Resistance training increases lower body negative pressure tolerance.

This study investigated whether whole body resistance training would increase tolerance to lower body negative pressure (LBNP). Twelve males (age = 19.6 +/- 0.4 yr; mean +/- SD) underwent an acute, 12-wk program of upper and lower body resistance training (ART). Pre- and posttraining, the ART group and a control group (CON; N = 8; age = 25.4 +/- 2.4 yr) underwent LBNP tolerance tests and neck pressure-suction testing. Additionally, a group of chronically resistance-trained individuals (CRT group; N = 5; age = 22.4 +/- 0.9 yr) were tested. LBNP tolerance was increased in the ART group after training and the CRT group exhibited a significantly higher LBNP tolerance than the other groups. The ART group exhibited a decreased leg circumference change at the same absolute negative pressure at which tolerance occurred pretraining. This indicated a decreased fluid pooling after ART. The CRT group exhibited a "flattened" hypotensive portion of the carotid sinus-heart rate baroreflex curve, but this appeared to be due to the increased neck muscle mass of the subjects. We conclude that whole body ART increases LBNP tolerance possibly mediated through alterations in vascular compliance. CRT results in even greater LBNP tolerance with the responsible mediating mechanisms unclear.

Ten weeks of aerobic training do not affect lower body negative pressure responses.

Based mostly on cross-sectional data, it has been suggested that aerobic training may decrease lower body negative pressure (LBNP) tolerance through a hypothesized attenuation in both high- and low-pressure baroreflex gain. An experimental group (EXP) of eight male subjects [22.1 +/- 1.4 (SD) yr] underwent a 10-wk treadmill and cycle ergometer training program, which resulted in a 21% increase in maximal O2 uptake (VO2 max), 45.7 +/- 1.5 vs. 55.2 +/- 1.7 (SE) ml.kg-1.min-1; P less than 0.05]. A control group, (CON; n = 7; 27.3 +/- 5.7 yr), which did not undergo training, had no significant changes in VO2 max (49.4 +/- 3.3 vs. 48.8 +/- 3.2 ml.kg-1.min-1). Before and after training the EXP and CON groups participated in LBNP tolerance tests (terminated at presyncope) and neck pressure-suction testing (to describe the carotid sinus-heart rate baroreflex). LBNP tolerance, as defined by three different indexes, and carotid sinus-heart rate baroreflex gain were not altered in either group after training. Furthermore, there were no changes in LBNP heart rate, blood pressure, leg circumference, forearm blood flow, or forearm vascular resistance responses at any level of LBNP challenge after training. In conclusion, 10 wk of aerobic training did not change LBNP tolerance or alter the reflex cardiovascular compensatory mechanisms activated during LBNP.