46
reported the beneficial effects of physical exercise in the rehabilitation of the dis-
ease, in particular, on the heart [ 20 , 21 ]. Beavers et al. tried to evaluate the effect of
long-term (6–12 months) physical excise intervention on inflammatory biomarkers
in the elder population [ 22 ]. In this study, a bundle of biomarkers includes a family
of interleukin-related cytokines (IL-1ra, IL-2sRα, IL-6sR, IL-8, IL-1sRII, IL-15),
adiponectin, and TNF- α were measured. They concluded that the IL-8 was the only
inflammatory biomarker in their study population was affected by the physical
activity. Similar results were observed in a short-term physical activity population.
Lund et al. tried to investigate the stability of inflammatory biomarkers in short-
term physical activity in middle-aged male [ 23 ]. Their data suggested that change
the style of exercise (withdrawal of highly active and the imposition of daily exer-
cise) will not elicit substantial changes in C-reactive protein (CRP), IL-6, and TNF-
α. In other words, these inflammatory markers (CRP, IL-6, and TNF-α) are relatively
stable and rarely affected by exercise behavior.
Notably, the latest data suggest that the inflammatory biomarkers may be affectedby exercise intensity. Another study has different answers. Different from the previ-
ous studies, in this study, the authors selected the change of maximal oxygen con-
sumption (VO 2 max) as the primary outcome and tried to determine if the response
of certain inflammatory biomarkers change (decrease or increase in the level of
biomarkers) to the diverse of the exercise intensity [ 24 – 26 ]. The inflammatory bio-
markers involved in this study include IL-1β, IL-6, IL-10, TNF- α, hs-CRP, soluble
intercellular adhesion molecule-1 (sICAM-1), and ratios of TNF- α/IL-10 in circu-
lating peripheral blood. The data clearly demonstrated that a single bout of exercise
with high-intensity induces a transient increase in IL-6 and the ratio of IL-6/IL-10,
and low-intensity can decrease the level of sICAM-1 [ 27 ].
3 Fibroblast Growth Factor 23 (FGF23): New Insight
into Links Between Bone and Heart
Several initial studies indicated that fibroblast growth factor 23 (FGF23), a major
regulator of phosphate homeostasis and vitamin D homeostasis, may play a unique
role in linking benefits of physical exercise on the heart [ 28 , 29 ]. FGF23 is a 32-kDa
protein with 251 amino acids that is synthesized and secreted by bone cell (mainly
osteoblasts) which was initially regarded as responsible for phosphate metabolism.
Unexpectedly, a recent study indicated that FGF23 has significantly expanded into
its present role as a key player in cardiovascular disease, though the study’s sample
size was very small [ 30 , 31 ]. It will, nevertheless, be valuable to confirm these find-
ings in additional settings, especially in athletes, fitness lovers or even community-
based, multi-race/ethnic regular physical exercise population. The data about the
FGF23 levels will itself be informative and be important in designing the future
exercise evaluation, and the findings may act as a potential direction of benefit to the
exercise on the heart function.
L. Che and D. Li