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The incidence of perturbed gastrointestinal integrity, as well as resulting systemic immune responses and gastrointestinal symptoms, otherwise known as exercised-induced gastrointestinal syndrome (EIGS), is common among individuals who partake in prolonged exercise. EIGS may cause the translocation of pathogenic material, including whole bacteria and bacterial endotoxins, from the lumen into circulation, which may progress into clinical consequences such as sepsis, and potentially subsequent fatality. However, further investigation is warranted to assess the possibility of food allergen and/or digestive enzyme luminal to circulatory translocation in response to exercise, and the clinical consequences. Findings from this narrative literature review demonstrate evidence that whole bacteria and bacterial endotoxins translocation from the gastrointestinal lumen to systemic circulation occurs in response to exercise stress, with a greater propensity of translocation occurring with accompanying heat exposure. It has also been demonstrated that food allergens can translocate from the lumen to systemic circulation in response to exercise stress and initiate anaphylaxis. To date, no research investigating the effect of exercise on the translocation of digestive enzymes from the lumen into systemic circulation exists. It is evident that EIGS and consequential pathogenic translocation presents life-threatening clinical implications, warranting the development and implementation of effective management strategies in at-risk populations. [ABSTRACT FROM AUTHOR]

The impact of a carbohydrate-electrolyte solution with sodium alginate and pectin for hydrogel formation (CES-HGel), was compared to a standard CES with otherwisematched ingredients (CES-Std), for blood glucose, substrate oxidation, gastrointestinal symptoms (GIS; nausea, belching, bloating, pain, regurgitation, flatulence, urge to defecate, and diarrhea), and exercise performance. Nine trained male endurance runners completed 3 hr of steady-state running (SS) at 60% ...O2max, consuming 90 g/hr of carbohydrate from CES-HGel or CES-Std (53 g/hr maltodextrin, 37 g/hr fructose, 16% w/v solution) in a randomized crossover design, followed by an incremental time to exhaustion (TTE) test. Blood glucose and substrate oxidation were measured every 30 min during SS and oxidation throughout TTE. Breath hydrogen (H2) was measured every 30 min during exercise and every 15 min for 2 hr postexercise. GIS were recorded every 15 min throughout SS, immediately after and every 15-min post-TTE. No differences in blood glucose (incremental area under the curve [mean ± SD]: CES-HGel 1,100 ± 96 mmol⋅L-1⋅150 min-1 and CES-Std 1,076 ± 58 mmol⋅L-1⋅150 min-1; p = .266) were observed during SS. There were no differences in substrate oxidation during SS (carbohydrate: p = .650; fat: p = .765) or TTE (carbohydrate: p = .466; fat: p = .633) and no effect of trial on GIS incidence (100% in both trials) or severity (summative rating score: CES-HGel 29.1 ± 32.6 and CES-Std 34.8 ± 34.8; p = .262). Breath hydrogen was not different between trials (p = .347), nor was TTE performance (CES-HGel 722 ± 182 s and CES-Std: 756 ± 187 s; p = .08). In conclusion, sodium alginate and pectin added to a CES consumed during endurance running does not alter the blood glucose responses, carbohydrate malabsorption, substrate oxidation, GIS, or TTE beyond those of a CES with otherwise matched ingredients. [ABSTRACT FROM AUTHOR]

Considering the recent growth of exercise gastroenterology research focusing on exercise-induced gastrointestinal syndrome mechanisms, response magnitude, prevention and management strategies, the standardized assessment of gastrointestinal symptoms (GIS) is warranted. The current methodological study aimed to test the reliability of a modified visual analog scale for assessing GIS during exercise, in response to a variety of exertional-stress scenarios, with and without dietary intervention. Recreational endurance runners (n = 31) performed one of the three exercise protocols, which included: 2-hr running at 70% VO2max in temperate (24.7 °C) ambient conditions, with fluid restriction; 2-hr running at 60% VO2max in hot (35.1 °C) ambient conditions, while consuming chilled water immediately before and every 15 min during exercise; and 2-hr running at 60% VO2max in temperate (23.0 °C) ambient conditions, while consuming 30 g/20 min carbohydrate (2:1 glucose:fructose, 10% temperate w/v), followed by a 1-hr distance test. GIS was monitored pre-exercise, periodically during exercise, and immediately postexercise. After wash out, participants were retested in mirrored conditions. No significant differences (p > .05) were identified between test-retest using Wilcoxon signed-rank test for all GIS (specific and categorized), within each exercise protocol and the combined protocols. Strong correlations were observed for gut discomfort, total GIS, upper GIS, and nausea (rs = .566 to rs = .686; p < .001), but not for lower GIS (rs = .204; p = .232). Cohen's magnitude of difference was minimal for all GIS (specific δ < 0.14 and categorized δ < 0.08). The modified visual analog scale for assessing GIS during exercise appears to be a reliable tool for identifying incidence and severity of GIS in cohort populations and is sensitive enough to detect exertional and intervention differences. [ABSTRACT FROM AUTHOR]

