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Tibialis anterior (TA) muscle has frequently been used for scientific experiments, particularly for muscle contractile assays, because of its anatomical advantages. However, classical evaluation methods for the TA muscle, such as EMG and force transducer, require experimental skills to acquire reliable results. Furthermore, because sacrificing experimental animals is usually indispensable for both methods, sequential observations cannot be performed. Therefore, developing a simple, objective, and animal friendly evaluation system was warranted. In this article, we introduce a novel, simple, and noninvasive in vivo evaluation method for the TA muscle called the toe-lift test (TLT), which is not only easy to perform but also capable of detecting contractile strength precisely. Because the TLT does not require experimental animal sacrifice, performing assessments over time, such as in sequential observation, is possible. This novel method represents a solution to the need for a simple, noninvasive, and effective method for TA muscle contractile evaluation.

Satellite cells, a population of skeletal muscular stem cells, are generally recognized as the main and, possibly, the sole source of postnatal muscle regeneration. Previous studies have revealed the potential of low-level laser (LLL) irradiation in promoting satellite cell proliferation, which, thereby, boosts the recovery of skeletal muscle from atrophy. The purpose of this study is to investigate the beneficial effect of LLL on disuse-induced atrophy. The optimal irradiation condition of LLL (808 nm) enhancing the proliferation of Pax7+ve cells, isolated from tibialis anterior (TA) muscle, was examined and applied on TA muscle of disuse-induced atrophy model of the rats accordingly. Healthy rats were used as the control. On one hand, transiently, LLL was able to postpone the progression of atrophy for 1 week through a reduction of apoptosis in Pax7−veMyoD+ve (myocyte) population. Simultaneously, a significant enhancement was observed in Pax7+veMyoD+ve population; however, most of the increased cells underwent apoptosis since the second week, which suggested an impaired maturation of the population. On the other hand, in normal control rats with LLL irradiation, a significant increase in Pax7+veMyoD+ve cells and a significant decrease of apoptosis were observed. As a result, a strengthened muscle contraction was observed. Our data showed the capability of LLL in postponing the progression of disuse-induced atrophy for the first time. Furthermore, the result of normal rats with LLL irradiation showed the effectiveness of LLL to strengthen muscle contraction in healthy control.

The aim of this study was to evaluate the response of satellite cells to muscular atrophies which possess different pathological characteristics and which were induced by distinct damages. Right lower limbs of rats were exposed to denervation or disuse and later its tibialis anterior (TA) or soleus (SOL) muscles were analyzed. After confirming their functional impairments indicated by common but distinct pathological and electrophysiological characteristics, the quantitative polymerase chain reaction analysis of Pax7 and Pax3 expressions and the number of Pax7+ve and Pax3+ve cells were analyzed sequentially at day 0, day 7, and day 14. TA muscles of both denervation- and disuse-induced atrophy models showed persisted low level of Pax7 expression from day 7 (0.91 ± 0.23 and 0.31 ± 0.07, P = 0.06, n = 6) through day 14 (1.09 ± 0.15 and 0.4 ± 0.09 [P < 0.05]). On the other hand, significant elevations were observed in Pax3 expression in both atrophy models (2.73 ± 0.46 and 2.75 ± 0.26 [P < 0.05]) at day 7. Similar to TA muscle, resembled pattern of Pax7 and Pax3 expression changes were observed between the SOL muscles of denervation- and disused-atrophy models. These trends were further confirmed by the changes in Pax7+ve and Pax3+ve cell numbers of TA and SOL muscles in both atrophy models. Despite the distinct pathological findings, similar patterns in the changes of Pax3 and Pax7 expressions and the changes of Pax7+ve and Pax3+ve cell numbers were observed between the denervation- and disuse-induced atrophy models and this commonality was admitted among the muscle type. Therefore, we claim that the muscle regeneration orchestrated by satellite cells was governed by the muscle type in which satellite cells reside.

Despite remarkable advancements in modern medicine, muscular atrophy remains as an unsolved problem. It is well known that pathological characteristics of different atrophy types could vary according to the pathophysiological causes. In fact, the lesion of atrophy is not always homogenously distributed but often predominantly evident in either fast or slow myofibers. As the focalization of the atrophic lesions, the existence and the functional impairment of each fast and slow progenitor/satellite cell (SC) are suspected though there are still controversies about this hypothesis. In this study, we isolated Pax7 positive (Pax7+ve) SCs from the tibia anterior (fast) and soleus (slow) muscles respectively and successfully demonstrated, for the first time, the difference between optimal exposure durations of photobiomodulation (PBM) which was known as low level laser irradiation (LLLI) in promoting proliferation of Pax7+ve SC which were acquired from fast and slow muscles respectively. Moreover, a hypertrophy-accompanied bidirectional change in myofiber composition with neuromuscular junction alteration, either from slow to fast or fast to slow, were achieved by applying different PBM durations. Simultaneously, PBM exhibited a synergistic effect with muscle exercise on the increase in myofiber size. Our data suggested the existence of at least two different populations of Pax7+ve SC which possess distinct sensitivities towards PBM. As our data revealed the capability of PBM in bidirectional changes of skeletal muscle composition and neuromuscular junction constitution thereby strengthen its contractility through altering the irradiation condition, we believe PBM showed the potential to be as a promising clinical treatment for muscular atrophy.