Background: Continuous-flow left ventricular assist devices (LVADs) and heart transplantation (HTX) improve survival and quality of life in advanced heart failure. However, restoration of central hemodynamics does not consistently normalize exercise capacity, physical performance, or body composition. Persistent skeletal muscle dysfunction, endothelial abnormalities, metabolic disturbances, and adverse body composition changes frequently limit functional recovery. Methods: This narrative review examines determinants of rehabilitation outcomes across the transition from advanced heart failure to LVAD support and subsequent HTX. Particular emphasis is placed on restoration of pulsatile circulation, vascular and microcirculatory adaptation, immunosuppressive therapy, body composition remodeling, and emerging immunometabolic mechanisms. Results: Rehabilitation outcomes appear to be increasingly determined by peripheral rather than central cardiovascular factors. Continuous-flow LVAD support induces vascular, endothelial, autonomic, and microcirculatory adaptations that may persist after transplantation. Although HTX restores physiological pulsatile circulation and cardiac output, recovery is often limited by skeletal muscle dysfunction, impaired mitochondrial capacity, chronotropic abnormalities, and adverse body composition changes. Immunosuppressive therapies further influence muscle plasticity, adipose tissue distribution, insulin sensitivity, endothelial function, and exercise adaptation, contributing to phenotypes such as sarcopenia, myosteatosis, and sarcopenic obesity. Conclusions: Functional recovery after LVAD support and HTX is a multidimensional process extending beyond restoration of cardiac function. We propose a hemodynamic–immunometabolic framework in which vascular adaptation, skeletal muscle biology, body composition remodeling, and immunosuppressive therapy interact to determine rehabilitation success and may inform personalized rehabilitation strategies.

The aim of study was to determine the influence of an experimental programme for grasping an effective swimming technique on the results of active swimming among youth swimmers at their initial stage of training. Methods: The subjects were 90 children of both sex aged 9–11 year and split into two groups: a) an experimental group (n = 45; girls: n = 18, boys: n = 27) that underwent the original programme and b) a controlled group (n = 45; girls: n = 18, boys: n = 27) that underwent a standard programme. The observation spanned 12 weeks, during which both groups had 24 training sessions. Swimming speed and effectiveness were assessed according to the following variants: A (full style), B (upper limbs), and C (lower limbs). Results: The intervention improved results for A (full style) among girls in the experimental group (F(2,68) = 6.37, p = 0.003; ηp2 = 0.16) and B (upper limbs) (F(2,68) = 7.78, p = 0. 001; ηp2 = 0.19). Among the boys in the experimental group, a trend towards significance (F(2,104) = 2.45, p = 0.091; ηp2 = 0.05) was observed regarding variant B. Regarding variant C (lower limbs), among girls, significant changes were noted in the relationship term*group (F(2,68) = 5.19, p = 0.008; ηp2 = 0.13) and in boys, among terms (F(2,104) = 8.71, p = 0.000; ηp2 = 0.14). No significant changes were noted in the control groups. Conclusions: The applied training improved performance in the experimental group, confirming the validity of introducing exercises to improve swimming technique at the initial stages of training.

Pulsatile blood flow is a fundamental characteristic of cardiovascular physiology that regulates endothelial function, vascular homeostasis, microcirculatory integrity, and organ adaptation through complex mechanobiological pathways. The widespread use of continuous-flow left ventricular assist devices (CF-LVADs) has created a unique clinical model of chronic pulsatility deprivation, whereas heart transplantation restores physiological pulsatile hemodynamics. This review examines the molecular, cellular, and systemic consequences of these contrasting circulatory states. Evidence from experimental and clinical studies indicates that reduced pulsatility during CF-LVAD support is associated with impaired endothelial mechanotransduction, glycocalyx disruption, oxidative stress, inflammatory activation, angiogenic dysregulation, acquired von Willebrand syndrome, and microvascular remodeling. These alterations contribute to bleeding, thrombosis, neurological events, and progressive end-organ dysfunction. In contrast, restoration of pulsatile flow following heart transplantation promotes recovery of endothelial signaling, nitric oxide bioavailability, vascular responsiveness, and tissue perfusion, although persistent immune-mediated injury may limit complete vascular normalization. Emerging concepts involving Piezo1 signaling, YAP/TAZ mechanotransduction, extracellular vesicles, immunometabolism, and multi-omics profiling further support the role of pulsatility as a biological regulator rather than a simple hemodynamic consequence of cardiac contraction. Understanding pulsatility-dependent cardiovascular remodeling may facilitate the development of next-generation circulatory support technologies and novel therapeutic strategies to preserve vascular health.