Damian Skrypnik, Katarzyna Skrypnik, José Casaña Granell, Dawid Woszczyk, Joanna Suliburska
Journal: Scientific reports 2025;15(1):38951
PMID: 41198895
After an acute coronary syndrome (ACS), such as a heart attack, patients are often referred to cardiac rehabilitation (CR). CR usually includes supervised exercise, education, and lifestyle advice to improve recovery and reduce future heart attack risk. Exercise causes muscles to release proteins called myokines, which can influence inflammation, metabolism, and cardiovascular health. However, it is not fully understood how CR affects myokine levels in patients recovering from ACS. The aim was to investigate the influence of a 2-week CR programme on indicators of inflammation and cardiovascular health.
The results showed that patients who completed CR had increased levels of myokines after the two-week programme. These findings suggest that exercise-based rehabilitation alters circulating myokine levels in patients after ACS.
In conclusion, cardiac rehabilitation appears to influence muscle-derived proteins that may play a role in cardiovascular recovery. While the study does not prove that changes in myokines directly improve long-term outcomes, it provides insight into possible biological mechanisms behind the benefits of cardiac rehabilitation. Healthcare professionals may use this information to understand how structured exercise contributes to recovery after acute coronary events.
The role of myokines as a link between cardiac rehabilitation (CR) and cardiovascular benefits in patients recovering from acute coronary syndrome (ACS) is important but not well understood. We investigated the effect of CR on circulating levels of myostatin, follistatin, apelin, and follistatin-related protein 1 (FSTL1) in post-ACS patients. A total of 110 patients underwent a 2-week CR programme (group S) and were compared with 110 non-CR patients (group K). In group S, blood pressure, heart rate, anthropometrics, body composition, and serum myokine levels were measured at baseline and post-CR; in group K, these were assessed once. After CR, apelin, myostatin, and FSTL1 increased in group S. Apelin and myostatin were higher in group S post-CR compared with group K, while follistatin remained higher in group K at both time points. FSTL1 was initially higher in group K but increased post-CR in STEMI patients only; myostatin increased in NSTEMI patients. Apelin increased in STEMI patients. Apelin and myostatin levels were independent of cardiovascular risk factors. Post-CR, follistatin correlated inversely with diastolic pressure; FSTL1 was related to fat tissue, muscle mass and body mass index. CR modulates key myokines and differential myokine responses in STEMI vs. NSTEMI patients support the need for personalised rehabilitation strategies. ClinicalTrials.gov registration number: NCT03935438.
© 2025. The Author(s).
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