Moderate exercise effects on orthostatic intolerance while wearing protective clothing.

INTRODUCTION: Wearing protective clothing can have deleterious effects on operational capacities and can cause non-compensable thermal stress. We studied the effects of moderate exercise on orthostatic tolerance while wearing protective clothing in eight healthy subjects tolerant to orthostatism. METHODS: Subjects performed a 60-min moderate exercise on a treadmill followed by a 45-min head-up tilt test. Subjects performed the moderate exercise either in a comfortable condition (control, CON) or wearing protective clothing (PRO) in a random order. RESULTS: Compared with the CON trial, exercise in the PRO trial induced higher body dehydration, heart rate, and rectal temperature and a decrease in plasma volume. Orthostatic tolerance was significantly reduced in the PRO trial (23.7 +/- 0.2 min) compared with the CON trial (40.7 +/- 1.0 min). Transition from supine to head-up position caused a significant decrease in blood pressure in the PRO compared with the CON. RR interval was smaller in the PRO trial compared with CON in both the supine and head-up positions. Spontaneous baroreflex sensitivity was decreased in the PRO, either supine or standing, compared to CON (4.6 +/- 0.5 ms x mmHg(-1) and 14.5 +/- 4.2 ms x mmHg(-1) in supine, and 3.3 +/- 0.6 ms x mmHg(-1) and 7.0 +/- 0.6 ms x mmHg(-1) in standing, for PRO and CON, respectively). DISCUSSION: These results suggest that the large decrease in the tolerance to orthostatism after exercise while wearing protective clothing was due to the impossibility of maintaining an adapted blood pressure induced by a conflict between the needs of peripherical vasoconstriction linked to the standing posture, the needs of vasodilatation linked to thermoregulation, and a drop in the sensibility of the spontaneous baroreflex.

Oxidative stress and 17-alpha- and 17-beta-estradiol modulate neurofilaments differently.

Oxidative stress plays an important role in the pathogenesis of neurodegenerative diseases such as Parkinson's disease (PD). Neuronal death in the substantia nigra of PD patients is partly caused by exacerbated oxidative damage. Our previous studies demonstrated that oxidative stress can alter the structure and stability of neurofilament (NF) proteins and that 17-alpha- and 17-beta-estradiol are potent neuroprotective agents. The aim of this study was to investigate the cytoskeletal target of neuroprotection by estrogens in neuronal PC12 cells. We induced oxidative stress by MPP+ administration for 24 h, and 17-alpha- and 17-beta-estradiol were used as neuroprotective drugs. We measured gene expression and protein expression of each NF subunit, NFL, NFM, and NFH, by semiquantitative RT-PCR, Western blot, and immunofluorescence. Our results demonstrate that NFL mRNA and protein levels are not modulated by MPP+ or estradiol isomers, whereas NFM gene expression, as well as protein expression, are strongly influenced by MPP+, 17-alpha-, and 17-beta-estradiol after a 24-h treatment. Finally, mRNA levels of the most phosphorylated subunits, NFH, are not changed by MPP+ or treatment with both estradiol isomers, whereas NFH protein expression is decreased by the same treatments. These results suggest that oxidative stress affects neuronal cytoskeleton, maybe though proteolysis and/or abnormal structural changes in NFs. Then, 17-alpha- and 17-beta-estradiol might help the neuronal cell in recovering after oxidative stress by inducing protein expression of NFM and NFH subunits.