Fibroblast growth factor 23 does not directly influence skeletal muscle cell proliferation and differentiation or ex vivo muscle contractility.

Skeletal muscle dysfunction accompanies the clinical disorders of chronic kidney disease (CKD) and hereditary hypophosphatemic rickets. In both disorders, fibroblast growth factor 23 (FGF23), a bone-derived hormone regulating phosphate and vitamin D metabolism, becomes chronically elevated. FGF23 has been shown to play a direct role in cardiac muscle dysfunction; however, it is unknown whether FGF23 signaling can also directly induce skeletal muscle dysfunction.

Skeletal Muscle, but not Cardiovascular Function, Is Altered in a Mouse Model of Autosomal Recessive Hypophosphatemic Rickets.

Autosomal recessive hypophosphatemic rickets (ARHR) is a heritable disorder characterized by hypophosphatemia, osteomalacia, and poor bone development. ARHR results from inactivating mutations in the DMP1 gene with the human phenotype being recapitulated in the Dmp1 null mouse model which displays elevated plasma fibroblast growth factor 23. While the bone phenotype has been well-characterized, it is not known what effects ARHR may also have on skeletal, cardiac, or vascular smooth muscle function, which is critical to understand in order to treat patients suffering from this condition.

Cardiac thromboxane A2 receptor activation does not directly induce cardiomyocyte hypertrophy but does cause cell death that is prevented with gentamicin and 2-APB.

Background: We have previously shown that the thromboxane (TXA2) receptor agonist, U46619, can directly induce ventricular arrhythmias that were associated with increases in intracellular calcium in cardiomyocytes. Since TXA2 is an inflammatory mediator and induces direct calcium changes in cardiomyocytes, we hypothesized that TXA2 released during ischemia or inflammation could also cause cardiac remodeling.

Methods: U46619 (0.

FGF23 directly impairs endothelium-dependent vasorelaxation by increasing superoxide levels and reducing nitric oxide bioavailability.

Fibroblast growth factor 23 (FGF23) is secreted primarily by osteocytes and regulates phosphate and vitamin D metabolism. Elevated levels of FGF23 are clinically associated with endothelial dysfunction and arterial stiffness in chronic kidney disease (CKD) patients; however, the direct effects of FGF23 on endothelial function are unknown. We hypothesized that FGF23 directly impairs endothelial vasorelaxation by hindering nitric oxide (NO) bioavailability.

Changes in α7β1 integrin signaling after eccentric exercise in heat-shocked rat soleus.

Introduction: α7β1 integrin links the extracellular matrix to the focal adhesion (FA) in skeletal muscle and serves as a stabilizing and signal relayer. Heat shock (HS) induces expression of proteins that interact with the FA.

Methods: Male Wistar rats were assigned to 1 of 3 groups: control (CON); eccentric exercise (EE); or EE+HS (HS).

Effects of an acute bout of resistance exercise on fiber-type specific to GLUT4 and IGF-1R expression.

The effects of resistance exercise on fiber-type-specific expression of insulin-like growth factor I receptor (IGF-1R) and glucose transporter 4 (GLUT4) was determined in 6 healthy males. The expression of both genes increased in Type I fibers (p < 0.05), but only GLUT4 increased (p < 0.

FGF23 is a novel regulator of intracellular calcium and cardiac contractility in addition to cardiac hypertrophy.

Fibroblast growth factor 23 (FGF23) is a hormone released primarily by osteocytes that regulates phosphate and vitamin D metabolism. Recent observational studies in humans suggest that circulating FGF23 is independently associated with cardiac hypertrophy and increased mortality, but it is unknown whether FGF23 can directly alter cardiac function. We found that FGF23 significantly increased cardiomyocyte cell size in vitro, the expression of gene markers of cardiac hypertrophy, and total protein content of cardiac muscle.

Acute heat stress prior to downhill running may enhance skeletal muscle remodeling.

