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Objectives The elderly are the most at-risk population for heat-related illness and mortality during the periods of hot weather. However, evidence-based elderly-specific cooling strategies to prevent heat-illness are limited. The aim of this investigation was to quantify the elderly's physiological and perceptual responses to cooling through cold water ingestion (COLD) or an L-menthol mouth rinse (MENT) during simulated activities of daily living in UK summer climatic conditions. Study design Randomised, controlled repeated measures research design. Methods A total of ten participants (men n = 7, women n = 3: age; 69 ± 3 yrs, height; 168 ± 10 cm, body mass; 68.88 ± 13.72 kg) completed one preliminary and three experimental trials; control (CON), COLD and MENT. Experimental trials consisted of 40 min rest followed by 30 min of cycling exercise at 6 metabolic equivalents and a 6-min walk test (6MWT), within a 35 °C, 50% relative humidity environment. Experimental interventions (every 10 min); cold water (4 °C) ingestion (total of 1.5L) or menthol (5 ml mouth swill for 5 s, menthol concentration of 0.01%). Results Peak rectal temperature (Tre) was significantly (P Conclusion The elderly have reduced physiological strain (Tre and HR) during activities of daily living and a 6MWT in hot UK climatic conditions, when they drink cold water. Furthermore, the elderly's perception (TS and TC) of the hot environment did not differ from CON at the end of exercise with COLD or MENT interventions. Menthol provided neither perceptual benefit to exercise in the heat nor functional gain. The TS data indicate that elderly may be at increased risk of heat illness, due to not feeling hot and uncomfortable enough to implement physiological strain reducing strategies such as cold-water ingestion.

This study aimed to examine the impact of extreme heat exposure frequency on inflammation and well-being in UK Fire Service personnel.136 Fire personnel and 14 controls (CON) were recruited [92 Firefighters (FF), 44 Breathing Apparatus Instructors (BAI)]. BAI were split into low (LBAI; ≤15 exposures per month) and high (HBAI; ≥20 exposures per month) categories. Measures of inflammation, mood and fatigue were collected at 0, 3 and 6 month times points. These variables were analysed for differences between groups and association with frequency of exposure.HBAI exhibited raised IL-1β, IL-6, IL-10, IgE and lower IgM (p 0.05). In addition, IL-1β, IL-6, IL-10 and IgM were associated with monthly exposure number, with exposures accounting for 15.4% of the variance in IL-6, 11.8% of IL-1β and 25.2% of IL-10. No differences in mood or fatigue were reported (p 0.05).High exposure firefighting consistently causes systemic inflammation without perceptual recognition of potential health risks.

Objectives To investigate the efficacy of heat acclimation (HA) in the young (YEX) and elderly (EEX) following exercise-HA, and the elderly utilising post-exercise hot water immersion HA (EHWI). Design Cross-sectional study. Method Twenty-six participants (YEX: n = 11 aged 22 ± 2 years, EEX: n = 8 aged 68 ± 3 years, EHWI: n = 7 aged 73 ± 3 years) completed two pre-/post-tests, separated by five intervention days. YEX and EEX exercised in hot conditions to raise rectal temperature (Trec) ≥38.5 °C within 60 min, with this increase maintained for a further 60 min. EHWI completed 30 min of cycling in temperate conditions, then 30 min of HWI (40 °C), followed by 30 min seated blanket wrap. Pre- and post-testing comprised 30 min rest, followed by 30 min of cycling exercise (3.5 W·kg−1 Ḣprod), and a six-minute walk test (6MWT), all in 35 °C, 50% RH. Results The HA protocols did not elicit different mean heart rate (HR), Trec, and duration Trec ≥ 38.5 °C (p > 0.05) between YEX, EEX, and EHWI groups. Resting Trec, peak skin temperature, systolic and mean arterial pressure, perceived exertion and thermal sensation decreased, and 6MWT distance increased pre- to post-HA (p 0.05). Conclusions Irrespective of age or intervention, HA induced thermoregulatory, perceptual and exercise performance improvements. Both exercise-HA (EEX), and post-exercise HWI (EHWI) are considered viable interventions to prepare the elderly for heat stress.

