Evaluation of the effect of oxidative stress on dynamics of cardiac biomarkers in Georgian elite athletes with overtraining syndrome

Abstract

Abstract Funding Acknowledgements Type of funding sources: None. Background Training of professional athletes comprises of repetitive overloading to initiate structural and functional changes for favorable adaptation to the workouts, but with an inadequate recovery overloading may produce non-functional overreaching(NFO) and then overtraining syndrome(OTS). It is important to study chronic effects of exercises via responses of biomarkers for understanding of muscle fatigue and cardiac damage to identify athletes at risk of poor adaptation to training[3,4]. The purpose was to study the effects of oxidative stress on dynamics of cardiac biomarkers in Georgian elite athletes with OTS. Methods On the initial stage in 43 athletes(37 with NFO, 6 with OTS) study of relationship between oxidative stress and OTS revealed imbalance between oxidant production and antioxidant protection via attenuation of antioxidant capacity in athletes with OTS[1,2]. On the current stage of our study,in 43 NFO/OTS athletes and 40 age-matched controls without NFO/OTS pre-season serum creatine kinase myocardial band(CK-MB) and cardiac troponin I(cTnI) were measured, followed by in-season evaluation of the dynamic of their changes(HUMAN,Germany). In-season levels of CK-MB and cTnI were obtained 24hrs before strenuous sport-specific exercise of peak-season intensity, immediately after the work-load,after 6, 48,and 72hrs. Baseline and post-execise clinical assessment and transthoracic echocardiography(TTE) were performed in 6 and 48hrs after strenuous session(6 hrs corresponds to the time when cTnI is typically detectable in ischemic models;48 hrs-CK concentrations recovery time). Results Similar rising trend of CK-MB and cTnI levels was observed immediately after exercise, reaching peak values after 6hrs in all athletes, though, significantly greater in NFO/OTS athletes than in controls, and slightly exceeded reference range of cTnI (in NFO 0.128±0.092ng/ml, in OTS 0.137±0.061ng/ml). After 48hrs of recovery CK-MB and cTnI in NFO/OTS athletes were significantly higher than on entry, showing slower recovery,though normalized in 72hrs. TTE 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 in OTS athletes(E/A pre-exercise:1.47±0.25, post-exercise:in 6hrs 1.06±0.14,in 48hrs 1.40±0.09,p<0,05). Elevated cardiac markers after strenuous exercise can be linked to increased cellular permeability and cardiac troponin leakage, amplified by oxidative stress existent in OTS athletes. Conclusions In our study intensive exercise caused transient increase of the CK-MB and cTnI in NFO/OTS athletes, 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.