Responses in muscle sympathetic activity to acute hypoxia in humans

Responses in muscle sympathetic activity (MSA) to acute hypoxia were studied in 13 healthy male subjects under hypobaric hypoxic conditions at a simulated altitude of 4,000, 5,000, and 6,000 m. Efferent postganglionic MSA was recorded directly with a tungsten microelectrode inserted percutaneously into the tibial nerve. Heart rate (HR) and respiratory rate (RR) were counted respectively from the R wave of an electrocardiogram and from the respiratory tracing recorded by the strain-gauge method. The average values of the MSA burst rate and total activity of MSA (burst rate x mean burst amplitude) at 4,000, 5,000, and 6,000 m were 36.4 +/- 2.6, 39.1 +/- 3.1, and 40.2 +/- 4.2 (SE) bursts/min and 616 +/- 138, 794 +/- 190, and 764 +/- 227 arbitrary units, respectively. These values were significantly higher than the values of 27.1 +/- 2.9 bursts/min and 446 +/- 28 at sea level. HR increased significantly at altitudes, but RR did not show significant change. Under severe hypoxic conditions beyond 5,000 m, there were large interindividual differences in the MSA responsiveness to hypoxia. The results indicate that MSA is activated under hypoxia by stimulating the chemoreceptors. However, the central controlling mechanisms that would be affected by hypoxia may also influence the MSA responsiveness under severe hypoxia.

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Influence of cilnidipine or nisoldipine on sympathetic activity in healthy male subjects

Heart and Vessels ◽

10.1007/s00380-007-0984-y ◽

2007 ◽

Vol 22 (6) ◽

pp. 404-409 ◽

Cited By ~ 10

Author(s):

Tsuyoshi Shiga ◽

Yuichiro Yamada ◽

Naoki Matsuda ◽

Takanori Tanaka ◽

Akinori Urae ◽

...

Keyword(s):

Sympathetic Activity ◽

Healthy Male ◽

Male Subjects

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Effects of five consecutive nocturnal hypoxic exposures on the cerebrovascular responses to acute hypoxia and hypercapnia in humans

Journal of Applied Physiology ◽

10.1152/japplphysiol.00977.2003 ◽

2004 ◽

Vol 96 (5) ◽

pp. 1745-1754 ◽

Cited By ~ 18

Author(s):

Jon C. Kolb ◽

Philip N. Ainslie ◽

Kojiro Ide ◽

Marc J. Poulin

Keyword(s):

Near Infrared ◽

Chronic Hypoxia ◽

Acute Hypoxia ◽

Transcranial Doppler Ultrasound ◽

Simulated Altitude ◽

Normoxic Control ◽

Highly Correlated ◽

End Tidal ◽

Cerebrovascular Regulation ◽

Male Subjects

The effects of discontinuous hypoxia on cerebrovascular regulation in humans are unknown. We hypothesized that five nocturnal hypoxic exposures (8 h/day) at a simulated altitude of 4,300 m (inspired O2 fraction = ∼13.8%) would elicit cerebrovascular responses that are similar to those that have been reported during chronic altitude exposures. Twelve male subjects (26.6 ± 4.1 yr, mean ± SD) volunteered for this study. The technique of end-tidal forcing was used to examine cerebral blood flow (CBF) and regional cerebral O2 saturation (SrO2) responses to acute variations in O2 and CO2 twice before, immediately after, and 5 days after the overnight hypoxic exposures. Transcranial Doppler ultrasound was used to assess CBF, and near-infrared spectroscopy was used to assess SrO2. Throughout the nocturnal hypoxic exposures, end-tidal Pco2 decreased ( P < 0.001) whereas arterial O2 saturation increased ( P < 0.001) compared with overnight normoxic control measurements. Symptoms associated with altitude illness were significantly greater than control values on the first night ( P < 0.001) and second night ( P < 0.01) of nocturnal hypoxia. Immediately after the nocturnal hypoxic intervention, the sensitivity of CBF to acute variations in O2 and CO2 increased 116% ( P < 0.01) and 33% ( P < 0.05), respectively, compared with control values. SrO2 was highly correlated with arterial O2 saturation ( R2 = 0.94 ± 0.04). These results show that discontinuous hypoxia elicits increases in the sensitivity of CBF to acute variations in O2 and CO2, which are similar to those observed during chronic hypoxia.

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