This study aimed to identify a pre-cooling method to reduce the physiological and perceptual strain, and the inflammatory response, experienced by individuals who wear personal protective equipment. Eleven males (age 20 ± 2 years, weight 75.8 ± 9.3 kg, height 177.1 ± 5.0 cm) completed 15min pre-cooling (phase change vest [PCV], forearm cooling [ARM], ice slurry consumption [ICE], or a no cooling control [CON]) and 45min intermittent walk (4 km h-1, 1% gradient) in 49.5 ± 0.6 °C and 15.4 ± 1.0% RH, whilst wearing firefighter ensemble. ICE reduced rectal temperature (Tre) before heat exposure compared to CON (ΔTre: 0.24 ± 0.09 °C, p < 0.001, d=0.38) and during exercise compared to CON, ARM, and PCV (p=0.026, ηp 2=0.145). Thermal sensation was reduced in ICE and ARM vs. CON (p=0.018, ηp 2=0.150). Interleukin-6 was not affected by precooling (p=0.648, ηp 2=0.032). It is recommended that those wearing protective equipment consume 500 ml of ice slurry 15min prior to work to reduce physiological and perceptual strain.

It is necessary to estimate the area of afforestation and deforestation in New Zealand, since 1990, to meet reporting obligations under the Kyoto Protocol. We describe a method for national mapping of forest change that achieves high accuracy, but only requires moderate effort. A national coverage of satellite imagery is standardised, classified (automatically) for land cover, and then compared with an existing 1990 land-use map to identify polygons (>1 ha) of possible forest change. Each one of these possible change polygons is checked by operators for actual or spurious change. The resulting forest change map showed the area of afforestation between 1990 and 2008 was 579,000 (±10,000) ha, and the area of deforestation was 75,000 (± 5000) ha. This means that reported emission credits can never be reported to better than plus or minus 2%. Likewise, reported liabilities for emissions can never be reported to better than plus or minus 6%.

Background: We previously showed that human muscle protein synthesis (MPS) increased during infusion of amino acids (AAs) and peaked at ≈120 min before returning to baseline rates, despite elevated plasma AA concentrations. Objective: We tested whether a protein meal elicited a similar response and whether signaling responses that regulate messenger RNA translation matched MPS changes. Design: Eight postabsorptive healthy men (=21 y of age) were studied during 8.5 h of primed continuous infusion of [1,2- 13 C 2 ] leucine with intermittent quadriceps biopsies for determination of MPS and anabolic signaling. After 2.5 h, subjects consumed 48 g whey protein. Results: At 45-90 min after oral protein bolus, mean (±SEM) myofibrillar protein synthesis increased from 0.03 ± 0.003% to 0.10 ± 0.01%/h; thereafter, myofibrillar protein synthesis returned to baseline rates even though plasma essential AA (EAA) concentrations remained elevated (+130% at 120 min, +80% at 180 min). The activity of protein kinase B (PKB) and phosphorylation of eukaryotic initiation factor 4G preceded the rise of MPS and increases in phosphorylation of ribosomal protein kinase S6 (S6K1), and 4E-binding protein 1 (4EBP1) was superimposable with MPS responses until 90 min. However, although MPS decreased thereafter, all signals, with the exception of PKB activity (which mirrored insulin responses), remained elevated, which echoed the slowly declining plasma EAA profile. The phosphorylation of eukaryotic initiation factor 2α increased only at 180 min. Thus, discordance existed between MPS and the mammalian target of rapamycin complex 1 (mTORC1) and signaling (ie, S6K1 and 4EBP1 phosphorylation). Conclusions: We confirm our previous findings that MPS responses to AAs are transient, even with oral protein bolus. However, changes in MPS only reflect elevated mTORC 1 signaling during the upswing in MPS.

