2013
DOI: 10.1117/1.jbo.18.9.095002
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Tissue deoxygenation kinetics induced by prolonged hypoxic exposure in healthy humans at rest

Abstract: This study aimed to investigate the effects of sustained hypoxic exposure on cerebral and muscle oxygenation and cardiorespiratory function at rest. Eleven healthy subjects inhaled a normobaric hypoxic (FiO2=0.12) or normoxic (FiO2=0.21) gas mixture for 4 h at rest, on two separated blinded sessions. Arterial oxygen saturation (SpO2), heart rate variability (HRV), end-tidal CO2 (EtCO2), and oxygenation of quadriceps muscle, prefrontal and motor cortices assessed by near-infrared spectroscopy (NIRS) were measur… Show more

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Cited by 23 publications
(23 citation statements)
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“…8,11,20,[22][23][24][25][26] The length of stay and type of rise to a simulated altitude could generate different cardiac autonomic modulation responses, as shown in the table 1. 12,27,28 Likewise, the different levels of oxygen used in the studies, ranging from 19% to 9.6% of FiO 2 10,21,23 also appear to induce different HRV responses.…”
Section: Intervening Factors Of Hypoxia In Hrvmentioning
confidence: 92%
See 2 more Smart Citations
“…8,11,20,[22][23][24][25][26] The length of stay and type of rise to a simulated altitude could generate different cardiac autonomic modulation responses, as shown in the table 1. 12,27,28 Likewise, the different levels of oxygen used in the studies, ranging from 19% to 9.6% of FiO 2 10,21,23 also appear to induce different HRV responses.…”
Section: Intervening Factors Of Hypoxia In Hrvmentioning
confidence: 92%
“…24 After this, they suggest two possible routes, one relates to a possible baroreflex response that may counterbalance the initial disturbance, preventing very high levels of HR 31 or even, in the possibility of fall in SpO 2 below a certain threshold, cause a negligible change in ANS activity. 24 Although SpO 2 was not been stabilized during 10-min exposure, the study by Rupp et al 28 indicates SpO 2 stabilization only after 20-minute exposure to a level of 12% FiO 2 at 4000 m, i.e., less than that achieved by Krejci et al 24 One only study 21 separated the sample into two groups, RG = SpO 2 ≥ 72.2% and SG = SpO 2 ≤ 72.2%, in addition to controlling RF and using an extreme level of hypoxia of ~6200m. In this study of rapid exposure to NH, the RG group had a decrease in LnHF but with maintenance of Ln LF/HF.…”
Section: Exposure To Hypoxia and Its Effects On Hrvmentioning
confidence: 96%
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“…This time point coincides with significant and near maximal reduction in cerebral oxygenation measured by near-infrared spectroscopy during a 4-hour hypoxic exposure (FiO 2 = 0.12) at rest. 16 Shortterm changes in cerebral volume are commonly caused by changes in tissue water content or perfusion. The absence of significant change in ADC after 30 minutes of exposure suggests that edema is not responsible for this early increase in whitematter volume.…”
Section: Correlationsmentioning
confidence: 99%
“…7 We also assessed potential early MRI changes after 30 minutes of passive hypoxic exposure, i.e., the hypoxic exposure duration eliciting maximal cerebral deoxygenation (assessed in a recent report from our group by near-infrared spectroscopy). 16 We hypothesized that (1) hypoxia would induce signs of cerebral edema as early as after 30 minutes and this would be exacerbated after 10 hours of exposure and (2) hypoxia associated with exercise would induce similar changes in brain volumes and ADC as hypoxia at rest with matched arterial oxygenation levels, i.e., demonstrating the primary role of hypoxemia regarding cerebral changes.…”
Section: Introductionmentioning
confidence: 99%