Introduction and objective: The study aimed to evaluate the physiological stress response, i.e. internal load to intermittent and continuous exercise performed during the treadmill running in professional female soccer players, and additionally to determine the most appropriate method for...

Calcium (Ca²⁺) release from the sarcoplasmic reticulum is central to excitation–contraction coupling and plays a critical role in the development of skeletal muscle fatigue. Altered Ca²⁺ dynamics may affect not only contractile function but also neuromuscular excitability. This study examined the effects of pharmacological modulation of Ca²⁺ channels on fatigue development and spinal reflex activity in rats. Using the Hoffmann reflex (H-reflex) as an indicator of motoneuron excitability, we evaluated the effects of Ca²⁺ channel blockers (Amiloride, Nifedipine) and an activator ((−)-Bay K8644) on the reflex responses of the plantar muscle before and after fatigue induction. The ratio of the maximum H-reflex to maximum M-wave (H_max/M_max) was used to assess alterations in spinal excitability. Compared with the control, both Amiloride and Nifedipine markedly reduce the H_max/M_max ratio (77% and 60%, respectively), whereas (−)-Bay K8644 elicited a robust 129% increase. These findings demonstrate that pharmacological modulation of Ca²⁺ channels has distinct and divergent effects on spinal excitability during fatigue. These results highlight the close interaction between intramuscular Ca²⁺ regulation and reflex pathways and suggest potential strategies for enhancing muscle performance through targeted Ca²⁺ channel modulation.

Background/Objectives: Spinal excitability may undergo adaptive modulation in response to training load, sport-specific demands, and fatigue. While high-impact sports are known to influence reflex responsiveness, the extent to which these changes differ from athletes in lower-impact disciplines remains unclear. This study aimed to investigate post-exercise changes in Hmax/Mmax ratio among trained runners with varied sport backgrounds, and to identify emergent physiological profiles that may reflect differential spinal adaptation to fatigue. Methods: Twenty-two trained athletes underwent unilateral H-reflex testing before and after treadmill running performed to voluntary exhaustion. Amplitudes of the H-reflex and M-wave were recorded, and Hmax/Mmax ratios were analyzed. Based on a physiologically relevant threshold commonly used to distinguish normal from suppressed reflex amplitudes, participants were post hoc classified into three groups: Group A (pre- and post-test ratios above threshold), Group B (pre above, post below), and Group C (both below). A two-way repeated-measures ANOVA was used to assess between-group effects. Results: Significant differences were found across groups and conditions (p < 0.001). Group A maintained reflex ratios above the threshold, indicating stable excitability. Group B showed the greatest suppression (approximately 66%), transitioning from normal to subthreshold values. Group C remained consistently below-threshold. A significant interaction (p < 0.0001) confirmed that reflex modulation varied by physiological profile. A small but statistically significant reduction in H-reflex latency was also observed; however, this change remained within normal physiological variability. Conclusions: Postexercise H-reflex modulation revealed heterogeneous neuromuscular responses among athletes. These findings may contribute to understanding how sport-specific demands and fatigue shape spinal excitability and may help identify individuals with adaptive or potentially pathological profiles relevant to sports diagnostics.

Traumatic muscle injuries often lead to prolonged functional impairments due to oxidative stress, metabolic disturbances, and structural damage. This study investigates the therapeutic potential of chronic administration of C₆₀ fullerene aqueous (C₆₀FAS) solutions in enhancing muscle recovery post-injury. Rats with experimentally induced gastrocnemius muscle trauma received C₆₀FAS orally at a daily dose of 1 mg/kg body weight. Functional assessments included measurements of maximal force generation and time to peak contraction. Biochemical analyses evaluated lactate, superoxide dismutase (SOD), and catalase (CAT) levels, while histological examinations assessed muscle fiber integrity and collagen deposition. Results demonstrated significant improvements in muscle function, with a 35–40% increase in maximal force and a 27–38% acceleration in contraction time. Biochemical analysis revealed a 25% decrease in lactate concentration, potentially indicating improved metabolic function. This change is in line with normalized SOD and CAT activities, suggesting enhanced redox balance following treatment. Histological analyses revealed preserved myofibrillar architecture and reduced fibrosis in treated muscles. These findings suggest that C₆₀ fullerene facilitates muscle recovery through antioxidant protection, metabolic support, and structural preservation, highlighting its potential as a therapeutic agent for muscle injuries.

An investigation of the central mechanisms underlying muscle inflammation and musculoskeletal pain is an important step to find means for the prevention or treatment of muscle inflammation. One of the insufficiently studied brain structures involved in the transmission of nociceptive information is the claustrum (CL). Therefore, the aim of the study was to reveal changes in the patterns of Fos-immunoreactivity and NADPH-diaphoreactivity in the nucleus claustrum (CL) and additionally in the ventral putamen (Pu) during chronic inflammation of m. gastrocnemius-soleus in cat, induced by intramuscular injection of complete Freund’s adjuvant (CFA). Immunohistochemical and histochemical techniques were used to detect Fos-immunoreactive (Fos-ir) and NADPH-diaphorase reactive (NADPH-dr) neurons within studied structures. It was revealed that nine days after CFA-induced muscle inflammation the level of Fos-immunoreactivity and NADPH-d reactivity within the CL and in the ventral part of Pu increased two-fold in comparison with the control. Because the CL is reciprocally connected with many structures of the brain cortex and subcortical structures, all these structures can be pathways of transmission of nociceptive information, nevertheless, it can be assume that the central amygdala nucleus may make the main nociceptive contribution to the activation of neurons within the CL. It is known that CL is mutually related to Pu, but it was not possible to assess their mutual influence in this study. The results of the study of the Fos-ir neurons distribution in CL and Pu under conditions of long-term muscles inflammation indicate the active involvement of the mentioned structures in the formation of adaptive reactions. The increase in the number of neurons with NADPH-d reactivity in CL and Pu indicates that NO-signals play a significant role in the formation and amplification of the response to painful impulses from inflamed muscles. In addition, further research is needed to accurately identify all possible nociceptive inputs to the CL and to separate the emotional, motor, auditory, and visual components that may accompany nociceptive processes.