Prescribing workload administration to optimise isothermic heat acclimation

Repeated exercise-heat exposures, known as heat acclimation (HA), are often implemented as an intervention to attenuate decrements in physiological strain and exercise tolerance prior to work in normothermic and hot, humid conditions. The fundamental potentiating stimuli for thermoregulatory adaptation are repeated, significant rises in core temperature. Targeting of a specific core temperature is known as isothermic, or controlled hyperthermic HA. Different methods of modulating the exercise component of isothermic HA have been implemented, with prescription previously based upon either peak oxygen uptake (VO2peak), power, or subjective ratings of perceived exertion or thermal sensation. Interestingly, metabolic heat production, a measure to determine changes in core temperature, has not been used to prescribe isothermic HA. The aim of this study was to determine the relationship between the rate of rectal (core) temperature (Trec) increase, and different methods for prescribing workload during an acute exercise-heat exposure, with the objective of trying to refine the prescription of isothermic HA workloads

Reliability and validity of skin temperature measurement by telemetry thermistors and a thermal camera during exercise in the heat

Abstract. New technologies afford convenient modalities for skin temperature (T SKIN ) measurement, notably involving wireless telemetry and non-contact infrared thermometry. The purpose of this study was to investigate the validity and reliability of skin temperature measurements using a telemetry thermistor system (TT) and thermal camera (TC) during exercise in a hot environment. Each system was compared against a certified thermocouple, measuring the surface temperature of a metal block in a thermostatically controlled waterbath. Fourteen recreational athletes completed two incremental running tests, separated by one week. Skin temperatures were measured simultaneously with TT and TC compared against a hard-wired thermistor system (HW) throughout rest and exercise. Post hoc calibration based on waterbath results displayed good validity for TT (mean bias [MB] = -0.18°C, typical error [TE] = 0.18°C) and reliability (MB = -0.05°C, TE = 0.31°C) throughout rest and exercise. Poor validity (MB = -1.4°C, TE = 0.35°C) and reliability (MB = -0.65°C, TE = 0.52°C) was observed for TC, suggesting it may be best suited to controlled, static situations. These findings indicate TT systems provide a convenient, valid and reliable alternative to HW, useful for measurements in the field where traditional methods may be impractical

Isothermic and fixed intensity heat acclimation methods induce similar heat adaptation following short and long-term timescales

Heat acclimation requires the interaction between hot environments and exercise to elicit thermoregulatory adaptations. Optimal synergism between these parameters is unknown. Common practise involves utilising a fixed workload model where exercise prescription is controlled and core temperature is uncontrolled, or an isothermic model where core temperature is controlled and work rate is manipulated to control core temperature. Following a baseline heat stress test; 24 males performed a between groups experimental design performing short term heat acclimation (STHA; five 90min sessions) and long term heat acclimation (LTHA; STHA plus further five 90min sessions) utilising either fixed intensity (50%), continuous isothermic (target rectal temperature 38.5°C for STHA and LTHA), or progressive isothermic heat acclimation (target rectal temperature 38.5°C for STHA, and 39.0°C for LTHA). Identical heat stress tests followed STHA and LTHA to determine the magnitude of adaptation. All methods induced equal adaptation from baseline however isothermic methods induced adaptation and reduced exercise durations (STHA=−66% and LTHA=−72%) and mean session intensity (STHA=−13%and LTHA=−9%) in comparison to fixed (p0.05). Only thermal sensation improved from baseline to STHA (−0.2), and then between STHA and LTHA (−0.5) (p<0.05). Both the continuous and progressive isothermic methods elicited exercise duration, mean session intensity, and meanTrecanalogous to more efficient administration for maximising adaptation. Short term isothermic methods are therefore optimal for individuals aiming to achieve heat adaptation most economically, i.e. when integrating heat acclimation into a pre-competition taper. Fixed methods may be optimal for military and occupational applications due to lower exercise intensity and simplified administration

Exercise hyperthermia induces greater changes in gastrointestinal permeability than equivalent passive hyperthermia

Hyperthermia and exertional heat illness increase gastrointestinal (GI) permeability, although whether the latter is only via hyperthermia is unclear. The aim of this pilot study was to determine whether different changes in GI permeability, characterized by an increased plasma lactulose:rhamnose concentration ratio ([L:R]), occurred in exercise hyperthermia in comparison to equivalent passive hyperthermia. Six healthy adult male participants (age 25 ± 5 years, mass 77.0 ± 6.7 kg, height 181 ± 6 cm, peak oxygen uptake [urn:x-wiley:2051817X:media:phy214945:phy214945-math-0001] 48 ± 8 ml.kg−1.min−1) underwent exercise under hot conditions (Ex-Heat) and passive heating during hot water immersion (HWI). Heart rate (HR), rectal temperature (TCORE), rating of perceived exertion (RPE), and whole-body sweat loss (WBSL) were recorded throughout the trials. The L:R ratio, peak HR, change in HR, and change in RPE were higher in Ex-Heat than HWI, despite no differences in trial duration, peak core temperature or WBSL. L:R was strongly correlated (p < 0.05) with HR peak (r = 0.626) and change in HR (r = 0.615) but no other variable. The greater L:R in Ex-Heat, despite equal TCORE responses to HWI, indicates that increased cardiovascular strain occurred during exercise, and exacerbates hyperthermia-induced GI permeability at the same absolute temperature

