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.

New insights into ocular blood flow at very high altitudes

2009 ◽  
Vol 106 (2) ◽  
pp. 454-460 ◽  
Author(s):  
Martina M. Bosch ◽  
Tobias M. Merz ◽  
Daniel Barthelmes ◽  
Benno L. Petrig ◽  
Frederic Truffer ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
High Altitude ◽  
Cerebral Edema ◽  
Arterial Oxygen Saturation ◽  
Acute Mountain Sickness ◽  
Fundus Photography ◽  
Arterial Oxygen ◽  
High Altitudes ◽  
Choroidal Blood Flow

Little is known about the ocular and cerebral blood flow during exposure to increasingly hypoxic conditions at high altitudes. There is evidence that an increase in cerebral blood flow resulting from altered autoregulation constitutes a risk factor for acute mountain sickness (AMS) and high-altitude cerebral edema (HACE) by leading to capillary overperfusion and vasogenic cerebral edema. The retina represents the only part of the central nervous system where capillary blood flow is visible and can be measured by noninvasive means. In this study we aimed to gain insights into retinal and choroidal autoregulatory properties during hypoxia and to correlate circulatory changes to symptoms of AMS and clinical signs of HACE. This observational study was performed within the scope of a high-altitude medical research expedition to Mount Muztagh Ata (7,546 m). Twenty seven participants underwent general and ophthalmic examinations up to a maximal height of 6,800 m. Examinations included fundus photography and measurements of retinal and choroidal blood flow, as well as measurement of arterial oxygen saturation and hematocrit. The initial increase in retinal blood velocity was followed by a decrease despite further ascent, whereas choroidal flow increase occurred later, at even higher altitudes. The sum of all adaptational mechanisms resulted in a stable oxygen delivery to the retina and the choroid. Parameters reflecting the retinal circulation and optic disc swelling correlated well with the occurrence of AMS-related symptoms. We demonstrate that sojourns at high altitudes trigger distinct behavior of retinal and choroidal blood flow. Increase in retinal but not in choroidal blood flow correlated with the occurrence of AMS-related symptoms.

Control of breathing in Sherpas at low and high altitude

1980 ◽  
Vol 49 (3) ◽  
pp. 374-379 ◽  
Author(s):  
P. H. Hackett ◽  
J. T. Reeves ◽  
C. D. Reeves ◽  
R. F. Grover ◽  
D. Rennie
Keyword(s):  
High Altitude ◽  
Ventilatory Response ◽  
Minute Ventilation ◽  
Acute Hypoxia ◽  
Arterial Oxygen Saturation ◽  
Carbon Dioxide Tension ◽  
Arterial Oxygen ◽  
Hypoxic Ventilatory Response ◽  
Oxygen Administration ◽  
End Tidal

Sherpas are well known for their physical performance at extreme altitudes, yet they are reported to have blunted ventilatory responses to acute hypoxia and relative hypoventilation in chronic hypoxia. To examine this paradox, we studied ventilatory control in Sherpas in comparison to that in Westerners at both low and high altitude. At low altitude, 25 Sherpas had higher minute ventilation, higher respiratory frequency, and lower end-tidal carbon dioxide tension than 25 Westerners. The hypoxic ventilatory response of Sherpas was found to be similar to that in Westerners, even though long altitude exposure had blunted the responses of some Sherpas. At high altitude, Sherpas again had higher minute ventilation and a tendency toward higher arterial oxygen saturation than Westerners. Oxygen administration increased ventilation further in Sherpas but decreased ventilation in Westerners. We conclude that Sherpas differ from other high-altitude natives; their hypoxic ventilatory response is not blunted, and they exhibit relative hyperventilation.

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.

scholarly journals Exercise exacerbates acute mountain sickness at simulated high altitude

2000 ◽  
Vol 88 (2) ◽  
pp. 581-585 ◽  
Author(s):  
R. C. Roach ◽  
D. Maes ◽  
D. Sandoval ◽  
R. A. Robergs ◽  
M. Icenogle ◽  
...  
Keyword(s):  
High Altitude ◽  
Minute Ventilation ◽  
Arterial Oxygen Saturation ◽  
Acute Mountain Sickness ◽  
Urine Volume ◽  
Barometric Pressure ◽  
Arterial Oxygen ◽  
Simulated High Altitude ◽  
Mountain Sickness ◽  
Exercise Induced

