Repeated maximal-intensity short-duration exercise (sprint interval training, SIT) can produce muscle adaptations similar to endurance training (ET) despite a much reduced training volume. However, most SIT data use cycling, and little is known about its effects on body composition or maximal cardiac output (Qmax). The purpose of this study was to assess body composition, 2000-m run time trial, VO(2max), and Q(max) effects of run SIT versus ET. Men and women (n = 10 per group; mean ± SD: age = 24 ± 3 yr) trained three times per week for 6 wk with SIT, 30-s all-out run sprints (manually driven treadmill), four to six bouts per session, 4-min recovery per bout, versus ET, 65% VO(2max) for 30 to 60 min·d(-1). Training improved (P < 0.05) body composition, 2000-m run time trial performance, and VO(2max) in both groups. Fat mass decreased 12.4% with SIT (mean ± SEM; 13.7 ± 1.6 to 12.0 ± 1.6 kg) and 5.8% with ET (13.9 ± 1.7 to 13.1 ± 1.6 kg). Lean mass increased 1% in both groups. Time trial performance improved 4.6% with SIT (-25.6 ± 8.1 s) and 5.9% with ET (-31.9 ± 6.3 s). VO(2max) increased 11.5% with SIT (46.8 ± 1.6 to 52.2 ± 2.0 mL·kg·(-1)·min(-1)) and 12.5% with ET (44.0 ± 2.0 to 49.5 ± 2.6 mL·kg·(-1)·min(-1)). None of these improvements differed between groups. In contrast, Q(max) increased by 9.5% with ET only (22.2 ± 2.0 to 24.3 ± 1.6 L·min(-1)). Despite a fraction of the time commitment, run SIT induces similar body composition, VO(2max), and performance adaptations as ET, but with no effect on Q(max). These data suggest that adaptations with ET are of central origin primarily, whereas those with SIT are more peripheral

Evidence indicates that skeletal muscle lipid droplet-associated proteins (PLINs) regulate lipolysis through protein-protein interactions on the lipid droplet surface. In adipocytes, PLIN1 is thought to regulate lipolysis by directly interacting with comparative gene identification-58 (CGI-58), an activator of adipose triglyceride lipase (ATGL). Upon lipolytic stimulation, PLIN1 is phosphorylated, releasing CGI-58 to fully activate ATGL and initiate triglyceride breakdown. The absence of PLIN1 in skeletal muscle leads us to believe that other PLIN family members undertake this role. Our purpose was to examine interactions between PLIN2, PLIN3, and PLIN5, with ATGL and its coactivator CGI-58 at rest and following contraction. Isolated rat solei were incubated for 30 min at rest or during 30 min of intermittent tetanic stimulation [150-ms volleys at 60 Hz with a train rate of 20 tetani/min (25°C)] to maximally stimulate intramuscular lipid breakdown. Results show that the interaction between ATGL and CGI-58 increased 128% following contraction (P = 0.041). Further, ATGL interacts with PLIN2, PLIN3, and PLIN5 at rest and following contraction. The PLIN2-ATGL interaction decreased significantly by 21% following stimulation (P = 0.013). Both PLIN3 and PLIN5 coprecipitated with CGI-58 at rest and following contraction, while there was no detectable interaction between PLIN2 and CGI-58 in either condition. Therefore, our findings indicate that in skeletal muscle, during contraction-induced muscle lipolysis, ATGL and CGI-58 strongly associate and that the PLIN proteins work together to regulate lipolysis, in part, by preventing ATGL and CGI-58 interactions at rest.

