Effect of intermittent hypoxia on muscle and cerebral oxygenation during a 20-km time trial in elite athletes: a preliminary report

2010 ◽  
Vol 35 (4) ◽  
pp. 548-559 ◽  
Author(s):  
Michael J. Hamlin ◽  
Helen C. Marshall ◽  
John Hellemans ◽  
Philip N. Ainslie
Keyword(s):  
Cerebral Oxygenation ◽  
Elite Athletes ◽  
Arterial Oxygen Saturation ◽  
Time Trial ◽  
Arterial Oxygen ◽  
Hypoxic Exposure ◽  
Post Intervention ◽  
Randomized Design ◽  
Improved Performance ◽  
End Tidal

The effects of intermittent hypoxic exposure (IHE) on cerebral and muscle oxygenation, arterial oxygen saturation (SaO2), and respiratory gas exchange during a 20-km cycle time trial (20TT) were examined (n = 9) in a placebo-controlled randomized design. IHE (7:3 min hypoxia to normoxia) involved 90-min sessions for 10 days, with SaO2 clamped at ∼80%. Prior to, and 2 days after the intervention, a 20TT was performed. During the final minute of the 20TT, in the IHE group only, muscle oxyhemoglobin (oxy-Hb) was elevated (mean ± 95% confidence interval 1.3 ± 1.2 ΔµM, p = 0.04), whereas cerebral oxy-Hb was reduced (–1.9% ± 1.0%, p < 0.01) post intervention compared with baseline. The 20TT performance was unchanged between groups (p = 0.7). In the IHE group, SaO2 was higher (1.0 ± 0.7Δ%, p = 0.006) and end-tidal PCO2 was lower (–1.2 ± 0.1 mm Hg, p = 0.01) during the final stage of the 20TT post intervention compared with baseline. In summary, reductions in muscle oxy-Hb and systemic SaO2 occurring at exercise intensities close to maximal at the end of a 20TT were offset by IHE, although this was not translated into improved performance.

Evidence of sustained forearm vasodilatation after brief isocapnic hypoxia

2004 ◽  
Vol 96 (5) ◽  
pp. 1782-1787 ◽  
Author(s):  
Renaud Tamisier ◽  
Daniel Norman ◽  
Amit Anand ◽  
Yoon Choi ◽  
J. Woodrow Weiss
Keyword(s):  
Vascular Resistance ◽  
Forearm Blood Flow ◽  
Muscle Sympathetic Nerve Activity ◽  
Arterial Oxygen Saturation ◽  
Arterial Oxygen ◽  
Hypoxic Exposure ◽  
Compensatory Response ◽  
The Mean ◽  
End Tidal ◽  
Forearm Vascular Resistance

Healthy subjects exposed to 20 min of hypoxia increase ventilation and muscle sympathetic nerve activity (MSNA). After return to normoxia, although ventilation returns to baseline, MSNA remains elevated for up to an hour. Because forearm vascular resistance is not elevated after hypoxic exposure, we speculated that the increased MSNA might be a compensatory response to sustained release of endogenous vasodilators. We studied the effect of isocapnic hypoxia (mean arterial oxygen saturation 81.6 ± 4.1%, end-tidal Pco2 44.7 ± 6.3 Torr) on plethysmographic forearm blood flow (FBF) in eight healthy volunteers while infusing intra-arterial phentolamine to block local α-receptors. The dominant arm served as control. Forearm arterial vascular resistance (FVR) was calculated as the mean arterial pressure (MAP)-to-FBF ratio. MAP, heart rate (HR), and FVR were reported at 5-min intervals at baseline, then while infusing phentolamine during room air, isocapnic hypoxia, and recovery. Despite increases in HR during hypoxia, there was no change in MAP throughout the study. By design, FVR decreased during phentolamine infusion. Hypoxia further decreased FVR in both forearms. With continued phentolamine infusion, FVR after termination of the exposure (17.47 ± 6.3 mmHg·min·ml-1·100 ml of tissue) remained lower than preexposure baseline value (23.05 ± 8.51 mmHg·min·ml-1·100 ml of tissue; P < 0.05). We conclude that, unmasked by phentolamine, the vasodilation occurring during hypoxia persists for at least 30 min after the stimulus. This vasodilation may contribute to the sustained MSNA rise observed after hypoxia.

scholarly journals Positive expiratory pressure improves arterial and cerebral oxygenation in acute normobaric and hypobaric hypoxia

