Low-intensity exercise with blood flow restriction (LI BFR) has been shown to release substances that play a key role in neuroplasticity and may be effective in improving rehabilitation outcomes in patients with neurodegenerative diseases. Researchers suggest that LI BFR engages high-threshold motor units even during low-intensity exercise, leading to increased motor unit end-state variability and a rapid onset of neuromuscular fatigue. However, the amplitude-frequency characteristics and motor unit recruitment strategies during LI BFR are not well understood. The aim of this study was to investigate the effects of blood flow restriction on motor unit activation patterns during low-intensity exercise to elucidate the physiological mechanisms underlying this novel training approach. Participants with a mean age of 33 years were subjected to blood flow restriction during isometric wrist flexion. High-density surface EMG (HD sEMG) activity was recorded from both the flexor carpi radialis and palmaris longus muscles. The study shows that blood flow restriction significantly shifted motor unit activation to high threshold motor units. These findings highlight the need to investigate the long-term effects of LI BFR on motor unit coordination in clinical populations.

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.

Acute kidney injury (AKI) is a life-threatening event prevalent in hospitalized patients but also not rare among endurance sports athletes. Hypoxia, oxidative stress, and sterile inflammation are the key pathophysiological factors driving kidney damage in AKI. Zinc is an essential trace element required for the intact function of approximately 3000 proteins (~10% of the human proteome), including over 300 enzymes for which zinc serves as a cofactor. Cell biological tasks of zinc signaling include adaptive responses to hypoxia and oxidative stress, as well as anti-inflammatory effects. The underlying molecular pathways involve modulation of hypoxia-inducible factor signaling, suppression of reactive oxygen species (ROS) generation, and inhibition of the nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB), the latter being the major pro-inflammatory transcription factor. As a catalytic cofactor for the “classical” histone deacetylases, zinc is essential for epigenetic control of gene expression, thereby exerting further adaptive effects. Apart from the intracellular zinc signaling, extracellular zinc elicits cytoprotective and anti-inflammatory effects via the G Protein-Coupled Receptor 39 (GPR39). GPR39 activation by zinc binding may exert antioxidant and anti-inflammatory effects mediated by the zinc-finger protein A20 (TNFAIP3) and NF-κB suppression, followed by reduced production of pro-inflammatory cytokines such as tumor necrosis factor (TNF), interleukin-1β (IL-1β), and IL-6. At the same time, GPR39 signaling may stimulates the release of the anti-inflammatory cytokine IL-10, thus shifting the kidney tissue towards an anti-inflammatory milieu, promoting renal recovery. The present review focuses on the role of zinc in AKI to identify potential therapeutic strategies targeting zinc signaling for renoprotection and biomarker-based risk stratification.

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.