According to our hypothesis, delayed onset muscle soreness (DOMS) is an acute compression axonopathy of the nerve endings in the muscle spindle. It is caused by the superposition of compression when repetitive eccentric contractions are executed under cognitive demand. The acute compression axonopathy could coincide with microinjury of the surrounding tissues and is enhanced by immune-mediated inflammation. DOMS is masked by sympathetic nervous system activity at initiation, but once it subsides, a safety mode comes into play to prevent further injury. DOMS becomes manifest when the microinjured non-nociceptive sensory fibers of the muscle spindle stop inhibiting the effects of the microinjured, hyperexcited nociceptive sensory fibers, therefore providing the ‘open gate’ in the dorsal horn to hyperalgesia. Reactive oxygen species and nitric oxide play a cross-talking role in the parallel, interlinked degeneration–regeneration mechanisms of these injured tissues. We propose that the mitochondrial electron transport chain generated free radical involvement in the acute compression axonopathy. ‘Closed gate exercises’ could be of nonpharmacological therapeutic importance, because they reduce neuropathic pain in addition to having an anti-inflammatory effect. Finally, DOMS could have an important ontogenetical role by not just enhancing ability to escape danger to survive in the wild, but also triggering muscle growth.

Unaccustomed or strenuous eccentric exercise is known to cause delayed-onset muscle soreness. A recent hypothesis postulated that mechano-energetic microinjury of the primary afferent sensory neuron terminals in the muscle spindles, namely a transient Piezo2 channelopathy, could be the critical cause of delayed-onset muscle soreness in the form of a bi-phasic non-contact injury mechanism. This theory includes that this microlesion could delay the medium-latency response of the stretch reflex. Our aim with this study was to investigate this hypothesis. According to our knowledge, no study has examined the effect of delayed-onset muscle soreness on the medium-latency response of the stretch reflex. Our findings demonstrated that a significant delay in the medium-latency stretch reflex could be observed right after a multi-stage fitness test in the quadriceps femoris muscles of Hungarian professional handball players who consequently experienced delayed-onset muscle soreness. The long-latency stretch reflex and most likely short-latency stretch reflex were unaffected by delayed-onset muscle soreness in our study, which is in line with earlier findings. We translate these findings as indicative of proprioceptive Type Ia terminal microdamage in the muscle spindle in line with the aforementioned new acute non-contact compression axonopathy theory of delayed-onset muscles soreness.

Anterior cruciate ligament injury occurs when the ligament fibers are stretched, partially torn, or completely torn. The authors propose a new injury mechanism for non-contact anterior cruciate ligament injury of the knee. Accordingly, non-contact anterior cruciate ligament injury could not happen without the acute compression microinjury of the entrapped peripheral proprioceptive sensory axons of the proximal tibia. This would occur under an acute stress response when concomitant microcracks-fractures in the proximal tibia evolve due to the same excessive and repetitive compression forces. The primary damage may occur during eccentric contractions of the acceleration and deceleration moments of strenuous or unaccustomed fatiguing exercise bouts. This primary damage is suggested to be an acute compression/crush axonopathy of the proprioceptive sensory neurons in the proximal tibia. As a result, impaired proprioception could lead to injury of the anterior cruciate ligament as a secondary damage, which is suggested to occur during the deceleration phase. Elevated prostaglandin E2, nitric oxide and glutamate may have a critical neuro-modulatory role in the damage signaling in this dichotomous neuronal injury hypothesis that could lead to mechano-energetic failure, lesion and a cascade of inflammatory events. The presynaptic modulation of the primary sensory axons by the fatigued and microdamaged proprioceptive sensory fibers in the proximal tibia induces the activation of N-methyl-D-aspartate receptors in the dorsal horn of the spinal cord, through a process that could have long term relevance due to its contribution to synaptic plasticity. Luteinizing hormone, through interleukin-1β, stimulates the nerve growth factor-tropomyosin receptor kinase A axis in the ovarian cells and promotes tropomyosin receptor kinase A and nerve growth factor gene expression and prostaglandin E2 release. This luteinizing hormone induced mechanism could further elevate prostaglandin E2 in excess of the levels generated by osteocytes, due to mechanical stress during strenuous athletic moments in the pre-ovulatory phase. This may explain why non-contact anterior cruciate ligament injury is at least three-times more prevalent among female athletes.