Long noncoding RNA forkhead box D3‐antisense RNA 1 (FOXD3‐AS1) is associated with cardiovascular diseases, but its roles in myocardial ischemia/reperfusion (I/R) injury and the related signaling pathway have not been fully reported. We aimed to investigate the roles and mechanism of action of FOXD3‐AS1 in myocardial I/R injury. An in vivo myocardial I/R injury mouse model and an in vitro hypoxia/reoxygenation (H/R) cardiomyocyte model was established. Quantitative reverse transcription‐polymerase chain reaction, western blotting, and immunofluorescent assays were performed to examine the expression levels of FOXD3‐AS1, microRNA (miR)‐128, thioredoxin‐interacting protein/regulation of development and DNA damage response 1/protein kinase B/glycogen synthase kinase 3β/nuclear factor erythroid 2‐related factor 2 (TXNIP/Redd1/AKT/GSK3β/Nrf2) pathway‐related proteins and apoptosis‐related proteins. The interactions between FOXD3‐AS1 and miR‐128 and miR‐128 and TXNIP were analyzed by Spearman's correlation test, predicted by ENCORI, and verified by dual‐luciferase reporter assay. In addition, the levels of cardiac injury markers and oxidative stress markers were evaluated by corresponding kits. Cell Counting Kit‐8 assays and flow cytometry were performed to assess cell viability and apoptosis. Hematoxylin and eosin staining was applied to observe the effect of FOXD3‐AS1 on the morphology of myocardial I/R injured tissues. The results showed that the FOXD3‐AS1 and TXNIP were highly expressed, whereas miR‐128 was expressed at low levels in I/R myocardial tissues and H/R‐induced H9c2 cells. FOXD3‐AS1 directly targeted miR‐128 to reduce its expression. TXNIP was confirmed as a downstream target of miR‐128. Knockdown of FOXD3‐AS1 led to the alleviation of I/R injury in vivo and in vitro. FOXD3‐AS1 enhanced the expression of TXNIP by sponging miR‐128, which inhibited the Redd1/AKT/GSK3β/Nrf2 pathway. Both inhibition of miR‐128 and overexpression of TXNIP reversed the cardioprotective effect of FOXD3‐AS1 small interfering RNA in H/R‐induced H9c2 cells. [ABSTRACT FROM AUTHOR]

New Findings: What is the topic of this review?The potential role of nutrition in exertional heat stroke.What advances does it highlight?Certain nutritional and dietary strategies used by athletes and workers may exert a protective effect the pathophysiological processes of exertional heat stroke, whereas others may be detrimental. While current evidence suggests that some of these practices may be leveraged as a potential countermeasure to exertional heat stroke, further research on injury‐related outcomes in humans is required. Exertional heat stroke (EHS) is a life‐threatening illness and an enduring problem among athletes, military servicemen and ‐women, and occupational labourers who regularly perform strenuous activity, often under hot and humid conditions or when wearing personal protective equipment. Risk factors for EHS and mitigation strategies have generally focused on the environment, health status, clothing, heat acclimatization and aerobic conditioning, but the potential role of nutrition is largely underexplored. Various nutritional and dietary strategies have shown beneficial effects on exercise performance and health and are widely used by athletes and other physically active populations. There is also evidence that some of these practices may dampen the pathophysiological features of EHS, suggesting possible protection or abatement of injury severity. Promising candidates include carbohydrate ingestion, appropriate fluid intake and glutamine supplementation. Conversely, some nutritional factors and low energy availability may facilitate the development of EHS, and individuals should be cognizant of these. Therefore, the aims of this review are to present an overview of EHS along with its mechanisms and pathophysiology, discuss how selected nutritional considerations may influence EHS risk focusing on their impact on the key pathophysiological processes of EHS, and provide recommendations for future research. With climate change expected to increase EHS risk and incidence in the coming years, further investigation on how diet and nutrition may be optimized to protect against EHS would be highly beneficial. [ABSTRACT FROM AUTHOR]

