## 1 Introduction  
The capacity of skeletal muscle to adapt to metabolic and environmental demands is remarkable. Notably, this tissue is able to increase or decrease its mass, and consequently the size of the contractile apparatus, in response to various stimuli, such as exercise [1], electrical stimulation [2], denervation [3], mechanical load [4], nutritional demands [5], or external factors such as hypoxia [6; 7]. Hypertrophy is the increase in skeletal muscle mass and force, which is characterized by increased protein synthesis and storage, resulting in larger muscle fibers [8; 9]. Among possible stimuli, resistance exercise is regarded as the most effective means of promoting hypertrophy. Under this sort of stimulation, the hypertrophic response is caused by the accumulation of anabolic bursts from numerous exercise sessions and recuperation rounds [10; 11; 12]. Resistance exercise training in humans typically consists of recurrent sessions (3-4 times per week) with high repetitions (3 to 10 sets of 1 to 12 repetitions per set) and moderate loading (65-85 percent of one maximum repetition--1 RM) with short rest periods (<90 s) [13; 14]. Notably, a recovery period (two to three days) is required to restore basal tissue homeostasis [12; 13; 15]. Throughout the years, various animal models have been created to examine this adaptive muscle response [15]. Compensatory hypertrophy was one of the earliest attempts to simulate resistance exercise (also described as functional overload and synergism ablation) [16; 17; 18; 19], and although this model produces a rapid (about one week) and substantial (30%) increase in the muscle mass, it has significant drawbacks, including an intense inflammatory response and persistent injury due to the extreme stretching imposed on the plantar muscle. A second animal model is squat training, which debuted in the late nineties and has been widely employed over the past two decades [20]; nonetheless, research employing this model focuses mostly on cardiac muscle hypertrophy [21; 22; 23]. This approach typically results in a 15-30% rise in mass after 8-12 weeks, with a greater hypertrophic response in the plantar muscle, which is not the focus of human squat exercises [20; 24]. In addition, the plantar muscle is rather tiny and profoundly confined in the posterior legs, limiting its utility for tissue, molecular, and functional-based investigation. The squat model has only been documented in rats, restricting its applicability to genetically modified models, which are often based on mice. Subsequently, a stretch-shortening contraction training strategy was modified to address athletic actions more specifically. In this model, electrical stimulation is utilized to induce concentric activation of the dorsiflexors, followed by the application of an opposing force (eccentric component), resulting in plantar flexion. After four-and-a-half weeks of training utilizing this strategy, around 20% hypertrophy is attained in TA [25; 26; 27]. Additionally, the usage of ladder-climbing as an alternative resistance exercise model has occurred. In this procedure, rats or mice are placed at the base of a vertical ladder with various loads attached to their tails [28; 29; 30; 31; 32; 33]. The majority of training protocols are lengthy, lasting 6 to 8 weeks, and muscle mass increase may vary greatly between research (11-23%), which may be related to the fact that animal motivation influences performance. Finally, a resistance-like exercise protocol based on electrical stimulation was first developed in rats by [PERSON] and [PERSON] (1988) [34; 35]; since then, their protocol has undergone several improvements [36], resulting in two major types of electrical stimulation in animal models: one in which the sciatic nerve is electrically stimulated via invasive procedures [2; 37] and another in which the muscle is directly stimulated [11; 38].