Fighter pilots flying high-performance aircraft are commonly exposed to high-sustained gravitoinertial force field in the head-to-seat direction (i.e., + Gz; henceforth G denotes + Gz), eliciting exaggerated hydrostatic pressure gradients in the vasculature, with markedly elevated intravascular pressures in the dependent vessels, and reduced pressures in the vessels above the heart. The capacity to, in a relaxed state (i.e., without the use of anti-G strategies/garments), withstand enhanced G loads (relaxed G tolerance) is, hence, determined by the arterial-pressure responsiveness, preserving adequate ocular and cerebral perfusion (Balldin
1986; Green
2016; Pollock et al.
2021). G tolerance, which describes large inter-individual variability, appears to be influenced by several anatomical and functional features, mainly including the basal levels of arterial pressure and the heart-to-head vertical distance (Klein et al.
1969), the wall stiffness of the lower-limb precapillary resistance vessels (Eiken et al.
2012,
2022 ), and, during gradual/slow increments of the G load, also the function of sympathetic circulatory reflexes (Newman et al.
1998; Sundblad et al.
2016; Convertino
2001; Scott et al.
2013). Thus, in regards to the latter, a cross-sectional study in a cohort of non-pilots, has indicated that, compared to individuals with low gradual onset G tolerance (< 4.2 G), those possessing high G tolerance (≥ 5.5 G) exhibit an augmented pressure response to an acute sympathoexcitatory stimulus, namely the hand cold-pressor test (Sundblad et al.
2014). These inherent differences in arterial-pressure regulation were attributable to between-group variations in vasoconstrictor sensitivity, presumably associated with higher myogenic responsiveness in the high-G-tolerant individuals, rather than to changes in sympathetic outflow.
Recently, we demonstrated that 5 weeks of repeated + G exposures (G training) in a relaxed state, improved G tolerance, especially during rapid onset-rate elevation of the G load (Eiken et al.
2022). Such a response was ascribed predominantly to local adaptations, described by the reduced pressure distensibility of leg arteries/arterioles, elicited by the recurrent transmural pressure increases. Still, whether the long-term iterative hypergravity exposures might also have modulated sympathetically mediated cardiovascular reflex responses, contributing, at least partly, to the enhanced G tolerance, remains unknown.
Accordingly, the present study tested the hypothesis that repetitive gravitoinertial stress would augment the arterial-pressure response to peripheral sympathetic stimulation. To this end, we employed a within-subject design, wherein systemic hemodynamic responses were monitored during a hand cold-pressor test, before and after a 5-weeks G-training regimen performed in a human-use centrifuge. On the basis of previous evidence (Sundblad et al.
2014), we hypothesized that iterative increments in total peripheral blood-flow resistance (TPR) induced during the G training, might amplify the cold-induced arterial-pressure elevation, due to a more pronounced increase in TPR. In view of our finding that the vasoadaptations evoked by the G training were limited to the lower-limb vasculature (Eiken et al.
2022), a foot cold-pressor test was also conducted by a subset of subjects, at the same time points.