The study aimed to determine if short-term high dose probiotic supplementation containing Lactobacillus casei (L.casei) attenuates the commonly reported exertional-heat stress (EHS) induced endotoxinaemia and cytokinaemia. Eight endurance trained male volunteers (mean± SD: age 26 ± 6 y, nude body mass 70.2 ± 8.8 kg, height 1.75 ± 0.05 m, VO2max 59 ± 5 ml⋅kg-1⋅min-1) completed a blinded randomized cross-over design, whereby oral ingestion of a commercially available probiotic beverage containing L.casei (volume equivalent for x1011 colony forming units⋅day-1) (PRO) or placebo (PLA) was consumed for 7 consecutive days before exposure to EHS, which comprised of 2h running exercise at 60% VO2max in hot ambient conditions (34.0 °C and 32% RH). Blood samples were collected at baseline (7 days before EHS), pre-EHS, post-EHS (1 hr, 2 hr, 4 hr, and at 24 hr). Plasma samples were analyzed for gram-negative bacterial endotoxin, cytokine profile (IL-6, IL-1β, TNF-α, IFN-γ, IL-8, and IL-10) and plasma osmolality. Plasma osmolality did not differ between trials. Seven days of L.casei supplementation did not show significant changes in resting circulatory endotoxin concentration or plasma cytokine profile compared with PLA. A main effect of time was observed for IL-6, TNF-α, IL-10 and IL-8; whereby levels increased in response to EHS (p < .05). Relative to pre-EHS concentrations, higher plasma concentrations of endotoxin (p = .05), and a trend for higher plasma TNF-α concentration (p = .09) was observed on PRO compared with PLA throughout recovery. Short-term high dose supplementation of a probiotic beverage containing L.casei before EHS did not attenuate EHS induced endotoxaemia and cytokinaemia; nor is it more positively favorable over a placebo. [ABSTRACT FROM AUTHOR]

We compared the impact of two different, but commonly consumed, beverages on integrative markers of exercise recovery following a 2 h high intensity interval exercise (i.e., running 70–80% V̇ O2max intervals and interspersed with plyometric jumps). Participants (n = 11 males, n = 6 females) consumed a chocolate flavored dairy milk beverage (CM: 1.2 g carbohydrate/kg BM and 0.4 g protein/kg BM) or a carbohydrate-electrolyte beverage (CEB: isovolumetric with 0.76 g carbohydrate/kg BM) after exercise, in a randomized-crossover design. The recovery beverages were provided in three equal boluses over a 30 min period commencing 1 h post-exercise. Muscle biopsies were performed at 0 h and 2 h in recovery. Venous blood samples, nude BM and total body water were collected before and at 0, 2, and 4 h recovery. Gastrointestinal symptoms and breath hydrogen (H2) were collected before exercise and every 30 min during recovery. The following morning, participants returned for performance assessment. In recovery, breath H2 reached clinical relevance of >10 ppm following consumption of both beverages, in adjunct with high incidence of gastrointestinal symptoms (70%), but modest severity. Blood glucose response was greater on CEB vs. CM (P < 0.01). Insulin response was greater on CM compared with CEB (P < 0.01). Escherichia coli lipopolysaccharide stimulated neutrophil function reduced on both beverages (49%). p-GSK-3β/total-GSK-3β was greater on CM compared with CEB (P = 0.037); however, neither beverage achieved net muscle glycogen re-storage. Phosphorylation of mTOR was greater on CM than CEB (P < 0.001). Fluid retention was lower (P = 0.038) on CEB (74.3%) compared with CM (82.1%). Physiological and performance outcomes on the following day did not differ between trials. Interconnected recovery optimization markers appear to respond differently to the nutrient composition of recovery nutrition, albeit subtly and with individual variation. The present findings expand on recovery nutrition strategies to target functionality and patency of the gastrointestinal tract as a prerequisite to assimilation of recovery nutrition, as well as restoration of immunocompetency. [ABSTRACT FROM AUTHOR]

