## 1 Introduction  
Exercise has beneficial effects in the prevention and treatment of a number of diseases, such as metabolic diseases, psychiatric diseases, neurological diseases, cardiovascular diseases, musculo-skeletal disorders, and cancer [1; 2; 3; 4]. Skeletal muscles, which are one of the major tissues used to perform exercise, are also affected by exercise causing increased insulin sensitivity, myokine secretion, muscle fiber type shifts, and increased muscle mass. In particular, mimicking physical exercise, achieved by neuromuscular electrical stimulation, has been shown to improve skeletal muscle regeneration in the elderly [5; 6]. During exercise, motoneuron firing induces intramyofibillar Ca\({}^{2+}\) release from the sarcoplasmic reticulum to trigger muscle contraction through myosin heavy chain ATPase activity, while systemic conditions, such as increased sympathetic nervous system activity, release of fatty acids, and glucocorticoid secretion, are changed. These stimuli synergistically or additively induce transcriptomic activation or repression in skeletal muscles [7; 8; 9]. Transcriptomic modification is classified by the expression patterns of two groups: acute response genes and slow response genes. Acute response genes are induced shortly after exercise and this gene induction does not last for a long time. _Ppargcla_ is a well-known acute exercise induced gene [10]. On the other hand, chronic reactive genes are not induced by a single bout of exercise; however, once the gene expression is modified, it is maintained for longer period of time, such as with _Myhl_ genes [11]. Calcium released from the sarcoplasmic reticulum acts as an important transcriptional regulator, which activates calcineurin, a calcium/calmodulin-regulated protein phosphatase, and CaMK, calcium- and calmodulin-dependent protein kinase. Calcineurin induces translocation of NFAT proteins to the nucleus and causes transcriptional activation. The calcineurin-NFAT pathway increases _Myh2_ expression in fast-type muscles and _Myh7_ in slow-type muscles. CaMK phosphorylates HDAC (histone deacetylase) to induce nuclear export, which complexes with MEF2 proteins to repress MEF2-dependent genes, such as _Myh7_. Both calcium-induced transcriptions lead fiber-type shifts to a slow type [12]. Adrenalin secretion is increased during exercise to satisfy the energy demand via increased heart rate, respiration, glycogenolysis in the liver, and lipolysis in white adipose tissue. Adrenaline acts through adrenoreceptors, which are found in skeletal muscles, cardiac muscle, smooth muscle, and the brain [13]. In particular, skeletal muscles express \(\beta\)2-adrenooreceptor, which plays a role in vasodilation and increased contraction velocity in skeletal muscle, as well as in carbohydrate degradation [14]. Clenbuterol is a specific agonist of \(\beta\)2-adrenoceptor and is usually used as a bronchodilator for airway obstructive disorders, such as bronchial asthma and chronic bronchitis; clenbuterol is also an anabolic steroid, which is a banned drug and has been designated by the World Anti-Doping Agency (WADA) as being used for doping. Clenbuterol has been shown to induce skeletal muscle hypertrophy and a type change from a slow to fast muscle type by increasing IGF-1 expression [15; 16; 17]. _Ppargca1a_ has been shown to also be under the control of clenbuterol in in vivo treatments [18]. To elucidate the molecular mechanisms of transcriptional regulation of _in vivo_ exercise, we factored the exercise into muscle contraction induced by motoneuron activity and the effect of endocrins. As an _in vitro_ muscle contraction model, electrical pulse stimulation (EPS) has been widely used [19; 20]. EPS induces calcium release from the sarcoplasmic reticulum, therefore EPS enables analysis of calcium signaling _in vitro_. Global transcriptional analyses of EPS have recently been published by two different groups [21; 22]. Both experiments focused on relatively short-term EPS treatments.