A. Pavyletraon et al., CARDIOVASCULAR-RESPONSES TO ORTHOSTATIC TESTS AFTER A 42-DAY HEAD-DOWN BED-REST, European journal of applied physiology and occupational physiology, 77(1-2), 1998, pp. 50-59
Cardiovascular responses to orthostatic tests were studied before and
after a prolonged 42 day-head-down bed-rest (HDBR:-6 degrees) experime
nt simulating a long duration space flight. Seven men participating in
the experiment underwent stand tests (10 min) and lower body negative
pressure (LBNP) tests (5 min at -25, -35, -45 mmHg). Heart rate varia
bility and spontaneous baroreflex response slope (SBS) were analysed t
o assess autonomic nervous system responses, Changes in plasma volume
(PV) were assessed at the end of HDBR, At the end of HDBR, four subjec
ts could not complete the stand tests and one could not complete the L
BNP test, A higher stressed heart rate with standing (+44% before and
+57% after HDBR) and LBNP exposure (+19% before and +34% after HDBR) w
ere observed. A decrease in blood pressure (BP) reflecting a reduced v
asomotor response was only observed with standing (mean BP +21% before
and -8% after HDBR); LBNP was less sensitive probably because it was
performed 6 h after the stand test, The PV decreased by 10.6%. A decli
ne in spectrum total power reflecting a reduced variance of RR-interva
l, a decrease in parasympathetic activity and an increase in sympathet
ic one were observed at the end of HDBR, The reduced. parasympathetic
indicator and SBS would suggest that the vagal nerve component of the
cardiovascular control had been diminished. Except for a lower BP when
standing after HDBR, no significant difference was observed between f
inishers and non-finishers. Autonomic nervous system changes including
reduced vasomotor responses constituted important contributors to the
orthostatic intolerance observed here and after space flights. Some a
utonomic and PV changes seemed to be opposite to those observed with t
raining and would suggest a role of reduced physical activity in cardi
ovascular changes induced by HDBR.