Subjects completed a medical history and physical activity questionnaire to determine eligibility. No subject was a smoker or had diagnosed metabolic or cardiovascular disease. Subjects were considered to be well-trained and Z-IETD-FMK supplier performed resistance exercise for 4.6 ± 2.2 hrs per week for 8.4 ± 6.6 yrs. Descriptive characteristics are provided in Table 1. Subjects were instructed not to deviate from their current training regimen during the course of the study with the exception of refraining from exercise for the 48 hours prior to each testing day. All experimental procedures were performed in accordance with the Helsinki Declaration.

The University of Memphis Human Subjects Committee approved all experimental procedures. All subjects provided both verbal and written consent prior to participating in this study. Table 1 Descriptive characteristics of www.selleckchem.com/products/CP-690550.html 10 exercise AZD0156 trained men. Variable Value Age (yrs) 27 ± 4 Height (cm) 175 ± 7 Weight (kg) 77 ± 11 Body mass index (kg·m-2) 25 ± 3 Body fat (%)* 9 ± 3 Years Resistance Exercise 8 ± 7 Hours/wk Resistance Exercise 5 ± 2 Data

are mean ± SD. * Determined from 7-site skinfold analysis use Lange calipers and Siri equation Conditions and Testing The dietary supplement used in this investigation (Meltdown®, Vital Pharmaceuticals, Inc., Davie, FL) included yohimbine, caffeine, and synephrine as the primary active ingredients. Please see Figure 1 for a description of the dietary supplement. All capsules used in this investigation were from the same bottle and produced in accordance with Good Manufacturing Practices (GMPs). Prior to production, all raw materials were tested for ingredient potency and the finished product was verified for label claims. Subjects consumed three capsules of the dietary supplement or an identical looking placebo (corn starch, microcrystalline

cellulose, super refined sesame oil, propylene glycol fatty acid ester, safflower oil, sunflower oil) in a double blind, cross-over design. No food was allowed until testing was completed, although water was allowed ad libitum and matched for both days of testing (mean intake = 500 mL). Subjects reported to the laboratory in a fasted state (> 8 hours), without caffeine consumption during the past 8 hours. All testing was done between 0600–1000 hours. Following a 10 minute quiet rest period, a baseline 5-FU ic50 blood sample was obtained (0 min). Subjects then ingested either the supplement or placebo, in the presence of an investigator. Subjects remained inactive during the entire 90 minute test period. At 30 minutes post ingestion, a second blood sample was taken (30 min). A measurement of resting metabolic rate, using indirect calorimetry, was then started and continued for 30 minutes. Subjects were positioned in a seated posture and gas analysis was performed with breath-by-breath collection using a SensorMedics Vmax 229 metabolic system (Yorba Linda, CA) and facemask.

CrossRefPubMed 24. selleckchem Kanamaru S, Kurazono H, Terai A, Monden K, Kumon H, Mizunoe Y, Ogawa O, Yamamoto S: Increased biofilm formation in learn more Escherichia coli isolated from acute prostatitis. Int J Antimicrob Agents 2006,28(Supplement 1):21–25.CrossRef 25. Naves P, del Prado G, Huelves L, Gracia M, Ruiz V, Blanco J, Dahbi G, Blanco M, del Carmen Ponte M, Soriano F: Correlation

between virulence factors and in vitro biofilm formation by Escherichia coli strains. Microb Pathog 2008,45(2):86–91.CrossRefPubMed 26. Danese P, Pratt L, Dove S, Kolter R: The outer membrane protein, Antigen 43, mediates cell-to-cell interactions within Escherichia coli biofilms. Mol Microbiol 2000,37(2):424–432.CrossRefPubMed 27. Ong C-LY, Ulett GC, Mabbett AN, Beatson SA, Webb RI, Monaghan W, Nimmo GR, Looke DF, McEwan AG, Schembri MA: Identification of Type 3 Fimbriae in Uropathogenic Escherichia coli Reveals a Role in Biofilm Formation. J Bacteriol 2008,190(3):1054–1063.CrossRefPubMed 28. Schembri MA, Dalsgaard D, Klemm P: Capsule Shields the Function of Short Bacterial Adhesins. J Bacteriol 2004,186(5):1249–1257.CrossRefPubMed 29. Soto SM, Smithson A, Martinez JA, Horcajada JP, Mensa J, Vila J: Biofilm Formation in Uropathogenic Escherichia coli Strains: Relationship With Prostatitis, Urovirulence Factors and Antimicrobial Resistance. J Urol