Characterization of Mycosphaerellaceae species associated with citrus greasy spot in Panama and Spain

[EN] Greasy spot of citrus, caused by Zasmidium citri-griseum (= Mycosphaerella citri), is widely distributed in the Caribbean Basin, inducing leaf spots, premature defoliation, and yield loss. Greasy spot-like symptoms were frequently observed in humid citrus-growing regions in Panama as well as in semi-arid areas in Spain, but disease aetiology was unknown. Citrus-growing areas in Panama and Spain were surveyed and isolates of Mycosphaerellaceae were obtained from citrus greasy spot lesions. A selection of isolates from Panama (n = 22) and Spain (n = 16) was assembled based on their geographical origin, citrus species, and affected tissue. The isolates were characterized based on multi-locus DNA (ITS and EF-1 alpha) sequence analyses, morphology, growth at different temperatures, and independent pathogenicity tests on the citrus species most affected in each country. Reference isolates and sequences were also included in the analysis. Isolates from Panama were identified as Z. citri-griseum complex, and others from Spain attributed to Amycosphaerella africana. Isolates of the Z. citri-griseum complex had a significantly higher optimal growth temperature (26.8 degrees C) than those of A. africana (19.3 degrees C), which corresponded well with their actual biogeographical range. The isolates of the Z. citri-griseum complex from Panama induced typical greasy spot symptoms in 'Valencia' sweet orange plants and the inoculated fungi were reisolated. No symptoms were observed in plants of the 'Ortanique' tangor inoculated with A. africana. These results demonstrate the presence of citrus greasy spot, caused by Z. citri-griseum complex, in Panama whereas A. africana was associated with greasy spot-like symptoms in Spain.Research was partially funded by 'Programa de Formacion de los INIA Iberoamerica' and INIA RTA2010-00105-00-00-FEDER to Vidal Aguilera Cogley.. We thank J. Martinez-Minaya (UV) for assistance with INLAAguilera-Cogley, VA.; Berbegal Martinez, M.; Català, S.; Collison Brentu, F.; Armengol Fortí, J.; Vicent Civera, A. (2017). Characterization of Mycosphaerellaceae species associated with citrus greasy spot in Panama and Spain. PLoS ONE. 12(12):1-19. https://doi.org/10.1371/journal.pone.0189585S1191212Crous, P. W., Summerell, B. A., Carnegie, A. J., Wingfield, M. J., Hunter, G. C., Burgess, T. I., … Groenewald, J. Z. (2009). Unravelling Mycosphaerella: do you believe in genera? Persoonia - Molecular Phylogeny and Evolution of Fungi, 23(1), 99-118. doi:10.3767/003158509x479487Mondal, S. N., & Timmer, L. W. (2006). Greasy Spot, a Serious Endemic Problem for Citrus Production in the Caribbean Basin. Plant Disease, 90(5), 532-538. doi:10.1094/pd-90-0532Whiteside, J. O. (1970). Etiology and Epidemiology of Citrus Greasy Spot. Phytopathology, 60(10), 1409. doi:10.1094/phyto-60-1409Huang, F., Groenewald, J. Z., Zhu, L., Crous, P. W., & Li, H. (2015). Cercosporoid diseases of Citrus. Mycologia, 107(6), 1151-1171. doi:10.3852/15-059Wellings, C. R. (1981). Pathogenicity of fungi associated with citrus greasy spot in New South Wales. Transactions of the British Mycological Society, 76(3), 495-499. doi:10.1016/s0007-1536(81)80080-0Marco, G. M. (1986). A Disease Similar to Greasy Spot but of Unknown Etiology on Citrus Leaves in Argentina. Plant Disease, 70(11), 1074a. doi:10.1094/pd-70-1074aVidal Aguilera-Cogley, & Antonio Vicent. (2015). FUNGAL DISEASES OF CITRUS IN PANAMA. Acta Horticulturae, (1065), 947-952. doi:10.17660/actahortic.2015.1065.118Honger J. Aetiology and importance of foliage diseases affecting citrus in the nursery at the Agricultural Research Station (ARS). PhD Thesis. Accra: University of Ghana; 2004.Vicent A, Álvarez A, León M, García-Jiménez J. Mycosphaerella sp. asociada a manchas foliares de cítricos en España. In: Proceedings of the 13th Congress of the Spanish Phytopathological Society. 