## 4 Discussion and Conclusions
Together with the fact that the increased ROM was strongly correlated with age-related increased fascia thickness [93] and with decreased sciatic nerve shear wave velocity [92], it seems possible that static stretching-induced changes in passive joint behavior is attributable, in part, to changes in the mechanical properties of the non-muscular structures (for review see [91; 94]). In addition to the possible mechanical contribution of the non-muscular structures, given that fasciae are densely innervated with sensory nerves, including proprioceptors and nociceptors [95; 96], the sensitivity of the sensory neurons responsible for the sensation of pain (e.g., nociceptors) may be altered in response to static stretching and thus may contribute to an increase in stretch tolerance. It is also plausible that an increase in stretch tolerance might result from some neural adaptations, which could be reflected in altered neural responses to static stretching. However, the results of our meta-analyses demonstrated no significant change in neural responses. Although a meta-analysis for the effects of chronic static stretching on neural responses was not conducted due to the limited data available from the reviewed studies, neural responses to chronic static stretching are seemingly not associated with increased stretch tolerance, which was evaluated at a stretched position. For example, the spinal reflex excitability (e.g., \(\mathrm{H_{max}/M_{max}}\) ratio) was significantly reduced in the resting lengths but not in the stretched lengths of both the SOL and MG after 3 weeks static of stretching training [72], and the maximum voluntary activation (e.g., RMS EMG) of the triceps surae did not change after a 12-week static stretch intervention [82]. Collectively, it appears that acute and chronic static stretching may not lead to a significant change in neural responses, and an increase in stretch tolerance may be possible without significant changes in reflex and voluntary responses. Decreases in maximum isometric force generation after acute static stretching, so called stretch-induced force loss, have received consistent attention, probably because reduced muscle performance after static stretching as a means of a warm-up before competitive exercise is undesirable. Two primary hypotheses have been developed to explain such stretching-induced force deficits: (1) mechanical factors such as altered MTU mechanical properties and (2) neural factors such as a reduced efferent neural drive and altered motor control strategies (for review see [97]). First, the results of our meta-analyses appear to support the mechanical hypothesis that more compliant tendons can lead to stretching-induced force loss, presumably shifting the fiber/fascicle operating range toward the ascending limb of the active force-length curve [98; 99]. In addition, the fact that the overall effect size was significant for the MTU mechanical properties and shear elastic modulus but not for muscle fascicle length suggests the possibility of stretching-induced changes in the mechanical properties of the intramuscular connective tissue (e.g., endomysium, perimysium, epimysium) [73; 100]. As these connective tissues connect adjacent fibers, fascicles, and muscles directly and indirectly, they are known to provide a route by which active contractile forces can be transmitted to the adjacent fibers/fascicles/muscles, also referred to as myofasical force transmission (for review see [101; 102; 103]). In this regard, more compliant connective tissues, as a result of static stretching if any, could compromise the efficiency of the force transmission, potentially resulting in decreased MVIT. The results of our meta-analyses did not support the possible contribution of corticospinal excitability and spinal reflex excitability to the stretching-induced force loss, as also suggested by previous studies [54; 56; 104].