Carotid-cardiac baroreflex response and LBNP tolerance following resistance training

TATRO, D. L., G. A. DUDLEY, and V. A. CONVERTINO. Carotid-cardiac baroreflex response and LBNP tolerance following resistance training. Med. Sci. Sports Exerc., Vol. 24, No. 7, pp. 789–796, 1992. The purpose of this study was to examine the effect of lower body resistance training on cardiovascular control mechanisms and blood pressure maintenance during an orthostatic challenge. Lower body negative pressure (LBNP) tolerance, carotid-cardiac baroreflex function (using neck chamber pressure), and calf compliance were measured in eight healthy males before and after 19 wk of knee extension and leg press training. Resistance training sessions consisted of four or five sets of 6–12 repetitions of each exercise, performed two times per week. Training increased strength 25 ± 3 (SE)% (P = 0.0003) and 31, ± 6% P = 0.0004), respectively, for the leg press and knee extension exercises. Average fiber size in biopsy samples of m. vastus lateralis increased 21 ± 5% (P = 0.0014). Resistance training had no significant effect on LBNP tolerance. However, calf compliance decreased in five of the seven subjects measured, with the group average changing from 4.4 ± 0.6 ml·mm Hg-1 to 3.9 ± 0.3 ml·mm Hg-‘ (P = 0.3826). The stimulus-response relationship of the carotid-cardiac baroreflex response shifted to the left on the carotid pressure axis as indicated by a reduction of 6 mm Hg in baseline systolic blood pressure (P = 0.0471). In addition, maximum slope increased from 5.4 ± 1.3 ms-mm Hg-1 before training to 6.6 ± 1.6 ms-mm Hg-1 after training (P = 0.0141). Our results suggest the possibility that high resistance, lower extremity exercise training can cause a chronic increase in sensitivity and resetting of the carotid-cardiac baroreflex. However, change in carotid-cardiac baroreflex function did not prove advantageous during a hypotensive challenge induced by LBNP. These findings may reflect the failure of the specific resistance training stimulus employed in our study to induce changes in other mechanisms important to blood pressure regulation.