Indirect evidence of CNS adrenergic pathways activation during spaceflight

Microgravity causes cephalad fluid shift and compensatory mechanisms. Hormonal changes suggestive of peripheral sympathetic (catecholaminergic) nervous system activation have been recently found in astronauts during flight. Simulation studies showed increased perivascular sympathetic fiber density in the rat brain.

Intracranial microcirculatory adaptations might also occur in astronauts, involving an increase in the turnover rate of catecholamines, i.e., norepinephrine (NE) and its precursor, Dopamine (DA). DA is known to inhibit prolactin (PRL) release and to enhance growth hormone (GH) secretion by the pituitary. Therefore, increased brain dopaminergic activity would result into lower circulating PRL concentrations. At the same time, plasma levels of GH and of its effector insulin-like growth factor-1 (IGF-1) would increase during flight.

Circulating cortisol (CS), PRL, GH and IGF-1 levels were measured 2 d preflight, inflight (4-5 d after launch) and on different days postflight in four astronauts involved in the Spacelab D-2 mission.

No significant changes were found in CS concentrations. PRL decreased while GH and IGF-1 increased inflight (p < 0.05). After flight no statistically relevant hormonal changes were found with respect to preflight.

The observed hormonal changes were consistent with the original hypothesis that spaceflight might activate CNS adrenergic pathways. They occurred in the absence of two typical markers of stress, namely CS and PRL increase, thus ruling out any non-specific effect of acute stress on the results. In agreement with the most recent results of real and simulated microgravity studies performed in both the experimental animal and in man, these data lend support to the hypothesis that the CNS adrenergic pathways are also activated in the human during spaceflight.