Effects of preload 4 repetition maximum on 100-m sprint times in collegiate women.

The purpose of this study was to determine the effects of postactivation potentiation (PAP) on track-sprint performance after a preload set of 4 repetition maximum (4RM) parallel back half-squat exercises in collegiate women. All subjects (n = 12) participated in 2 testing sessions over a 3-week period. During the first testing session, subjects performed the Controlled protocol consisting of a 4-minute standardized warm-up, followed by a 4-minute active rest, a 100-m track sprint, a second 4-minute active rest, finalized with a second 100-m sprint. The second testing session, the Treatment protocol, consisted of a 4-minute standardized warm-up, followed by 4-minute active rest, sprint, a second 4-minute active rest, a warm-up of 4RM parallel back half-squat, a third 9-minute active rest, finalized with a second sprint. The results indicated that there was a significant improvement of 0.19 seconds (p < 0.05), when the second sprint was preceded by a 4RM back-squat protocol during Treatment. The standardized effect size, d, was 0.82, indicating a large effect size. Additionally, the results indicated that it would be expected that mean sprint times would increase 0.04-0.34 seconds (p < 0.05), when using a preload 4RM squat protocol. There were no significant differences between Control pre and posttests (p > 0.05). The findings suggest that performing a 4RM parallel back half-squat warm-up before a track sprint will have a positive PAP affect on decreased track-sprint times. Track coaches, looking for the "competitive edge" (PAP effect) may re-warm up their sprinters during meets.

Dendritic cells potently purge latent HIV-1 beyond TCR-stimulation, activating the PI3K-Akt-mTOR pathway.

BACKGROUND: The latent HIV-1 reservoir in treated patients primarily consists of resting memory CD4+ T cells. Stimulating the T-cell receptor (TCR), which facilitates transition of resting into effector T cells, is the most effective strategy to purge these latently infected cells. Here we supply evidence that TCR-stimulated effector T cells still frequently harbor latent HIV-1. METHODS: Primary HIV-1 infected cells were used in a latency assay with or without dendritic cells (DCs) and reversion of HIV-1 latency was determined, in the presence or absence of specific pathway inhibitors. FINDINGS: Renewed TCR-stimulation or subsequent activation with latency reversing agents (LRAs) did not overcome latency. However, interaction of infected effector cells with DCs triggered further activation of latent HIV-1. When compared to TCR-stimulation only, CD4+ T cells from aviremic patients receiving TCR + DC-stimulation reversed latency more frequently. Such a "one-two punch" strategy seems ideal for purging the reservoir. We determined that DC contact activates the PI3K-Akt-mTOR pathway in CD4+ T cells. INTERPRETATION: This insight could facilitate the development of a novel class of potent LRAs that purge latent HIV beyond levels reached by T-cell activation.