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.

The aim of the study was to investigate any indication of diminished orthostatic tolerance as a result of fatiguing intensive acute concentric exercise with a successive isometric wall-sit followed by an orthostatic stress test, with a special focus on any distinguishable alterations due to a delayed-onset muscle soreness effect. The exercise protocol was carried out among nineteen (10 female, 9 male) junior swimmers from the Hungarian National Swim Team. All athletes showed a positive orthostatic stress test right after our exercise protocol. The diastolic blood pressure was significantly lower due to the delayed-onset muscle soreness effect in the standing position after the supine position of the orthostatic stress test, in contrast to the athletes who did not experience delayed-onset muscle soreness. Furthermore, the heart rate was dysregulated in athletes with a delayed-onset muscle soreness effect when they assumed a supine position after the sustained standing position during the orthostatic stress test, in contrast to the athletes without delayed-onset muscle soreness. Interesting to note is that, in three subjects, the sustained standing position decreased the heart rate below the level of the initial supine position and six athletes experienced dizziness in the standing position, and all of these athletes were from the group that experienced delayed-onset muscle soreness. Accordingly, this study, for the first time, demonstrated that delayed-onset muscle soreness impairs orthostasis after unaccustomed fatiguing intensive acute concentric exercise with a successive isometric weight-loaded wall-sit; however, validation of this association should be investigated in a larger sample size.

The purpose of the study was to carry out an immunophenotypical characterization with a special focus on natural killer cells of junior swimmers from the Hungarian National Swim Team before and after an intensive acute exercise. Nineteen swimmers, ten females and nine males, completed the exercise protocol. Sixteen swimmers experienced delayed-onset muscle soreness. Most of our findings substantiated earlier results, such as the increase in the percentage of the CD3⁻/CD56⁺ natural killer cells and the CD3⁻/CD56^dim+ NK cells, and the decrease in the percentage of CD3⁺ T cells among lymphocytes after the exercise protocol. The drop of natural killer cell activity back to the pre-exercise level was in line with earlier findings. Interestingly, the percentage of CD3⁺/CD56⁺ NKT-like cells did not change significantly in those three swimmers who did not report delayed-onset muscle soreness. On the contrary, the percentage of CD3⁺/CD56⁺ NKT-like cells among lymphocytes increased in fourteen and decreased in two swimmers reporting delayed-onset muscle soreness. This study for the first time demonstrated a link between the delayed-onset muscle soreness and the imbalanced control of CD3⁺/CD56⁺ NKT-like cells among lymphocytes. However, validation of this association in a larger sample size study will be necessary.

Cancer patients often experience loss in body weight and also a decrease in muscle mass, which results in the reduction of physical activity and mobilization of the patient. To decelerate the loss of muscle mass, as part of the cancer treatment patients frequently undergo physical therapy and considering the physical capabilities of the patients, with moderate loads. Moreover, frequent studies also observed for cancer patients, together with the decrease in muscle mass a shift into fast-twitch muscle fibers from slow-twitch fibers. The aim of our study therefore was to determine how motor fibers behave under moderate isometric load executed until total exhaustion. 11 university students (G1), and 14 elite athletes (G2) participated in the study. 65% of the maximal voluntary contraction (MVC) was determined for the biceps brachii muscle, and with this load holding a weight, participants had to sustain a 90 deg. isometric elbow flexion in a standing posture until complete fatigue occurred. EMG activity for the biceps brachii muscle was measured and frequency analysis was performed. 3 windows were determined in the fatiguing protocol: the first (W1), middle (W2), and last (W3) 5 s, and also frequency analysis for MVC was performed (MAX) between 0 and 260 Hz with 20 Hz wide frequency bands. The results indicate, that as the protocol progressed in time and the effect of fatigue increased (from W1 to W3) the activity of low frequency muscle fibers significantly increased (0-40 Hz) while activity of high frequency muscle fibers (60-260 Hz) significantly decreased for G1 and G2 groups identically. We can conclude, that training applied with constant moderate tension as fatigue increases will result in the increased activation of the lower frequency slow–twitch muscle fibers, but the increase of fatigue in the lower frequency fibers will not result in the increase in the activation level of the higher frequency fast-twitch fibers. Consequently, because as slow-twitch fibers are being used at moderate loads and even when fatigue occurs in these fibers the fast-twitch fibers will not work, higher muscle loads are needed if the aim is to activate fast-twitch fibers. Considering the shift into fast-twitch muscle fibers from slow-twitch fibers for cancer patients, in some cases if the patient’s age and physical status allows during the physical treatment, higher loads and consequently higher levels of activation might be beneficial for the retardment of loss concerning the fast-twitch fiber mass.

Heart rate variability (HRV) is often modulated by pain; therefore, the objective of this study was to assess whether the induction of delayed-onset muscle soreness (DOMS) is already affected by HRV alterations during exercise, in spite of the fact that pain evolves only post-exercise. An isokinetic dynamometer was used to induce DOMS in this study on 19 young male elite handball players who were subjected to HRV measurements throughout a DOMS-inducing exercise session. The result of this study indicated that the heart rate (HR) dependence of time–frequency domain parameters could be described by an exponential-like function, while entropy showed a V-shaped function, with a minimum “turning point” separated by descending and ascending intervals. The DOMS protocol upshifted the time–frequency domain HRV parameters in the entire HR range, contrary to the sample entropy values that were systematically downshifted, indicative of an upregulated sympathetic tone. The group-averaged HR-dependent sample entropy function showed a nonlinear character under exercise, with lower values for higher DOMS than for the group with lower DOMS below the turning-point HR, and vice versa above it. The differences between the respective HRV(HR) point sets representing the low-DOMS and high-DOMS groups were quantified using a statistical method and found to be significant at the current sample size for all the HRV parameters used. Since oxidative stress is implicated in DOMS, we are the first to report that nonlinear alterations may impact HRV in a HR-dependent manner in DOMS using a Piezo2 interpretation. This finding provides further indirect evidence for an initiating neural microdamage that prevails under DOMS-inducing exercise, and the diagnostic detection of this point may provide control for avoiding further injury risk in sports and exercise activities.

This study aimed at analyzing the corneal neural regeneration in ankylosing spondylitis patients using in vivo corneal confocal microscopy in correlation with Langerhans cell density, morphology, and dry eye parameters. Approximately 24 ankylosing spondylitis subjects and 35 age- and gender-matched control subjects were enrolled. Data analysis showed that all corneal nerve-fiber descriptives were lower in the ankylosing spondylitis group, implicating disrupted neural regeneration. Peripheral Langerhans cell density showed a negative correlation with nerve fiber descriptions. A negative correlation between tear film break-up time and corneal nerve fiber total branch density was detected. The potential role of somatosensory terminal Piezo2 channelopathy in the pathogenesis of dry eye disease and ankylosing spondylitis is highlighted in our study, exposing the neuroimmunological link between these diseases. We hypothesized earlier that spinal neuroimmune-induced sensitization due to this somatosensory terminal primary damage could lead to Langerhans cell activation in the cornea, in association with downregulated Piezo1 channels on these cells. This activation could lead to a Th17/Treg imbalance in dry eye secondary to ankylosing spondylitis. Hence, the corneal Piezo2 channelopathy-induced impaired Piezo2-Piezo1 crosstalk could explain the disrupted neural regeneration. Moreover, the translation of our findings highlights the link between Piezo2 channelopathy-induced gateway to pathophysiology and the gateway reflex, not to mention the potential role of spinal wide dynamic range neurons in the evolution of neuropathic pain and the flare-ups in ankylosing spondylitis and dry eye disease.