umans evolved from species that walked on all 4 limbs, which means that experiments in quadrupeds can guide andsupport experiments in humans. This is particularly helpful for neural rehabilitation because the central nervous system isplastic in nature, meaning that activities promoting central nervous system activity can alter subsequent output properties. Thisis known as neuroplasticity and can be measured as changes in spinal cord excitability through reflexes as a proxy. By targetingevolutionarily conserved pathways that act on similar interneurons within the spinal cord to either increase or decrease excitability,it may be possible to preferentially modulate spinal cord excitability based on a desirable outcome. For example, rhythmicmovement reduces spinal cord excitability whereas brief sensory input to cutaneous afferents increases spinal cord excitability.Alterations in spinal cord excitability have been shown to outlast the activity duration, suggesting that neuroplasticity is nottransient. This evidence suggests that both rhythmic movement and sensory input can induce acute neuroplasticity of spinalcord excitability. The overall purpose of this dissertation was 2-fold: (i) to provide reviews of how evolutionarily conservedpathways are studied in humans and how they contribute to human rhythmic movement; and (ii) experimentally examine howthese conserved pathways, which converge onto similar interneuron circuitry, can be exploited to cause bidirectional changesin spinal cord excitability. Reviews indicate that humans have retained characteristics of quadrupedal locomotion and, inparticular, activity of the arms affects the excitability of the legs, and vice versa. Cutaneous input is integrated throughout thebody during locomotion, such that cutaneous sensations elicit neuromechanical responses that are nerve-specific and modulatedaccording to the phase of movement. In experiment 1, there was increased spinal cord excitability following patternedstimulation of cutaneous afferents innervating the bottom of the foot. In experiment 2, stimulation to cutaneous afferentsinnervating both the top and bottom of the foot amplified voluntary plantar- and dorsiflexion. In experiment 3, cervicolumbarconnections were exploited to amplify plasticity in spinal cord excitability induced by rhythmic movement. Finally, in experiment4, there were interactions of rhythmic movement and fatigue, which both reduce spinal cord excitability, with cutaneousstimulation, which increases spinal cord excitability, such that reductions in spinal cord excitability associated with fatigue weremitigated by cutaneous stimulation. Taken together, these experiments suggest that cutaneous stimulation can increase spinalcord excitability, whereas quadrupedal locomotor activity can decrease spinal cord excitability. These conserved pathways canbe exploited to intentionally modify spinal cord excitability in a bidirectional fashion, which provides fruitful information forthe exploration of rehabilitation and sport performance practices. [ABSTRACT FROM AUTHOR]

The study of heat adaptation in military personnel offers generalizable insights into a variety of sporting, recreational and occupational populations. Conversely, certain characteristics of military employment have few parallels in civilian life, such as the imperative to achieve mission objectives during deployed operations, the opportunity to undergo training and selection for elite units or the requirement to fulfill essential duties under prolonged thermal stress. In such settings, achieving peak individual performance can be critical to organizational success. Short-notice deployment to a hot operational or training environment, exposure to high intensity exercise and undertaking ceremonial duties during extreme weather may challenge the ability to protect personnel from excessive thermal strain, especially where heat adaptation is incomplete. Graded and progressive acclimatization can reduce morbidity substantially and impact on mortality rates, yet individual variation in adaptation has the potential to undermine empirical approaches. Incapacity under heat stress can present the military with medical, occupational and logistic challenges requiring dynamic risk stratification during initial and subsequent heat stress. Using data from large studies of military personnel observing traditional and more contemporary acclimatization practices, this review article (1) characterizes the physical challenges that military training and deployed operations present (2) considers how heat adaptation has been used to augment military performance under thermal stress and (3) identifies potential solutions to optimize the risk-performance paradigm, including those with broader relevance to other populations exposed to heat stress. [ABSTRACT FROM AUTHOR]

