As the brain is limited in its capacity to store glucose or oxygen, adequate cerebral perfusion is fundamental to normal brain functioning. Rapid alterations in the gravitational gradient cause shifts in blood volume and pressure that can affect cerebral perfusion and leave high-performance aircraft pilots prone to various degrees of compromised brain function (e.g. loss of vision or consciousness). Characterizing how shifts in blood volume and pressure affect cerebral perfusion is not only important for the safety of aircraft pilots, but also adds to our understanding of how systemic and local haemodynamic factors work together to coordinate cerebral perfusion under various stressors. Exaggerated adjustments to the cardio- and cerebrovascular systems are observed during flight manoeuvres such as the push–pull manoeuvre, which consists of transitioning from negative g-forces along the longitudinal axis of the body (−Gz) during a ‘push’ phase, to positive g-forces (+Gz) during a ‘pull’ phase. During −Gz to +Gz transitions, a reduced physiological tolerance to changes in the gravitational gradient occurs, which is otherwise not present during transitions from 1 Gz to >1 Gz, and the reduced physiological tolerance is called the ‘push–pull effect’. Although mechanisms underlying the push–pull effect are not completely understood, an articulate review by Scott et al. (2007) summarizes how the arterial baroreflex may play an important part in the push–pull effect. Specifically, during the push phase, vessels above the heart experience an increase in intravascular hydrostatic forces, which initiates baroreflex-mediated bradycardia and peripheral vasodilation that leads to a reduction in mean arterial pressure (MAP). Upon transitioning to the pull phase, the (slow-to-reverse) baroreflex-induced drop in MAP is carried through to the initial segment of the pull phase. Swift transition from the push to pull phase causes brief mechanical reductions in carotid artery pressure which build on existing baroreflex-mediated reductions in MAP, potentially exaggerating +Gz-related reductions in eye-level perfusion pressures and impacting cerebral perfusion. Current strategies for protecting cerebral perfusion during flight manoeuvres include donning anti-gravity suits targeted at increasing venous return to the heart or performing a Valsalva-like anti-gravity straining manoeuvre that increases both arterial pressure and venous return. The aforementioned strategies target blood pressure drops during the +Gz or pull phase and may even augment haemodynamic changes during the push phase, which could exaggerate drops in blood pressure during the subsequent pull phase. What if instead of targeting blood pressure drops during the pull phase, cerebral perfusion preservation methods could instead focus on minimizing haemodynamic changes during the push phase? In this issue of The Journal of Physiology, Xing et al. (2020) implemented an elegant and straightforward strategy for preserving cerebral perfusion during the push–pull manoeuvre. As moderate levels of lower body negative pressure (LBNP) redistributes blood volume without affecting arterial pressure, Xing et al. (2020) measured systemic and cerebral haemodynamics during a simulated push–pull manoeuvre at two levels of hypogravity (−0.50 G and −0.87 G), with and without (control) application of LBNP at −40 mmHg. Two variations of the push phase consisted of a head down tilt (HDT) at −30° or −60° corresponding to −0.50 G or −0.87 G, respectively. The pull phase involved a rapid transition to an upright 90° position (HUT). During each push phase, and compared to control conditions, application of LBNP seemed to counteract the blood shift caused by HDT and reduced mean middle cerebral artery blood velocity (MCAv) and estimated MAP at the MCA level. When it comes to investigating loss of consciousness during a push–pull manoeuvre, the rapid transition from push to pull phase becomes the epoch of interest. During the transition from HDT to HUT, MCAv increased with LBNP for both levels of push–pull transitions. Finally, during the initial 10 s of HUT, MCAv (specifically diastolic MCAv) was higher for the LBNP condition before returning to similar levels as the control condition. Interestingly, the MCAv pulsatility index was lower for the LBNP condition than in control, which may allude to changes in brain vascular compliance following transition to the HUT. It may be the case that during the HDT or push phase, LBNP allowed for baroreceptor unloading, and during the transition, release of LBNP may have slowed the blood volume shift towards the legs which could contribute to the higher blood pressures during this transition. The respective lag times for haemodynamic control mechanisms add complexity when discriminating contributions for each mechanism during stressors like the push–pull manoeuvre. Continued refinement of experimental and analytical methods adds to our knowledge of the complex interplay between neurogenic, autoregulatory, metabolic and mechanical haemodynamic control factors. For example, Tymko et al. (2020) developed a means to relate cerebrovascular resistance to sympathetic nerve activity. Moir et al. (2020) provided data to support cerebrovascular compliance as a factor which not only partakes in dynamic autoregulatory processes but precedes changes in cerebrovascular resistance. Finally, Klein et al. (2020) used second-by-second analysis, rather than traditional time-averaged approaches, to demonstrate that MCAv is transient during changes in gravity which may be due to changes in hydrostatic gradient rather than systemic pressure. Xing et al. (2020) found that application of LBNP prior to and during transition from HDT to HUT could serve as a means to preserve cerebral perfusion during a simulated push–pull manoeuvre. Such findings provide novel and necessary information when considering future strategies for preserving cerebral perfusion during airflight manoeuvres. More broadly, these findings provoke stimulating research questions surrounding the interplay between various haemodynamic factors during dynamic stimuli. None declared. Sole author. None applicable.