Blood flow and pressure relationships which determine vo_2max

Blood flow and pressure relationships which determine VO_2max. Med. Sci. Sports Exerc., Vol. 27, No. 1, pp. 37-42, 1995. The role of O₂ delivery in regulating VO_2max has been studied in an isolated gastrocnemius-plantaris muscle preparation contracting insitu; recent data addressing this issue are presented. VO₂ increases nonlinearly 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 stimulation 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 directly related to the level of blood flow attained as VO₂/Q (arterial-venous O₂ difference) is fixed by some unknown mechanism. Increasing blood flow, with a pump, during 1·s⁻¹ tetanic contractions increases O₂ diffusive conductance and peak VO₂. When O₂ delivery is reduced, ischemic hypoxia appears to result in more rapid reductions in muscle performance than hypoxic hypoxia because of decreases in perfusion pressure and Q.³¹P-NMR studies reveal that reductions in creatine phosphate and energy charge are similar between ischemia and hypoxia suggesting a common regulator, O₂. We conclude that VO_2max is limited by O₂ delivery as a result of a limited and uneven distribution of muscle blood flow. These limitations appear secondary to mechanical restraints imposed by contraction duty cycle and vascular compression.