Ventilatory Responses to Acute and Chronic Hypoxia

Bisgard, G. E.; Forster, H. V.

doi:10.1002/cphy.cp040252

Cited by 27 publications

(36 citation statements)

References 348 publications

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“…After CBD, this acclimatization is attenuated and/or eliminated, and it remains attenuated even after the peripheral chemoreflex and eupneic Pa CO 2 have returned partially and completely to normal, respectively (8,10,25,26). Thus there is no plasticity of this function, which is not unexpected from the evidence that acclimatization results from increased gain of the carotid chemoreceptors (7,14,71).…”

Section: Denervation Of Peripheral Chemoreceptorsmentioning

confidence: 91%

“…Most contemporary physiologists do not view the carotid body as an accessory mechanism, but these receptors are still viewed as the major sensors for the excitatory effect on breathing of a few breaths or minutes (acute) of hypoxemia. In quantitating this excitatory effect (known as the peripheral chemoreflex), the response of only a few breaths or minutes of hypoxia is considered because, after a few minutes, the hypoxia-induced hyperpnea will result in hypocapnia, which, along with a depressant effect of hypoxemia on neurons, will dampen the hyperpnea due to the increased carotid stimulation (7). Because of these time-dependent and multiple effects of hypoxia, the peripheral chemoreflex is often assessed by administering only a few breaths of low or high O 2 or by intravenous bolus injection of sodium cyanide (NaCN), which transiently activates excitatory oxygen chemoreceptors.…”

Section: Denervation Of Peripheral Chemoreceptorsmentioning

confidence: 99%

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Invited Review: Plasticity in the control of breathing following sensory denervation

Forster

2003

Journal of Applied Physiology

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Forster, H. V. Invited Review: Plasticity in the control of breathing following sensory denervation. J Appl Physiol 94: 784-794, 2003; 10.1152/japplphysiol.00602.2002.-The purpose of this manuscript is to review the results of studies on the recovery or plasticity following a denervation-or lesion-induced change in breathing. Carotid body denervation (CBD), lung denervation (LD), cervical (CDR) and thoracic (TDR) dorsal rhizotomy, dorsal spinal column lesions, and lesions at pontine, medullary, and spinal sites all chronically alter breathing. The plasticity after these is highly variable, ranging from near complete recovery of the peripheral chemoreflex in rats after CBD to minimal recovery of the Hering-Breuer inflation reflex in ponies after LD. The degree of plasticity varies among the different functions of each pathway, and plasticity varies with the age of the animal when the lesion was made. In addition, plasticity after some lesions varies between species, and plasticity is greater in the awake than in the anesthetized state. Reinnervation is not a common mechanism of plasticity. There is evidence supporting two mechanisms of plasticity. One is through upregulation of an alternate sensory pathway, such as serotonin-mediated aortic chemoreception after CBD. The second is through upregulation on the efferent limb of a reflex, such as serotonin-mediated increased responsiveness of phrenic motoneurons after CDR, TDR, and spinal cord injury. Accordingly, numerous components of the ventilatory control system exhibit plasticity after denervation or lesion-induced changes in breathing; this plasticity is uniform neither in magnitude nor in underlying mechanisms. A major need in future research is to determine whether "reorganization" within the central nervous system contributes to plasticity following lesion-induced changes in breathing.receptors; recovery of function; redundancy; chemoreflexes; mechanoreflexes DENERVATION OR LESIONING OF a receptor or neural pathway that normally contributes to the regulation of a physiological function will result in loss of or altered function. Thereafter, a time-dependent recovery of function is a manifestation of plasticity within the regulatory system. The purpose of this review is to summarize research on this type of plasticity within the system regulating breathing. Lesions are one of several means of inducing plasticity; a review of these and a general discussion of plasticity are presented elsewhere (66). Nevertheless, it seems appropriate to emphasize here that recovery of function can be due to restoration of the same mechanism or substitution of another mechanism. Also, recovery refers specifically to the return of a function, whereas plasticity refers to the process or mechanism of the restoration (i.e., capability of building new tissue or formative). A related phenomenon, redundancy, refers to two or more mechAddress for reprint requests and other correspondence:

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Section: Denervation Of Peripheral Chemoreceptorsmentioning

confidence: 91%

Section: Denervation Of Peripheral Chemoreceptorsmentioning

confidence: 99%

Invited Review: Plasticity in the control of breathing following sensory denervation

Forster

2003

Journal of Applied Physiology

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“…Ventilatory acclimatization (VEacc) can be characterized by the progressive decrease in the end-tidal PCO 2 (PET CO 2 ) that leads to an increase in arterial O 2 saturation (Sa O 2 ) during the first several days of moderate-to high-altitude residence [hypobaric hypoxia (HH), reduced barometric pressure (P B ) and 20.9% O 2 ] (7,28). The enhanced oxygenation is closely linked with reduced acute mountain sickness (AMS) and improved exercise performance during HH residence (1,11,12,14).…”

mentioning

confidence: 99%

Effect of repeated normobaric hypoxia exposures during sleep on acute mountain sickness, exercise performance, and sleep during exposure to terrestrial altitude

