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The research aimed to investigate back pain (BP) prevalence in a large cohort of young athletes with respect to age, gender, and sport discipline. BP (within the last 7days) was assessed with a face scale (face 1-2=no pain; face 3-5=pain) in 2116 athletes (m/f 61%/39%; 13.3 +/- 1.7years; 163.0 +/- 11.8cm; 52.6 +/- 13.9kg; 4.9 +/- 2.7 training years; 8.4 +/- 5.7 training h/week). Four different sports categories were devised (a: combat sports, b: game sports; c: explosive strength sport; d: endurance sport). Analysis was described descriptively, regarding age, gender, and sport. In addition, 95% confidence intervals (CI) were calculated. About 168 (8%) athletes were allocated into the BP group. About 9% of females and 7% of males reported BP. Athletes, 11-13years, showed a prevalence of 2-4%; while prevalence increased to 12-20% in 14- to 17-year olds. Considering sport discipline, prevalence ranged from 3% (soccer) to 14% (canoeing). Prevalences in weight lifting, judo, wrestling, rowing, and shooting were 10%; in boxing, soccer, handball, cycling, and horse riding, 6%. 95% CI ranged between 0.08-0.11. BP exists in adolescent athletes, but is uncommon and shows no gender differences. A prevalence increase after age 14 is obvious. Differentiated prevention programs in daily training routines might address sport discipline-specific BP prevalence.
We sought to investigate the effects of wearing a mobile respiratory gas analysis system during a treadmill test on blood lactate (bLa) concentrations and commonly applied bLa thresholds. A total of 16 recreational athletes (31 +/- 3 years, V0205: 58 6 ml min(-1)-kg(-1)) performed one multistage treadmill test with and one without gas exchange measurements (GEM and noGEM). The whole bLa curve, the lactate threshold (LT), the individual anaerobic thresholds according to Stegmann(IAT(sr)) and Dickhuth (IAT(Di)), and a fixed bLa concentration of 4 mmob.l(-1) (OBLA) were evaluated. The bLa curve was shifted slightly leftward in GEM compared to noGEM (P<0.05), whereas the heart rate response was not different between conditions (P= 0.89). There was no difference between GEM and noGEM for LT (2.61 +/- 0.34 vs. 2.64 +/- 0.39 m(-1) s(-1) P=0.49) and IAT(st) (3.47 +/- 0.42 vs. 3.55 +/- 0.47m-s(-1), P=0.12). However, IATD(Di) (3.57 +/- 0.39 vs. 3.66 +/- 0.44m-s(-1), P<0.01) and OBLA (3.85 +/- 0.46 vs. 3.96 +/- 0.47m-s-1, P<0.01) occurred at slower running velocities in GEM. The bLa response to treadmill tests is mildly affected by wearing a mobile gas analysis system. This also applies to bLa thresholds located at higher exercise intensities. While the magnitude of the effects is of little importance for recreational athletes, it might be relevant for elite athletes and scientific studies.
Following stroke, neuronal death takes place both in the infarct region and in brain areas distal to the lesion site including the hippocampus. The hippocampus is critically involved in learning and memory processes and continuously generates new neurons. Dysregulation of adult neurogenesis may be associated with cognitive decline after a stroke lesion. In particular, proliferation of precursor cells and the formation of new neurons are increased after lesion. Within the first week, many new precursor cells die during development. How dying precursors are removed from the hippocampus and to what extent phagocytosis takes place after stroke is still not clear. Here, we evaluated the effect of a prefrontal stroke lesion on the phagocytic activity of microglia in the dentate gyrus (DG) of the hippocampus. Three-months-old C57BL/6J mice were injected once with the proliferation marker BrdU (250 mg/kg) 6 hr after a middle cerebral artery occlusion or sham surgery. The number of apoptotic cells and the phagocytic capacity of the microglia were evaluated by means of immunohistochemistry, confocal microscopy, and 3D-reconstructions. We found a transient but significant increase in the number of apoptotic cells in the DG early after stroke, associated with impaired removal by microglia. Interestingly, phagocytosis of newly generated precursor cells was not affected. Our study shows that a prefrontal stroke lesion affects phagocytosis of apoptotic cells in the DG, a region distal to the lesion core. Whether disturbed phagocytosis might contribute to inflammatory- and maladaptive processes including cognitive impairment following stroke needs to be further investigated.