Cardiovascular deconditioning during long-term spaceflight through multiscale modeling

Abstract

Human spaceflight has been fascinating man for centuries, representing the intangible need to explore the unknown, challenge new frontiers, advance technology, and push scientific boundaries further. A key area of importance is cardiovascular deconditioning, that is, the collection of hemodynamic changes-from blood volume shift and reduction to altered cardiac function-induced by sustained presence in microgravity. A thorough grasp of the 0G adjustment point per se is important from a physiological viewpoint and fundamental for astronauts' safety and physical capability on long spaceflights. However, hemodynamic details of cardiovascular deconditioning are incomplete, inconsistent, and poorly measured to date; thus a computational approach can be quite valuable. We present a validated 1D-0D multiscale model to study the cardiovascular response to long-term 0G spaceflight in comparison to the 1G supine reference condition. Cardiac work, oxygen consumption, and contractility indexes, as well as central mean and pulse pressures were reduced, augmenting the cardiac deconditioning scenario. Exercise tolerance of a spaceflight traveler was found to be comparable to an untrained person with a sedentary lifestyle. At the capillary-venous level significant waveform alterations were observed which can modify the regular perfusion and average nutrient supply at the cellular level. The present study suggests special attention should be paid to future long spaceflights which demand prompt physical capacity at the time of restoration of partial gravity (e.g., Moon/Mars landing). Since spaceflight deconditioning has features similar to accelerated aging understanding deconditioning mechanisms in microgravity are also relevant to the understanding of aging physiology on the Earth.

Keywords: Biomedical engineering; Medical research.

Fig. 1. Pressures and flow rates throughout the body in 1G supine and 0G conditions.

Time-series of the pressure, P(t), and flow rate, Q(t), at different sites: left vertebral artery (cerebral), right ventricle and left brachial artery (cardio-thoracic region), left renal artery (abdominal region), leg veins (lower limbs). Blue: supine 1G configuration on the Earth; red: 0G spaceflight configuration. Mean pressure ($\overline{P}$), mean flow rate ($\overline{Q}$), together with maximum pressure ($P_{\max }$), and pulse pressure (PP) relative variations between 1G and 0G configurations are reported in each panel.

Fig. 2. Volumes throughout the body in 1G supine and 0G conditions.

Time-series of the volume, V(t), at different 0D sites: venules (upper body), left ventricle and pulmonary artery (cardio-thoracic region), veins below VIP (abdominal region), capillaries (lower limbs). Blue: supine 1G configuration on the Earth; red: 0G spaceflight configuration. Mean volume ($\overline{V}$) relative variations between 1G and 0G configurations are reported for each region (colored values refer to the corresponding time-series shown).

Fig. 3. Pressure and flow rate waveform alterations.

Normalized time-series $P^{\prime }\left(t^{\prime }\right)$ and $Q^{\prime }\left(t^{\prime }\right)$ at different sites: left internal carotid artery (cerebral), left ventricle and inferior vena cava (cardio-thoracic region), celiac artery (abdominal region), posterior tibial artery (lower limbs). Blue: supine 1G configuration on the Earth; red: 0G spaceflight configuration. NSD (normalized signal difference) values for $Q^{\prime }$ and $P^{\prime }$ are reported in each panel.

Fig. 4. Proximal-to-distal arterial tree: pressures and flow rates in 1G supine and 0G conditions.

Time-series P(t), Q(t), $P^{\prime }\left(t^{\prime }\right)$, and $Q^{\prime }\left(t^{\prime }\right)$ at the extremes of the 1D arterial proximal-to-distal tree: ascending aorta and anterior tibial artery. Blue: supine 1G configuration on the Earth; red: 0G spaceflight configuration. NSD values for $Q^{\prime }$ and $P^{\prime }$, together with mean pressure ($\overline{P}$), mean flow rate ($\overline{Q}$), max pressure ($P_{\max }$), and pulse pressure (PP) relative variations between 1G and 0G configurations are reported in the panels.

Fig. 5. Scheme of the multiscale model.

The sketch includes the arterial tree (right), the structure of the 0D compartments (left), the arteriolar 0D–1D interface (dashed box), and the baroreceptor mechanisms (top). Details of the 0D compartments are depicted in the bottom panels. According to VIP, the model is divided into upper body (RH right heart, PC pulmonary circulation, LH left heart, U ABD and HA upper body arteries and arterioles; upper abdomen, head and arms venous return, SVC superior vena cava,) and lower body (L ABD and LEGS lower body arteries and arterioles; lower abdomen and legs venous return, IVC inferior vena cava). Modeling parameters and variables are defined in the Supplementary Information, see Supplementary Table 1 for the legend.