.—We hypothesized that exercise would cause greater severity and incidence of acute mountain sickness (AMS) in the early hours of exposure to altitude. After passive ascent to simulated high altitude in a decompression chamber [barometric pressure = 429 Torr, ∼4,800 m (J. B. West, J. Appl. Physiol. 81: 1850–1854, 1996)], seven men exercised (Ex) at 50% of their altitude-specific maximal workload four times for 30 min in the first 6 h of a 10-h exposure. On another day they completed the same protocol but were sedentary (Sed). Measurements included an AMS symptom score, resting minute ventilation (V˙e), pulmonary function, arterial oxygen saturation ([Formula: see text]), fluid input, and urine volume. Symptoms of AMS were worse in Ex than Sed, with peak AMS scores of 4.4 ± 1.0 and 1.3 ± 0.4 in Ex and Sed, respectively ( P < 0.01); but restingV˙e and[Formula: see text] were not different between trials. However, [Formula: see text] during the exercise bouts in Ex was at 76.3 ± 1.7%, lower than during either Sed or at rest in Ex (81.4 ± 1.8 and 82.2 ± 2.6%, respectively, P< 0.01). Fluid intake-urine volume shifted to slightly positive values in Ex at 3–6 h ( P = 0.06). The mechanism(s) responsible for the rise in severity and incidence of AMS in Ex may be sought in the observed exercise-induced exaggeration of arterial hypoxemia, in the minor fluid shift, or in a combination of these factors.

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.

Re: “Positional Changes in Arterial Oxygen Saturation and End-Tidal Carbon Dioxide at High Altitude: Medex 2015” by Kuenzel et al.

2020 ◽  
Vol 21 (3) ◽  
pp. 305-306
Author(s):  
Ulrich Limper ◽  
Vera Fiala ◽  
Eva M. Elmenhorst ◽  
Jens Tank ◽  
Gereon Schaelte ◽  
...  
Keyword(s):  
Carbon Dioxide ◽  
Oxygen Saturation ◽  
High Altitude ◽  
Arterial Oxygen Saturation ◽  
Arterial Oxygen ◽  
End Tidal Carbon Dioxide ◽  
End Tidal

scholarly journals Spleen contraction elevates hemoglobin concentration at high altitude during rest and exercise

2020 ◽  
Vol 120 (12) ◽  
pp. 2693-2704
Author(s):  
Erika Schagatay ◽  
Alexander Lunde ◽  
Simon Nilsson ◽  
Oscar Palm ◽  
Angelica Lodin-Sundström
Keyword(s):  
High Altitude ◽  
Acute Hypoxia ◽  
Arterial Oxygen Saturation ◽  
Hemoglobin Concentration ◽  
Step Test ◽  
Arterial Oxygen ◽  
Spleen Volume ◽  
Spleen Contraction ◽  
Response To Exercise ◽  
Rest And Exercise

Abstract Purpose Hypoxia and exercise are known to separately trigger spleen contraction, leading to release of stored erythrocytes. We studied spleen volume and hemoglobin concentration (Hb) during rest and exercise at three altitudes. Methods Eleven healthy lowlanders did a 5-min modified Harvard step test at 1370, 3700 and 4200 m altitude. Spleen volume was measured via ultrasonic imaging and capillary Hb with Hemocue during rest and after the step test, and arterial oxygen saturation (SaO2), heart rate (HR), expiratory CO2 (ETCO2) and respiratory rate (RR) across the test. Results Resting spleen volume was reduced with increasing altitude and further reduced with exercise at all altitudes. Mean (SE) baseline spleen volume at 1370 m was 252 (20) mL and after exercise, it was 199 (15) mL (P < 0.01). At 3700 m, baseline spleen volume was 231 (22) mL and after exercise 166 (12) mL (P < 0.05). At 4200 m baseline volume was 210 (23) mL and after exercise 172 (20) mL (P < 0.05). After 10 min, spleen volume increased to baseline at all altitudes (NS). Baseline Hb increased with altitude from 138.9 (6.1) g/L at 1370 m, to 141.2 (4.1) at 3700 m and 152.4 (4.0) at 4200 m (P < 0.01). At all altitudes Hb increased from baseline during exercise to 146.8 (5.7) g/L at 1370 m, 150.4 (3.8) g/L at 3700 m and 157.3 (3.8) g/L at 4200 m (all P < 0.05 from baseline). Hb had returned to baseline after 10 min rest at all altitudes (NS). The spleen-derived Hb elevation during exercise was smaller at 4200 m compared to 3700 m (P < 0.05). Cardiorespiratory variables were also affected by altitude during both rest and exercise. Conclusions The spleen contracts and mobilizes stored red blood cells during rest at high altitude and contracts further during exercise, to increase oxygen delivery to tissues during acute hypoxia. The attenuated Hb response to exercise at the highest altitude is likely due to the greater recruitment of the spleen reserve during rest, and that maximal spleen contraction is reached with exercise.

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