BLOOD-FLOW AND PRESSURE RELATIONSHIPS WHICH DETERMINE VO2MAX

The role of O-2 delivery in regulating VO2max has been studied in an i solated gastrocnemius-plantaris muscle preparation contracting in situ ; recent data addressing this issue are presented. VO2 increases nonli nearly with stimulation frequency reaching a peak at 5 twitches.s(-1) or 1 tet.s(-1) (200 ms trains, 50 imp.s(-1)). Further increases in sti mulation frequency result in a lower VO2. Measured VO2 maxima are less than predicted VO2 capacity, and peak VO2 during tetanic contractions is greater than that during twitches. Above 150 imp min(-1), VO2 is d irectly related to the level of blood flow attained as VO2/Q (arterial -venous O-2 difference) is fixed by some unknown mechanism. Increasing blood flow, with a pump, during 1.s(-1) tetanic contractions increase s O-2 diffusive conductance and peak VO2. When O-2 delivery is reduced , ischemic hypoxia appears to result in more rapid reductions in muscl e performance than hypoxic hypoxia because of decreases in perfusion p ressure and Q. P-31-NMR studies reveal that reductions in creatine pho sphate and energy charge are similar between ischemia and hypoxia sugg esting a common regulator, O-2. We conclude that VO2max is limited by O-2 delivery as a result of a limited and uneven distribution of muscl e blood flow. These limitations appear secondary to mechanical restrai nts imposed by contraction duty cycle and vascular compression.