Cited by 647Cardiovascular and exercise physiologyHemoglobin structure and functionHigh Altitude and Hypoxia

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Myoglobin O2 desaturation during exercise. Evidence of limited O2 transport.

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Richardson, R S, Noyszewski, E A, Kendrick, K F, Leigh, J S, Wagner, P D·1995·Journal of Clinical Investigation

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Abstract

The assumption that cellular oxygen pressure (PO2) is close to zero in maximally exercising muscle is essential for the hypothesis that O2 transport between blood and mitochondria has a finite conductance that determines maximum O2 consumption. The unique combination of isolated human quadriceps exercise, direct measures of arterial, femoral venous PO2, and 1H nuclear magnetic resonance spectroscopy to detect myoglobin desaturation enabled this assumption to be tested in six trained men while breathing room air (normoxic, N) and 12% O2 (hypoxic, H). Within 20 s of exercise onset partial myoglobin desaturation was evident even at 50% of maximum O2 consumption, was significantly greater in H than N, and was then constant at an average of 51 +/- 3% (N) and 60 +/- 3% (H) throughout the incremental exercise protocol to maximum work rate. Assuming a myoglobin PO2 where 50% of myoglobin binding sites are bound with O2 of 3.2 mmHg, myoglobin-associated PO2 averaged 3.1 +/- .3 (N) and 2.1 +/- .2 mmHg (H). At maximal exercise, measurements of arterial PO2 (115 +/- 4 [N] and 46 +/- 1 mmHg [H]) and femoral venous PO2 (22 +/- 1.6 [N] and 17 +/- 1.3 mmHg [H]) resulted in calculated mean capillary PO2 values of 38 +/- 2 (N) and 30 +/- 2 mmHg(H). Thus, for the first time, large differences in PO2 between blood and intracellular tissue have been demonstrated in intact normal human muscle and are found over a wide range of exercise intensities. These data are consistent with an O2 diffusion limitation across the 1-5-microns path-length from red cell to the sarcolemma that plays a role in determining maximal muscle O2 uptake in normal humans.

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Authors: Richardson, R. S., Noyszewski, E. A., Kendrick, K. F., Leigh, J. S., & Wagner, P. D.
Affiliations: University of California System (US)
ORCID: Richardson, R S
Wagner, P D
Venue: Journal of Clinical Investigation
Publisher: American Society for Clinical Investigation
Published: 1995-10-01
Volume: 96
Issue: 4
Pages: 1916-1926
ISSN: 0021-9738 (ISSN-L)
DOI: 10.1172/jci118237
PMC: PMC185828
OpenAlex: W2074243670
Cited by: 647
References: 47
Citations by year: 2026: 19 · 2025: 16 · 2024: 29 · 2023: 27 · 2022: 16 · 2021: 19 · 2020: 28 · 2019: 23 · 2018: 20 · 2017: 26 · 2016: 14 · 2015: 31 · 2014: 19 · 2013: 21 · 2012: 24
FWCI: 27.28
Type: journal article
Language: en
Open access: bronze
doi.org
Locations: Journal of Clinical Investigation (publishedVersion)
PubMed Central (publishedVersion)
PubMed (publishedVersion)
Funders: Tobacco-Related Disease Research Program
National Heart, Lung, and Blood Institute (R01HL044125, HL 44125, P01HL017731, HL17731)
Topics: Health Sciences › Medicine › Physiology (medical) › Cardiovascular and exercise physiology
Life Sciences › Biochemistry, Genetics and Molecular Biology › Biochemistry › Hemoglobin structure and function
Health Sciences › Medicine › Physiology (medical) › High Altitude and Hypoxia
Keywords: oxygen transport, physical activity, hypoxia, capillary oxygen tension, muscle oxygenation, oxygen diffusion limitation, VO2max, quadriceps, arterial oxygen tension, 1H NMR, trained men
MeSH terms: Adult, Biological Transport, Humans, Hydrogen-Ion Concentration, Leg, Male, Muscles, Myoglobin, Oxygen, Oxygen Consumption, Exercise, Cell Respiration

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Myoglobin O2 desaturation during exercise. Evidence of limited O2 transport.

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