Brain-derived neurotrophic factor (BDNF) and its high-affinity receptor tropomyosin receptor kinase B (TrkB) are classically associated with neuroplasticity, but increasing evidence suggests a broader role for BDNF/TrkB signaling in systemic stress adaptation beyond the central nervous system. Strenuous exercise is a model of functional stress that may become a clinically relevant renal challenge under conditions such as dehydration, heat stress, vascular vulnerability, and repeated exposure. Neuroendocrine stress activation, hemodynamic perturbations, and cytoskeletal instability are key factors that may contribute to glomerular barrier dysfunction in this setting. BDNF biogenesis is complex, and circulating BDNF largely reflects platelet-associated pools and context-dependent release. At the tissue level, BDNF/TrkB signaling can activate actin-regulatory pathways involved in cellular resilience. The podocyte is of particular interest because its actin-dependent architecture functionally parallels that of neurons and is essential for maintenance of the glomerular filtration barrier. Within this framework, BDNF/TrkB signaling may stabilize podocyte actin dynamics, reduce foot process effacement, and attenuate proteinuria. The present review focuses on the brain–kidney axis and the potential renoprotective role of BDNF/TrkB signaling, while highlighting major knowledge gaps regarding BDNF availability to glomerular cells, isoform-specific TrkB actions, and causal inference in humans exposed to repeated exercise-related renal stress. However, current human evidence is insufficient to define the dominant source and delivery route of BDNF to glomerular cells during exercise-related renal stress. Therefore, BDNF/TrkB is discussed here as a candidate modulatory/resilience pathway rather than an established causal driver.

Aging disrupts postural control through impaired cognitive–motor integration, increasing fall risk. In this study, we examined whether sports training is associated with attenuated age-related balance decline. A total of 44 individuals participated: 24 were under 45 years and 20 were over 45 years; regardless of age, 24 had no sport experience and 20 had experience. Postural stability was assessed using a stabilometric target-test on firm and soft surfaces. Pronounced group differences emerged only on the firm surface; no effects were observed on the soft surface, which reduces proprioceptive input. The center of pressure (CoP) velocity fluctuation was significantly lower in both younger and sports-experienced groups (q < 0.05), indicating higher postural stability. Regression analysis further confirmed that athletes exhibit significantly lower CoP velocity (p < 0.0001) regardless of age. These data suggest that regular sports training may attenuate age-related postural decline, boosting cognitive–motor integration and neuromotor reserve.

Unilateral transtibial amputation (TTA) is associated with knee strength deficits and inter-limb asymmetry (ILA), but multi-velocity isokinetic profiling in competitive para-athletes remains limited. Eight competitive male para-athletes with unilateral TTA (C2–C4; body mass 68.9 ± 7.9 kg; 31.1 ± 10.4 months post-amputation) were assessed on an IsoMed 2000 dynamometer at 60, 180, 240, and 300°·s⁻¹. Peak torque (PT) was normalised to body mass. The intact limb served as an internal cohort reference (n = 8), while paired bilateral comparisons were available in four athletes (n = 4). Amputated-side PT was lower across all velocities, with flexion deficits of 31–42% and extension deficits of 33–39%. ILA was velocity-dependent, with minima at 240°·s⁻¹ for flexion and 300°·s⁻¹ for extension. H/Q showed a modest amputated-side upward shift at 60–240°·s⁻¹ (+2.5 to +8.0 pp), consistent with relative flexor preservation and a predominant extensor deficit. This pilot descriptive dataset supports future multi-velocity screening and controlled trials of velocity-matched resistance training while highlighting substantial between-athlete variability.