Breath-by-breath O(2) uptake (VO2, L min(-1)) and blood lactate concentration were measured before, during exercise, and recovery in six kata and six kumite karate Word Champions performing a simulated competition. VO2max, maximal anaerobic alactic, and lactic power were also assessed. The total energy cost (VO2TOT mL kg(-1) above resting) of each simulated competition was calculated and subdivided into aerobic, lactic, and alactic fractions. Results showed that (a) no differences between kata and kumite groups in VO2max, height of vertical jump, and Wingate test were found; (b) VO2TOT were 87.8 +/- 6.6 and 82.3 +/- 12.3 mL kg(-1) in kata male and female with a performance time of 138 +/- 4 and 158 +/- 14 s, respectively; 189.0 +/- 14.6 mL kg(-1) in kumite male and 155.8 +/- 38.4 mL kg(-1) in kumite female with a predetermined performance time of 240 +/- 0 and 180 +/- 0 s, respectively; (c) the metabolic power was significantly higher in kumite than in kata athletes (p < or = 0.05 in both gender); (d) aerobic and anaerobic alactic sources, in percentage of the total, were significantly different between gender and disciplines (p < 0.05), while the lactic source was similar; (e) HR ranged between 174 and 187 b min(-1) during simulated competition. In conclusion, kumite appears to require a much higher metabolic power than kata, being the energy source with the aerobic contribution predominant.

Sundowning syndrome (SDS) in patients with Alzheimer's disease (AD) is characterized by the intensification of behavioral disorders at sunset. Despite SDS etiology being unclear, a strong relationship between high cortisol levels and SDS has been reported. Aerobic exercise (AE) and cognitive training (CT) can reduce cortisol levels. However, whether SDS would benefit from AE and CT is still unknown. Therefore, the aim of this study was to investigate whether AE and CT treatments are effective in reducing SDS via downregulation of cortisol levels. The possible additive effects of combined AE+CT were also assessed. Eighty AD patients were randomly assigned to AE (n = 20), CT (n = 20), AE+CT (n = 20), and standard therapy (no treatment, NT; n = 20). Treatments were administered for 3 months, 5 days/week, 1 hour before sunset. Before and after treatments, salivary cortisol levels were sampled at 7, 11, 15, at sunset, and 20 (time of day). Blind assessment of behavioral disorders (neuropsychiatric inventory, NPI) and agitation (agitated behavior scale, ABS) were also performed. After interventions, cortisol levels were reduced in AE and AE+CT by ∼26%. In the same groups, NPI and ABS decreased by ∼50%. By contrast, cortisol and behavioral disorders were similar to baseline in CT and NT. Changes in NPI and ABS were significantly correlated with the reduction in cortisol levels. AE or AE+CT effects on SDS and cortisol levels and the lack of effect of CT alone indicate the effectiveness of an exercise-based treatment on SDS, suggesting a possible hypothalamic-pituitary-adrenal axis dysregulation underpinning SDS.

While fatigue increased all EMD components, muscle cooling affected only the electrochemical but not the mechanical processes of EMD.

Acute passive stretching has been shown to alter muscle-tendon unit (MTU) stiffness and to reduce peak tetanic force (pF). MTU mechanical properties and electro-mechanical delay (EMD) are closely related. Thus, EMD changes would be expected after stretching. The aim of the study was to assess the stretching-induced changes in both contractile and viscoelastic contributors to EMD. The time course of these changes will be also evaluated. Tetanic stimulations were delivered on the medial gastrocnemius muscle of 16 active males, before and after (every 15 min, for 2 h) passive stretching administration. During contractions, electromyographic (EMG), mechanomyographic (MMG) and force signals were recorded. The delays between EMG and force (Δt EMG-F, which corresponds to EMD), EMG and MMG (Δt EMG-MMG) and MMG and force (Δt MMG-F) signals were calculated, together with pF and EMG conduction velocity (CV). After stretching (i) pF decreased by 31% (P < 0.05) and remained depressed for the entire recovery period, while EMG CV did not change; (ii) Δt EMG-F, Δt EMG-MMG and Δt MMG-F increased significantly from 45.4 ± 3.0 ms, 2.2 ± 0.3 ms and 42.4 ± 3.1 ms to 52.7 ± 3.4 ms, 2.4 ± 0.3 ms and 50.3 ± 3.5 ms, respectively; (iii) Δt EMG-F and Δt MMG-F remained lengthened for the entire recovery period, while Δt EMG-MMG recovered to its pre-stretching condition within 15 min. These findings suggest that after stretching, the reduction in pF was accompanied by an elongation of the overall EMD. However, stretching had effects of short duration at the contractile level, but more persisting effects on MTU viscoelastic characteristics.