Metabolic and lactate responses to supramaximal exercise in elite junior soccer players and distance runners

Aim: Elite soccer players are considered not as excellent but as good endurance athletes. Because of the characteristics of the game which is faster and is played at higher intensity, a high anaerobic power is also required characteristic of elite soccer players. Hence, the purpose of the present study was to compare the metabolic and lactate responses to 30s maximal cycle ergometer tests in high school soccer players and distance runners. Methods: Ten elite high school male soccer players (SP) and ten elite high school male distance runners (DR) volunteered as subjects in this study. Anaerobic power measures were obtained using Wingate anaerobic test including peak power (PP) and mean power (MP). The oxygen uptake (VO_2) was recorded breath-by-breath during the test (30s) and during the first 30s of recovery. Blood samples for lactate concentrations were drawn at rest before the test and during the 30-min recovery period. Results: Values (±SEM) of PP were 647 (±27) and 568 (±24) W in the SP and DR, respectively being significant (P<0.05). During the test, the DR had a significantly greater VO_2 than the SP (P<0.01). Blood lactate concentrations, on the other hand in recovery after the test were higher in the SP than DR. Conclusion: Those results would indicate that the energy supply for the 30s supramaximal exercise depended on the competitive specialty. The energy supply of the SP was more provided by the anaerobic metabolism and in the DR by the aerobic system

Clinical and pathologic features of focal segmental glomerulosclerosis with mitochondrial tRNALeu(UUR) gene mutation

Clinical and pathologic features of focal segmental glomerulosclerosis with mitochondrial tRNALeu(UUR) gene mutation.BackgroundSeveral families have been described in which an A to G transition mutation at position 3243 (A3243G) of the mitochondrial DNA (mtDNA) is associated with focal and segmental glomerulosclerosis (FSGS). However, the prevalence, clinical features, and pathophysiology of FSGS carrying mtDNA mutations are largely undefined.MethodsAmong 11 biopsy-proven primary FSGS patients of unknown etiology, we examined seven FSGS patients to determine whether any of the clinical and pathological features of FSGS were associated with an A3243G mtDNA mutation. In four subjects in whom the A3243G mtDNA mutation was discovered in blood leukocytes, as well as in urine sediments, we retrospectively reviewed the medical records and re-evaluated the renal biopsy specimen using light and electron microscopy. We further screened the patient's family members for the presence and degree of heteroplasmy for this mtDNA mutation and obtained medical histories that were consistent with mitochondrial cytopathy.ResultsThe four individuals identified with the A3243G mtDNA mutation were female. Proteinuria was diagnosed in these individuals during a routine annual health checkup in their teenage years. None of the patients showed any symptoms related to mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-like episode, whereas diabetes mellitus in two of the patients and a hearing disturbance in one patient became manifest within a 3- to 13-year follow-up period. Strict maternal transmitted inheritance was confirmed by pedigree studies in all of these patients. Steroid therapy was ineffective in all four patients. In two of these patients, renal function declined slowly to end-stage renal failure. Histologic examination of biopsy specimens revealed that glomeruli were not hypertrophied, while electron microscopic examination identified severely damaged, multinucleated podocytes containing extremely dysmorphic abnormal mitochondria in all patients.ConclusionsFSGS may belong to the spectrum of renal involvement in A3243G mtDNA mutation in humans. Severely injured podocytic changes containing abnormal mitochondria may explain the pathogenesis of FSGS in association with the A3243G mtDNA mutation

Structural and dynamic behavior of lithium iron polysulfide Li₈FeS₅ during charge–discharge cycling

Lithium sulfide (Li₂S) is one of the promising positive electrode materials for next-generation rechargeable lithium batteries. To improve the electrochemical performance of electronically resistive Li₂S, a Fe-doped Li₂S-based positive electrode material (Li₈FeS₅) has been recently designed and found to exhibit excellent discharge capacity close to 800 mAh g⁻¹. In the present study, we investigate the structural and dynamic behavior of Li₈FeS₅ during charge–discharge cycling. In Li₈FeS₅, Fe ions are incorporated into the Li₂S framework structure. The Li₂S-based structure is found to transform to an amorphous phase during the charge process. The delithiation-induced amorphization is associated with the formation of S-S polysulfide bonds, indicating charge compensation by S ions. The crystalline to non-crystalline structural transformation is reversible, but Li ions are extracted from the material via a two-phase reaction, although they are inserted via a single-phase process. These results indicate that the delithiation/lithiation mechanism is neither a topotactic extraction/insertion nor a conversion-type reaction. Moreover, the activation energies for Li ion diffusion in the pristine, delithiated, and lithiated materials are estimated to be in the 0.30–0.37 eV range, which corresponds to the energy barriers for local hopping of Li ions along the Li sublattice in the Li₂S framework