The interaction of strength and aerobic fitness on sympathetic nervous system activity in simulated weightlessness and reentry

The purpose of this study was to investigate the interactive effects of various levels of aerobic fitness and leg strength on the plasma catecholamine concentrations during simulated weightlessness and reentry. Twenty-four male subjects (30.8±3.9 years old, 178.9±4.9 cm, and 81.0±0.2 kg) were classified into four groups by their aerobic capacity and leg strength . If the subject's VO₂max was ≤50 ml 02/(kg-min) or ≥45 ml O₂/(kg-min), he was classified as high fit (HF) or low fit (LF), respectively. Using a Cybex dynanometer, if the subject could lift ≥103% or ≤97% of his bodyweight with each leg, he was classified as high strength (HS) or low strength (LS), respectively. The subjects underwent a 90 min., -6° head-down tilt (HDT), preceded by a 20 minute baseline period and followed by a lower body negative pressure (LBNP) test to -50 mm Hg. Heart rate (HR), plasma norepinephrine (NE) and epinephrine (E) levels were measured. Mean arterial pressure (MAP) was calculated using systolic and diastolic blood pressures. During the first 15 minutes of HDT, there were no changes in NE, E, or HR in any of the groups. During 90 minutes of HDT, there were no differences in E and NE levels among the groups. NE responses during LBNP were not different among the groups. While the E responses of the HFHS, LFHS, and LFLS groups to LBNP increased similarly, E levels in the HFLS group did not change during LBNP. The low fit, high strength group (LFHS) exhibited a significantly higher MAP during LBNP than the other three groups. The head-down tilt responses indicate that early exposure to head-down tilt does not result in a load on the cardiac baroreceptors sufficent to trigger changes in sympathetic nervous activity and heart rate. The data also indicate that the sympathetic nervous system response to head-down tilt does not differ in individuals with different combinations of aerobic fitness and strength levels. The similar increases in NE in all the subjects during LBNP IV suggested that the stress did not recruit trained systems in the subjects (stress specificity). Similarity of E responses during LBNP in the LF and HFHS groups was also attributed to stress specificity. The LBNP protocol did not stress the HFLS group sufficently to increase the E levels during LBNP. The increased MAP in the LFHS group during LBNP was speculated to be due to an augmentation of blood pressure with high strength levels. The augmentation could be due to increased muscle tone in the LFHS group.