• Neuromuscular transmission and pharmacological modulation emerge as central drivers of muscle activity, demonstrated by direct end-plate transmission (acetylcholine), ion sensitivity, and drug actions (prostigmine, quinine) shaping contraction and disease across poliomyelitis and myasthenia/myotonia studies [10], [5], [19], [17], [2].

• Denervation-linked fibrillation and atrophy reveal the plastic response of skeletal muscle under neuromuscular disruption, with observed fibrillation after denervation, its relation to atrophy, and disease-related electrolyte shifts informing pathophysiology and prognosis [1], [14], [15], [13].

• Cellular contraction is modulated by intracellular biochemistry, with ATP-triggered release of contraction in isolated fibres and localization of adenine derivatives supporting a biophysical basis for contraction regulation [4], [12].

• Cross-species motor control and locomotion reveal conserved principles of reflex-posture generation, rhythm, and zonation of contraction areas in invertebrates and elasmobranchs, highlighting comparative neurophysiology of movement [3], [8], [9], [11], [18].

• Human motor innervation and performance metrics show a baseline tonic state and preparatory-tension effects on reaction time, linking structural innervation with functional output [13], [6].