Possible Explanation of "Association of Episodic Physical and Sexual Activity With Triggering of Acute Cardiac Events,"
Copyright 2011, James Michael Howard, Fayetteville, Arkansas
The common factor is increased prolactin. Prolactin is increased by sexual stimulation and exercise in horses (Journal of Animal Science, Vol 69, Issue 6 2556-2562). PRL is increased as a "sustained PRL surge after sexual climax in males and females" (Reproduction. 2010 Nov;140(5):643-54). Also, "patients with acute myocardial infarction as a subgroup of acute coronary syndromes showed the highest prolactin levels" (Horm Metab Res 2006; 38(11): 767-772). I think prolactin as a common factor in your report may be supported.
Since prolactin has been identified as a specific stimulator of DHEA, I think the real mechanism involves DHEA. I suggest a case may be that prolactin stimulates DHEAS, the precursor of DHEA, which then produces DHEA, which then reduces prolactin. A cycle of production and inhibition involves PRL, DHEAS, and DHEA. Some studies report increases in DHEAS following exercise, etc.
If a person of low DHEA is stimulated to produce a bolus of DHEAS, then the DHEAS momentarily reduces the ratio of DHEA to DHEAS. Therefore, moment occurs in which DHEA availability is reduced. DHEA is the active molecule. DHEA, DHEAS and myocardial infarction has been connected: "Similar relationships between concentrations of DHEA-S and risk [of myocardial infarction] were observed, with an RR of 1.58 (95% CI 1.13-2.21; P for trend = 0.06) for myocardial infarction in the highest vs lowest quartile." (Clin Chem. 2008 Jul;54(7):1190-6).
I suggest the increased probability of MI following episodic exercise or sexual activity is caused by the momentary increase in the DHEAS to DHEA ratio in individuals of low DHEA. The momentary decrease in available DHEA is the cause.