The time course and magnitude of blood flow changes in the human quadriceps muscles following isometric contraction.

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Abstract
Blood velocities in the human femoral artery were measured using pulsed bidirectional Doppler‐ultrasound equipment before, during and after single isometric contractions of the quadriceps muscle group. After contraction periods lasting more than 20 s (long) and of tensions from 10% up to 75% of maximal voluntary contraction (m.v.c.), an increase in blood velocities of seven to eight times the resting level was observed. Estimated maximal volume flow to the whole leg during the post‐contraction hyperaemic phase calculated from these blood velocity measurements and vessel diameter (measured with echo‐ultrasound equipment) was in two of the subjects 2.4 l/min (female) and 4.4 l/min (male), respectively. In the latter, this estimate fitted very well with results obtained using a venous thermo‐dilution method. When using computer tomography to estimate the volume of the quadriceps muscle group, the calculated maximum flow to this muscle group in the post‐contraction hyperaemic phase was approximately 175 (female) and 185 (male) ml/min. 100 ml muscle, respectively. This was about forty times the estimated resting volume flow to this muscle of 4.7 (female) and 4.5 (male) ml/min. 100 ml muscle. The length of the post‐contraction hyperaemia after short (less than 10 s) contraction periods was 12‐13 s, by which time velocities had reached 25% above the precontraction level. After long contractions, the corresponding values were 23‐25 s. By contrast, previous plethysmographic observations by others indicate that postcontraction hyperaemias following long contractions last 10‐15 min. There was a marked difference between the times taken to reach maximal velocity in the hyperaemic phase when comparing short and long contractions. Maximal velocity was reached four to six cardiac cycles following short periods of contraction but during the very first heart beat after long periods of contractions. The present observations are compatible with the hypothesis that locally released metabolites or hormones play a dominant role in the regulation of the post‐contraction hyperaemia. Since during the short contraction periods maximal velocity was reached only after some seconds, whereas with the longer contraction periods it was reached during the first heart beat, it is suggested that these metabolites are released at some distance from the resistance vessels and that some time is needed for diffusion.