47
Though initial studies show that FGF23 is secreted from bone cells, and imme-diately circulated into peripheral blood to reach the whole-body [ 32 – 34 ]. FGF23 is
regulated by bone proteins PHEX and DMP1 [ 35 ]. A recent study based on an ani-
mal model showed only chronic exercise or calorie restriction upregulates FGF23
mRNA and protein expression in skeletal muscle [ 36 , 37 ]. FGF23 mRNA and pro-
tein expression may vary in different exercise patterns, or models, including acute
exercise, exhaustive exercise, and chronic exercise. Li et al. used C57BL/6 J mice to
evaluate the exercise performance, H 2 O 2 production, reactive oxygen species (ROS),
and functional mitochondrial biomarkers in muscle, the gene expression of sirtuin
1, and mitochondrial transcription factor A, PGC-1α, PPAR-δ, and citrate synthase
activity was assayed. There have been some unexpected findings such as only
chronic exercise upregulated the level of FGF23 mRNA and protein expression. In
addition, the exogenous FGF23 can significantly extend the time to exhaustion,
which associated with VO 2 and VO 2 max. As a matter of fact, this issue is extremely
important to the evaluation of exercise promotes exercise performance by pro-
teomics technologies, in particular for chronic exercise evaluation.
4 Troponins Proteins—A Novel Biomarker of Myocardial
Injury in Physical Exercise
The benefit of physical exercise on heart function has been accepted with minimal
debate. However, the intensity and amount of exercise vary widely, and another pos-
sibility exists, that is the physical exertion or exercise above a certain threshold may
paradoxically worsen heart health. Thus far, some small studies from clinical have
been performed that documented adverse cardiac and vascular events with high
levels of endurance exercise. Investigating the potential role of prolonged exercise
and endurance training elevations in adverse cardiovascular early reports focused on
the serum concentrations of troponins proteins, a family of acidic regulatory mole-
cules found in cardiac muscle. This phenomenon was partly due to cTns are highly
specific biomarkers of response to myocardial cell damage [ 38 – 41 ]. So far, two
high-sensitive regulatory proteins, which can be measured from serum, cardiac tro-
ponin T (cTnT) and troponin I (cTnI) have been found related to the mechanisms of
actin-mediated regulation [ 42 ]. There is little good evidence from clinical data that
cardiac troponins may as a potential biomarker in response to exercise [ 43 ]. The
objective of this study was to determine if prolonged exercise resulted in the appear-
ance of cardiac troponin T (cTnT) in serum and whether this was associated with
elevated levels of myocardial oxidative stress. The initial evidence was derived from
animal experiments [ 44 ]. Li et al. using a myocardial oxidative stress model built in
Sprague-Dawley rats, their data clearly indicated that serum cardiac troponin T is
significantly associated with the myocardial oxidative stress after prolonged exer-
cise [ 45 ]. A pilot study from clinical trials leads by Lee et al., using a novel high-
sensitivity cardiac troponin I (hs-cTnI) as a biomarker to investigate whether the
3 The Effects of Exercise on Cardiovascular Biomarkers: New Insights, Recent Data...