This work presents the results obtained for a thioether derivative of bipyridine, (E,Z)-1-(4′-methyl-[2,2′-bipyridine]-4-yl)-N-(4(methylthio)phenyl)methanimine (4-mbpy-Bz-SMe), and its copper complex [CuII(4-mbpy-Bz-SMe)2]2+. Electronic spectra acquired at 183 K of the cuprous complex [CuI(4-mbpy-Bz-SMe)2]+ generated in situ indicated the formation of the peroxodicopper compound {[CuII(4-mbpy-Bz-SMe)2]2(μ-O22−)}2+. A gold electrode modified with [CuII(4-mbpy-Bz-SMe)2]2+ (Au/[Cu]) was fully characterized by SERS spectroscopy, electrochemistry and impedance spectroscopy thus showing adsorption occurs through the sulfur atom of the 4-mbpy-Bz-SMe moieties. DNA cleavage assays showed the copper complex, in solution and adsorbed on gold, degrades DNA if reducing conditions are maintained, i.e. ascorbic acid (H2AA) in solution or applied potentials more negative than 0.12 V vs. Ag/AgCl (CuI form). The electron paramagnetic resonance (EPR) spectra obtained for the electrolyzed solution (Eapl = −0.2 V, no H2O2) and for the solution containing [CuII(4-mbpy-Bz-SMe)2]2+ and H2O2 showed hydroxyl radical, HO˙, generation had occurred. The cyclic voltammograms obtained with H2AA in solution at Au/[CuII(4-mbpy-Bz-SMe)2]2+ as the working electrode showed a one-electron reaction leading to the ascorbyl radical (HA˙), which was detected by EPR. The current assigned to the electrode oxidation of HA˙ to AA decreased with the addition of catalase, a scavenger of H2O2, meaning peroxide is involved in the mechanism. [ABSTRACT FROM AUTHOR]

Ultra-endurance activities (≥ 4h) present unique challenges that, beyond fatigue, may be exacerbated by sub-optimal nutrition during periods of increased requirements and compromised gastrointestinal function. The causes of fatigue during ultra-endurance exercise are multi-factorial. However, mechanisms can potentially include central or peripheral fatigue, thermal stress, dehydration, and/or endogenous glycogen store depletion; of which optimising nutrition and hydration can partially attenuate. If exercise duration is long enough (e.g. ≥ 10h) and exercise intensity low enough (e.g. 45-60% of maximal oxygen uptake), it is bio-energetically plausible that ketogenic adaptation may enhance ultra-endurance performance, but this requires scientific substantiation. Conversely, the scientific literature has consistently demonstrated that daily dietary carbohydrates (3-12g/kg/day) and carbohydrate intake (30-110g/h) during ultra-endurance events can enhance performance at individually tolerable intake rates. Considering gastrointestinal symptoms are common in ultra-endurance activities, effective dietary prevention and management strategies may provide functional, histological, systemic, and symptomatic benefits. Taken together, a well-practiced and individualized fuelling approach is required to optimize performance in ultra-endurance events. [ABSTRACT FROM AUTHOR]

This repeated-measures case series describes the changes in cardiorespiratory fitness, body composition and systemic inflammation in 4 well-trained athletes pre- and post-completion of an unsupported transatlantic rowing race. The acute effects of endurance exercise have been well described previously, but the enduring consequences of ultra-endurance on the cardiorespiratory, metabolic and immune systems are largely unknown. This study explores these physiological adaptations following 2 weeks of recovery. Cardiorespiratory fitness testing, body composition analysis, and blood sampling for inflammatory cytokines were recorded immediately before race departure and repeated 14 days following race completion. Mean VO2max (ml/kg/min) was similar pre- (48.2±2.8) and post-race (46.7±1.5). Heart rate responses were equivalent at incremental workloads. Mean blood lactate (mmol/L) was higher at low to moderate power outputs and lower at maximal effort (14.6±1.85 vs. 13.1±2.5). Percentage body fat (17.7 ± 7.9 vs. 16.2±7.4) was analogous to pre-race analysis. Low-grade inflammation persisted, indicated by an increase in IL-1β (69%), IL-8 (10%), TNF-α (8%), IL-6 (5.4%), and C-reactive protein (22.4%). VO2max and heart rate responses were similar pre- and post-race, but sub-maximal efficiency measures of cardiorespiratory fitness were consistent with persistent fatigue. Body composition had returned to baseline but low-grade systemic inflammation persisted. Persistent pro-inflammatory cytokinaemia is known to exert deleterious consequences on immune, metabolic, and psychological function. Adequate recovery is necessary to re-establish inflammatory homeostasis, and the results of this study may inform these decisions. [ABSTRACT FROM AUTHOR]

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It is highly attractive to construct natural enzyme-free nanoarray architecture as a 3D catalyst for hydrogen peroxide detection due to its great specific surface area and easy accessibility to target molecules. In this communication, we demonstrate that nickel borate nanoarray supported on carbon cloth (Ni−Bi/CC) behaves as an efficient catalyst electrode for H2O2 electro-reduction in neutral media. As a non-enzymatic electrochemical H2O2 sensor, such Ni−Bi/CC shows superior sensing performances with a fast response time (less than 3 s), a low detection limit (0.85 n m, S/ N=3), and a high sensitivity (18320 μA m m cm−2). Importantly, it also demonstrates favourable reproducibility and long-term stability. [ABSTRACT FROM AUTHOR]

