Optimal Load Magnitude and Placement for Peak Power Production in a Vertical Jump: A Segmental Contribution Analysis.

ABSTRACT: Bordelon, NM, Jones, DH, Sweeney, KM, Davis, DJ, Critchley, ML, Rochelle, LE, George, AC, and Dai, B. Optimal load magnitude and placement for peak power production in a vertical jump: A segmental contribution analysis. J Strength Cond Res 36(4): 911-919, 2022-Weighted jumps are widely used in power training, however, there are discrepancies regarding which loading optimizes peak jump power. The purpose was to quantify the effects of load magnitudes and placements on the force, velocity, and power production in a countermovement vertical jump. Sixteen male and 15 female subjects performed vertical jumps in 7 conditions: no external load, 10 and 20% dumbbell loads, 10 and 20% vest loads, and 10 and 20% barbell loads with load percentages relative to body weight. Arm swing was encouraged for all, but the barbell load conditions. Kinematics were collected to quantify the whole-body (the person and external loads) forces, velocities, and power as well as segments' contributions to the whole-body forces and velocities. Repeated-measure analyses of variance were performed followed by paired comparisons. Jump heights were the greatest for the no external load and 10% dumbbell conditions. The 10 and 20% dumbbell conditions demonstrated the greatest peak whole-body power, while the 2 barbell conditions showed the lowest peak whole-body power. At the time of peak whole-body power, the 2 dumbbell and 2 vest conditions resulted in greater whole-body forces. Whole-body velocities were the greatest for the no external load and 10% dumbbell conditions. Holding the dumbbells in the hands magnified the effects of external loads in producing forces and velocities. The constraint of arm movements in the barbell conditions limited power production. These findings highlight the importance of load placement and arm swing in identifying the optimal configuration for power production in weighted jumps.

Longitudinal assessments of balance and jump-landing performance before and after anterior cruciate ligament injuries in collegiate athletes.

The purpose was to quantify the effect of an anterior cruciate ligament (ACL) injury on balance and jump-landing performance and bilateral asymmetries. Among 500 collegiate athletes who performed a reaching test and a double-leg counter-movement jump-landing test at baseline, 8 male and 6 female athletes suffered ACL injuries. In the follow-up, they performed the reaching test 3 and 6 months after ACL reconstruction (ACLR) and the jump-landing test 6 months after ACLR. Less reaching distances for the injured leg and increased reaching distance asymmetries were observed 3 and 6 months after ACLR compared to baseline. Less peak jumping and landing forces for the injured leg and increased jumping and landing force asymmetries were found 6 months after ACLR compared to baseline. The decreased performance of the injured leg and increased asymmetries may contribute to the high ACL re-injury rates. Baseline assessments would be useful for establishing an individual's pre-injury performance.

Loss of neprilysin function promotes amyloid plaque formation and causes cerebral amyloid angiopathy.

Cerebral deposition of the amyloid beta protein (Abeta), an invariant feature of Alzheimer's disease, reflects an imbalance between the rates of Abeta production and clearance. The causes of Abeta elevation in the common late-onset form of Alzheimer's disease (LOAD) are largely unknown. There is evidence that the Abeta-degrading protease neprilysin (NEP) is down-regulated in normal aging and LOAD. We asked whether a decrease in endogenous NEP levels can prolong the half-life of Abeta in vivo and promote development of the classic amyloid neuropathology of Alzheimer's disease. We examined the brains and plasma of young and old mice expressing relatively low levels of human amyloid precursor protein and having one or both NEP genes silenced. NEP loss of function 1) elevated whole-brain and plasma levels of human Abeta(40) and Abeta(42), 2) prolonged the half-life of soluble Abeta in brain interstitial fluid of awake animals, 3) raised the concentration of Abeta dimers, 4) markedly increased hippocampal amyloid plaque burden, and 5) led to the development of amyloid angiopathy. A approximately 50% reduction in NEP levels, similar to that reported in some LOAD brains, was sufficient to increase amyloid neuropathology. These findings demonstrate an important role for proteolysis in determining the levels of Abeta and Abeta-associated neuropathology in vivo and support the hypothesis that primary defects in Abeta clearance can cause or contribute to LOAD pathogenesis.

The vacuolar-ATPase inhibitor bafilomycin and mutant VPS35 inhibit canonical Wnt signaling.

Endosomal acidification and transport are essential functions in signal transduction. Recent data suggest that Wnt signaling requires intact endosomal transport machinery but the effects of endosomal acidification on Wnt signal transduction have not been evaluated. Here we report that bafilomycin, a specific inhibitor of the vacuolar proton ATPase that blocks endosomal acidification, inhibits canonical Wnt signal transduction initiated by Wnt ligand and partially inhibits signaling initiated by disheveled. Bafilomycin does not affect Tcf promoter activation by beta-catenin. These data indicate that endosomal acidification is necessary for Wnt signaling. To identify interactions between endosomal transport proteins and Wnt receptors, we performed a GST fusion protein pulldown experiment and identified a possible indirect interaction between the LRP6 intracellular domain and vacuolar protein sorting protein 35 (VPS35). We show that an N-terminal deletion mutant of VPS35 reduces canonical Wnt signaling in HEK-293 cells expressing exogenous Wnt-1. These data suggest that endosomal V-type ATPase activity and retromer trafficking proteins are functionally important in Wnt signal transduction.

Insulin degrading enzyme is localized predominantly at the cell surface of polarized and unpolarized human cerebrovascular endothelial cell cultures.

Insulin degrading enzyme (IDE) is expressed in the brain and may play an important role there in the degradation of the amyloid beta peptide (Abeta). Our results show that cultured human cerebrovascular endothelial cells (HCECs), a primary component of the blood-brain barrier, express IDE and may respond to exposure to low levels of Abeta by upregulating its expression. When radiolabeled Abeta is introduced to the medium of cultured HCECs, it is rapidly degraded to smaller fragments. We believe that this degradation is largely the result of the action of IDE, as it can be substantially blocked by the presence of insulin in the medium, a competitive substrate of IDE. No inhibition is seen when an inhibitor of neprilysin, another protease that may degrade Abeta, is present in the medium. Our evidence suggests that the action of IDE occurs outside the cell, as inhibitors of internalization fail to affect the rate of the observed degradation. Further, our evidence suggests that degradation by IDE occurs on the plasma membrane, as much of the IDE present in HCECs was biotin-labeled by a plasma membrane impermeable reagent. This activity seems to be polarity dependent, as measurement of Abeta degradation by each surface of differentiated HCECs shows greater degradation on the basolateral (brain-facing) surface. Thus, IDE could be an important therapeutic target to decrease the amount of Abeta in the cerebrovasculature.