Spinal stabilisation exercises are commonly used in the management of low back pain (LBP). There is limited evidence relating to patients' experiences of their involvement in such programmes. The aim of this study was to explore the experiences of a sample of individuals with chronic LBP who participated in a randomised controlled trial (RCT) investigating the most efficacious dosage and frequency of spinal stabilisation exercises. The qualitative study involved nine participants who took part in focus group discussions. The data were analysed using thematic content analysis and provided insights into the experiences of the participants. Four themes emerged: Physical dimensions of the LBP experience, emotional and psychological dimensions of the LBP experience and perceived effects of the programme and lastly, the impact of the treatment programme on participants' knowledge, understanding and adherence. In conclusion participants' experiences were not limited to the positive effects of stabilisation exercises on pain, functional disability and quality of life, but also reflected increases in confidence, the formulation of self help strategies and the ability to exert better control over their LBP. The findings highlight the importance of well planned associated educational support packages in the treatment of LBP paving the way for future qualitative research.

Objective.—The effect hydration status has on exposure to hypoxia is unclear. The purpose of the study was to identify how hydration status, above and below euhydrated levels, affects the physiological responses and onset of acute mountain sickness symptoms during acute normobaric hypoxia. Methods.—Eight males completed intermittent walking tests under normobaric hypoxic conditions (FIO2 0.13) after controlled hyperhydration, hypohydration, and euhydration protocols. A range of physiological, psychological, and altitude illness markers were monitored throughout the 125-minute exposure. Results.—Heart rate, core temperature, peripheral arterial oxygen saturation, urine osmolality, and mean self-reported Lake Louise Questionnaire acute mountain sickness scores were significantly different between euhydration, hypohydration, and hyperhydration, respectively, and closely correlated with environmental symptoms questionnaire, Lake Louise questionnaire, and headache scores (P .05). Other measures of ventilation and lung function were also significantly different between hydration conditions (P .05). Conclusions.—Hydration state above and below euhydration has detrimental consequences on physiological strain and onset of acute mountain sickness symptoms when exposed to acute normobaric hypoxia.

A protein phosphorylated efficiently in vitro by MAP kinase-activated protein kinase-2 (MAPKAP-K2) was purified from skeletal muscle extracts and identified as the calcium/calmodulin-dependent myosin light chain kinase (MLCK). The phosphorylation site was mapped to Ser 161 , a residue shown previously to be autophosphorylated by MLCK. The residue equivalent to Ser 161 became phosphorylated in vivo when rat hindlimbs were stimulated electrically. However, phosphorylation was triggered within seconds, whereas activation of MAPKAP-K2 required several minutes. Moreover, contraction-induced Ser 161 phosphorylation was similar in wild-type or MAPKAP-K2−/− mice. These results indicate that contraction-induced phosphorylation is probably catalyzed by MLCK and not MAPKAP-K2. Ser 161 phosphorylation induced the binding of MLCK to 14-3-3 proteins, but did not detectably affect the kinetic properties of MLCK. The sequence surrounding Ser 161 is unusual in that residue 158 is histidine. Previously, an arginine located three residues N-terminal to the site of phosphorylation was thought to be critical for the specificity of MAPKAP-K2.