Copyright of Applied Physiology, Nutrition & Metabolism is the property of Canadian Science Publishing and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

While coronary angioplasty represents an effective treatment option following acute myocardial infarction, the reperfusion of the occluded coronary artery can prompt ischemia-reperfusion (I/R) injury that significantly impacts patient outcomes. As ω-3 polyunsaturated fatty acids (PUFAs) have proven, yet limited cardioprotective abilities, an optimized polymer-conjugation approach is reported that improves PUFAs bioavailability to enhance cardioprotection and recovery in animal models of I/R-induced injury. Poly-l-glutamic acid (PGA) conjugation improves the solubility and stability of di-docosahexaenoic acid (diDHA) under physiological conditions and protects rat neonatal ventricular myocytes from I/R injury by reducing apoptosis, attenuating autophagy, inhibiting reactive oxygen species generation, and restoring mitochondrial membrane potential. Enhanced protective abilities are associated with optimized diDHA loading and evidence is provided for the inherent cardioprotective potential of PGA itself. Pretreatment with PGA-diDHA before reperfusion in a small animal I/R model provides for cardioprotection and limits area at risk (AAR). Furthermore, the preliminary findings suggest that PGA-diDHA administration in a swine I/R model may provide cardioprotection, limit edema and decrease AAR. Overall, the evaluation of PGA-diDHA in relevant preclinical models provides evidence for the potential of polymer-conjugated PUFAs in the mitigation of I/R injury associated with coronary angioplasty., (© 2021 Wiley-VCH GmbH.)

High-mobility group box 1 (HMGB1) plays a key role in the development of acute lung injury (ALI). Propofol, a general anesthetic with anti-inflammatory properties, has been suggested to be able to modulate lipopolysaccharide (LPS)-induced ALI. In this study, we investigated the effects of propofol on the expression of HMGB1 in a rat model of LPS-induced ALI. Rats underwent intraperitoneal injection of LPS to mimic sepsis-induced ALI. Propofol bolus (1, 5, or 10 mg/kg) was infused continuously 30 min after LPS administration, followed by infusion at 5 mg/(kg · h) through the left femoral vein cannula. LPS increased wet to dry weight ratio and myeloperoxidase activity in lung tissues and caused the elevation of total protein and cells, neutrophils, macrophages, and neutrophils in bronchoalveolar lavage fluid (BALF). Moreover, HMGB1 and other cytokine levels were increased in BALF and lung tissues and pathological changes of lung tissues were excessively aggravated in rats after LPS administration. Propofol inhibited all the above effects. It also inhibited LPS-induced toll-like receptor (TLR)2/4 protein upexpression and NF-κB activation in lung tissues and human alveolar epithelial cells. Propofol protects rats and human alveolar epithelial cells against HMGB1 expression in a rat model of LPS-induced ALI. These effects may partially result from reductions in TLR2/4 and NF-κB activation. [ABSTRACT FROM AUTHOR]

Purpose: The efficacy of myocardial conditioning strategies is compromised in patients with advanced age, diabetes, or low ejection fraction. We conducted a single-centre parallel-arm blinded randomized-controlled trial to determine whether propofol provides perioperative myocardial protection.Methods: Patients enrolled in this study were scheduled for primary aortocoronary bypass surgery utilizing normothermic cardiopulmonary bypass (CPB) with blood cardioplegia. The participants were stratified by diabetic status and left ventricular ejection fraction and randomly assigned to receive either an elevated dose of propofol -previously associated with experimental cardioprotection- or an isoflurane preconditioning regime. The primary endpoint was the coronary sinus (CS) concentration of 15-F2t-isoprostane (isoP). Secondary endpoints included in-hospital low cardiac output syndrome (LCOS) and major adverse cardiac events, 12- and 24-hr CS cardiac troponin I (cTnI) release, and myocardial B-cell lymphoma 2 (Bcl-2) protein expression.Results: Data were analyzed from 125 of 137 randomized participants. Participants receiving propofol experienced a greater mean (SD) increase from baseline in CS 15-F2t-isoP levels compared with those receiving isoflurane [26.9 (10.9) pg·mL(-1) vs 12.1 (10.4) pg·mL(-1), respectively; mean difference, 14.8; 95% confidence interval (CI), 11.0 to 18.6; P < 0.001] but a decreased incidence of LCOS (20.9% vs 57.1%, respectively; relative risk [RR],0.37; 95% CI, 0.22 to 0.62; P < 0.001). The incidence of LCOS was similar between groups in participants without type 2 diabetes mellitus (DM2) (P = 0.382) but significantly decreased in the propofol DM2 subgroup compared with the isoflurane DM2 subgroup (17.9% vs 70.3%, respectively; RR, 0.26; 95% CI, 0.13 to 0.52; P < 0.001). Propofol was associated with an increase in myocardial Bcl-2 protein expression (P = 0.005), a lower incidence of a CS cTnI threshold for myocardial infarction (P = 0.014), and fewer heart failure events (P < 0.001).Conclusion: Propofol may be a preemptive intraoperative cardioprotectant for patients with DM2 under conditions of normothermic CPB and blood cardioplegic arrest. The study is registered at www.clinicaltrials.gov (NCT00734383) and www.controlled-trials.com (ISRCTN70879185). [ABSTRACT FROM AUTHOR]