2019 ◽  
Vol 317 (5) ◽  
pp. R754-R762 ◽  
Author(s):  
Thomas Rupp ◽  
Jonas J. Saugy ◽  
Nicolas Bourdillon ◽  
Samuel Verges ◽  
Grégoire P. Millet
Keyword(s):  
Near Infrared ◽  
Cerebral Oxygenation ◽  
Arterial Oxygen Saturation ◽  
Cardiovascular Responses ◽  
Barometric Pressure ◽  
Free Breathing ◽  
Arterial Oxygen ◽  
Hypoxic Exposure ◽  
Time Points ◽  
Positive Expiratory Pressure

Positive expiratory pressure (PEP) has been shown to limit hypoxia-induced reduction in arterial oxygen saturation, but its effectiveness on systemic and cerebral adaptations, depending on the type of hypoxic exposure [normobaric (NH) versus hypobaric (HH)], remains unknown. Thirteen healthy volunteers completed three randomized sessions consisting of 24-h exposure to either normobaric normoxia (NN), NH (inspiratory oxygen fraction, [Formula: see text] = 13.6%; barometric pressure, BP = 716 mmHg; inspired oxygen partial pressure, [Formula: see text] = 90.9 ± 1.0 mmHg), or HH (3,450 m, [Formula: see text] = 20.9%, BP = 482 mmHg, [Formula: see text] = 91.0 ± 0.6 mmHg). After the 6th and the 22nd hours, participants breathed quietly through a facemask with a 10-cmH2O PEP for 2 × 5 min interspaced with 5 min of free breathing. Arterial ([Formula: see text], pulse oximetry), quadriceps, and cerebral (near-infrared spectroscopy) oxygenation, middle cerebral artery blood velocity (MCAv; transcranial Doppler), ventilation, and cardiovascular responses were recorded continuously. [Formula: see text]without PEP was significantly lower in HH (87 ± 4% on average for both time points, P < 0.001) compared with NH (91 ± 3%) and NN (97 ± 1%). PEP breathing did not change [Formula: see text] in NN but increased it similarly in NH and HH (+4.3 ± 2.5 and +4.7 ± 4.1% after 6h; +3.5 ± 2.2 and +4.1 ± 2.9% after 22h, both P < 0.001). Although MCAv was reduced by PEP (in all sessions and at all time points, −6.0 ± 4.2 cm/s on average, P < 0.001), the cerebral oxygenation was significantly improved ( P < 0.05) with PEP in both NH and HH, with no difference between conditions. These data indicate that PEP could be an attractive nonpharmacological means to improve arterial and cerebral oxygenation under both normobaric and hypobaric mild hypoxic conditions in healthy participants.

Effect of sildenafil and acclimatization on cerebral oxygenation at altitude

2005 ◽  
Vol 109 (3) ◽  
pp. 319-324 ◽  
Author(s):  
Colin W. M. Chan ◽  
Helen Hoar ◽  
Kyle Pattinson ◽  
Arthur R. Bradwell ◽  
Alexander D. Wright ◽  
...  
Keyword(s):  
Oxygen Saturation ◽  
Cerebral Oxygenation ◽  
Hypoxic Pulmonary Vasoconstriction ◽  
Arterial Oxygen Saturation ◽  
Arterial Oxygen ◽  
Pulmonary Vasoconstriction ◽  
Partial Pressure Of Co2 ◽  
Rapid Ascent ◽  
End Tidal ◽  
Phosphodiesterase 5

Phosphodiesterase-5 inhibitors decrease hypoxic pulmonary vasoconstriction under hypobaric hypoxia, but are not known to affect cerebral blood flow or oxygenation. The present study was designed to evaluate the effect of sildenafil on cerebral haemodynamics during acute exposure to altitude and after acclimatization. Ten subjects were studied 1 and 3 days after rapid ascent to 3480 m before and for two consecutive hours after taking sildenafil (50 mg). Before acclimatization, HR (heart rate) rose at 1 h (76.3±1.0 beats/min compared with 72.5±1.5 beats/min at baseline; P<0.05) and had returned to baseline at 2 h (71.3±1.1 beats/min; P>0.05). Mean BP (blood pressure) fell from 96.0±2.0 mmHg at baseline to 91.7±2.5 (P<0.001) at 1 h and 89.8±1.8 mmHg (P<0.0001) at 2 h, whereas SaO2 (arterial oxygen saturation) increased from 83.9±0.5% at baseline to 85.3±0.4% (P<0.0001) at 1 h and 85.0±0.5% (P<0.01) at 2 h. MCAV [MCA (middle cerebral artery) velocity] and PETCO2 (end-tidal partial pressure of CO2) were unchanged, but rSO2 (regional cerebral oxygen saturation) rose progressively at 1 h (62.7±0.8%; P<0.05) and 2 h (65.3±0.9%; P<0.0001) compared with baseline (59.3±1.3%). After 3 days of acclimatization, resting rSO2 and RMCA (MCA resistance) increased and oxygen delivery fell. Changes in HR and mean BP after sildenafil were similar to day 1, but SaO2 did not change. However, rSO2 increased [61.7±0.9% at baseline to 65.0±1.0% (P<0.0001) at 1 h and 64.0±0.9% (P<0.001) at 2h], despite a reduction in MCAV [65.3±1.8 cm/s at baseline to 61.3±1.5 cm/s (P<0.01) at 1 h and 60.9±1.7 cm/s (P<0.0001) at 2 h] and PETCO2 [4.1±0.05 kPa at baseline to 4.0±0.04 kPa at 2 h (P<0.01)]. These observations suggest that sildenafil improves cerebral oxygenation at altitude. Whereas the early changes before acclimatization may be largely pulmonary in origin, the later observations may be a direct cerebral effect which warrants further study.

