In brief, it occur chemically by triggering with increased Ca++ concentrations in the cytosol of muscle fibers. At the molecular level, it occur by sliding of myosin and actin filaments on each other.
I was not sure exactly what you wanted to know, neuromuscular or intracellular? I found the following quote from the reference below. Perhaps this reference will answer your question more completely.
Regards,
Christopher
"There is strong evidence now that force production does not exclusively depend on the actin-myosin overlap (as currently assumed, [3]), that actin-myosin interactions depend on the contractile history (and that this history is stored in a molecular memory, [4]), and that passive (non actin-myosin related) force production is variable and an important component of contractility [5]."
If you mean the molecular basis of neuromuscular contraction of a skeletal muscle, then as described in textbooks of physiology it will start by having an action potential at the motor nerve which will secrete acetylcholine at the neuromuscular junction. acetylcholine will bind postsynaptic nicotinc receptors on the muscle and cause changes in membrane permeability to sodium leading to sodium influx which in turn will cause a depolarization of the muscle when it reaches it reaches its threshold level. this depolarization will travel along the t-tubules to cause opening of voltage gated calcium channels (DHP R) which in turn will cause opening of sarcoplasmic reticulum rayanodine receptors causing outflux of stored calcium to the cytosol. available calcium will bind to the calcium subunit of the troponin leading to conformational change of the troponin-tropomyosin complex that will uncover the sites for myosin head to bind on actin... power stroke occurs and sliding of actin over myosin occurs.. Z lines become shorter which means that the sarcomere shortens causing the whole muscle to contract.
you may find these in Guyton and Hall textbook of medical physiology.