Background: In the search for parameters to predict motion sickness that can be measured in the laboratory, we performed a longitudinal investigation in aviators. Since the vestibular system is involved in the generation of motion sickness as well as eye movements, vestibulo-ocular reflex (VOR) parameters seemed relevant. We investigated three topics: 1) the effect of axis orientation and its orientation to gravity on the VOR; 2) changes in VOR parameters depending on flight experience; and 3) differences in VOR parameters in aircrew with high and low susceptibility to motion sickness. Hypothesis: Nystagmus decay after angular velocity steps would be faster for non-susceptible and trained aviators. Methods: We recorded eye movements evoked by angular on-axis velocity steps (±90° · s-2, to and from 90° · s-1) in yaw, pitch, and roll, about both the Earth vertical and Earth horizontal axes in 14 subjects with a low susceptibility to motion sickness. These data were compared with those of 10 subjects with a high susceptibility. Results: Horizontal axis rotations are nauseogenic. We found that during (per) and post-condition, left- and rightward rotation responses were equal, and the orientation with respect to gravity did not alter the basic nystagmus decay, apart from a sinusoidal modulation. Moreover, pitch and roll rotations show equal nystagmus decays, significantly faster than for yaw; yaw and pitch peak velocities were equal and were larger than for roll. With regard to changes in VOR parameters depending on flight experience, we found that repeated vestibular stimulation reduced nystagmus decay as well as the otolith modulation. With respect to the changes in VOR parameters and motion sickness susceptibility, we found that subjects highly susceptible to motion sickness showed a slower decay of nystagmus with a larger peak velocity than less susceptible subjects. Conclusions: Group averages indicate a difference in eye movement parameters, only in yaw, depending on flight experience; and between subjects with low and high susceptibility to motion sickness. The involvement of the velocity storage mechanism as realized by an internal model is given as a plausible explanation.