Effect of exercise on cerebral perfusion in humans at high altitude

2005 ◽  
Vol 99 (2) ◽  
pp. 699-706 ◽  
Author(s):  
C. H. E. Imray ◽  
S. D. Myers ◽  
K. T. S. Pattinson ◽  
A. R. Bradwell ◽  
C. W. Chan ◽  
...  
Keyword(s):  
High Altitude ◽  
Oxygen Delivery ◽  
Cerebral Perfusion ◽  
Cerebral Oxygenation ◽  
Arterial Oxygen Saturation ◽  
Acute Mountain Sickness ◽  
Cycle Ergometer ◽  
Submaximal Exercise ◽  
Arterial Oxygen ◽  
End Tidal

The effects of submaximal and maximal exercise on cerebral perfusion were assessed using a portable, recumbent cycle ergometer in nine unacclimatized subjects ascending to 5,260 m. At 150 m, mean (SD) cerebral oxygenation (rSo2%) increased during submaximal exercise from 68.4 (SD 2.1) to 70.9 (SD 3.8) ( P < 0.0001) and at maximal oxygen uptake (V̇o2 max) to 69.8 (SD 3.1) ( P < 0.02). In contrast, at each of the high altitudes studied, rSo2 was reduced during submaximal exercise from 66.2 (SD 2.5) to 62.6 (SD 2.1) at 3,610 m ( P < 0.0001), 63.0 (SD 2.1) to 58.9 (SD 2.1) at 4,750 m ( P < 0.0001), and 62.4 (SD 3.6) to 61.2 (SD 3.9) at 5,260 m ( P < 0.01), and at V̇o2 max to 61.2 (SD 3.3) at 3,610 m ( P < 0.0001), to 59.4 (SD 2.6) at 4,750 m ( P < 0.0001), and to 58.0 (SD 3.0) at 5,260 m ( P < 0.0001). Cerebrovascular resistance tended to fall during submaximal exercise ( P = not significant) and rise at V̇o2 max, following the changes in arterial oxygen saturation and end-tidal CO2. Cerebral oxygen delivery was maintained during submaximal exercise at 150 m with a nonsignificant fall at V̇o2 max, but at high altitude peaked at 30% of V̇o2 max and then fell progressively at higher levels of exercise. The fall in rSo2 and oxygen delivery during exercise may limit exercise at altitude and is likely to contribute to the problems of acute mountain sickness and high-altitude cerebral edema.

Intermittent hypoxia increases ventilation and SaO2 during hypoxic exercise and hypoxic chemosensitivity

2001 ◽  
Vol 90 (4) ◽  
pp. 1431-1440 ◽  
Author(s):  
Keisho Katayama ◽  
Yasutake Sato ◽  
Yoshifumi Morotome ◽  
Norihiro Shima ◽  
Koji Ishida ◽  
...  
Keyword(s):  
Intermittent Hypoxia ◽  
Minute Ventilation ◽  
Acute Hypoxia ◽  
Arterial Oxygen Saturation ◽  
Submaximal Exercise ◽  
Arterial Oxygen ◽  
Hypoxic Exposure ◽  
Hypoxic Ventilatory Response ◽  
Ventilatory Equivalent ◽  
Hypoxic Exercise

