Dissociation of peak vascular conductance and V(O2) max among highly trained athletes

Previously, a strong relationship has been found between whole body maximal aerobic power (VO(2 max)) and peak vascular conductance in the calf muscle (J. L. Reading, J. M. Goodman, M. J. Plyley, J. S. Floras, P. P. Liu, P. R. McLaughlin, and R. J. Shephard. J. Appl. Physiol. 74: 567-573, 1993; P. G. Snell, W. H. Martin, J. C. Buckley, and C. G. Blomqvist. J. Appl. Physiol. 62: 606-610, 1987), suggesting a matching between maximal exercise capacity and peripheral vasodilatory reserve across a broad range of aerobic power. In contrast, long-term training could alter this relationship because of the unique demands for muscle blood flow and cardiac output imposed by different types of training. In particular, the high local blood flows but relatively low cardiac output demand imposed by the type of resistance training used by bodybuilders may cause a relatively greater development in peripheral vascular reserve than in aerobic power. To examine this possibility, we studied the relationship between treadmill VO(2 max) and vascular conductance in the calf by using strain-gauge plethysmography after maximal ischemic plantar flexion exercise in 8 healthy sedentary subjects (HS) and 28 athletes. The athletes were further divided into three groups: 10 elite middle-distance runners (ER), 11 power athletes (PA), and 7 bodybuilders (BB). We found that both BB and ER deviate from the previously demonstrated relationship between VO(2 max) and vascular conductance. Specifically, for a given vascular conductance, BB had a lower VO(2 max), whereas ER had a higher VO(2 max) than did HS and PA. We conclude that the relationship between peak vascular conductance and aerobic power is altered in BB and ER because of training-specific effects on central vs. peripheral cardiovascular adaptation to local skeletal muscle metabolic demand.