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Effects of training on the ventilatory response to hypoxia

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The purpose of the present study was to examine the influence of systematical training on the ventilatory response to hypoxia. A rebreathing technique - progressive isocapnic hypoxia - was used to measure hypoxic chemoreflex reactivity. The ventilatory response was measured in a group of 22 world class adult kayakers (22.6 ±1.9 yr), 16 young kayakers (17.8 ±1.1 yr), and 38 control subjects (21.9 ±1.9 yr). The ventilatory response to hypoxia - analyzed as the relationship (slope) MV/SaO2 (minute ventilation/oxygen arterial blood saturation) - in the adult kayakers was significantly lower (-1.03 ±0.28 L/min/%, P<0.01) compared with those in the control group (-1.81 ±0.54 L/min/%) and the young kayakers (-1.54 ±0.6 L/min/%; the difference between the latter two was insignificant). The following values of P0.1/SaO2 (mouth occlusion pressure/oxygen arterial blood saturation) relationship were found for the investigated groups: adult kayakers (-0.20 ±0.1 cmH2O/%, P<0.05), young kayakers (-0.47 ±0.1 cmH2O/%, N.S.), control group (-0.48 ±0.18 cm H2O/%). Correlation between the hypoxic ventilatory response and VO2max was significant in both groups of kayakers. These findings indicate that tolerance for hypoxia was elevated in the group of athletes compared with the control group. Hypoxic tolerance correlates with the duration of training.
Ventilatory responses to progressive hypercapnia were analyzed in the normocapnic and hypercapnic obstructive sleep apnea patients (OSA). The rebreathing hypercapnic and hypoxic tests were performed using the computerized equipment (Lungtest, MES), according to Read's method. The ventilatory response to hypoxia was impaired in all OSA patients. Concerning the hypercapnic ventilatory response, there were no differences between the OSA patients with normal end-tidal PCO2 and controls. Nine moderately hypercapnic OSA patients showed a right shift with a normal slope of the regression curve describing the relationship between the end-tidal PCO2 and minute ventilation. In contrast, three severely hypercapnic OSA patients showed a right shift with a decreased slope of this regression curve. We conclude that awake OSA patients who developed hypercapnic ventilatory insufficiency showed an impaired hypercapnic defense reaction.
In the present study we investigated whether classical or non-classical statistical methods might be useful in the diagnosis of early changes evoked by intermittent hypoxia (IH) in an experimental model. The experiments were carried out in anesthetized, spontaneously breathing rabbits. IH consisted of 5 cycles of breathing 14% O2 in N2 for 1 min interspersed with 3 min normoxic intervals. The following ventilatory variables were evaluated: frequency breathing, tidal volume, and minute ventilation. The results indicate that IH had a progressively stimulatory effect on the baseline ventilation and on the hypoxic ventilatory responses. Further, the algorithms of the pattern recognition theory might be a suitable tool for the recognition of early ventilatory effects of recurrent hypoxic events in the IH model. The recognition of IH states may be useful in clinical and sports medicine.
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The aging corotid body

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The respiratory system is subject to the aging process, which could limit its responsiveness to hyperventilatory stimuli. Attenuation of the ventilatory response to hypoxia in old age is, as yet, an unresolved issue. Such attenuation may be germane for the pathogenesis of respiratory disorders developing more often in elderly subjects. The aim of this study was to determine the potential adverse effects of age on the morphology and function of carotid bodies. Morphology was studied at the level of electron microscopy on carotid bodies dissected from adult young (3 months) and old (>2 years) rats and function by comparing the hypoxic ventilatory response in populations of young (mean age 24 years) and old (mean age 71 years) female subjects. The human protocol consisted of a progressive hypoxia test, based on a rebreathing technique in a closed system. The hypoxic ventilatory response was evaluated from the slopes of minute ventilation on arterial oxygen saturation. The results of the morphological study showed degenerative changes developing with age in the ultrastructure of carotid bodies. On the other side, respiratory responses to hypoxia in old women were well preserved and were no less than those in young women. Therefore, a discrepancy appeared between the morphological and functional aspects. These findings suggest development of compensatory mechanisms in brain respiratory areas which maintain primary defensive reflexes, such as the hyperventilation of hypoxia.
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Ventilatory response to hypoxia in experimental pathology of the diaphragm

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In this study, we examined the usefulness of arterial blood gas variables, as changed by the hypoxic stimulus, in discerning various experimentally-induced conditions of diaphragm weakness in anesthetized cats. We defined three experimental situations (models): (i) intact muscle, statistical Class I, (ii) four degrees of muscle dysfunction (after sequential diaphragm denervation), Classes II-V, and (iii) entirely paralyzed muscle, Class VI. Responses to a hypoxic stimulus in the above-mentioned conditions were evaluated by using the methods of the pattern recognition theory. We found that before the hypoxic stimulus, with partial but of different severity denervation of the diaphragm, the k-nearest neighbor classifier (k-NN) assigned 100% of the classified cases to Class II (one phrenic nerve rootlet cut). In contrast, during hypoxia only 67% of cases were assigned to Class II, the remaining being spread throughout other classes of muscle weakness. When one limits the procedure to the extreme classes: Class I (intact diaphragm) and Class VI (totally denervated diaphragm), the k-NN picks out 33% and 50% cases of bilateral diaphragm paralysis before and during hypoxia, respectively. We conclude that any remaining innervations of the diaphragm ensure the functionally optimal level of lung ventilation that may waver when hypoxia develops.
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Transient O2-dependent effects of CO2 on ventilation in the anesthetized mouse

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In this study we sought to determine the effects of background hyperoxia on the ventilatory response to hypercapnia. We addressed this issue by examining the temporal profile of the first minute transients of minute ventilation, and its frequency and tidal components, in response to 5% and 10% CO2 each co-applied with the natural (balanced with air) and hyperoxic (balanced with O2) levels of oxygen. The study was performed on the urethane-anesthetized, tracheostomized, spontaneously breathing mouse, placed in a flow-through body plethysmograph. We identified an early suppressant effect of CO2-in-O2 on breathing frequency. The frequency declined to 88.5 ±1.4% and 87.8 ±1.9% relative to the pre-test, baseline level for 5% and 10% CO2, respectively. There was a compensatory rise in tidal volume and no major change in the overall ventilation. In contrast, CO2-in-Air resulted in ventilatory stimulation caused in equal measure by frequency and tidal components. Thus, the inhibitory effect on breathing frequency of the CO2-in-O2 resulted from the O2 content in the mixture and had the temporal characteristics consistent with carotid body function. In conclusion, transient O2-dependent effects can bear on the nascent hypercapnic ventilatory response. The complexity of the O2-CO2 interaction regarding the breathing pattern components should be taken into account while designing the optimal conditions for a hypercapnic test.
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