The purpose of this study was 1) to test the hypothesis that ventilation and arterial oxygen saturation (SaO2 ) during acute hypoxia may increase during intermittent hypoxia and remain elevated for a week without hypoxic exposure and 2) to clarify whether the changes in ventilation and SaO2 during hypoxic exercise are correlated with the change in hypoxic chemosensitivity. Six subjects were exposed to a simulated altitude of 4,500 m altitude for 7 days (1 h/day). Oxygen uptake (V˙o 2), expired minute ventilation (V˙e), and SaO2 were measured during maximal and submaximal exercise at 432 Torr before (Pre), after intermittent hypoxia (Post), and again after a week at sea level (De). Hypoxic ventilatory response (HVR) was also determined. At both Post and De, significant increases from Pre were found in HVR at rest and in ventilatory equivalent for O2(V˙e/V˙o 2) and SaO2 during submaximal exercise. There were significant correlations among the changes in HVR at rest and inV˙e/V˙o 2 and SaO2 during hypoxic exercise during intermittent hypoxia. We conclude that 1 wk of daily exposure to 1 h of hypoxia significantly improved oxygenation in exercise during subsequent acute hypoxic exposures up to 1 wk after the conditioning, presumably caused by the enhanced hypoxic ventilatory chemosensitivity.

Obstructive Sleep Apnea in Children With Down Syndrome

PEDIATRICS ◽  
1991 ◽  
Vol 88 (1) ◽  
pp. 132-139
Author(s):  
Carole L. Marcus ◽  
Thomas G. Keens ◽  
Daisy B. Bautista ◽  
Walter S. von Pechmann ◽  
Sally L. Davidson Ward
Keyword(s):  
Obstructive Sleep Apnea ◽  
Down Syndrome ◽  
Sleep Apnea ◽  
Arterial Oxygen Saturation ◽  
Sleep Apnea Syndrome ◽  
Arterial Oxygen ◽  
Children With Down Syndrome ◽  
Obstructive Sleep ◽  
Apnea Syndrome ◽  
End Tidal

Children with Down syndrome have many predisposing factors for the obstructive sleep apnea syndrome (OSAS), yet the type and severity of OSAS in this population has not been characterized. Fifty-three subjects with Down syndrome (mean age 7.4 ± 1.2 [SE] years; range 2 weeks to 51 years) were studied. Chest wall movement, heart rate, electrooculogram, end-tidal Po2 and Pco2, transcutaneous Po2 and Pco2, and arterial oxygen saturation were measured during a daytime nap polysomnogram. Sixteen of these children also underwent overnight polysomnography. Nap polysomnograms were abnormal in 77% of children; 45% had obstructive sleep apnea (OSA), 4% had central apnea, and 6% had mixed apneas; 66% had hypoventilation (end-tidal Pco2, &gt;45 mm Hg) and 32% desaturation (arterial oxygen saturation &lt;90%). Overnight studies were abnormal in 100% of children, with OSA in 63%, hypoventilation in 81%, and desaturation in 56%. Nap studies significantly underestimated the presence of abnormalities when compared to overnight polysomnograms. Seventeen (32%) of the children were referred for testing because OSAS was clinically suspected, but there was no clinical suspicion of OSAS in 36 (68%) children. Neither age, obesity, nor the presence of congenital heart disease affected the incidence of OSA, desaturation, or hypoventilation. Polysomnograms improved in all 8 children who underwent tonsilletomy and adenoidectomy, but they normalized in only 3. It is concluded that children with Down syndrome frequently have OSAS, with OSA, hypoxemia, and hypoventilation. Obstructive sleep apnea syndrome is seen frequently in those children in whom it is not clinically suspected. It is speculated that OSAS may contribute to the unexplained pulmonary hypertension seen in children with Down syndrome.

Two patterns of daily hypoxic exposure and their effects on measures of chemosensitivity in humans

2007 ◽  
Vol 103 (6) ◽  
pp. 1973-1978 ◽  
Author(s):  
Michael S. Koehle ◽  
A. William Sheel ◽  
William K. Milsom ◽  
Donald C. McKenzie
Keyword(s):  
Oxygen Saturation ◽  
Intermittent Hypoxia ◽  
Ventilatory Response ◽  
Arterial Oxygen Saturation ◽  
Arterial Oxygen ◽  
Hypoxic Exposure ◽  
Hypoxic Ventilatory Response ◽  
The Third ◽  
Long Duration ◽  
The Mean

