Oxygen transport in rest-work transition illustrates new functions for myoglobin.

Myoglobin (Mb) saturation was measured spectroscopically in 1,950 randomly selected cells from dog gracilis muscles frozen in situ during the transition from rest to steady twitch contraction at approximately 70% maximum rate of O2 consumption (VO2max). Measurements were made at the center of muscle-cell profiles in cross section, with spatial resolution approximately 5 X 5 X 3 micron. PO2 was calculated from saturation by use of the oxymyoglobin dissociation curve. Flow increased more rapidly than VO2 (half-times 5 and 14 s, respectively). Mb saturation changed little through 15 s. Saturation was lowest at 30 s and rose somewhat between 30 s and steady state. The lowest intracellular PO2 at any time or location was 1.5 Torr, and only 5% of loci were below 2 Torr. Since 1.5 Torr is about 10 times the minimum PO2 required for the observed VO2 (Connett et al. An upper bound on the minimum PO2 for O2 consumption in red muscle in vivo. Adv. Exp. Med. Biol. In press.), neither anoxia nor hypoxia was present. The observed fall in saturation and intracellular PO2 during exercise permits Mb to 1) promote transcapillary O2 flux, 2) facilitate intracellular O2 diffusion, 3) minimize convective and diffusive shunting, and 4) buffer intracellular PO2 above the tension that limits cytochrome turnover.