2007,177(1):365–368.CrossRefPubMed 30. Ulett GC, Mabbett AN, Fung KC, Webb RI, Schembri MA: The role of F9 fimbriae of uropathogenic selleck chemicals Escherichia coli in biofilm formation. Microbiology 2007,153(7):2321–2331.CrossRefPubMed 31. Ulett GC, Valle J, Beloin C, Sherlock O, Ghigo J-M, Schembri MA: Functional Analysis of Antigen 43 in Uropathogenic Escherichia coli Reveals a Role in Long-Term Persistence in the Urinary Tract. Infect Immun 2007,75(7):3233–3244.CrossRefPubMed 32. Vianney A, Jubelin G, Renault S, Dorel C, Lejeune P, Lazzaroni JC:Escherichia coli tol and rcs genes participate in the complex network affecting curli synthesis. Microbiology 2005,151(7):2487–2497.CrossRefPubMed 33. Bidet P, Mahjoub-Messai F, Blanco J, Blanco J, Dehem M, Aujard Interleukin-3 receptor Y, Bingen E, Bonacorsi S: Combined multilocus sequence typing

and O serogrouping distinguishes Escherichia coli subtypes associated with infant urosepsis and/or meningitis. J Infect Dis 2007,196(2):297–303.CrossRefPubMed 34. Xie Y, Kim KJ, Kim KS: Current concepts on Escherichia coli K1 translocation of the blood-brain barrier. FEMS Immunol Med Microbiol 2004,42(3):271–279.CrossRefPubMed 35. Boudeau J, Barnich N, Darfeuille-Michaud A: Type 1 pili-mediated adherence of Escherichia coli strain LF82 isolated from Crohn’s disease is involved in bacterial invasion of intestinal epithelial cells. Mol Microbiol 2001,39(5):1272–1284.CrossRefPubMed 36. Clermont O, Bonacorsi S, Bingen E: Rapid and Simple Determination of the Escherichia coli Phylogenetic Group. Appl Environ Microbiol 2000,66(10):4555–4558.CrossRefPubMed 37.

The most affected Semaxanib clinical trial villages were Muangmuay, Vangkham and Vangmat (a subdivision of Bouammi village2). Between April and July 2010 the official company produced up to 7 kg of gold. The villagers were equally interested in gold extraction. Between July and September 2010, 30 villagers from Muangmuay invested in a village-based gold concession. According to villagers, in little more than 4 months, the village production reached almost 1 kg of gold. But the most vulnerable families were worried about food resources particularly fish and other water resources (i.e. river algae, crabs, shrimp, molluscs). The official company confirmed the villagers’

fears that it would not be possible to harvest such resources for several years after the mining finished. Discussion To achieve collaborative monitoring, it is important to reach a shared understanding among the different stakeholders, especially decision makers see more (in our case district authorities) and natural resource managers at the village level, of what needs to be monitored. Of equal importance is how to test and refine the monitoring system and embed it into the local governance, taking into account all stakeholders’ concerns and practical choices. Participatory monitoring

as a negotiation tool Communities are rarely in a position strong enough to negotiate with decision-makers under pressure from the private sector, especially in Laos, where top-down governance is combined with the economic interests of neighbouring countries looking for land HSP90 (i.e. Thailand, Vietnam, and China) (Baird 2010). The example of the gold mining illustrates well the impact of new commercial activities and the limited capacity and power of the local people to react to the transformation of the landscape around their villages. Villagers selleck chemicals llc living in close proximity to the gold mining were in fact more interested in short-term

benefits through small-scale gold extraction than worried about long-term impacts on their important NTFPs. Villagers not directly involved in the mining activity were more aware of its impact on the river conditions and their main source of food and livelihoods. At the time of the gold mining activities, however, PLUP had not been entirely implemented in Muangmuay kumban. We believe that its full implementation would have enhanced local people’s capacity for negotiation, and level of understanding of environmental risks and impacts. A system that takes into account local governance and reflects all stakeholders’ concerns In the past, local perceptions were rarely taken into account when dealing with natural resource management (Fraser et al. 2006). In Laos, until 2011, the priority was generally given to what was considered important by the district authorities and conservation institutions. Government authorities still consider ‘informing’ villagers about the government’s decisions as a form of ‘local participation’.

