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

TLDR

The assumption that cellular oxygen pressure (PO₂) is near zero in maximally exercising muscle underpins the hypothesis that finite O₂ transport conductance between blood and mitochondria limits maximal O₂ consumption. The authors tested this assumption by exercising isolated human quadriceps, directly measuring arterial and femoral venous PO₂, and using ¹H NMR spectroscopy to detect myoglobin desaturation in six trained men breathing room air and 12 % O₂; partial desaturation appeared within 20 s of exercise onset, was greater in hypoxia, and remained constant at ~51 % (normoxia) and ~60 % (hypoxia) during incremental work. The study found myoglobin‑associated PO₂ averaged 3.1 mmHg in normoxia and 2.1 mmHg in hypoxia; at maximal exercise arterial PO₂ fell from 115 mmHg to 46 mmHg and femoral venous PO₂ from 22 mmHg to 17 mmHg, yielding mean capillary PO₂ of 38 mmHg (normoxia) and 30 mmHg (hypoxia), thereby demonstrating large PO₂ differences between blood and intracellular tissue across exercise intensities and indicating an O₂ diffusion limitation across the 1–5 µm path from red cell to sarcolemma that limits maximal muscle O₂ uptake.

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.