The pivotal role of phosphatidylinositol 3-kinase (PI 3-kinase) in signal transduction has been well established in recent years. Receptor-regulated forms of PI 3-kinase are thought to phosphorylate phosphatidylinositol 4,5-bisphosphate (PtdIns(4,5)P2) at the 3-position of the inositol ring to give the putative lipid second messenger, phosphatidylinositol 3,4,5-trisphosphate (PtdIns(3,4, 5)P3). Cellular levels of PtdIns(3,4,5)P3 are currently measured by time-consuming procedures involving radiolabeling with high levels of 32PO4, extraction, and multiple chromatography steps. To avoid these lengthy and hazardous procedures, many laboratories prefer to assay PI 3-kinase activity in cell extracts and/or appropriate immunoprecipitates. Such approaches are not readily applied to measurements of PtdIns(3,4,5)P3 in extracts of animal tissues. Moreover, they can be misleading since the association of PI 3-kinases in molecular complexes is not necessarily correlated with the enzyme's activity state. Direct measurements of PtdIns(3,4,5)P3 would also be desirable since its concentration may be subject to additional control mechanisms such as activation or inhibition of the phosphatases responsible for PtdIns(3,4,5)P3 metabolism. We now report a simple, reproducible isotope dilution assay which detects PtdIns(3,4,5)P3 at subpicomole sensitivity, suitable for measurements of both basal and stimulated levels of PtdIns(3,4,5)P3 obtained from samples containing approximately 1 mg of cellular protein. Total lipid extracts, containing PtdIns(3,4,5)P3, are first subjected to alkaline hydrolysis which results in the release of the polar head group Ins(1,3,4,5)P4. The latter is measured by its ability to displace [32P]Ins(1,3,4,5)P4 from a highly specific binding protein present in cerebellar membrane preparations. We show that this assay solely detects PtdIns(3,4,5)P3 and does not suffer from interference by other compounds generated after alkaline hydrolysis of total cellular lipids. Measurements on a wide range of cells, including rat-1 fibroblasts, 1321N1 astrocytoma cells, HEK 293 cells, and rat adipocytes, show wortmannin-sensitive increased levels of PtdIns(3,4,5)P3 upon stimulation with appropriate agonists. The enhanced utility of this procedure is further demonstrated by measurements of PtdIns(3,4,5)P3 levels in tissue derived from whole animals. Specifically, we show that stimulation with insulin increases PtdIns(3,4,5)P3 levels in rat skeletal muscle in vivo with a time course which parallels the activation of protein kinase B in the same samples.

A potential influence of gas chromatographic parameters on measured 13C/12C-isotope ratios of saturated fatty acid methyl esters in gas chromatography-combustion-isotope ratio mass spectrometry (GC-C-IRMS) has been studied. A dependence of measured isotope ratios on temperature gradients was observed and differences in measured δ13C-values for individual fatty acid methyl esters varied by 0.5 to 3‰. Possible reasons for this isotopic fractionation and its implications for 13C natural abundance work are discussed.

Intramuscular glutamine falls with injury and disease in circumstances associated with increases in blood corticosteroids. We have investigated the effects of corticosteroid administration (0.44 mg/kg dexamethasone daily for 8 days, 200 g female rats) on intramuscular glutamine and Na+, muscle glutamine metabolism and sarcolemmal glutamine transport in the perfused hindlimb. After dexamethasone treatment intramuscular glutamine fell by 45% and Na+ rose by 25% (the respective muscle/plasma distribution ratios changed from 8.6 to 4.5 and 0.12 to 0.15); glutamine synthetase and glutaminase activities were unchanged at 475 +/- 75 and 60 +/- 19 nmol/g muscle per min. Glutamine output by the hindlimb of anaesthetized rats was increased from 31 to 85 nmol/g per min. Sarcolemmal glutamine transport was studied by paired-tracer dilution in the perfused hindlimb: the maximal capacity (Vmax) for glutamine transport into muscle (by Na(+)-glutamine symport) fell from 1058 +/- 310 to 395 +/- 110 nmol/g muscle per min after dexamethasone treatment, accompanied by a decrease in the Km (from 8.1 +/- 1.9 to 2.1 +/- 0.4 mM glutamine). At physiological plasma glutamine concentration (0.75 mM) dexamethasone appeared to cause a proportional increase in sarcolemmal glutamine efflux over influx. Addition of dexamethasone (200 nM) to the perfusate of control rat hindlimbs caused acute changes in Vmax and Km of glutamine transport similar to those resulting from 8-day dexamethasone treatment. The reduction in muscle glutamine concentration after dexamethasone treatment may be primarily due to a reduction in the driving force for intramuscular glutamine accumulation, i.e., in the Na+ electrochemical gradient. The prolonged increase in muscle glutamine output after dexamethasone treatment (which occurs despite a reduction in the size of the intramuscular glutamine pool) appears to be due to a combination of (a) accelerated sarcolemmal glutamine efflux and (b) increased intramuscular synthesis of glutamine.