Saline was added to make the volume to 11 ml to which 2 ml diethyl ether was added and centrifuged at 10,000 rpm for 10 minutes. This procedure was repeated twice after which the supernatant was discarded and the sediment preserved in sterile containers in normal saline. Ether is classed as an extremely flammable reagent requiring storage in suitable flammable-liquid storage cabinets; therefore, we used ethyl acetate

as an alternative. Formalin was not used as it leads to a reduction in the fluorescence intensity of stained spores and being a Polymerase Chain Reaction (PCR) inhibitor, it may interfere with the molecular study of the parasites to be conducted later [4]. After concentration the saline and iodine MK0683 purchase find more preparations of the samples were microscopically observed as above. Staining The concentrated samples were used for staining. Thin smears from all the samples were prepared on two different slides. The first slide was stained by Modified safranin technique [3]. In this method 3% acid alcohol was used for fixation. Safranin was used for staining and counterstaining was done by Malachite green. Kinyoun’s staining was used to stain the second slide [3]. The smear was fixed with absolute methanol and stained with Kinyoun’s carbol fuschin. Destaining was done by

10% alcohol and the smear was counterstained by Malachite green. At least 200 oil immersion fields of the above smears were examined for the parasites. Fluorescence microscopy A wet mount preparation of the concentrated samples was made and checked for autoflourescence of Cyclospora cayetanensis at 200× magnification with a 330 to 380 nm UV filter. The use of Calcoflour White (Sigma, USA) for fluorescent labeling of Microsporidia spores based on the presence of α-chitin in the inner endospore layer of the spore wall was first introduced by Vávra et al [5]. Calcoflour White stain (10 μl)

was added to the same amount of concentrated samples taken on clean, dry slides. The working solution was prepared by making 1:10 dilution of the stock (1%) and adding 0.05% Evan’s Blue dye. Slides were examined with the help Decitabine in vitro of UV fluorescence microscope at an excitation wavelength of 405 nm. A modification of the above method was performed by using a fluorescent probe 4, 6-diamidine-2-phenylindole (DAPI). Equal quantities (10 μl) of stool sample and DAPI (Sigma, USA) were put on a slide and left for 5 minutes. Thereafter, 10 μl of Calcoflour White was added and the slides were air dried. The slides were screened with the help of a fluorescence microscope using 435-485 BA filter. Antigen detection The third part of the unconcentrated stool samples was Selleck HDAC inhibitor subjected to sandwich ELISA for Cryptosporidium parvum antigen detection. The procedure was performed as per the instructions given in the commercially available kit (IVD Research Inc. CA, USA).

In the present work, we obtained clear evidence of the operation of qE when we added the uncoupler CCCP (Fig. 6). Addition of CCCP resulted in a sharp incline of the fluorescence signal as it collapsed the ∆pH gradient, dissipating qE. Nevertheless, the NPQ kinetics during the dark to light transient were not as expected. After a dark to buy SN-38 light transition, Selleck eFT-508 electron transport activity

is expected to cause an increase in the ∆pH gradient, which leads to an increase in qE. Activation of photosynthesis and PSII activity in D. tertiolecta operates according to expectations as can be seen from ∆F/F m ′ and F′ kinetics. Photosynthetic electron transport was, therefore, expected to elevate NPQ during the early phase of the dark to light transient, where a high photoprotective potential is required due to insufficient photosynthetic energy quenching. The initial rise of F m ′ (NPQ down-regulation) is not in accordance to the expected decrease in both fluorescence parameters as a result of an increase in qE: one would expect a decrease. Casper-Lindley and Björkman (1998) showed for D. tertiolecta that exposure to saturating PF-induced de-epoxidation

of violaxanthin, at very strong PF (1,200 μmol photons m−2 s−1), after a minimum of 5 min. The same authors also showed that after 45 min of high PF treatment only 60% of the violaxanthin pool was de-epoxidised, while maximal NPQ values were reached after approximately 15 min, indicating A-769662 datasheet the effective potential of this species to quench excess absorbed quanta. This also demonstrates that in this species slow NPQ is not strictly connected to xanthophyll cycle de-epoxidation. Nevertheless, a sudden exposure to 440 μmol photons m−2 s−1 caused

