The Impact of 12 Weeks Exercise Training on Circulating Soluble-Klotho and Pro - BNP in Coronary Artery Disease Patients

Abstract

Background: Klotho protein is a membrane-based circulating protein that regulates cell metabolism, as well as the lifespan modulating activity of Fibroblast Growth Factors (FGFs). Higher plasma circulating Klotho levels reduce cardiovascular risk, suggesting Klotho has a protective role in cardiovascular diseases. Brain natriuretic peptide is a prognostic marker in coronary artery disease (CAD) patients, and in particular in CAD patients with heart failure. Aerobic exercise reduces the risk of cardiovascular events and mortality in patients with proven coronary artery disease (CAD), thus, S-Klotho serum levels were assessed in order to find out whether exercise can modulate its activity. Purpose: to assess the impact of 12 weeks exercise training program on S-Klotho and pro-BNP levels in coronary artery disease patients, and to assess possible correlation between S-Klotho and pro-BNP II. Methods: S-Klotho and pro-BNP serum were assessed in 2 groups: gr. A = 41 coronary artery disease patients (CAD), age 59.6 years ± 2.2 sd, all with recent (< 45 days) aorto coronary bypass surgery (CABG) years, myocardial infarction (MI), or percutaneous intervention (PCI) who were recruited to a 12 weeks supervised aerobic exercise program (45 min/4-5 sessions/week), and gr. B, a control group consisting of 17 CAD patients, age 61 years ± 2.4sd who continued their usual treatment and lifestyle with no active exercise intervention. Assessment was done twice, prior to exercise program and at the end of 12 weeks intervention. Blood samples were drawn from a forearm vein after overnight fasting, s-Klotho levels in the serum were analyzed using an α-klotho enzyme linked immunosorbent assay Elisa kit (IBL, Immuno-Biological Laboratories Co., Japan) and the pro-BNP was measured as well by an immunoassay method using the Cobas e-411 analyzer,

Sixteen weeks of aerobic training influence spirometry, s-klotho, and hemodynamic responses to sub-maximal exercise testing in obese men with severe obstructive sleep apnea

“…[46][47][48] While resistance training showed no to little effect on s-klotho levels, aerobic training, especially chronic aerobic training has been proven to increase the biomarker's levels. 25,[46][47][48] The current study further suggest that s-klotho levels increase from baseline to immediate-post exercise and then decrease. Levels of s-klotho are higher immediatepost and decrease faster in healthy compared to OSA subjects.…”

“…[18][19][20] On the other hand, aerobic exercise improves cardiorespiratory aspects of function in people with OSA. [21][22][23][24][25] The six Minute Walk Test (6MWT) is an exercise test that may be sub-maximal and/or maximal according to extent of effort on the participant's behalf. As part of the 6MWT the participant is instructed to achieve the greatest distance possible within 6minutes of walking.…”

Klotho: An Emerging Factor With Ergogenic Potential

“…Accordingly, aerobic exercise training interventions have been shown to increase sKlotho and tissue expression of Klotho. Significant increases in sKlotho have been reported following 12 weeks of aerobic exercise in trained young women (182), postmenopausal women (129) and in patients with coronary artery disease (190).…”

The effects of partial sleep deprivation and the sub-maximal NDKS exercise testing protocol on S-Klotho and hemodynamic responses in women

“…[20][21][22][23][24] Furthermore, S-Klotho is a role-player in determining the sensitivity to insulin, mediating the binding of FGF19, FGF20, and FGR23 to their receptors as part of the growth process at the cellular level. 23 In addition, S-Klotho is suggested as a cardiovascular system "protector" via means of endothelium-derived NO production, 25,26 and has been proven to affect cellular calcium homeostasis via increased expression of TRPV5, and decreased TRPC6; and increases membrane expression of inward rectifier ROMK. In mice, under-expression causes hypervitaminosis of vitamin D; altered mineral-ion homeostasis resulting in accelerated aging; a syndrome of accelerated aging; arteriosclerosis; impaired endothelium-dependent vasodilation; and impaired angiogenesis.…”