Heat shock proteins (HSPs) are chaperones that are known to have important roles in facilitating protein synthesis, protein assembly and cellular protection. While HSPs are known to be induced by damaging exercise, little is known about how HSPs actually mediate skeletal muscle adaption to exercise. The purpose of this study was to determine the effects of a heat shock pretreatment and the ensuing increase in HSP expression on early remodeling and signaling (2 and 48 h) events of the soleus (Sol) muscle following a bout of downhill running.

Store-operated calcium entry is present in HL-1 cardiomyocytes and contributes to resting calcium.

Store-operated Ca(2+) entry (SOCE) has recently been shown to be of physiological and pathological importance in the heart, particularly during cardiac hypertrophy. However, measuring changes in intracellular Ca(2+) during SOCE is very difficult to study in adult primary cardiomyocytes. As a result there is a need for a stable and reliable in vitro model of SOCE which can be used to test cardiac drugs and investigate the role of SOCE in cardiac pathology.

Salivary IgA is not a reliable indicator of upper respiratory infection in collegiate female soccer athletes.

It has been shown that mucosal immunity measures such as salivary immunoglobulin A (s-IgA) can be affected by sport activities and has resulted in an increased susceptibility to infection. However, there is limited research that has evaluated the change in s-IgA throughout a full sport training season. The purpose of the study was to evaluate the change in s-IgA levels and incidence of upper respiratory infection in the National Collegiate Athletic Association Division I level female soccer athletes compared to age matched controls over an entire sport training season.

Acute heat treatment improves insulin-stimulated glucose uptake in aged skeletal muscle.

Aging is associated with insulin resistance and decreased insulin-stimulated glucose uptake into skeletal muscle. Although the mechanisms underlying age-related insulin resistance are not clearly defined, impaired defense against inflammation and tissue oxidative stress are likely causes. Heat shock proteins (HSPs) have been shown to protect tissue from oxidative stress and inhibit the activation of stress kinases such as JNK, known to interfere with the insulin signaling pathway.

Phosphatidylinositol 3,5-bisphosphate (PI(3,5)P2) potentiates cardiac contractility via activation of the ryanodine receptor.

Phosphatidylinositol 3,5-bisphosphate (PI(3,5)P2) is the most recently identified phosphoinositide, and its functions have yet to be fully elucidated. Recently, members of our muscle group have shown that PI(3,5)P2 plays an important role in skeletal muscle function by altering Ca(2+) homeostasis. Therefore, we hypothesized that PI(3,5)P2 may also modulate cardiac muscle contractility by altering intracellular Ca(2+) ([Ca(2+)](i)) in cardiac myocytes.

Forskolin attenuates the action of insulin on the Akt-mTOR pathway in human skeletal muscle.

Forskolin (FSK) is capable of both stimulating and inhibiting the intracellular signaling pathways of protein synthesis tissues other than skeletal muscle. The purpose of this investigation was to determine if FSK administration affects various elements of the protein kinase B (Akt)-mammalian target of rapamycin (mTOR) pathway in human skeletal muscle. Ten (n = 10) healthy, young (21.

Supplemental carbohydrate ingestion does not improve performance of high-intensity resistance exercise.

The effects of supplemental carbohydrate (CHO) ingestion on the performance of squats to exhaustion (STE) were investigated with eight resistance-trained men. Subjects participated in a randomized, counterbalanced, double-blind, placebo-controlled protocol with testing separated by 7 days. Subjects consumed 0.

Age-related changes in relative expression of real-time PCR housekeeping genes in human skeletal muscle.

The purpose of this investigation was to examine the expression of three commonly used housekeeping genes -- glyceraldehyde-3-phosphate dehydrogenase (GAPDH), beta(2)-microglobulin (beta(2)M), and RNA polymerase 2a (polR2a) -- in elderly (E) compared to young (Y) subjects. Nine young subjects (22.7 +/- 3.

Training alterations in elite cyclists may cause transient changes in glomerular filtration rate.

Training alterations in elite cyclists may cause transient changes in glomerular filtration rate. To these authors' knowledge, no biochemical investigation of chronic renal function in athletes during a training cycle exists. The purpose of the present archival study was to evaluate the effects of training on homeostatic renal function, evaluated predicted glomerular filtration rate (GFR).