a decrease in NPQ during the first 4 min (Fig. 2) which might attribute to the disappearance of chlororespiration due to its influence on the ∆pH gradient. Chlororespiration can maintain a ∆pH gradient that is suitable to allow qE activation in the dark as this process uses the photosynthetic electron AZD9291 order transport chain and result in a partly reduced PQ pool and H+ translocation over the thylakoid membrane in darkness (e.g. Peltier and Cournac 2002). Exposure to sub-saturating PF caused an even more rapid NPQ decrease, followed by an overshoot in NPQ, and steady values after approximately 7 min (Fig. 3). During following light increments the overshoot was not observed. However, in the following light increments the NPQ decrease occurred with similar kinetics to the dark–light transition, suggesting that down-regulation of NPQ in PF treatments is not primarily due to activation procedures of photosynthetic reactions. Exposure to 50 μmol photons m−2 s−1 (50% of growth light) for 10 min during the first light increment is expected to have resulted in significant activation of photosynthetic processes. Repetitive down-regulation of NPQ in increasing PF also rejects the hypothesis of an active NPQ in the dark due to chlororespiration.

Typhimurium. MAPK inhibitor To successfully colonise such a broad range of different hosts, S. Enteritidis has acquired genes which are frequently clustered at particular parts of chromosome called Salmonella Pathogenicity Islands (SPI). Although there are up to 14 different pathogenicity islands, the presence of which varies among different serovars of Salmonella enterica (S. enterica), 5 of these can be found in all S. enterica serovars. The SPI-1 and SPI-2 pathogenicity islands are considered as the most important for S. enterica virulence. Proteins encoded by SPI-1 form a type III secretion system (TTSS) which mediates the translocation of S. enterica proteins into a host cell across its cytoplasmic membrane. The translocated

proteins induce cytoskeletal rearrangements which results in S. enterica uptake even

by non-professional phagocytes [1, 2]. Genes localised within SPI-2 encode proteins of another TTSS expressed by S. enterica inside host cells where it translocates its proteins across the phagosomal membrane and increases intracellular survival [3]. The functions of the genes localised on the CH5424802 purchase remaining SPIs are less well characterised; for SPI-3 genes conflicting information has been published suggesting their role both in gut colonisation and intracellular survival [4, 5]. SPI-4 genes are required for the intestinal phase of disease [5] although a SPI-4 requirement for systemic infection of mice has been also reported [6]. Genes localised at SPI-5 are co-regulated with either SPI-1 selleckchem or SPI-2 genes and therefore represent a dually controlled system [7, 8]. After oral ingestion, S. enterica comes into contact with the intestinal epithelial lining and using the SPI-1 encoded TTSS it enters M-cells and enterocytes. After crossing the epithelium S. enterica interacts with neutrophils and macrophages. The result of these initial events is critical for Ureohydrolase the outcome of the disease. If S. enterica is not recognised by host cells, and the proinflammatory immune response in the gut is not induced, it

is likely that the infection will develop into a typhoid-like disease [9–11]. During the course of the typhoid-like infection of mice, S. enterica colonises internal organs such as liver and spleen where it is found in macrophages, neutrophils, and T- and B-lymphocytes [12]. Why the immune system of a host does not respond properly to S. enterica infection during the typhoid disease has never been explained in sufficient detail although it is known that S. enterica is capable of induction of apoptosis in macrophages [13, 14], inhibition of antigen presentation by dendritic cells [15] and also NK cell depletion [16]. Except for the role of SPI-1 in invasiveness the non-professional phagocytes and SPI-2 in intracellular survival, roles of the remaining 3 major pathogenicity islands in the interactions of S. enterica with host immune system are not too much elucidated.

The calculated β is 7.0 × 10-8 cm/W, which is comparable to the value reported previously [12]. For sample B after 800°C annealing, it is noted that the α-Si sublayers begin to be crystallized as revealed by Raman spectra, as shown in Figure 4, and the crystallinity is about 61%. The NLA coefficient is reduced to 4.2 × 10-8 cm/W, which can be explained in terms as two factors. First, we find that the optical

bandgap slightly increases from 1.89 eV (sample A) to 2.07 eV (sample B), which means that the density of states at the same energy level in conduction band decreases due to the enlargement of the bandgap; therefore, the number of absorbed photon via two photon buy SHP099 selleck compound absorption (TPA) process is reduced at the same incident intensity. Second, due to the formation of nc-Si dots after annealing, part of incident photons can be absorbed to excite carriers from the valence band to localized states existing in the interfacial region of nc-Si and SiO2 layers, which may reduce the two photon absorption process between valence and conduction band. Consequently, the nonlinear absorption β is reduced in sample B. Figure 4 Normalized Raman spectra Fedratinib ic50 of samples A to D. As-deposited Si/SiO2 multilayers