2006; Murcia; Spain.Abdelfattah, A., Cacciola, S. O., Mosca, S., Zappia, R., & Schena, L. (2016). Analysis of the Fungal Diversity in Citrus Leaves with Greasy Spot Disease Symptoms. Microbial Ecology, 73(3), 739-749. doi:10.1007/s00248-016-0874-xQuaedvlieg, W., Binder, M., Groenewald, J. Z., Summerell, B. A., Carnegie, A. J., Burgess, T. I., & Crous, P. W. (2014). Introducing the Consolidated Species Concept to resolve species in the Teratosphaeriaceae. Persoonia - Molecular Phylogeny and Evolution of Fungi, 33(1), 1-40. doi:10.3767/003158514x681981Edgar, R. C. (2004). MUSCLE: multiple sequence alignment with high accuracy and high throughput. Nucleic Acids Research, 32(5), 1792-1797. doi:10.1093/nar/gkh340Darriba, D., Taboada, G. L., Doallo, R., & Posada, D. (2012). jModelTest 2: more models, new heuristics and parallel computing. Nature Methods, 9(8), 772-772. doi:10.1038/nmeth.2109Ronquist, F., Teslenko, M., van der Mark, P., Ayres, D. L., Darling, A., Höhna, S., … Huelsenbeck, J. P. (2012). MrBayes 3.2: Efficient Bayesian Phylogenetic Inference and Model Choice Across a Large Model Space. Systematic Biology, 61(3), 539-542. doi:10.1093/sysbio/sys029Rambaut A. FigTree v1. 4.0, a graphical viewer of phylogenetic trees. Edinburgh, Scotland: University of Edinburgh; 2016.Spiegelhalter, D. J., Best, N. G., Carlin, B. P., & van der Linde, A. (2002). Bayesian measures of model complexity and fit. Journal of the Royal Statistical Society: Series B (Statistical Methodology), 64(4), 583-639. doi:10.1111/1467-9868.00353Rue, H., Martino, S., & Chopin, N. (2009). Approximate Bayesian inference for latent Gaussian models by using integrated nested Laplace approximations. Journal of the Royal Statistical Society: Series B (Statistical Methodology), 71(2), 319-392. doi:10.1111/j.1467-9868.2008.00700.xChristensen RH. Ordinal—regression models for ordinal data. R package version 2015.1–21. 2015. http://www.cran.r-project.org/package=ordinal/ Accessed 8 May 2017.Hunter, G. C., Wingfield, B. D., Crous, P. W., & Wingfield, M. J. (2006). A multi-gene phylogeny for species of Mycosphaerella occurring on Eucalyptus leaves. Studies in Mycology, 55, 147-161. doi:10.3114/sim.55.1.147Braun, U., & Urtiaga, R. (2013). New species and new records of cercosporoid hyphomycetes from Cuba and Venezuela (Part 2). Mycosphere, 4(2), 172-214. doi:10.5943/mycosphere/4/2/3Braun, U., Crous, P. W., & Nakashima, C. (2014). Cercosporoid fungi (Mycosphaerellaceae) 2. Species on monocots (Acoraceae to Xyridaceae, excluding Poaceae). IMA Fungus, 5(2), 203-390. doi:10.5598/imafungus.2014.05.02.04Aptroot A. Mycosphaerella and its anamorphs: conspectus of Mycosphaerella CBS Biodiversity Series 5. Utrecht: CBS-KNAW Fungal Biodiversity Centre; 2006.Crous, P. W., & Wingfield, M. J. (1996). Species of Mycosphaerella and Their Anamorphs Associated with Leaf Blotch Disease of Eucalyptus in South Africa. Mycologia, 88(3), 441. doi:10.2307/3760885Aguín, O., Sainz, M. J., Ares, A., Otero, L., & Pedro Mansilla, J. (2013). Incidence, severity and causal fungal species of Mycosphaerella and Teratosphaeria diseases in Eucalyptus stands in Galicia (NW Spain). Forest Ecology and Management, 302, 379-389. doi:10.1016/j.foreco.2013.03.021Maxwell, A., Dell, B., Neumeister-Kemp, H. G., & Hardy, G. E. S. J. (2003). Mycosphaerella species associated with Eucalyptus in south-western Australia: new species, new records and a key. Mycological Research, 107(3), 351-359. doi:10.1017/s0953756203007354Otero L, Aguín O, Mansilla J, Hunter G, Wingfield M. Identificación de especies de Mycosphaerella en Eucalyptus globulus y E. nitens en Galicia. In: Proceedings of the 13th Congress of the Spanish Phytopathological Society; 2006; Murcia, Spain.ZHAN, J., & McDONALD, B. A. (2011). Thermal adaptation in the fungal pathogen Mycosphaerella graminicola. Molecular Ecology, 20(8), 1689-1701. doi:10.1111/j.1365-294x.2011.05023.xPeel, M. C., Finlayson, B. L., & McMahon, T. A. (2007). Updated world map of the Köppen-Geiger climate classification. Hydrology and Earth System Sciences, 11(5), 1633-1644. doi:10.5194/hess-11-1633-200