The purpose of this study was to compare chemoresponses following two different intermittent hypoxia (IH) protocols in humans. Ten men underwent two 7-day courses of poikilocapnic IH. The long-duration IH (LDIH) protocol consisted of daily 60-min exposures to normobaric 12% O2. The short-duration IH (SDIH) protocol comprised twelve 5-min bouts of 12% O2, separated by 5-min bouts of room air, daily. Isocapnic hypoxic ventilatory response (HVR) was measured daily during the protocol and 1 and 7 days following. Hypercapnic ventilatory response (HCVR) and CO2 threshold and sensitivity (by the modified Read rebreathing technique) were measured on days 1, 8, and 14. Following 7 days of IH, the mean HVR was significantly increased from 0.47 ± 0.07 and 0.47 ± 0.08 to 0.70 ± 0.06 and 0.79 ± 0.06 l·min−1·%SaO2−1 (LDIH and SDIH, respectively), where %SaO2 is percent arterial oxygen saturation. The increase in HVR reached a plateau after the third day. One week post-IH, HVR values were unchanged from baseline. HCVR increased from 3.0 ± 0.4 to 4.0 ± 0.5 l·min−1·mmHg−1. In both the hyperoxic and hypoxic modified Read rebreathing tests, the slope of the CO2/ventilation plot was unchanged by either intervention, but the CO2/ventilation curve shifted to the left following IH. There were no correlations between the changes in response to hypoxia and hypercapnia. There were no significant differences between the two IH protocols for any measures, indicating that comparable changes in chemoreflex control occur with either protocol. These results also suggest that the two methods of measuring CO2 response are not completely concordant and that the changes in CO2 control do not correlate with the increase in the HVR.

scholarly journals Hypoxaemia following Sustained Low-Volume Venous Air Embolism in Sheep

1988 ◽  
Vol 16 (2) ◽  
pp. 164-170 ◽  
Author(s):  
J. Pfitzner ◽  
S. P. Petito ◽  
A. G. McLean
Keyword(s):  
Arterial Oxygen Saturation ◽  
Air Embolism ◽  
Arterial Oxygen ◽  
Venous Air Embolism ◽  
Minute Period ◽  
Volume Ventilation ◽  
Gas Measurements ◽  
Respiratory Disturbance ◽  
Upright Head ◽  
End Tidal

In six upright (head above thorax) anaesthetised sheep, serial blood gas measurements were made over a 100-minute period during which repeated small-volume air emboli were injected intravenously to lower and maintain the end-tidal CO 2 concentration approximately 0.5% below its initial baseline level. With constant volume ventilation and an inspired N 2 O:O 2 ratio of 2:1, the arterial PCO 2 progressively increased and the arterial PO 2 progressively decreased with significant arterial hypoxaemia ensuing in three out of the six animals. It is suggested that during neurosurgery performed in the sitting position and with an inspired oxygen concentration of 33%, the degree of cardio-respiratory disturbance caused by venous air embolism should be assessed by continuous monitoring not only of end-tidal CO 2 concentration but also of arterial oxygen saturation using pulse oximetry.

Relationship of ovarian hormones to hypoxemia in women residents of 4,300 m

2001 ◽  
Vol 280 (2) ◽  
pp. R488-R493 ◽  
Author(s):  
F. León-Velarde ◽  
M. Rivera-Chira ◽  
R. Tapia ◽  
L. Huicho ◽  
C. Monge-C
Keyword(s):  
Luteal Phase ◽  
Arterial Oxygen Saturation ◽  
Premenopausal Women ◽  
Arterial Oxygen ◽  
Chronic Mountain Sickness ◽  
Physiological Variables ◽  
Cerro De Pasco ◽  
End Tidal ◽  
Hb Concentration ◽  
Relationship Of

Prevalence of excessive erythrocytosis, the main sign of chronic mountain sickness (CMS), is greater in postmenopausal Andean women than in premenopausal women. It is uncertain whether this greater prevalence is related to the decline in female hormones and ventilatory function after the occurrence of the menopause. To study this, we compared the physiological variables involved in the physiopathology of CMS [end-tidal CO2 (Pet CO2 , Torr) and end-tidal O2 (Pet O2 , Torr), arterial oxygen saturation (SaO2 , %), and Hb concentration (g/dl)] and progesterone and estradiol levels between postmenopausal and premenopausal women, both in the luteal and follicular phases. Women residing in Cerro de Pasco ( n= 33; 4,300 m) aged 26–62 yr were studied. Postmenopausal women compared with premenopausal women in the luteal phase had lower Pet O2 (48 ± 4 vs. 53 ± 2 Torr, P = 0.005) and SaO2 levels (82 ± 12 vs. 88 ± 12%, P < 0.005) and higher Pet CO2 (34 ± 2 vs. 29 ± 3 Torr, P = 0.005) and Hb concentration (19 ± 1 vs. 14 ± 2 g/dl, P < 0.005). In addition, plasma progesterone was negatively correlated with Pet CO2 and positively correlated with Pet O2 and SaO2 . No clear relationship was found among the cycle phases between estradiol and the variables studied. In conclusion, our results reveal that, before menopause, there is better oxygenation and lower Hb levels in women long residing at altitude, and this is associated with higher levels of progesterone in the luteal phase of the cycle.

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