The physiological adaptations that take place during and after sports performance result in an increase in effective volemia (reduction in hematocrit and hemoglobin), increase in muscle mass (increase in creatine kinase [CK], aspartate aminotransferase [AST], γ-glutamyltransferase [GGT]), bio chemical evidence of muscle trauma (increased CK and myoglobin, AST, alanine aminotransferase [ALT], lactate dehydrogenase [LDH], K+), hypercatabolism, increased energy substrates demand (decreased glucose, triglycerides, and increased cortisol and testosterone), and, finally, cardio vascular overload (increased troponins).
It has been documented that after a marathon, athletes show a reduction in estimated glomerular filtration rate (eGFR) and an increase in creatinine and lipocalin-2, also known as neutrophil gelatinase-associated lipocalin (NGAL). The prolonged physical activity effect on renal function is transient, and values of these parameters tend to return to pre-marathon levels within 24–48 h.
Similarly, some traditional markers of hepatic damage also show transient increases following endurance sports competitions. In particular, the most marked increases are in total and direct bilirubin, LDH, and ALT. No significant variations are observed in AST, alkaline phosphatase (ALP), and GGT. These increases, however, are transitory, and the parameters involved tend to reduce again within 24 h of the competition end. The transitory nature of these variations raises questions about their pathophysiological nature. They may be the expression of physiological mechanisms of adaptation to physical stress.
Physical exercise, especially endurance practiced at an amateur and professional level (running, cycling, and swim ming), involves increased cardiac output, heart rate, and systolic pressure for several hours. This increase in cardiac work sustained over time generates myocardial stress accompanied by the physiological release of oxygen-free radicals (OFRs) and alterations in intracellular pH, which, in turn, support and amplify the damage of myocardiocytes.
It has been extensively documented that an acute increase in cardiac troponins (cTn) is observed in subjects practicing endurance sports, immediately after a marathon. In most observations, circulating cTn levels return to baseline 24–48 h after the athletic performance end. The advent of high-sensitivity cTn assays made possible to confirm this phenomenon in several studies. However, it is not yet clear whether this increase is physiological or indicative of irreversible myocardial damage. Hypotheses have been put forward on the mechanisms leading to this transient increase in cTn, which involve the release of cTn from cell vesicles. It is known that in the myocardiocyte, there are two intracellular pools of cTn: cytosolic, consisting of soluble cTn (6–8% for cTnT and 3% for cTnI), and structural, consisting of cTn complexed with tropomyosin and actin. The cTn derived from the structural pool is responsible for the peak observed during myocardial necrosis, which is diagnostic of acute myocardial infarction. On the other hand, release from the cytoplasmic pool is responsible for the transient small increase observed following moderate- to high-intensity physical performance accompanied by transient myocardial stress. In this case, the release of cTn occurs following an increase in membrane permeability, accompanied by the detachment of membrane vesicles containing cytoplasmic proteins and not as a result of cell necrosis. When the appropriate tissue oxygenation is restored, this phenomenon ceases, with the consequent return of circulating cTn within the reference limits. Therefore, the myocardial stress observed during physical exercise is not so prolonged or severe as to cause myocardial damage irreversible but is sufficient to cause the release of vesicles and their contents, including cTn, into the circulation.
In addition, the reduced renal clearance observed during exercise could prolong the catabolic elimination of cTn and other proteins released from the myocardiocyte, increasing their stay in circulation.
Even the main hematological parameters obtained by blood count show altered values immediately after sports performance. In particular, an increase in white blood cells (WBC), neutrophils, and monocytes, together with a decrease in lymphocytes and eosinophils, have been documented in several studies. These changes are mainly attributable to the release of catecholamines and cortisol typically observed during exercise. In addition, a decrease in red blood cells (RBC) and hemoglobin (Hb) can be observed along with an increase in platelets (PLT) and mean platelet volume (MPV).
The main changes in biochemical-clinical parameters observed following a medium-high intensity sports performance are summarized in Table 1.
Table1. Changes in the main biomarkers in response to endurance sports performance (assessed within 3 h of the competition end)