Background: Alzheimer’s disease (AD) mortality rates have steadily increased over time. Lithium, the current gold standard treatment for bipolar disorder, can exert neuroprotective effects against AD. Objective: We examined the relationship between trace levels of lithium in drinking water and changes in AD mortality across several Texas counties. Methods: 6,180 water samples from public wells since 2007 were obtained and averaged for 234 of 254 Texas counties. Changes in AD mortality rates were calculated by subtracting aggregated age-adjusted mortality rates obtained between 2000–2006 from those obtained between 2009–2015. Using aggregated rates maximized the number of counties with reliable mortality data. Correlational analyses between average lithium concentrations and changes in AD mortality were performed while also adjusting for gender, race, education, rural living, air pollution, physical inactivity, obesity, and type 2 diabetes. Results: Age-adjusted AD mortality rate was significantly increased over time (+27%, p < 0.001). Changes in AD mortality were negatively correlated with trace lithium levels (p = 0.01, r = –0.20), and statistical significance was maintained after controlling for most risk factors except for physical inactivity, obesity, and type 2 diabetes. Furthermore, the prevalence of obesity and type 2 diabetes positively correlated with changes in AD mortality (p = 0.01 and 0.03, respectively), but also negatively correlated with trace lithium in drinking water (p = 0.05 and <0.0001, respectively). Conclusion: Trace lithium in water is negatively linked with changes in AD mortality, as well as obesity and type 2 diabetes, which are important risk factors for AD.

Alzheimer’s disease (AD) has traditionally been discussed as a disease where serious cognitive decline is a result of Aβ-plaque accumulation, tau tangle formation, and neurodegeneration. Recently, it has been shown that metabolic dysregulation observed with insulin resistance and type-2 diabetes actively contributes to the progression of AD. One of the pathologies linking metabolic disease to AD is the release of inflammatory cytokines that contribute to the development of brain neuroinflammation and mitochondrial dysfunction, ultimately resulting in amyloid-beta peptide production and accumulation. Improving these metabolic impairments has been shown to be effective at reducing AD progression and improving cognitive function. The polyphenol resveratrol (RSV) improves peripheral metabolic disorders and may provide similar benefits centrally in the brain. RSV reduces inflammatory cytokine release, improves mitochondrial energetic function, and improves Aβ-peptide clearance by activating SIRT1 and AMPK. RSV has also been linked to improved cognitive function; however, the mechanisms of action are less defined. However, there is evidence to suggest that chronic RSV-driven AMPK activation may be detrimental to synaptic function and growth, which would directly impact cognition. This review will discuss the benefits and adverse effects of RSV on the brain, highlighting the major signaling pathways and some of the gaps surrounding the use of RSV as a treatment for AD.

Ments in insulin action; however, others have provided evidence that IL-6 has anti-inflammatory properties. Purpose This study aimed to examine the relation between IL-6 signaling, macrophage infiltration, and polarization and insulin action in inguinal fat after acute exercise in obese, insulin-resistant mice. Methods Male C57BL/6 mice were fed a low-fat diet (10% kcal lard) or a high-fat diet (HFD, 60% kcal lard) for 7 wk and then underwent an acute bout of exercise (2-h treadmill running: 15 m·min−1, 5% incline). Results The HFD resulted in increased body mass, glucose intolerance, and attenuated insulin-induced AKT Thr308 phosphorylation in inguinal fat. This was accompanied by increases in indices of macrophage infiltration (F4/80, CD68, and monocyte chemoattractant protein-1 expression) and polarization toward an M1 phenotype (increased expression of CD11c, CD11c/galactose-type C-type lectin 1, and inducible nitric oxide synthase). Immunofluorescence imaging demonstrated increased F4/80- and CD11c-positive cells with the HFD. Two hours after exercise, the insulin-induced activation of AKT Th308 phosphorylation was recovered in HFD mice. This was accompanied by an upregulation of IL-6 and IL-10 signaling, as demonstrated by increased expression of IL-6, IL-10, and SOCS3 as well as STAT3 phosphorylation. Furthermore, acute exercise resulted in a shift toward reduction in M1 polarization indicated by a decrease in the ratio of CD11c to galactose-type C-type lectin 1 mRNA as well as a decline in F4/80- and CD11c-positive cells. Conclusions The results suggest a link between exercise-induced increases in IL-6, reductions in indices of M1 macrophages, and increased IL-10, a reputed anti-inflammatory cytokine with insulin-sensitizing properties....