Background: After the increasingly common anterior cruciate ligament reconstruction (ACLR) procedure in competitive athletes, rehabilitation is crucial for facilitating a timely return to sports (RTS) and preventing re-injury. This pilot study investigates the patient-reported outcomes of postoperative rehabilitation in competitive athletes, comparing supervised rehabilitation (SVR) and home-based rehabilitation (HBR). Methods: After ACLR, 60 (out of 74 screened) athletes were recruited and equally divided into HBR and SVR groups using non-probability convenience sampling, with each group comprising 15 males and 15 females. The rehabilitation outcomes in the respective groups were evaluated at 8 months using measures (Tegner Activity Scale [TAS], International Knee Documentation Committee subjective knee form [IKDC-SKF], ACL Return to Sport after Injury [ACL-RSI]) and objective parameters (isometric muscle strength, hamstring/quadricep asymmetry). RTS was evaluated at 9 months, with ACL re-injury rates recorded approximately 6 months post-RTS. Results: Both groups exhibited decreased TAS scores (HBR: 8 to 6, SVR: 8 to 7), with the SVR group demonstrating superior postoperative IKDC-SKF scores (81.82 vs. 68.43) and lower ACL-RSI scores (49.46 vs. 55.25). Isometric and isokinetic muscle strength, along with asymmetry values, was higher in the SVR group 8 months post-ACLR (p < 0.05). The SVR group showed a higher RTS rate to the same level (76.6% vs. 53.3%), while the re-injury rate was the same in both the rehabilitation groups (3.3%). Conclusions: Although both rehabilitation approaches yielded comparable outcomes, SVR may demonstrate some superior biomechanical improvements in athletes, resulting in a higher RTS rate. However, the psychological outcomes and re-injury rates did not significantly differ between the groups, emphasizing the need to address individual psychological needs during rehabilitation. Further investigation is recommended with a larger sample size to address the differences of gender among competitive athletes.

Background: Biomechanical factors behind non-contact anterior cruciate ligament (ACL) injury in soccer and handball are still not fully understood. Unfortunately, ACL injuries more frequently appear in game situations. Aim: To describe a possible ACL injury mechanism in male professional handball players using MRI images and our own biomechanical model. Hypothesis: The friction parameters of the surface have extreme importance in the non-contact ACL injury mechanism. If the surface is more slippery, the horizontal component of the ground reaction force (GRF) will be smaller, consequently the torque originating from the GRF acting on the knee will be greater during the landing phase of a vertical jump, resulting in greater abduction effect on the knee. Consequently, the risk of knee injury increases. Methods: We have collected MRI images and anthropometric data of 15 healthy male individuals (age 19–23) to create a biomechanical model to calculate the torques in the knee to obtain more knowledge about ACL injury mechanism. Results: The lower extremity lean angle during the landing phase of a jump and friction parameters substantially affect abduction torques in the knee and consequently the risk of ACL injury occurrence. Conclusions: The landing posture when the knee is fully extended during landing is highly unfortunate for the ACL, compared to when the knee is partially flexed. If the knee is fully extended, greater hip abduction will increase the risk of an ACL injury, and if the surface is more slippery, e.g., the surface is wet, the possibility of ACL injury is even greater. In addition, we also applied a molecular working hypothesis through acquired Piezo2 channelopathy theory, as the proposed preceding neuromuscular disruptor prior to non-contact ACL injury.

Background: Biomechanical factors behind non-contact Anterior Cruciate Ligament (ACL) injury in soccer are still not fully understood. Unfortunately, ACL injuries almost always appear in game situations. Aim: To describe a possible ACL injury mechanism in male professional soccer players using MRI images and our own biomechanical model. Hypothesis: The friction parameters of the surface have extreme importance in the ACL injury mechanism. If the surface is more slippery, the horizontal component of the ground reaction force (GRF) will be smaller, consequently the torque originated from the GRF acting on the knee will be greater during the landing phase of a vertical jump, resulting in greater abduction effect on the knee. Consequently, the risk of knee injury increases. Methods: We have collected Magnetic Resonance Image images and anthropometric data of 15 healthy male individuals (age 19-23) to create a biomechanical model to calculate the torques in the knee to obtain more knowledge about ACL injury mechanism. Results: Lower extremity lean angle during the landing phase of a jump and friction parameters substantially affect abduction torques in the knee and consequently the risk of ACL injury occurrence. Conclusions: The landing posture when the knee is fully extended during landing is highly unfortunate for the ACL, compared to when the knee is partially flexed. If the knee is fully extended, greater hip abduction will increase the risk of an ACL injury, and if the surface is more slippery e.g. the surface is wet, the possibility of ACL injury is even greater. In addition, we also applied a molecular interpretation through acquired Piezo2 channelopathy, as the proposed preceding neuromuscular disruptor prior to non-contact ACL injury.