Based on over forty years of experience with human body donations, this narrative review proposes that myofascial trigger points represent local rigor contractures in living tissue. Previous descriptions of the so-called “rigour trigger” situate the lesion within the sarcomere. The mechanism under consideration involves persistent actomyosin attachment resulting from inadequate ATP at the contractile apparatus. These attachments may sustain tension even after the initial activity has ceased. An endplate disturbance may initiate the skeletal muscle focus. The rigor hypothesis addresses the sustained state of tension. A myocardial rigour trigger is introduced as a focal ATP-limited contracture in viable heart tissue. Experimental metabolic deprivation has demonstrated that cardiomyocytes can develop contracture. The role of connective tissue in transmitting this tension warrants inclusion in the investigation. Previous fascia-focused analyses of muscle, along with the subsequent paper on fascia and its role in rigor mortis, provide a strong anatomical foundation. This review integrates the clinical characterization of myofascial trigger points with experimental findings on cardiac rigor. This review recommends targeted measurements at the identified focus, including assessment of adjacent tissue responses. Myocardial trigger points have not yet been established in living humans. Identifying a viable focal contracture and quantifying the sustaining attachments would directly test this hypothesis.