Short-term heat acclimation prior to a multi-day desert ultra-marathon improves physiological and psychological responses without compromising immune status

Multistage, ultra-endurance events in hot, humid conditions necessitate thermal adaptation, often achieved through short term heat acclimation (STHA), to improve performance by reducing thermoregulatory strain and perceptions of heat stress. This study investigated the physiological, perceptual and immunological responses to STHA prior to the Marathon des Sables. Eight athletes (age 42 ± 4 years and body mass 81.9 ± 15.0 kg) completed 4 days of controlled hyperthermia STHA (60 min·day‒1, 45°C and 30% relative humidity). Pre, during and post sessions, physiological and perceptual measures were recorded. Immunological measures were recorded pre-post sessions 1 and 4. STHA improved thermal comfort (P = 0.02), sensation (P = 0.03) and perceived exertion (P = 0.04). A dissociated relationship between perceptual fatigue and Tre was evident after STHA, with reductions in perceived Physical (P = 0.04) and General (P = 0.04) fatigue. Exercising Tre and HR did not change (P > 0.05) however, sweat rate increased 14% (P = 0.02). No changes were found in white blood cell counts or content (P > 0.05). Four days of STHA facilitates effective perceptual adaptations, without compromising immune status prior to an ultra-endurance race in heat stress. A greater physiological strain is required to confer optimal physiological adaptations

Gene array of VHL mutation and hypoxia shows novel hypoxia-induced genes and that cyclin D1 is a VHL target gene

Gene expression analysis was performed on a human renal cancer cell line (786-0) with mutated VHL gene and a transfectant with wild-type VHL to analyse genes regulated by VHL and to compare with the gene programme regulated by hypoxia. There was a highly significant concordance of the global gene response to hypoxia and genes suppressed by VHL. Cyclin D1 was the most highly inducible transcript and 14-3-3 epsilon was downregulated. There were some genes regulated by VHL but not hypoxia in the renal cell line, suggesting a VHL role independent of hypoxia. However in nonrenal cell lines they were hypoxia regulated. These included several new pathways regulated by hypoxia, including RNase 6PL, collagen type 1 alpha 1, integrin alpha 5, ferritin light polypeptide, JM4 protein, transgelin and L1 cell adhesion molecule. These were not found in a recent SAGE analysis of the same cell line. Hypoxia induced downregulation of Cyclin D1 in nonrenal cells via an HIF independent pathway. The selective regulation of Cyclin D1 by hypoxia in renal cells may therefore contribute to the tissue selectivity of VHL mutation

Neuronal circuitry for pain processing in the dorsal horn

Neurons in the spinal dorsal horn process sensory information, which is then transmitted to several brain regions, including those responsible for pain perception. The dorsal horn provides numerous potential targets for the development of novel analgesics and is thought to undergo changes that contribute to the exaggerated pain felt after nerve injury and inflammation. Despite its obvious importance, we still know little about the neuronal circuits that process sensory information, mainly because of the heterogeneity of the various neuronal components that make up these circuits. Recent studies have begun to shed light on the neuronal organization and circuitry of this complex region

Synaptic Connections of the Neurokinin 1 Receptor-Like Immunoreactive Neurons in the Rat Medullary Dorsal Horn

The synaptic connections between neurokinin 1 (NK1) receptor-like immunoreactive (LI) neurons and γ-aminobutyric acid (GABA)-, glycine (Gly)-, serotonin (5-HT)- or dopamine-β-hydroxylase (DBH, a specific marker for norepinephrinergic neuronal structures)-LI axon terminals in the rat medullary dorsal horn (MDH) were examined under electron microscope by using a pre-embedding immunohistochemical double-staining technique. NK1 receptor-LI neurons were observed principally in laminae I and III, only a few of them were found in lamina II of the MDH. GABA-, Gly-, 5-HT-, or DBH-LI axon terminals were densely encountered in laminae I and II, and sparsely in lamina III of the MDH. Some of these GABA-, Gly-, 5-HT-, or DBH-LI axon terminals were observed to make principally symmetric synapses with NK1 receptor-LI neuronal cell bodies and dendritic processes in laminae I, II and III of the MDH. The present results suggest that neurons expressing NK1 receptor within the MDH might be modulated by GABAergic and glycinergic inhibitory intrinsic neurons located in the MDH and 5-HT- or norepinephrine (NE)-containing descending fibers originated from structures in the brainstem