Cerebral desaturation during exercise reversed by O2 supplementation

American Journal of Physiology - Heart and Circulatory Physiology - Tập 277 Số 3 - Trang H1045-H1052 - 1999
Henning B. Nielsen1, Robert Boushel1, Per Lav Madsen1, Niels H. Secher1
1Copenhagen Muscle Research Center, Department of Anesthesia, Rigshospitalet, University of Copenhagen, 2100 Copenhagen Ø, Denmark

Tóm tắt

The combined effects of hyperventilation and arterial desaturation on cerebral oxygenation ([Formula: see text]) were determined using near-infrared spectroscopy. Eleven competitive oarsmen were evaluated during a 6-min maximal ergometer row. The study was randomized in a double-blind fashion with an inspired O2 fraction of 0.21 or 0.30 in a crossover design. During exercise with an inspired O2 fraction of 0.21, the arterial CO2 pressure (35 ± 1 mmHg; mean ± SE) and O2 pressure (77 ± 2 mmHg) as well as the hemoglobin saturation (91.9 ± 0.7%) were reduced ( P < 0.05).[Formula: see text] was reduced from 80 ± 2 to 63 ± 2% ( P < 0.05), and the near-infrared spectroscopy-determined concentration changes in deoxy- (ΔHb) and oxyhemoglobin (ΔHbO2) of the vastus lateralis muscle increased 22 ± 3 μM and decreased 14 ± 3 μM, respectively ( P < 0.05). Increasing the inspired O2fraction to 0.30 did not affect ventilation (174 ± 4 l/min), but arterial CO2 pressure (37 ± 2 mmHg), O2 pressure (165 ± 5 mmHg), and hemoglobin O2saturation (99 ± 0.1%) increased ( P < 0.05).[Formula: see text] remained close to the resting level during exercise (79 ± 2 vs. 81 ± 2%), and although the muscle ΔHb (18 ± 2 μM) and ΔHbO2 (−12 ± 3 μM) were similar to those established without O2 supplementation, work capacity increased from 389 ± 11 to 413 ± 10 W ( P < 0.05). These results indicate that an elevated inspiratory O2fraction increases exercise performance related to maintained cerebral oxygenation rather than to an effect on the working muscles.

Từ khóa


Tài liệu tham khảo

10.1113/jphysiol.1949.sp004403

10.1177/026765919501000407

10.1249/00005768-199504000-00008

10.1007/BF00634377

10.1007/s004210050471

10.2466/pms.1997.85.3.1019

10.1152/ajpcell.1992.262.3.C766

10.1249/00005768-199406000-00010

Cunningham D. A., 1975, Med. Sci. Sports, 7, 37

10.1113/jphysiol.1984.sp015412

10.1152/jappl.1994.77.6.2753

10.1152/jappl.1994.77.5.2408

10.1152/jappl.1997.83.1.11

10.1080/02640418608732108

10.1152/jappl.1994.77.2.912

10.1046/j.1365-201X.1998.0280f.x

10.1111/j.1600-0838.1993.tb00391.x

10.1126/science.929199

10.1152/jappl.1992.73.5.1825

10.1152/jappl.1992.72.3.1123

10.1152/jappl.1985.59.4.1061

10.1097/00004647-199609000-00006

10.1152/jappl.1993.75.6.2586

10.1113/jphysiol.1989.sp017500

10.1152/jappl.1995.78.1.12

10.1152/jappl.1999.86.2.687

10.1111/j.1475-097X.1995.tb00541.x

10.1046/j.1365-201X.1998.0308f.x

10.1016/S0301-0082(98)00093-8

10.1152/jappl.1993.74.1.245

10.1152/jappl.1994.77.6.2740

10.1161/01.STR.22.5.596

10.1046/j.1365-201x.1999.00485.x

10.1046/j.1365-201X.1998.00405.x

10.1152/jappl.1996.81.3.1174

10.1152/jappl.1992.73.5.1838

10.1249/00005768-199504000-00016

Pollard V., 1996, Anesth. Analg., 82, 269

Pollard V., 1996, Anesth. Analg., 82, 278

10.1046/j.1365-201X.1997.00144.x

10.1152/jappl.1989.66.6.2491

Prieur F., 1998, Med. Sci. Sports Exerc., 30, 958

10.1249/00005768-199112000-00005

10.1249/00005768-198706000-00010

10.1213/00000539-199704000-00005

10.1006/nimg.1996.0034

10.1152/jappl.1977.42.3.385

10.1152/jappl.1981.51.3.725

10.1016/0005-2728(88)90069-2

Thông tin
Thông tin xuất bản

American Journal of Physiology - Heart and Circulatory Physiology

Tập 277 Số 3

H1045-H1052

Thông tin tác giả