We hypothesized that an acute bout of strenuous, non-damaging exercise would increase rates of protein synthesis of collagen in tendon and skeletal muscle but these would be less than those of muscle myofibrillar and sarcoplasmic proteins. Two groups (n = 8 and 6) of healthy young men were studied over 72 h after 1 h of one-legged kicking exercise at 67% of maximum workload (W max ). To label tissue proteins in muscle and tendon primed, constant infusions of [1-
Abstract. We present a new model for the global tropospheric chemistry of inorganic bromine (Br y ) coupled to oxidant-aerosol chemistry in the GEOS-Chem chemical transport model (CTM). Sources of tropospheric Br y include debromination of sea-salt aerosol, photolysis and oxidation of short-lived bromocarbons, and transport from the stratosphere. Comparison to a GOME-2 satellite climatology of tropospheric BrO columns shows that the model can reproduce the observed increase of BrO with latitude, the northern mid-latitudes maximum in winter, and the Arctic maximum in spring. This successful simulation is contingent on the HOBr + HBr reaction taking place in aqueous aerosols and ice clouds. Bromine chemistry in the model decreases tropospheric ozone mixing ratios by < 1-8 nmol mol −1 (6.5 % globally), with the largest effects in the northern extratropics in spring. The global mean tropospheric OH concentration decreases by 4 %. Inclusion of bromine chemistry improves the ability of global models (GEOS-Chem and p-TOMCAT) to simulate observed 19th-century ozone and its seasonality. Bromine effects on tropospheric ozone are comparable in the present-day and pre-industrial atmospheres so that estimates of anthropogenic radiative forcing are minimally affected. Br atom concentrations are 40 % higher in the pre-industrial atmosphere due to lower ozone, which would decrease by a factor of 2 the atmospheric lifetime of elemental mercury against oxidation by Br. This suggests that historical anthropogenic mercury emissions may have mostly deposited to northern mid-latitudes, enriching the corresponding surface reservoirs. The persistent rise in background surface ozone at northern mid-latitudes during the past decades could possibly contribute to the observations of elevated mercury in subsurface waters of the North Atlantic.
SummaryThe National Institute on Aging Interventions Testing Program (ITP) evaluates agents hypothesized to increase healthy lifespan in genetically heterogeneous mice. Each compound is tested in parallel at three sites, and all results are published. We report the effects of lifelong treatment of mice with four agents not previously tested: Protandim, fish oil, ursodeoxycholic acid (UDCA) and metformin – the latter with and without rapamycin, and two drugs previously examined: 17‐α‐estradiol and nordihydroguaiaretic acid (NDGA), at doses greater and less than used previously. 17‐α‐estradiol at a threefold higher dose robustly extended both median and maximal lifespan, but still only in males. The male‐specific extension of median lifespan by NDGA was replicated at the original dose, and using doses threefold lower and higher. The effects of NDGA were dose dependent and male specific but without an effect on maximal lifespan. Protandim, a mixture of botanical extracts that activate Nrf2, extended median lifespan in males only. Metformin alone, at a dose of 0.1% in the diet, did not significantly extend lifespan. Metformin (0.1%) combined with rapamycin (14 ppm) robustly extended lifespan, suggestive of an added benefit, based on historical comparison with earlier studies of rapamycin given alone. The α‐glucosidase inhibitor, acarbose, at a concentration previously tested (1000 ppm), significantly increased median longevity in males and 90th percentile lifespan in both sexes, even when treatment was started at 16 months. Neither fish oil nor UDCA extended lifespan. These results underscore the reproducibility of ITP longevity studies and illustrate the importance of identifying optimal doses in lifespan studies.
Muscle is a site of lactate production and utilization with shuttling and oxidation occurring both among (Brooks, 1985) and within (Brooks, 1998) muscles. Additionally, during moderate-intensity exercise lactate turnover often exceeds that of glucose (Brooks, 1991), and lactate rate of oxidation (R ox ) can represent as much as 25 % of whole body carbohydrate (CHO) R ox (Bergman et al. 1999b). Whereas the importance of lactate as a fuel is recognized, the interactions of lactate and glucose as CHO sources for exercising muscle are relatively unexplored. Pearce & Connett (1980) demonstrated in isolated, noncontracting, rat soleus muscle that 8 mM lactate resulted in a decreased oxidation of glucose compared to no lactate. Further, a series of studies on rats Vettor et al. 1997) demonstrated that lactate infusion decreased glucose rate of disappearance (R d ) in skeletal muscle ) during a euglycaemichyperinsulinaemic clamp, and a lactate infusion during hyperglycaemia resulted in increased glucose R d with increased glycogen synthesis, but unchanged flux through glycolysis . More recently the same group (Lombardi et al. 1999) demonstrated that a 24 h lactate infusion decreased GLUT-4 mRNA and protein content, offering a possible mechanism for decreased glucose disposal in disease states with chronic elevated lactate levels. Whereas the data on resting rats are in good agreement, data in humans are less consistent.Lactate infusion in resting humans during a euglycaemichyperinsulinaemic clamp had no effect on glucose exchange across an inactive forearm (Ferrannini et al. 1993). We (Miller et al. 2002) recently demonstrated with a lactate clamp (LC) procedure that exogenous lactate infusion resulted in decreased glucose oxidation during rest after an 8-12 week training programme. We also reported decreased glucose oxidation with exogenous lactate infusion during exercise at the same absolute, but not relative, exercise intensity after training. Additionally, during exogenous lactate infusion the percentage of glucose R d oxidized decreased during rest pre-and posttraining and during exercise at the same absolute intensity
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
customersupport@researchsolutions.com
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
This site is protected by reCAPTCHA and the Google Privacy Policy and Terms of Service apply.
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.