The purpose of this study was to clarify the time course of the viscoelasticity of gastrocnemius medialis muscle and tendon after stretching. In 11 male participants, displacement of the myotendinous junction on the gastrocnemius medialis muscle was measured ultrasonographically during the passive dorsiflexion test, in which the ankle was passively dorsiflexed at a speed of 1°/s to the end of the range of motion (ROM). Passive torque, representing resistance to stretch, was also measured using an isokinetic dynamometer. On five different days, passive dorsiflexion tests were performed before and 0, 15, 30, 60 or 90 min after stretching, which consisted of dorsiflexion to end ROM and holding that position for 1 min, five times. As a result, end ROM was significantly increased at 0, 15 and 30 min (P<0.05 each) after stretching as compared with each previous value. Passive torque at end ROM was also significantly increased after stretching. Although the stiffness of the muscle-tendon unit was significantly decreased immediately after stretching (P<0.05), this shift recovered within 15 min. These results showed that the retention time of the effect of stretching on viscoelasticity of the muscle-tendon unit was shorter than the retention time of the effect of stretching on end ROM.

The purpose of this study was to clarify the temporal course of stiffness in the muscle-tendon unit after stretching. In 11 male participants, displacement of the myotendinous junction on the gastrocnemius medialis muscle was measured ultrasonographically during the passive-dorsiflexion test, with the ankle was passively dorsiflexed at 1?/s to the end of the range of motion. Passive torque, representing resistance to stretch, was also measured using an isokinetic dynamometer. On 4 different days, passive-dorsiflexion tests were performed before and immediately, 5, 10 or 15?min after stretching, which comprised dorsiflexion to end range of motion and holding that position for 1?min, 5 times. As a result, end range of motion and passive torque at end range of motion were significantly increased after stretching (P<0.05) as compared with each previous value. Although stiffness of the muscle-tendon unit was significantly decreased immediately and 5?min after stretching (P<0.05), this change recovered within 10?min. These results suggest that static stretching for 5?min results in significantly increased range of motion over 30?min, but significant decreases in stiffness of the muscle-tendon unit returned to baseline levels within 5?10?min.

Understanding the cellular dynamics of Aire-expressing lineage(s) among medullary thymic epithelial cells (AEL-mTECs) is essential for gaining insight into the roles of Aire in establishment of self-tolerance. In this study, we monitored the maturation program of AEL-mTECs by temporal lineage tracing, in which bacterial artificial chromosome transgenic mice expressing tamoxifen-inducible Cre recombinase under control of the Aire regulatory element were crossed with reporter strains. We estimated that the half-life of AEL-mTECs subsequent to Aire expression was ∼7–8 d, which was much longer than that reported previously, owing to the existence of a post-Aire stage. We found that loss of Aire did not alter the overall lifespan of AEL-mTECs, inconsistent with the previous notion that Aire expression in medullary thymic epithelial cells (mTECs) might result in their apoptosis for efficient cross-presentation of self-antigens expressed by AEL-mTECs. In contrast, Aire was required for the full maturation program of AEL-mTECs, as exemplified by the lack of physiological downregulation of CD80 during the post-Aire stage in Aire-deficient mice, thus accounting for the abnormally increased CD80high mTECs seen in such mice. Of interest, increased CD80high mTECs in Aire-deficient mice were not mTEC autonomous and were dependent on cross-talk with thymocytes. These results further support the roles of Aire in the differentiation program of AEL-mTECs.

Aire controls the fate of autoreactive thymocytes (i.e., clonal deletion or development into regulatory T cells [Tregs]) through transcriptional control of the expression of tissue-restricted self-antigens (TRAs) from medullary thymic epithelial cells (mTECs) and bone marrow (BM)-derived cells. Although TRAs expressed by mTECs and BM-derived cells are suggested to complement each other to generate a full spectrum of TRAs, little is known about the relative contribution of TRAs from each component for establishment of self-tolerance. Furthermore, the precise role of Aire in specific types of Aire-expressing APCs remains elusive. We have approached these issues by generating two different types of transgenic mouse (Tg) model, which express a prefixed model self-antigen driven by the insulin promoter or the Aire promoter. In the insulin-promoter Tg model, mTECs alone were insufficient for clonal deletion, and BM-derived APCs were required for this action by utilizing Ag transferred from mTECs. In contrast, mTECs alone were able to induce Tregs, although at a much lower efficiency in the absence of BM-derived APCs. Importantly, lack of Aire in mTECs, but not in BM-derived APCs, impaired both clonal deletion and production of Tregs. In the Aire-promoter Tg model, both mTECs and BM-derived APCs could independently induce clonal deletion without Aire, and production of Tregs was impaired by the lack of Aire in mTECs, but not in BM-derived APCs. These results suggest that the fate of autoreactive thymocytes together with the requirement for Aire depend on the cell types that express self-antigens and the types of APCs involved in tolerance induction.

The purpose of this study was to clarify the time course of the stretching-induced decrease in maximal isometric plantar flexion torque. Nineteen women participated in 2 randomly ordered experimental trials: static 5-minute stretching or control with no stretching. The participants performed isometric maximal voluntary contractions (MVCs) of the right plantar flexor muscles, whereas electromyographic (EMG) amplitude (root mean square) was calculated for the medial and lateral gastrocnemius muscles. Measurements were conducted preintervention; immediately after intervention; and 5, 10, 15, and 30 minutes postintervention. The static 5-minute stretching trial consisted of dorsiflexion to the end range of motion and holding that position for 1 minute, 5 times, whereas the control trial consisted of 5 minutes of resting. As a result, the MVC torque was significantly decreased immediately after, and 5 minutes after the static 5-minute stretching intervention compared with the preintervention value (p < 0.05), and this change recovered within 10 minutes. However, the EMG amplitude did not change from preintervention to postintervention under any conditions. These results suggest that the deficits of static stretching are disabled in a short time after static stretching.