Effect of heat stress on LPS-induced febrile response in D-galactosamine-sensitized rats

. In the present study we have tested whether inhibition of protein synthesis in the liver can reduce the effect of this heat conditioning on the LPS-induced febrile response in the rat. D-galactosamine (D-gal) was used to selectively inhibit liver protein synthesis. D-gal (500 mg/kg) or PBS as control was administered intraperitoneally 1 h before heat stress. LPS (50 g/kg ip) was injected 24 h post-heat exposure. Treatment with D-gal blunted the febrile response to LPS. Moreover, heat-conditioned rats treated first with D-gal and subsequently with LPS demonstrated a profound fall in core temperature 10-18 h post-LPS. A significant increase of serum TNF-␣ accompanied this effect of D-gal on fever. Heat-conditioned animals receiving D-gal showed an inhibition in inducible HSP-70 in the liver. These data support the role of hepatic function in modulating the febrile response to LPS. heat shock proteins; liver; heart; kidney; tumor necrosis factor-␣, interleukin-6, temperature regulation; fever; lipopolysaccharide HEAT STRESS PROVOKES metabolic adaptations in the whole organism. One such response is the production of heat shock proteins (HSPs) (26). The accumulation of HSPs within cells helps both cells and the whole organism survive subsequent, otherwise lethal, thermal stress. Interestingly, heat conditioning sufficient to cause cellular HSP accumulation has also been shown to be protective in a subsequent, otherwise lethal, endotoxin challenge (30). Several studies have demonstrated that HSPs regulate cytokine production in peripheral blood monocytes. Intracellular HSP accumulation is associated with a decrease in synthesis of tumor necrosis factor-␣ (TNF-␣) and interleukin (IL)-1␤ (6, 32). Impaired HSP production causes enhanced TNF-induced cytotoxicity in cells Whereas heat conditioning is protective, pretreatment with D-galactosamine (D-gal) increases sensitivity to subsequent LPS (2, 10). D-gal inhibits protein synthesis primarily in the live

Effect of Branched-Chain Amino Acid Supplementation on Recovery Following Acute Eccentric Exercise

This study investigated the effect of branched-chain amino acid (BCAA) supplementation on recovery from eccentric exercise. Twenty males ingested either a BCAA supplement or placebo (PLCB) prior to and following eccentric exercise. Creatine kinase (CK), vertical jump (VJ), maximal voluntary isometric contraction (MVIC), jump squat (JS) and perceived soreness were assessed. No significant (p \u3e 0.05) group by time interaction effects were observed for CK, soreness, MVIC, VJ, or JS. CK concentrations were elevated above baseline (p \u3c 0.001) in both groups at 4, 24, 48 and 72 hr, while CK was lower (p = 0.02) in the BCAA group at 48 hr compared to PLCB. Soreness increased significantly from baseline (p \u3c 0.01) in both groups at all time-points; however, BCAA supplemented individuals reported less soreness (p \u3c 0.01) at the 48 and 72 hr time-points. MVIC force output returned to baseline levels (p \u3e 0.05) at 24, 48 and 72 hr for BCAA individuals. No significant difference between groups (p \u3e 0.05) was detected for VJ or JS. BCAA supplementation may mitigate muscle soreness following muscle-damaging exercise. However, when consumed with a diet consisting of ~1.2 g/kg/day protein, the attenuation of muscular performance decrements or corresponding plasma CK levels are likely negligible

Understanding the factors that effect maximal fat oxidation

Abstract Lipids as a fuel source for energy supply during submaximal exercise originate from subcutaneous adipose tissue derived fatty acids (FA), intramuscular triacylglycerides (IMTG), cholesterol and dietary fat. These sources of fat contribute to fatty acid oxidation (FAox) in various ways. The regulation and utilization of FAs in a maximal capacity occur primarily at exercise intensities between 45 and 65% VO2max, is known as maximal fat oxidation (MFO), and is measured in g/min. Fatty acid oxidation occurs during submaximal exercise intensities, but is also complimentary to carbohydrate oxidation (CHOox). Due to limitations within FA transport across the cell and mitochondrial membranes, FAox is limited at higher exercise intensities. The point at which FAox reaches maximum and begins to decline is referred to as the crossover point. Exercise intensities that exceed the crossover point (~65% VO2max) utilize CHO as the predominant fuel source for energy supply. Training status, exercise intensity, exercise duration, sex differences, and nutrition have all been shown to affect cellular expression responsible for FAox rate. Each stimulus affects the process of FAox differently, resulting in specific adaptions that influence endurance exercise performance. Endurance training, specifically long duration (>2 h) facilitate adaptations that alter both the origin of FAs and FAox rate. Additionally, the influence of sex and nutrition on FAox are discussed. Finally, the role of FAox in the improvement of performance during endurance training is discussed

Intestinal epithelial barrier function and tight junction proteins with heat and exercise

A single layer of enterocytes and tight junctions (intercellular multiprotein complexes) form the intestinal epithelial barrier that controls transport of molecules through transcellular and paracellular pathways. A dysfunctional or “leaky” intestinal tight junction barrier allows augmented permeation of luminal antigens, endotoxins, and bacteria into the blood stream. Various substances and conditions have been shown to affect the maintenance of the intestinal epithelial tight junction barrier. The primary focus of the present review is to analyze the effects of exertional or nonexertional (passive hyperthermia) heat stress on tight junction barrier function in in vitro and in vivo (animals and humans) models. Our secondary focus is to review changes in tight junction proteins in response to exercise or hyperthermic conditions. Finally, we discuss some pharmacological or nutritional interventions that may affect the cellular mechanisms involved in maintaining homeostasis of the intestinal epithelial tight junction barrier during heat stress or exercise