3.1. Evaluation of Pre- and Post-Ride Anthropometric and Serum Biochemical Parameters
Primarily, we observed expected changes in anthropometric parameters in response to exercise. A decrease in detected muscle content is connected to dehydration, which is most commonly seen after strenuous exercise, in which heavy sweating has occurred [18
]. Exercise also increases blood flow and vascular perfusion in skeletal muscles, which can result in a decrease in bioimpedance and muscle resistivity. This phenomenon can further affect the concentration of minerals in serum or disturb the functions of the cardiovascular system [19
]. It can be stated that there is a general agreement that the systolic blood pressure is increased after aerobic exercise; nevertheless, diastolic blood pressure exhibits negligible changes only [20
Lactate accumulation has been for a long time linked with disturbed sports performance, connected with the hypothesis about lactate acidosis [21
]. Nevertheless, the lactate-shuttle mechanism enables the use of lactate as an energetic substrate in both type I and type II skeletal muscles, providing them for physical exercise [22
]; thus, lactate is considered as a well-established indicator of fatigue more than as its cause. Based on the above-mentioned facts, the post-ride elevation of lactate level confirms that the level of physical exercise of the cyclist was sufficient.
Looking at the effects of bicycle riding on the determined biochemical markers, we found that levels of the main androgen steroid hormone testosterone were increased. It is well known that testosterone levels vary after an intensive and prolonged physical exercise [23
], and it was found that strenuous running or weight-lifting resulted in an increase of testosterone levels [24
]. On the other hand, Saka and coworkers showed that rigorous cycling decreased testosterone levels (p
= 0.001); nevertheless, why serum testosterone is reduced is not clear [9
]. They hypothesized that hormone production can be affected by constant abrasion of the testicles, leading to elevation of intrascrotal temperature or testicular microtrauma, and indeed, all of these factors impact the testicular functions [25
]. Contrary to that, our results show a post-ride elevation of testosterone, which can be partly a result of a transient hemoconcentration of circulating testosterone, reduced metabolic clearance and/or a possible hormone-mediated increase of testicular production [26
Further, we detected modest differences in pre- and post-ride bilirubin values of cyclists. Although we did not investigate specific mechanisms involved in this phenomenon, the literature suggests that exercise may increase the activity of heme-oxygenase-1, which converts biliverdin to bilirubin [27
]. Since bilirubin can be produced through its pre-cursor heme [28
], another plausible mechanism of bilirubin elevation is the stimulation of heme catabolism through an exercise-induced hemolysis and subsequent increased heme bio-availability, promoting the increased bilirubin concentrations. There is a major lack of studies concerning the effects of aerobic exercise on the bilirubin levels; however, we can find the support in a study by Swift and coworkers [29
], who concluded the possible beneficial effect on the decrease of cardiovascular risk through an increase in bilirubin concentrations.
Uric acid has a pivotal influence on vascular control by elevating oxidative stress (O2−
production) and NO-scavenging, which lead to vasodilatation [30
]. Our results demonstrate increased post-ride serum uric acid. It is worth noting that all participants carried out regular aerobic exercise, which increases the activity of xanthine oxidase, contributing to the oxidative stress [31
]. This enzyme is connected in the oxidation of hypoxanthine to xanthine and subsequently to uric acid after degradation of adenosine triphosphate (ATP) to adenosine monophosphate (AMP) and inosine-5′-monophosphate (IMP). Thus, the post-ride elevation of uric acid (the end product of purine nucleotide catabolism) is a result of physical exercise-induced purine degradation. Taken together, although physical activity improves cardiovascular risk, on the other hand, the impact of immediate uric acid formation on hyperuricemia or chronic gout is still not yet elucidated.
Our analyses revealed very low levels of CRP in pre-ride and post-ride serum specimens. It was found that bicycle riding resulted in a modest elevation of CRP; however, its amount was still very low and classified as a normal systemic CRP level [32
]. The available literature provides contradictory results on CRP levels post-physical exercise, since both an increase [33
] and a decrease [34
] have already been described. This phenomenon is likely due to the various types of activities tested in studies; however, it seems that CRP elevation is mostly associated with an exercise-induced inflammatory sequelae and is more significant during activities that are longer or more aerobically demanding, such as bicycle riding for longer distances.
3.3. The Effect of Physical Exercise on PCa Biomarkers
In the examination of PCa biomarkers, the study design resulted in an increase of both analyzed forms of PSA (tPSA; fPSA). By testing participants of the same age (about ≥50 years old), we mention two essential studies based on measurements of PSA in men after bicycle riding. Although the level of physical activity differed modestly, both studies describe an elevation in post-ride specimens [3
] and, thus, are consistent with our findings. It is noteworthy that Kindermann et al.
showed that one hour cycle ergometer activity increased not only tPSA, but also fPSA [5
Contrary to that, our study concurs with the data obtained in other studies. For instance, Saka and colleagues determined that a 300-km bicycle ride does not impact the performance of tPSA and fPSA [9
]; nevertheless, the study design is not comparable to our study, due to the tested cohort. In contrast to our cohort, they involved athletes and student volunteers with an average age of 22.4 and 24.4 years, respectively. Other studies with contradictory results can be found [2
]; nevertheless, a closer look reveals that their methodologies varied in many parameters, including the age, timing of the blood sampling and the duration and intensity of physical exercise; thus, the comparison is considerably hindered. Overall, it can be stated that similarly to a disorganization of prostate cells during PCa development, physical activity can irritate the cells to form transient pores for the leakage of PSA into blood (Figure 4
The stability of a biomarker belongs to its most fundamental properties. By means of physical exercise, both urinary and serum sarcosine exhibited no differences among pre- and post-ride sampling. The rationale of testing sarcosine is its possible utilization as an auxiliary diagnostic tool for PCa diagnostics [17
]. Contrary to PSA, which is a secretory protein, sarcosine is a common intermediate metabolite and by-product in glycine synthesis and degradation through the activity of glycine-N
-methyltransferase (GNMT) [16
]. Thus, it is expected that the sarcosine amount is highly dependent on the action of GNMT, which is encoded by tumor-susceptible gene GNMT [39
]. To the best of our knowledge, there is a lack of evidence about the effects of physical exercise on GNMT enzymatic activity; however, our results indirectly illustrate no significant changes in the degradation of glycine (Table 3
) and the elevation of sarcosine. Obviously, the impact on other biochemical markers does not interfere with the sarcosine urinary/serum levels, either. Hence, sarcosine seems to be applicable in prostate examinations, especially in the cases where PSA is expected to be undesirably influenced (per-rectal examination, bladder catheterization, sexual activity or bicycle riding).