The physiological cost of wearing the propellant handler's ensemble at the Kennedy Space Center

The potential for exposure to toxins used in the propulsion systems of spacecraft dictates the use of a whole body protective suit, the Propellant Handler's Ensemble (PHE) during preflight preparation and launching. The weight, structure, and operating parameters of the PHE may be expected to have a significant impact upon the metabolic, cardiovascular, and thermal responses of the user, especially during ambient temperature extremes and high workload situations. Four male subjects participated in tests in -7, 23, and 43 C (20, 74, and 110 F) environments in two versions of the PHE, the autonomous backpack (BP) and the hoseline (HL) supplied configuration. Measurements included heart rate (HR) rectal temperature, four skin temperatures, oxygen (O2), and carbon dioxide (CO2) in the helmet area, interior suit temperature, and suit pressure. Exercise metabolism was estimated from HR, PHE weight, and treadmill speed and grade. The HR responses between each PHE configuration were not statistically different. As a percentage of HR maximum, the mean values were 79 percent (COLD), 84 percent (LAB), and 90 percent (HOT). Helmet O2 and CO2 levels were correlated with percent HR max (P less than 0.001). Rectal temperatures were similar for each PHE configuration, except in the HOT exposure where the BP version exceeded the HL configuration (P less than 0.05). In nearly every instance the HR was driven to moderately high levels, the supplied respiratory gases were not optimum, and thermal adversity was a primary stressor. Our findings suggest that medical and physical fitness standards, along with operational restrictions, should be imposed upon PHE users to avoid situations that could adversely affect the worker

An Occupational Performance Test Validation Program for Fire Fighters at the Kennedy Space Center

We evaluated performance of a modified Combat Task Test (CTT) and of standard fitness tests in 20 male subjects to assess the prediction of occupational performance standards for Kennedy Space Center fire fighters. The CTT consisted of stair-climbing, a chopping simulation, and a victim rescue simulation. Average CTT performance time was 3.61 +/- 0.25 min (SEM) and all CTT tasks required 93% to 97% maximal heart rate. By using scores from the standard fitness tests, a multiple linear regression model was fitted to each parameter: the stairclimb (r(exp 2) = .905, P less than .05), the chopping performance time (r(exp 2) = .582, P less than .05), the victim rescue time (r(exp 2) = .218, P = not significant), and the total performance time (r(exp 2) = .769, P less than .05). Treadmill time was the predominant variable, being the major predictor in two of four models. These results indicated that standardized fitness tests can predict performance on some CTT tasks and that test predictors were amenable to exercise training

Metabolic pathways promoting intrahepatic fatty acid accumulation in methionine and choline deficiency:implications for the pathogenesis of steatohepatitis

The pathological mechanisms that distinguish simple steatosis from steatohepatitis (or NASH, with consequent risk of cirrhosis and hepatocellular cancer) remain incompletely defined. Whereas both a methionine- and choline-deficient diet (MCDD) and a choline-deficient diet (CDD) lead to hepatic triglyceride accumulation, MCDD alone is associated with hepatic insulin resistance and inflammation (steatohepatitis). We used metabolic tracer techniques, including stable isotope ([13C4]palmitate) dilution and mass isotopomer distribution analysis (MIDA) of [13C2]acetate, to define differences in intrahepatic fatty acid metabolism that could explain the contrasting effect of MCDD and CDD on NASH in C57Bl6 mice. Compared with control-supplemented (CS) diet, liver triglyceride pool sizes were similarly elevated in CDD and MCDD groups (24.37 ± 2.4, 45.94 ± 3.9, and 43.30 ± 3.5 μmol/liver for CS, CDD, and MCDD, respectively), but intrahepatic neutrophil infiltration and plasma alanine aminotransferase (31 ± 3, 48 ± 4, 231 ± 79 U/l, P < 0.05) were elevated only in MCDD mice. However, despite loss of peripheral fat in MCDD mice, neither the rate of appearance of palmitate (27.2 ± 3.5, 26.3 ± 2.3, and 28.3 ± 3.5 μmol·kg−1·min−1) nor the contribution of circulating fatty acids to the liver triglyceride pool differed between groups. Unlike CDD, MCDD had a defect in hepatic triglyceride export that was confirmed using intravenous tyloxapol (142 ± 21, 122 ± 15, and 80 ± 7 mg·kg−1·h−1, P < 0.05). Moreover, hepatic de novo lipogenesis was significantly elevated in the MCDD group only (1.4 ± 0.3, 2.3 ± 0.4, and 3.4 ± 0.4 μmol/day, P < 0.01). These findings suggest that important alterations in hepatic fatty acid metabolism may promote the development of steatohepatitis. Similar mechanisms may predispose to hepatocyte damage in human NASH