ASSESSMENT OF EFFECTS OF NON-FUNCTIONAL OVERREACHING AND OVERTRAINING ON RESPONSES OF SKELETAL MUSCLE AND CARDIAC...

The aim was to study the effects of non-functional overreaching and overtraining on responses of biomarkers of the skeletal muscle cell (CK-NAC) and cardiomyocyte injury (cTnI and CK-MB) and their use in monitoring OTS. In 43 athletes with non-functional overreaching (NFO)/overtraining syndrome (OTS) and 40 athletes without NFO/OTS -control athletes (CA) off-season measurements of creatine kinaze (CK-NAC and CK-MB) were performed, followed by peak-season evaluation of the dynamic of CK-NAC, CK-MB and cardiac troponin I (cTnI) changes. CK and cTnI levels were obtained 24 hrs before the strenuous exercise appropriate to the sport-specific peak-season intensity, immediately after completion of the work-load, after 6, 48, and 72hrs. Baseline and post-exercise clinical assessment and echocardiography were performed in 6 and 48 hrs after strenuous session. Similar rising trend of CK-NAC, CK-MB, and cTnI levels was observed immediately after exercise, reaching peak values after 6 hours in all athletes, though, significantly greater in NFO/OTS athletes than in controls. After 48 hours of recovery in athletes with NFO/OTS CK-NAC, CK-MB, and cTnI values were significantly higher than on entry, showing slower recovery. CK-NAC fell within the "possible overtraining and muscle damage" levels in OTS athletes, even after 72 hours of recovery. Most of the athletes noted continuous trauma during game/combat contact events, though, mostly recovered after 48 or 72 hours. Two year follow-up showed no signs of full recovery in the OTS athletes. Echocardiography didn't reveal any sustained alterations of systolic and diastolic functions, or clinically threatening myocardial damage, only minor diastolic changes due to adaptation to the post-exercise haemodynamic. Elevated values of cardiac markers after strenuous exercise can be linked to increased cellular permeability and cardiac troponin leakage, amplified by oxidative stress existent in OTS athletes. In our study sport-specific intensive exercise caused mild injury to skeletal muscle and transient increase of the CK-MB and cTnI, without irreversible pathophysiological and clinical consequences, suggesting mostly benign cardiac involvement, though amplified by existent oxidative stress in athletes with OTS. Monitoring responses via alterations of biochemical parameters can be helpful to guide athletic training, and prevent OTS or interrupt NFO to OTS progression.