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Impairment of 3000-m Run Time at Altitude Is Influenced by Arterial Oxyhemoglobin Saturation

CHAPMAN, ROBERT F.1; STAGER, JOEL M.1; TANNER, DAVID A.1; STRAY-GUNDERSEN, JAMES2; LEVINE, BENJAMIND D.2

Medicine & Science in Sports & Exercise: September 2011 - Volume 43 - Issue 9 - p 1649-1656
doi: 10.1249/MSS.0b013e318211bf45
Basic Sciences

The decline in maximal oxygen uptake (ΔV˙O2max) with acute exposure to moderate altitude is dependent on the ability to maintain arterial oxyhemoglobin saturation (SaO2).

Purpose: This study examined if factors related to ΔV˙O2max at altitude are also related to the decline in race performance of elite athletes at altitude.

Methods: Twenty-seven elite distance runners (18 men and 9 women, V˙O2max = 71.8 ± 7.2 mL·kg−1·min−1) performed a treadmill exercise at a constant speed that simulated their 3000-m race pace, both in normoxia and in 16.3% O2 (∼2100 m). Separate 3000-m time trials were completed at sea level (18 h before altitude exposure) and at 2100 m (48 h after arrival at altitude). Statistical significance was set at P ≤ 0.05.

Results: Group 3000-m performance was significantly slower at altitude versus sea level (48.5 ± 12.7 s), and the declines were significant in men (48.4 ± 14.6 s) and women (48.6 ± 8.9 s). Athletes grouped by low SaO2 during race pace in normoxia (SaO2 < 91%, n = 7) had a significantly larger ΔV˙O2 in hypoxia (−9.2 ± 2.1 mL·kg−1·min−1) and Δ3000-m time at altitude (54.0 ± 13.7 s) compared with athletes with high SaO2 in normoxia (SaO2 > 93%, n = 7, ΔV˙O2 = −3.5 ± 2.0 mL·kg−1·min−1, Δ3000-m time = 38.9 ± 9.7 s). For all athletes, SaO2 during normoxic race pace running was significantly correlated with both ΔV˙O2 (r = −0.68) and Δ3000-m time (r = −0.38).

Conclusions: These results indicate that the degree of arterial oxyhemoglobin desaturation, already known to influence ΔV˙O2max at altitude, also contributes to the magnitude of decline in race performance at altitude.

1Human Performance Laboratory, Department of Kinesiology, Indiana University, Bloomington, IN; and 2Institute for Exercise and Environmental Medicine, Presbyterian Hospital of Dallas, The University of Texas Southwestern Medical Center at Dallas, Dallas, TX

Address for correspondence: Robert F. Chapman, Ph.D., HPER 112, Bloomington, IN 47405; E-mail: rfchapma@indiana.edu.

Submitted for publication October 2010.

Accepted for publication January 2011.

©2011The American College of Sports Medicine