Skeletal muscle capillary hemodynamics from rest to contractions: implications for oxygen transfer.

Muscle contractions evoke an immediate rise in blood flow. Distribution of this hyperemia within the capillary bed may be deterministic for muscle O(2) diffusing capacity and remains unresolved. We developed the exteriorized rat (n = 4) spinotrapezius muscle for evaluation of capillary hemodynamics before (rest), during, and immediately after (post) a bout of twitch contractions to resolve (second-by-second) alterations in red blood cell velocity (V(RBC)) and flux (f(RBC)). Contractions increased (all P < 0.05) capillary V(RBC) (rest: 270 +/- 62 microm/s; post: 428 +/- 47 microm/s), f(RBC) (rest: 22.4 +/- 5.5 cells/s; post: 44.3 +/- 5.5 cells/s), and hematocrit but not the percentage of capillaries supporting continuous RBC flow (rest: 84.0 +/- 0.7%; post: 89.5+/-1.4%; P > 0.05). V(RBC) peaked within the first one or two contractions, whereas f(RBC) increased to an initial short plateau (first 12-20 s) followed by a secondary rise to steady state. Hemodynamic temporal profiles were such that capillary hematocrit tended to decrease rather than increase over the first approximately 15 s of contractions. We conclude that contraction-induced alterations in capillary RBC flux and distribution augment both convective and diffusive mechanisms for blood-myocyte O(2) transfer. However, across the first 10-15 s of contractions, the immediate and precipitous rise in V(RBC) compared with the biphasic and prolonged increase of f(RBC) may act to lower O(2) diffusing capacity by not only reducing capillary transit time but by delaying the increase in the instantaneous RBC-to-capillary surface contact thought crucial for blood-myocyte O(2) flux.