Enhancing Body Balance and Performance in Elite Archery Athletes: The Impact of Atlasprofilax Intervention on Suboccipital Myofascia.

BACKGROUND High-performance athletes, such as archers, require optimal proprioception and balance. Subclinical or underestimated metabolic and pathomechanic alterations in the suboccipital myofascia could lead to loss of performance in balance and proprioception. Therapeutic optimization of myofascia and its complex structures through noninvasive stimulation by mechanotransductive vibropressure could be a preliminary key factor in high-performance athletes for high-performance sport. CASE REPORT This study was conducted with 6 athletes from the Brazilian Olympic archery team to evaluate the impact of the Atlasprofilax intervention on body balance. The results were measured using a standardized medical stabilometric platform, which assessed static balance and proprioception capacity. One athlete underwent the intervention before the entire team was tested for balance and reflexes in their archery performance. The study found that the intervened athlete showed improved balance and reflexes, as indicated by superior scores in the risk of fall assessment and fall index. The results suggest the potential for the Atlasprofilax intervention to improve body balance and proprioception in high-performance athletes. CONCLUSIONS A single intervention using the Atlasprofilax method in 1 of 6 Olympic archers resulted in significant improvement in balance and proprioception when compared with that of the non-intervened athletes. This preliminary evidence suggests that the Atlasprofilax intervention on the suboccipital myofascia may have a positive impact on enhancing balance and performance in elite athletes by improving proprioception.

Total Resorption of a Chronic L4-L5 Disc Extrusion After Application of the Atlasprofilax Method: A Case Report.

BACKGROUND The intervertebral disc extrusion resorption has been described in the literature by various authors. It occurs in up to 75% of patients with symptomatic extruded lumbar discs. The Atlasprofilax method favors osteo-musculo-articular rehabilitation processes, mainly impacting on 2 levels: the first is the bone anatomy of the atlanto-occipital joint, and the second is the fasciae located in the cervical region. CASE REPORT A 42-year-old male patient diagnosed by MRI with dehydration of L2-L3 to L5-S1 intervertebral discs, disc bulging at L2-L3 and L3-L4, and disc extrusion at L4-L5, received a one-time neuromuscular treatment, called the Atlasprofilax method, to the suboccipital region. In a repeat MRI 6 months later, the disc extrusion at L4-L5 was totally resorbed and improvement in the L3-L4 and L4-L5 disc bulges was seen. The patient's symptoms prior to the Atlasprofilax treatment included bilateral trapezius pain, right brachialgia, constant chronic low back pain, right sciatica, gait claudication, and paresthesia and dysesthesias in the lower limbs with associated pain and numbness in the calves. These symptoms were ameliorated after the treatment. The sciatica disappeared 1 week after the treatment and did not recur. In a follow-up 5 years later, the remaining symptoms had improved even further. CONCLUSIONS We propose that alterations of the cervical musculature and deep fascia could predispose to the development of lumbar disc abnormalities. We therefore also propose that improvements in this patient, both in symptoms and in imaging findings, are due to a reduction of the asymmetric distribution of forces and elastic loading as a result of the Atlasprofilax treatment.

Mthfr deficiency induces endothelial progenitor cell senescence via uncoupling of eNOS and downregulation of SIRT1.

Hyperhomocysteinemia (HHcy) has been shown to induce endothelial dysfunction in part as a result of enhanced oxidative stress. Function and survival of endothelial progenitor cells (EPCs, defined as sca1(+) c-kit(+) flk-1(+) bone marrow-derived cells), which significantly contribute to neovascularization and endothelial regeneration, depend on controlled production of reactive oxygen species (ROS). Mice heterozygous for the gene deletion of methylenetetrahydrofolate reductase (Mthfr(+/-)) have a 1.5- to 2-fold elevation in plasma homocysteine. This mild HHcy significantly reduced the number of circulating EPCs as well as their differentiation. Mthfr deficiency was also associated with increased ROS production and reduced nitric oxide (NO) generation in Mthfr(+/-) EPCs. Treatment of EPCs with sepiapterin, a precursor of tetrahydrobiopterin (BH(4)), a cofactor of endothelial nitric oxide synthase (eNOS), significantly reduced ROS and improved NO production. mRNA and protein expression of eNOS and the relative amount of eNOS dimer compared with monomer were decreased by Mthfr deficiency. Impaired differentiation of EPCs induced by Mthfr deficiency correlated with increased senescence, decreased telomere length, and reduced expression of SIRT1. Addition of sepiapterin maintained cell senescence and SIRT1 expression at levels comparable to the wild type. Taken together, these results demonstrate that Mthfr deficiency impairs EPC formation and increases EPC senescence by eNOS uncoupling and downregulation of SIRT1.

Endothelial nitric oxide synthase uncoupling and perivascular adipose oxidative stress and inflammation contribute to vascular dysfunction in a rodent model of metabolic syndrome.

The metabolic syndrome represents a constellation of cardiovascular risk factors that promote the development of cardiovascular disease. Oxidative stress is a mediator of endothelial dysfunction and vascular remodeling. We investigated vascular dysfunction in the metabolic syndrome and the oxidant mechanisms involved. New Zealand obese (NZO) mice with metabolic syndrome and New Zealand black control mice were studied. NZO mice showed insulin resistance and increased visceral fat and blood pressure compared with New Zealand black mice. Mesenteric resistance arteries from NZO mice exhibited increased media:lumen ratio and media cross-sectional area, demonstrating hypertrophic vascular remodeling. Endothelium-dependent relaxation to acetylcholine, assessed by pressurized myography, was impaired in NZO mice, not affected by N(G)-nitro-l-arginine methyl ester, inhibitor of endothelial NO synthase, and improved by the antioxidant Tempol, suggesting reduced NO bioavailability and increased oxidative stress. Dimer:monomer ratio of endothelial NO synthase was decreased in NZO mice compared with New Zealand black mice, suggesting endothelial NO synthase uncoupling. Furthermore, vascular superoxide and peroxynitrite production was increased, as well as adhesion molecule expression. Perivascular adipose tissue of NZO mice showed increased superoxide production and NADPH oxidase activity, as well as adipocyte hypertrophy, associated with inflammatory Mac-3-positive cell infiltration. Vasoconstriction to norepinephrine decreased in the presence of perivascular adipose tissue in New Zealand black mice but was unaffected by perivascular adipose tissue in NZO mice, suggesting loss of perivascular adipose tissue anticontractile properties. Our data suggest that this rodent model of metabolic syndrome is associated with perivascular adipose inflammation and oxidative stress, hypertrophic resistance artery remodeling, and endothelial dysfunction, the latter a result of decreased NO and enhanced superoxide generated by uncoupled endothelial NO synthase.