Existing data supporting or disputing the validity of the Hashin-Shtrikman bounds on the elastic properties of multiphase aggregates often do not consider porosity, elastic anisotropy, or experimental errors. In this experiment, two-phase aggregates of KCl + (NH4Br, TlBr, CsCl, NaCl, Cu, and LiF) at every 20% volume fraction were vacuum hot-pressed and the compressional and shear velocities were measured with a computer-controlled ultrasonic interferometer to ±0.2%. The ratio of the shear moduli, μ, (phase 2/KCl) varied from about 1 to 5, producing a range of separations between the theoretical two-phase Hashin-Shtrikman bounds for the composites. Samples were generally 99% or better of the theoretical density, with less than 1% velocity anisotropy. Porosity corrections were applied assuming spherical pores, based on the observed velocity-pressure behaviour. Velocities agreed with the HS bounds calculated from the end-member single-crystal stiffnesses when anisotropy was taken into account. The velocity data were also used to estimate the bulk modulus, K, and shear modulus of the second phase by means of the matrix method — taking the K and μ of KCl as known and calculating the moduli of the other phase assuming that the measured velocities were the two-phase Hashin-Shtrikman bounds or the Voigt-Reuss-Hill average. A narrow range of moduli estimates results only if the μ's of both phases are fairly closely matched. For μ's mismatched by a factor of 5, the theoretical uncertainty in the estimates can be 10 times larger than the experimental uncertainty. Estimates using the VRH average can lie outside the HS-based results.

Stretching a muscle results in a rapid addition of sarcomeres at the ends of the muscle fibers. The effect of a pattern of electrical stimulation resembling that of a slow motoneuron on the newly formed muscle tissue in a stretched, fast-contracting muscle was investigated. We found that after a period as short as 4 days, the type of sarcomeres which were added on to the ends of the existing myofibrils differed from those in the middle regions of the experimental muscles: there was a much higher proportion of type I and type IIA sarcomeres in the stretch-stimulated ends. This study showed that reprogramming of the synthesis of fiber type-specific contractile proteins can be achieved and detected within a very short time by using electrical stimulation combined with stretch.

A carrier for glutamine, identified in rat muscle, has properties in terms of kinetics, ion dependence and hormone sensitivity, and effects of endotoxin and branched-chain aminoacids that point to an important function in the control of whole-body aminoacid metabolism. The existence of a link between the size of the glutamine pool in muscle and the rate of muscle protein synthesis raises possibilities for therapeutic interventions to limit protein loss in injury, sepsis, and chronic disease.

This article reviews work we have carried out to investigate (1) the transport mechanisms responsible for the high distribution ratio of free glutamine commonly observed in skeletal muscle; (2) the fall in the distribution ratio that accompanies starvation, injury and chronic disease, whether directly involving muscle or not; and (3) the effect of modulation of intracellular free-glutamine concentration on protein synthesis and breakdown in skeletal muscle. We suggest that the results are consistent with the controlling role of the muscle membrane glutamine-sodium cotransporter in the regulation of the intracellular glutamine pool, the existence of pathophysiological mechanisms for the modulation of intramuscular glutamine and anabolic effects of glutamine in promoting protein synthesis, with a smaller effect in reducing protein breakdown. The mechanisms by which glutamine affects skeletal muscle protein turnover, and thus muscle protein balance, and the extent of the net flow of amino acids between the periphery and the viscera are unknown as yet, but the results suggest that modulation of transporter activity may offer the possibility of therapeutic intervention to reduce muscle wasting associated with injury and disease.