(sample A) and samples after annealing with various temperatures (B: 800°C, C: 900°C, D: 1,000°C). The Raman spectra of sample D are decomposed by three components: the crystallized phase component peaked at 516 cm-1 (wine dash line), transition phase 506 cm-1 (cyan dash line), and the amorphous component peaked at 480 cm-1 (magenta

dash line). It is interesting to find that the nonlinear absorption coefficient becomes negative in samples C and D due to the SA process. As shown in Figure 4, it is found that with increasing the annealing temperature, the relative Raman signal of crystallized Si phases (centered at 516 and 506 cm-1) becomes stronger compared to that of amorphous Si phase (approximately 480 cm-1) and the band width becomes narrower; GPX6 meanwhile, the Raman peak of nc-Si shifts toward the higher wave number, which indicates that samples C and D are further crystallized after annealing at higher temperature due to the formation of more nc-Si. The high density of nc-Si dots results in much more interface states of nc-Si dots, which in consistent with the linear absorption properties, as shown in Figure 2. Therefore, the single photon transition from valence band to the interface states has been a main route to generate nonlinear absorption behaviors and the two photon absorption process can be neglected in this case. Consequently, the SA occurs to cause the negative nonlinear absorption coefficient.

The

elevation of PV in the present study is mirrored by the measured increase in DXA whole-body www.selleckchem.com/products/Belinostat.html lean mass. In the DXA two-component soft tissue model, lean mass comprises water, proteins, glycogen and non-bone minerals [27]. As increases in protein, glycogen and non-bone minerals can virtually be excluded (see below), the increase in whole-body lean mass must have resulted from an increase in whole body water, which led to an expansion in PV. Our findings are in accordance with the report of Lands et al.[39] who found a significantly higher value for DXA-derived whole-body lean mass after saline infusion given to healthy male participants. Finally, our finding that HRCLT was reduced lends further credence to our result that PV increased as a consequence of NVP-HSP990 order NaHCO3 supplementation, because PV expansion simultaneously AZD9291 increases stroke volume and reduces sympathetic nervous activity, leaving V̇ O2,CLT unaffected [40]. In our study, DXA-derived leg lean mass did neither change between interventions nor over time (Table 2). As with each gram of glycogen stored in muscle tissue 3–4 g of water is bound [28], and body water is present within the lean soft tissue compartment [27], a decrease in leg

lean mass in such a short time (2 days) would indicate a loss of glycogen. In turn, glycogen loss would implicate incomplete regeneration, which would manifest itself in a reduced anaerobic work capacity and, accordingly, decreased performance [41]. Since our participants displayed neither a reduction in leg lean mass nor performance, the provided regeneration drink and the participants’

daily nutritional Ureohydrolase intake were sufficient to restore glycogen from day to day, allowing them to perform maximally on each day. Our results have at least two practical implications. First, since the [HCO3 -] gradient between intramyocellular compartment and blood did not decrease over time, NaHCO3 can be taken daily in multiday competitions or tournaments lasting ≤ 5 d without the risk of reducing performance. Second, the apparent PV expansion in response to the high ion intake (see above) blunted any further increase in [HCO3 -]. If the same mechanism would be true for the chronic supplementation protocol, the effectiveness of this protocol should be questioned, as it seems that [HCO3 -] cannot be increased limitlessly, i.e. that it probably reaches a ceiling. The observed ceiling effect was probably based on a metabolic compensation mechanism preventing a disproportionate increase in [HCO3 -]. A respiratory compensation mechanism is unlikely to have occurred in our study because there were no differences between the NaHCO3 and placebo intervention for V̇ CO2 (P = 0.903, data not shown) and RER (P = 0.556, data not shown) during the resting measurements before the constant-load tests.

888 8.08 235 B CP1 2.217 5.62 130   CP2 2.666 6.44 198   CP3 2.817 SC79 mw 6.51 207 Samples A and B are both with GaAs-like and InSb-like alternate IFs and even number of InAs and GaSb MLs. The SLs possess C 2v symmetry in the ideal condition. At successive IFs, if In-Sb bonds lie in the (110) plane, while In-As bonds lie in the (1 0) plane. Linearly polarized light propagates along the (001) direction. When the polarized direction is parallel to [110] and [1 0] directions, it feels different chemical bonds at IFs. As a result, the optical properties

