Electrical muscle stimulation (EMS) is a widely used method in sports and rehabilitation
therapies to simulate physical exercise. EMS treatment via skeletal muscle activity
improves the cardiovascular functions and the overall physical condition of the patients.
However, the cardioprotective effect of EMS has not been proven so far, therefore,
the aim of this study was to investigate the potential cardiac conditioning effect
of EMS in an animal model. Low-frequency 35-min EMS was applied to the gastrocnemius
muscle of male Wistar rats for three consecutive days. Their isolated hearts were
then subjected to 30 min global ischemia and 120 min reperfusion. At the end of reperfusion
cardiac specific creatine kinase (CK-MB) and lactate dehydrogenase (LDH) enzyme release
and myocardial infarct size were determined. Additionally, skeletal muscle-driven
myokine expression and release were also assessed. Phosphorylation of cardioprotective
signaling pathway members AKT, ERK1/2, and STAT3 proteins were also measured. EMS
significantly attenuated cardiac LDH and CK-MB enzyme activities in the coronary effluents
at the end of the ex vivo reperfusion. EMS treatment considerably altered the myokine
content of the stimulated gastrocnemius muscle without altering circulating myokine
levels in the serum. Additionally, phosphorylation of cardiac AKT, ERK1/2, and STAT3
was not significantly different in the two groups. Despite the lack of significant
infarct size reduction, the EMS treatment seems to influence the course of cellular
damage due to ischemia/reperfusion and favorably modifies skeletal muscle myokine
expressions. Our results suggest that EMS may have a protective effect on the myocardium,
however, further optimization is required.
