FIFA 11+ Kids program effects on jump kinetics in soccer players - A randomized controlled clinical trial.

This study aimed to analyse the effects of the FIFA 11+ Kids programme on jump kinetics in soccer players. Twenty-four athletes (aged 9-11 years) were randomly allocated to the following groups: 1) the FIFA 11+ Kids programme (FT, n = 12), and 2) control training (CT, n = 12). Kinetic assessments of vertical jump (VJ), drop landing (DL), and anterior jump + maximum vertical jump (AJ) were performed on a force platform before and after eight weeks of training. Post-intervention impulse peak force and maximum impulse force (VJ) were significantly greater than the baseline values in the FT group (P < 0.001). Post-intervention landing peak force values for the first and second landings (DL) were significantly greater than the baseline values in the FT group (P = 0.01 and P = 0.05, respectively). Post-intervention landing peak force in the first landing (AJ) was significantly greater than the baseline values in the FT group (P = 0.005). The FT was effective in improving the impulsion performance during VJ. However, it increased the landing forces during DL and VJ.

Physical therapy management of an athlete with a Kim lesion using physical agents, manual therapy, and therapeutic exercise: a case report.

BACKGROUND: Several operative procedures have been described for treating a Kim lesion. However, no physical therapy intervention has been documented as conservative treatment for these cases. OBJECTIVE: The purpose of this report was to describe a physical therapy management protocol for an athlete with a Kim lesion. CASE DESCRIPTION: A 22-year-old female volleyball athlete presented to physical therapy with an 8-month history of right shoulder pain when performing the serve and attack sports gestures. Pain was 5/10 on the visual analogue scale (VAS). Pain was localized along the glenohumeral joint, around the long head of the biceps brachii tendon, and at the subscapularis tendon insertion. Shoulder range of motion (ROM) was limited to flexion (150°), abduction (158°), and internal rotation (80°). Kim lesion was confirmed by clinical tests (Kim test and Jerk test) and via magnetic resonance imaging. Shoulder functional outcomes were verified through the University of California Los Angeles (UCLA) shoulder rating scale. Upper extremity sensorimotor control was verified in bimanual support by stabilometry on a baropodometer. Core function was assessed through a plank test and a side plank test. The 8-week course of treatment included manual therapy, physical agents, shoulder and scapular mobilizations, resistance and sensorimotor exercises, core strengthening, and functional exercises. OUTCOMES: Physical therapy interventions resulted in a decrease in VAS pain (3/10), an increase in shoulder ROM (10.8°) and in UCLA shoulder score (from 22 to 33 points), a reduction in the center of pressure displacement (27-56%), and an increase in plank test (45%) and side plank test (21-29%) performance. The athlete had a full return to sport after the treatment. CONCLUSION: We concluded that the protocol used for conservative management of Kim lesion resulted in clinical satisfactory physical and functional outcomes for the athlete.

Decrease in APP and CP mRNA expression supports impairment of iron export in Alzheimer's disease patients.

Alzheimer's disease (AD) is a neurodegenerative disorder of still unknown etiology and the leading cause of dementia worldwide. Besides its main neuropathological hallmarks, a dysfunctional homeostasis of transition metals has been reported to play a pivotal role in the pathogenesis of this disease. Dysregulation of iron (Fe) metabolism in AD has been suggested, particularly at the level of cellular iron efflux. Herein, we intended to further clarify the molecular mechanisms underlying Fe homeostasis in AD. In order to achieve this goal, the expression of specific Fe metabolism-related genes directly involved in Fe regulation and export was assessed in peripheral blood mononuclear cells (PBMCs) from 73AD patients and 74 controls by quantitative PCR. The results obtained showed a significant decrease in the expression of aconitase 1 (ACO1; P=0.007); ceruloplasmin (CP; P<0.001) and amyloid-beta precursor protein (APP; P=0.006) genes in AD patients compared with healthy volunteers. These observations point out to a significant downregulation in the expression of genes associated with ferroportin-mediated cellular Fe export in PBMCs from AD patients, when compared to controls. Taken together, these findings support previous studies suggesting impairment of Fe homeostasis in AD, which may lead to cellular Fe retention and oxidative stress, a typical feature of this disease.

Genetic and biochemical markers in patients with Alzheimer's disease support a concerted systemic iron homeostasis dysregulation.

Alzheimer's disease (AD) is the most common form of dementia in the elderly individuals, resulting from a complex interaction between environmental and genetic factors. Impaired brain iron homeostasis has been recognized as an important mechanism underlying the pathogenesis of this disease. Nevertheless, the knowledge gathered so far at the systemic level is clearly insufficient. Herein, we used an integrative approach to study iron metabolism in the periphery, at both genotypic and phenotypic levels, in a sample of 116 patients with AD and 89 healthy control subjects. To assess the potential impact of iron metabolism on the risk of developing AD, genetic analyses were performed along with the evaluation of the iron status profile in peripheral blood by biochemical and gene expression studies. The results obtained showed a significant decrease of serum iron, ferritin, and transferrin concentrations in patients compared with the control subjects. Also, a significant decrease of ferroportin (SLC40A1) and both transferrin receptors TFRC and TFR2 transcripts was found in peripheral blood mononuclear cells from patients. At the genetic level, significant associations with AD were found for single nucleotide polymorphisms in TF, TFR2, ACO1, and SLC40A1 genes. Apolipoprotein E gene, a well-known risk factor for AD, was also found significantly associated with the disease in this study. Taken together, we hypothesize that the alterations on systemic iron status observed in patients could reflect an iron homeostasis dysregulation, particularly in cellular iron efflux. The intracellular iron accumulation would lead to a rise in oxidative damage, contributing to AD pathophysiology.

Electrophysiological studies in healthy subjects involving caffeine.

We review the electrophysiological studies concerning the effects of caffeine on muscle, lower and upper motor neuron excitability and cognition. Several different methods have been used, such as electromyography, recruitment analysis, H-reflex, transcranial magnetic stimulation (TMS), electroencephalography and event-related potentials. The positive effect of caffeine on vigilance, attention, speed of reaction, information processing and arousal is supported by a number of electrophysiological studies. The evidence in favor of an increased muscle fiber resistance is not definitive, but higher or lower motor neuron excitability can occur as a consequence of a greater excitation of the descending input from the brainstem and upper motor neurons. TMS can address the influence of caffeine on the upper motor neuron. Previous studies showed that cortico-motor threshold and intracortical excitatory and inhibitory pathways are not influenced by caffeine. Nonetheless, our results indicate that cortical silent period (CSP) is reduced in resting muscles after caffeine consumption, when stimulating the motor cortex with intensities slightly above threshold. We present new data demonstrating that this effect is also observed in fatigued muscle. We conclude that CSP can be considered a surrogate marker of the effect of caffeine in the brain, in particular of its central ergogenic effect.