along the [110] and [1 0] directions are different. In the RDS spectra, InSb features were not observed learn more clearly in room temperature, since the features of E 0, E 1, and E 1+Δ 1CPs are very broadening with few ML [24]. This effect is identified as the spread of carrier wave function of the ultra-thin IF to surrounding layers. Figure 6a shows the Δ E c and Δ E v of unstrained GaAs, InAs, InSb, and GaSb system at Γ point [25, 26]. E 1and E 1+Δ 1take place Temsirolimus in vivo along the Λ directions of the Brillouin zone

where the valence and conduction bands are nearly parallel. The energy gap of L and Λ are nearly equal. We have inferred the band alignment of L point in Figure 6b. The reflectance peaks of L transitions are not observed, since these transitions are too weak or hidden in the Λ transition structures [22]. In Figure 6b, the Λ 1conduction band offset between InAs and GaSb is 0.234 eV, and the Λ 3valence band offset is 0.544 eV. The staggered band alignment of bulk materials imply that in every InAs/GaSb SL, there is a InAs-like conduction band minimum and GaSb-like valence

band maximum. The Λ 3valence band of InSb is much higher than GaSb, and the Λ 1conduction band is much higher than InAs. The Λ 3valence band splits into Λ (4,5)and Λ 6since the spin-orbital interaction. The red lines show the Λ 6energy positions. The Λ 6band of InSb is higher than Λ (4,5)band of InAs. As the thickness of InSb layers is increasing Palbociclib in vivo from 0.43 to 1.29 ML, compared to sample A, the effect of quantum well structures is enhanced. More holes are localized in InSb layers. However, there is no such effect for the GaAs layer. The IPOA intensities of CP1, CP2, and the shoulder-like CP about InSb are increased. While the IPOA intensities of CP3 are decreased and the transition energy position of CP2 are anomalous, blue shift may attribute to the coupling of these states. Figure 6 Band alignments of InAs, GaAs, GaSb and InSb binary system. (a) At Γ point of Brillouin zone. (b) At L point of Brillouin zone. The red lines are the spin-orbital splitting energies at L point. Conclusions The IPOA of InAs/GaSb SLs with InAs-like and GaSb-like alternate IFs were observed by RDS. The main mechanism can attribute to the symmetry reduction to C 2v .

Both EPA and placebo groups had an increase in IL-6, in agreement with previous research [2]; however, the increment in the EPA group was significantly greater than that in the placebo group. Our findings of elevated IL-6 post-exercise contradict the previous research of Phillips et al. [20] and Bloomer et al. [21], who demonstrated a reduction in cytokines IL-6 and TNF-α 48 h post exercise. It should however be noted that Phillips et al. [20] used a combination of EPA, docasahexaenoate Selinexor molecular weight (DHA), tocopherols and Dactolisib in vivo flavonoids,

and Bloomer et al. [21] used EPA and DHA in the supplement groups. This therefore raises the question of whether it was this combination of fish oils, or whether it was EPA, DHA, tocopherols or flavonoids, which were individually responsible for the reduction in IL-6, TNF-α and CRP. The variability of the fish oil used may be a

possible explanation for the discrepancy between the findings of Phillips et al. [20] and Bloomer et al. [21] and the findings of the present study. As mentioned above, the IL-6 response post exercise appears to be associated with greater generated torques [14] and muscle soreness post resistance exercise [3]. Notwithstanding the data from Lenn et al. [3] it is unclear whether there is a direct link between IL-6 and muscle soreness experienced post resistance exercise. Anidulafungin (LY303366) The work of Graven-Nielsen et al. [7] CHIR98014 purchase demonstrated that muscle soreness significantly reduces MVC, possibly due to cytokines, such as IL-6 affecting nerve endings and activating

nocieoceptors [6]. Therefore if IL-6 is associated with pain, then any reduction in IL-6 through EPA supplementation should be reflected in a reduction in pain. This, however, was not the case in the present study. In fact, our data show no association between IL-6 and any of the generally accepted markers of DOMS. The lack of any clear link between IL-6 and pain sensation is evidenced in data provided by Phillips et al. [20] which suggests that whilst a fish oil-treated group had a significantly reduced IL-6 level 72 h post exercise, this was not matched with a reduction in perceived pain. The data provided both here and in Phillips et al. [20] suggest that IL-6 may not be involved in the muscle soreness experienced post resistance exercise, and that other pro-inflammatory cytokines such as TNF-α or IL-1β may be responsible, however this was beyond the scope of the current study to determine and requires further research. The data from the present study agrees with the findings from Lenn et al. [3], who suggested that EPA may not be beneficial at ameliorating the effects of DOMS and reducing levels of IL-6.