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In skeletal muscle capillaries, red blood cell (RBC) flux (F(RBC)), velocity (V(RBC)) and haematocrit (Hct(CAP)) are key determinants of microvascular O2 exchange. However, the mechanisms leading to the changes in F(RBC), V(RBC) and Hct(CAP) during muscle contractions and recovery thereafter are not fully understood. To address this issue we used intravital microscopy to investigate the temporal profile of the rat spinotrapezius muscle (n = 5) capillary haemodynamics during recovery from 3 min of twitch muscle contractions (1 Hz, 4-6 V). Specifically, we hypothesized that (1) during early recovery F(RBC) and V(RBC) would decrease rapidly and F(RBC) would display a biphasic response (consistent with a muscle pump effect on capillary haemodynamics), and (2) there would be a dynamic relationship between changes (Delta) in V(RBC) and Hct(CAP). The values at rest (R) and end-recovery (ER) were significantly lower (P < 0.05) than at end-contraction (EC) for F(RBC) (in cells s(-1), R = 30.1 +/- 7.8, EC = 46.2 +/- 7.3 and ER = 26.0 +/- 6.1), V(RBC) (in microm s(-1), R = 368 +/- 83, EC = 497 +/- 62 and ER = 334 +/- 59) and Hct(CAP) (R = 0.193 +/- 0.016, EC = 0.214 +/- 0.023 and ER = 0.185 +/- 0.019). The first data point where a significant decrease in F(RBC), Hct(CAP) and V(RBC) occurred was at 5, 5 and 20 s post-contraction, respectively. The decrease in F(RBC) approximated a monoexponential response (half-time of approximately 26 s). The relationship between DeltaV(RBC) and DeltaHct(CAP) was not significant (P > 0.05). Based on the early decrease in F(RBC) (within 5 s), overall dynamic profile of F(RBC) and the approximately 20 s 'delay' to the decrease in V(RBC) we conclude that the muscle pump does not appear to contribute substantially to the steady-state capillary haemodynamics in the contracting rat spinotrapezius muscle. Moreover, our findings suggest that alterations in V(RBC) do not obligate proportional changes in Hct(CAP) within individual capillaries following muscle contractions.

In response to an elevated metabolic rate ((.-)V(O(2)), increased microvascular blood-muscle O(2) flux is the product of both augmented O(2) delivery ((.-)Q(O(2)), and fractional O(2) extraction. Whole body and exercising limb measurements demonstrate that (.-)Q(O(2) and fractional O(2) extraction increase as linear and hyperbolic functions, respectively, of (.-)V(O(2). Given the presence of disparate vascular control mechanisms among different muscle fibre types, we tested the hypothesis that, in response to muscle contractions, (.-)Q(O(2) would be lower and fractional O(2) extraction (as assessed via microvascular O(2) pressure, P(mvO(2))) higher in fast- versus slow-twitch muscles. Radiolabelled microsphere and phosphorescence quenching techniques were used to measure (.-)Q(O(2) and P(mvO(2)), respectively at rest and across the transition to 1 Hz twitch contractions at low (Lo, 2.5 V) and high intensities (Hi, 4.5 V) in rat (n = 20) soleus (Sol, slow-twitch, type I), mixed gastrocnemius (MG, fast-twitch, type IIa) and white gastrocnemius (WG, fast-twitch, type IIb) muscle. At rest and for Lo and Hi (steady-state values) transitions, P(mvO(2)) was lower (all P < 0.05) in MG (mmHg: rest, 22.5 +/- 1.0; Lo, 15.3 +/- 1.3; Hi, 10.2 +/- 1.6) and WG (mmHg: rest, 19.0 +/- 1.3; Lo, 12.2 +/- 1.1; Hi, 9.9 +/- 1.1) than in Sol (rest, 33.1 +/- 3.2 mmHg; Lo, 19.0 +/- 2.3 mmHg; Hi, 18.7 +/- 1.8 mmHg), despite lower (.-)V(O(2) and (.-)Q(O(2) in MG and WG under each set of conditions. These data suggest that during submaximal metabolic rates, the relationship between (.-)Q(O(2) and O(2) extraction is dependent on fibre type (at least in the muscles studied herein), such that muscles comprised of fast-twitch fibres display a greater fractional O(2) extraction (i.e. lower P(mvO(2))) than their slow-twitch counterparts. These results also indicate that the greater sustained P(mvO(2)) in Sol may be important for ensuring high blood-myocyte O(2) flux and therefore a greater oxidative contribution to energetic requirements.

To determine whether fibre type affects the O2 exchange characteristics of skeletal muscle at the microcirculatory level we tested the hypothesis that, following the onset of contractions, muscle comprising predominately type I fibres (soleus, Sol, 86 % type I) would, based on demonstrated blood flow responses, exhibit a blunted microvascular PO2 (PO2,m, which is determined by the O2 delivery (QO2) to O2 uptake (VO2) ratio) profile (assessed via phosphorescence quenching) compared to muscle of primarily type II fibres (peroneal, Per, 84 % type II). PO2,m was measured at rest, and following the rest-contractions (twitch, 1 Hz, 2-4 V for 120 s) transition in Sol (n = 6) and Per (n = 6) muscles of Sprague-Dawley rats. Both muscles exhibited a delay followed by a mono-exponential decrease in PO2,m to the steady state. However, compared with Sol, Per demonstrated (1) a larger change in baseline minus steady state contracting PO2,m (DeltaPO2,m) (Per, 13.4 +/- 1.7 mmHg; Sol, 8.6 +/- 0.9 mmHg, P < 0.05); (2) a faster mean response time (i.e. time delay (TD) plus time constant (tau); Per, 23.8 +/- 1.5 s; Sol, 39.6 +/- 4.3 s, P < 0.05); and therefore (3) a greater rate of PO2,m decline (DeltaPO2,m/tau; Per, 0.92 +/- 0.08 mmHg s-1; Sol, 0.42 +/- 0.05 mmHg s-1, P < 0.05). These data demonstrate an increased microvascular pressure head of O2 at any given point after the initial time delay for Sol versus Per following the onset of contractions that is probably due to faster QO2 dynamics relative to those of VO2.