isoflurane; P &lt; 0.01). The central carbon dioxide sensitivities (control 1.20 +/- 0.12 vs. isoflurane 1.04 +/- 0.11 l.min-1.mmHg-1) and off-sets (control 36.0 +/- 0.1 mmHg vs. isoflurane 34.5 +/- 0.2 mmHg) did not differ between treatments. Study 2: Within 30 s of exposure to 0.1 MAC isoflurane, ventilation decreased significantly, from 17.7 +/- 1.6 (hypoxia, awake) to 15.0 +/- 1.5 l.min-1 (hypoxia, isoflurane). Study 3: At the initiation of hypoxia ventilation increased by 7.7 +/- 1.4 (control), 4.1 +/- 0.8 (0.1 MAC; P &lt; 0.05 vs. control), and 2.8 +/- 0.6 (0.2 MAC; P &lt; 0.05 vs. control) l.min-1. The subsequent ventilatory decrease averaged 4.9 +/- 0.8 (control), 3.4 +/- 0.5 (0.1 MAC; difference not statistically significant), and 2.0 +/- 0.4 (0.2 MAC; P &lt; 0.05 vs. control) l.min-1. There was a good correlation between the acute hypoxic response and the hypoxic ventilatory decrease (r = 0.9; P &lt; 0.001). Conclusions The results of all three studies indicate a selective and profound effect of subanesthetic isoflurane on the peripheral chemoreflex loop at the site of the peripheral chemoreceptors. We relate the reduction of the ventilatory decrease of sustained hypoxia to the decrease of the initial ventilatory response to hypoxia.

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