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.

Coratella, G, Beato, M, Milanese, C, Longo, S, Limonta, E, Rampichini, S, Cè, E, Bisconti, AV, Schena, F, and Esposito, F. Specific adaptations in performance and muscle architecture after weighted jump-squat vs. body mass squat jump training in recreational soccer players. J Strength Cond Res 32(4): 921-929, 2018-The aim of the present study was to compare the effects of weighted jump-squat training (WJST) vs. body mass squat jump training (BMSJT) on quadriceps' muscle architecture, lower-limb lean-mass (LM) and muscle strength, performance in change of direction (COD), and sprint and jump in recreational soccer players. Forty-eight healthy soccer players participated in an offseason randomized controlled trial. Before and after an 8-week training intervention, vastus lateralis pennation angle, fascicle length, muscle thickness, LM, squat 1RM, quadriceps and hamstrings isokinetic peak torque, agility T-test, 10-and 30-m sprints, and squat-jump (SJ) were measured. Although similar increases were observed in muscle thickness, fascicle length increased more in WJST (Effect size [ES] = 1.18, 0.82-1.54) than in BMSJT (ES = 0.54, 0.40-0.68), and pennation angle increased only in BMSJT (ES = 1.03, 0.78-1.29). Greater increases in LM were observed in WJST (ES = 0.44, 0.29-0.59) than in BMSJT (ES = 0.21, 0.07-0.37). The agility T-test (ES = 2.95, 2.72-3.18), 10-m (ES = 0.52, 0.22-0.82), and 30-m sprints (ES = 0.52, 0.23-0.81) improved only in WJST, whereas SJ improved in BMSJT (ES = 0.89, 0.43-1.35) more than in WJST (ES = 0.30, 0.03-0.58). Similar increases in squat 1RM and peak torque occurred in both groups. The greater inertia accumulated within the landing phase in WJST vs. BMSJT has increased the eccentric workload, leading to specific eccentric-like adaptations in muscle architecture. The selective improvements in COD in WJST may be related to the increased braking ability generated by the enhanced eccentric workload.

Purpose: Whether or not the homologous contralateral muscle (CM) undergoes stretch-induced force reduction as the stretched muscle (SM) is still unclear. The neuromuscular and mechanical factors underlying the force reduction in CM and SM were investigated. Methods: Twenty-one participants underwent unilateral knee extensors passive stretching. In both CM and SM, before, immediately after (POST), 5 (POST 5 ), and 10 min (POST 10 ) after passive stretching, maximum voluntary contraction (MVC), peak force (pF), and voluntary activation (VA) were measured. During MVC, the electromyographic and mechanomyographic root mean square (EMG RMS and MMG RMS, respectively) was calculated in rectus femoris, vastus lateralis, and vastus medialis, together with M-wave. The total electromechanical delay (EMD), divided in time delay (Δt) EMG-MMG and Δt MMG-F was calculated. Results: In CM at POST, the decrease in MVC (−11%; 95% confidence interval [CI], −13 to −9; effect size [ES], −2.27) was accompanied by a fall in VA (−7%; 95% CI, −9 to −4; ES, −2.29), EMG RMS (range, −22% to −11%; ES, −3.92 to −2.25), MMG RMS (range, −10% to −8%; ES, −0.52 to −0.39) and an increase in Δt EMG-MMG (≈+10%; ES, 0.73 to 0.93). All changes returned to baseline at POST 5 . In SM, decrease in MVC (−19%; 95% CI, −24 to −18; ES, −3.08), pF (−25%; 95% CI, −28 to −22; ES, −4.90), VA (−10%; 95% CI, −11 to −9; ES, −5.71), EMG RMS (≈−33%; ES, −5.23 to −3.22) and rise in MMG RMS (range, +25% to +32%; ES, 4.21 to 4.98) and EMD (≈+28%; ES, 1.59 to 1.77) were observed at POST and persisted at POST 10. No change in M-wave occurred. Conclusions: The contralateral central motor drive stretch-induced inhibition seems to account for the force reduction in CM. In SM, both central inhibition and mechanical factors concurred.

Key points Vascular function and arterial stiffness are important markers of cardiovascular health and cardiovascular co‐morbidity. Transitional phases of hypoemia and hypermia, with consequent fluctuations in shear rate, occuring during repetitive passive stretching adminstration (passive stretching training) may constitute an effective stimulus to induce an amelioration in vascular function, arterial stiffness and vascular remodelling by improving central and local blood flow control mechanisms. Vascular function, arterial stiffness and vascular remodelling were evaluated before and after 12 weeks of passive stretching training and after 6 weeks from training cessation, in the femoral, popliteal (treated with stretching), and brachial arteries (untreated) of both sides. After passive stretching training, vascular function and arterial remodelling improved, and arterial stiffness decreased in all the arteries, suggesting modifications of both central and local blood flow control mechanisms. Passive stretching‐induced improvements related to central mechanisms seemed to have a short duration, as they returned to pre‐training baseline within 6 weeks from training cessation, whereas those more related to a local mechanism persisted in the follow‐up. Abstract Acute passive stretching (PS) effects on blood flow (trueQ̇), shear rate (trueẎ), and vascular function in the feeding arteries of the stretched muscle have been extensively investigated; however, few data are available on vascular adjustments induced by long‐term PS training. We investigated the effects of PS training on vascular function and stiffness of the involved (femoral and popliteal) and uninvolved (brachial) arteries. Our hypothesis was that PS‐induced changes in trueQ̇ and trueẎ would improve central and local mechanisms of trueQ̇ control. Thirty‐nine participants were randomly assigned to bilateral PS (n = 14), monolateral PS (n = 13) or no PS training (n = 12). Vascular function was measured before and after 12 weeks of knee extensor and plantar flexor muscles’ PS training by single passive limb movement and flow‐mediated dilatation (FMD). Central (carotid‐femoral artery PWV, PWVCF) and peripheral (carotid‐radial artery PWV, PWVCR) arterial stiffness was measured by pulse‐wave velocity (PWV), together with systolic (SBP) and diastolic (DBP) blood pressure. After PS training, increases of 30%, 25% and 8% (P < 0.05) in femoral ΔtrueQ̇, popliteal and brachial artery FMD%, respectively, occurred in both PS training groups. A decrease in PWVCF, PWVCR, SBP and DBP (−25%, −17%, −4% and −8%, respectively; P < 0.05) was noted. No changes occurred in controls. Vascular function improved and arterial stiffness reduced in the arteries involved and uninvolved with PS training, suggesting modifications in both central and local trueQ̇ control mechanisms. PS‐induced improvements had a short duration in some of vascular function parameters, as they returned to baseline within 6 weeks of PS training cessation.