Fulco

Muza

Beidleman

et al. 2011

American Journal of Physiology-Regulatory, Integrative and Comp

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Fulco CS, Muza SR, Beidleman BA, Demes R, Staab JE, Jones JE, Cymerman A. Effect of repeated normobaric hypoxia exposures during sleep on acute mountain sickness, exercise performance, and sleep during exposure to terrestrial altitude. Am J Physiol Regul Integr Comp Physiol 300: R428 -R436, 2011. First published December 1, 2010; doi:10.1152/ajpregu.00633.2010.-There is an expectation that repeated daily exposures to normobaric hypoxia (NH) will induce ventilatory acclimatization and lessen acute mountain sickness (AMS) and the exercise performance decrement during subsequent hypobaric hypoxia (HH) exposure. However, this notion has not been tested objectively. Healthy, unacclimatized sea-level (SL) residents slept for 7.5 h each night for 7 consecutive nights in hypoxia rooms under NH [n ϭ 14, 24 Ϯ 5 (SD) yr] or "sham" (n ϭ 9, 25 Ϯ 6 yr) conditions. The ambient percent O2 for the NH group was progressively reduced by 0.3% [150 m equivalent (equiv)] each night from 16.2% (2,200 m equiv) on night 1 to 14.4% (3,100 m equiv) on night 7, while that for the ventilatory-and exercise-matched sham group remained at 20.9%. Beginning at 25 h after sham or NH treatment, all subjects ascended and lived for 5 days at HH (4,300 m). End-tidal PCO 2, O2 saturation (Sa O 2 ), AMS, and heart rate were measured repeatedly during daytime rest, sleep, or exercise (11.3-km treadmill time trial). From pre-to posttreatment at SL, resting end-tidal PCO 2 decreased (P Ͻ 0.01) for the NH (from 39 Ϯ 3 to 35 Ϯ 3 mmHg), but not for the sham (from 39 Ϯ 2 to 38 Ϯ 3 mmHg), group. Throughout HH, only sleep Sa O 2 was higher (80 Ϯ 1 vs. 76 Ϯ 1%, P Ͻ 0.05) and only AMS upon awakening was lower (0.34 Ϯ 0.12 vs. 0.83 Ϯ 0.14, P Ͻ 0.02) in the NH than the sham group; no other between-group rest, sleep, or exercise differences were observed at HH. These results indicate that the ventilatory acclimatization induced by NH sleep was primarily expressed during HH sleep. Under HH conditions, the higher sleep Sa O 2 may have contributed to a lessening of AMS upon awakening but had no impact on AMS or exercise performance for the remainder of each day. ventilatory acclimatization; physical performance; hypobaric hypoxia; arterial oxygen saturation ALTITUDE ACCLIMATIZATION RESULTS from numerous interrelated physiological adjustments that compensate for hypoxemia, with augmented ventilation being one of the most important and consistently reported (17,18,22,28). Ventilatory acclimatization (VEacc) can be characterized by the progressive decrease in the end-tidal PCO 2 (PET CO 2 ) that leads to an increase in arterial O 2 saturation (Sa O 2 ) during the first several days of moderate-to high-altitude residence [hypobaric hypoxia (HH), reduced barometric pressure (P B ) and 20.9% O 2 ] (7, 28). The enhanced oxygenation is closely linked with reduced acute mountain sickness (AMS) and improved exercise performance during HH residence (1,11,12,14). Some studies show that VEacc can also be induced by 1-4 h of HH exposure repeated daily at altitudes of 4,300 -4,500 m ...

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“…67 Initially, this increased ventilation leads to a decreased arterial partial pressure of CO2 and respiratory alkalosis. However, at altitudes below 3,000m this phenomenon appears to be alleviated within the first few days, partially by an increased urinary excretion of sodium.…”

Section: -61mentioning

confidence: 99%

Short-Term Arrival Strategies for Endurance Exercise Performance at Moderate Altitude

Foss

Constantini

Mickleborough

et al. 2015

Medicine &Amp; Science in Sports &Amp; Exercise

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Ventilatory Responses to Acute and Chronic Hypoxia

Cited by 27 publications

References 348 publications

Invited Review: Plasticity in the control of breathing following sensory denervation

Invited Review: Plasticity in the control of breathing following sensory denervation

Effect of repeated normobaric hypoxia exposures during sleep on acute mountain sickness, exercise performance, and sleep during exposure to terrestrial altitude

Short-Term Arrival Strategies for Endurance Exercise Performance at Moderate Altitude

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