i3?8 



HANDBOOK OF PHYSIOLOGY 



CIRCULATION II 



140 



ML/MIN 



I20 



IOO 



5 



o 



80 



8 6 ° 



40 

 20 



IO 

 ML/MIN 

 8 



z 

 O 



E 6 



io 4 



Z 



o 



O 25 SO 75 IOO% 



WORK PERFORMED AS °/ c MAXIMUM 



fig. 23. Results showing that blood flow and oxygen con- 

 sumption in the dog's gastrocnemius muscle were proportional 

 to the work done during rhythmic contraction. [From Kramer 

 el al. (132).] 



So much for Kramer's experiments. It is worth 

 recalling that Barger el al. (31) in their experiments 

 on the regulation of the circulation in exercise in 

 the normal clog also concluded, though from less 

 direct evidence, that muscle blood flow and oxygen 

 consumption were directly related. 



It is worth noting that in hyperthyroid subjects 

 the postexercise blood flow following a standard 

 exercise is much increased (1). Here again an ex- 

 planation might take us to the very center of the 

 mechanism of exercise hyperemia. 



But now we must "jot down" some results which 

 make it difficult to picture a relationship between 

 tissue oxygen tension and blood flow. Let us begin 

 with experiments by Dornhorst & Whelan (68). 

 They studied the effect of reduction of femoral arterial 

 blood pressure on postexercise hyperemia in the calf 

 muscles. The effective arterial pressure could be 

 halved by means of a pressure plethysmograph. 

 Figure 24 shows a typical result. After the arterial 

 pressure was reduced by one-half, the postexercise 

 hyperemia flows and "blood debt" were lowered but 

 the hyperemia was not prolonged. The changes in 

 the peripheral vascular resistance of the calf were 



exactly similar to those found in the limb with normal 

 blood pressure. Thus, if postexercise hyperemia 

 depended on the local concentration of a metabolite, 

 its removal or destruction could not depend on the 

 rate of blood flow nor could its oxidation depend upon 

 local oxygen tension. They concluded that for post- 

 exercise hyperemia, as for reactive hyperemia (see 

 above), the vasodilatation could be due to an intra- 

 cellular metabolite the removal of which from the 

 tissue of the vessel wall is limited more criticallv by 

 its diffusion gradient than by the rate of blood flow 

 through the vessel lumen. Such a metabolite, they 

 suggested, would be deactivated primarily by intra- 

 cellular oxidation. 



Holling & Verel (125) studied the effect of lowering 

 the effective arterial pressure on the forearm blood 

 flow. Arterial pressure was lowered by elevating the 

 forearm. There was a linear relation between pressure 

 and flow. Peripheral vascular resistance did not 

 change. Compensation for reduction of perfusion 

 pressure by vasodilatation did not occur. Oxygen 

 tension in the elevated forearm was reduced as 

 shown by the polarograph, but oxygen uptake was 

 unaltered because of increased utilization. Their 

 findings did not support the concept that metabolism 

 of resting muscle played a prominent role in the 

 regulation of its blood flow. In line with this, Blair 

 et al. (40) showed that compression of the brachial 

 arterv for 5 min beginning at the end of 1 min 

 rhythmic exercise of the forearm muscles altogether 

 abolished postcontraction hyperemia. They concluded 

 that it was not necessary to have an increase in blood 

 flow after exercise to "repay" the "debt" incurred in 

 exercise. This agrees with their observations following 

 postocclusive (reactive) hyperemia (see above). 

 However, by supplying the tissues with an excess of 

 blood, postexercise hyperemia does return the tissues 

 to the resting state more quickly than does the resting 

 flow. 



If oxygen lack of the arterial tree opens the vessels 

 in exercise, then asphyxiating skeletal muscle should 

 cause hyperemia. Bayliss (34), however, found that 

 the blood flow through the denervated hind limb 

 did not alter when the arterial blood was made 

 asphyxial. Yerzar (176) studied the effect of ven- 

 tilating the cat with 8 to 1 o per cent oxygen on the 

 gaseous metabolism of the gastrocnemius muscle. 

 Partial asphyxia of the muscle greatly reduced its 

 rate of oxygen consumption but had no effect on the 

 rate of the blood flow. The venous blood seldom 

 became less than 30 per cent saturated with oxygen, 

 nevertheless tissue oxvgen tension in regions farthest 



