Effects of dietary creatine supplementation on systemic microvascular density and reactivity in healthy young adults.

BACKGROUND: Dietary creatine supplementation (CrS) is a practice commonly adopted by physically active individuals. However, the effects of CrS on systemic microvascular reactivity and density have never been reported. Additionally, CrS is able to influence blood levels of homocysteine, resulting in presumed effects on vascular endothelial function. Thus, we investigated the effects of CrS on the systemic microcirculation and on homocysteine levels in healthy young individuals. METHODS: This open-label study was performed on a group of 40 healthy male, moderately physically active subjects aged 27.7 ± 13.4 years who received one week of CrS at a dose of 20 g/day of commercially available micronized creatine monohydrate. Laser speckle contrast imaging was used in the evaluation of cutaneous microvascular reactivity, and intra-vital video microscopy was used to evaluate skin capillary density and reactivity, before and after CrS. RESULTS: CrS did not alter plasma levels of homocysteine, although CrS increased creatinine (p = 0.0001) and decreased uric acid (p = 0.0004) plasma levels. Significant changes in total cholesterol (p = 0.0486) and LDL-cholesterol (p = 0.0027) were also observed along with a reduction in plasma levels of T3 (p = 0.0074) and an increase in T4 levels (p = 0.0003). Skin functional capillary density (p = 0.0496) and capillary recruitment during post-occlusive reactive hyperemia (p = 0.0043) increased after CrS. Increases in cutaneous microvascular vasodilation induced by post-occlusive reactive hyperemia (p = 0.0078) were also observed. CONCLUSIONS: Oral supplementation with creatine in healthy, moderately physically active young adults improves systemic endothelial-dependent microvascular reactivity and increases skin capillary density and recruitment. These effects are not concurrent with changes in plasma homocysteine levels.

Alterations of the kidney cortex proteome in response to exercise training in normoglycemic and hyperglycemic conditions.

Hyperglycemia induces systemic vascular endothelial dysfunction and renal damage through the overproduction of reactive oxygen species (ROS). Regular aerobic exercise decreases the incidence of ROS-associated diseases and is involved in protection against systemic and renal vascular alterations. To investigate the impact of exercise training on renal protein expression in hyperglycemic conditions, we performed gel-based proteomic analyses of the rabbit kidney cortex from sedentary and exercised rabbits after exposure to normal or high glucose concentrations. Abundance of proteins in the renal cortex was determined by two-dimensional polyacrylamide gel electrophoresis followed by protein identification with mass spectrometry, using peptide mass and fragment fingerprintings. We identified the differential abundance of twenty seven proteins in exercise trained animals among the total of 324 spots, from which five proteins are related to the down-regulation of cellular oxidative stress (albumin, protein disulfide isomerase, heat shock protein 60-like chaperonin, DJ-1 and ubiquinol-cytochrome-c reductase), and three proteins are involved in energy metabolism (shortchain acyl-coenzyme A dehydrogenase, malate dehydrogenase and L-arginine-glycine amidinotransferase). We concluded that exercise training induces an increase in the abundance of five antioxidant proteins in the renal cortex, which could explain the well-known increase in endothelial-dependent vasodilation that results from exercise and the consequential protective effect against increased oxidative stress of the hyperglycemic milieu. Moreover, this protective effect could be important in the prevention of kidney vascular damage associated with diabetes pathophysiology.