Apocynum venetum, a Chinese medicinal herb, is reported to be neuroprotective. However, whether Apocynum venetum leaf extract (AVLE) protects against ischemic myocardium remains elusive. Our present study was aimed to observe the effects of AVLE preconditioning on myocardial ischemia/reperfusion (MI/R) injury and to investigate the possible mechanisms. Rats were treated with AVLE (500 mg/kg/d, o. g.) or distilled water once daily for one week. Afterward, all the animals were subjected to 30 min of myocardial ischemia followed by 4 h of reperfusion. AVLE preconditioning for one week significantly improved cardiac function following MI/R. Meanwhile, AVLE reduced infarct size, plasma creatine kinase (CK)/lactate dehydrogenase (LDH) activities and myocardial apoptosis at the end of reperfusion in rat hearts. Moreover, AVLE preconditioning significantly inhibited superoxide generation, gp91phox expression, malonaldialdehyde formation and enhanced superoxide dismutase (SOD) activity in I/R hearts. Furthermore, AVLE treatment increased Akt and extracellular regulated protein kinases 1/2 (ERK1/2) phosphorylations in I/R rat heart. Either the Phosphatidylinositide 3-kinase (PI3K) inhibitor wortmannin or the ERK1/2 inhibitor PD98059 blocked AVLE-stimulated anti-oxidative effects and cardioprotection. Our study demonstrated for the first time that AVLE reduces oxidative stress and exerts cardioprotection against MI/R injury in rats. [ABSTRACT FROM AUTHOR]

Baicalein, a flavonoid derived from Scutellaria baicalensis Georgi, possesses cardioprotection against oxidant injury by scavenging reactive oxygen species (ROS). Few studies investigate whether baicalein protection is mediated by attenuating mitochondrial ROS and modulating the prosurvival and proapoptotic signaling. Primary cultured chick cardiomyocytes were used to study the role of baicalein in mitochondrial superoxide (O2·- generation and signaling of Akt and JNK. Cells were exposed to H2O2 for 2 h and baicalein was given 2 h prior to and during 2 h of H2O2 exposure. Cell viability was assessed by propidium iodide and DNA fragmentation. H2O2 (500 μM) significantly induced 45.3 ± 6.2% of cell death compared to the control (p < 0.001) and resulted in DNA laddering. Baicalein (10, 25 or 50 μM) dose-dependently reduced the cell death to 38.7 ± 5.6% (p = 0.226); 31.2 ± 3.9% (p < 0.01); 30.3 ± 5.3% (p < 0.01), respectively. It also attenuated DNA laddering. Further, baicalein decreased intracellular ROS and mitochondrial O2·-generation that was confirmed by superoxide dismutase PEG-SOD and mitochondria electron transport chain complex III inhibitor stigmatellin. In addition, baicalein increased Akt phosphorylation and decreased JNK phosphorylation in H2O2-exposed cells. Moreover, baicalein augmented mitochondrial phosphorylation of Akt Thr308 and GSK3β Ser9, and prevented mitochondrial cytochrome c release assessed by cellular fractionation. Our results suggest that baicalein cardioprotection may involve an attenuation of mitochondrial O2·- and an increase in mitochondrial phosphorylation of Akt and GSK3β while decreasing JNK activation. [ABSTRACT FROM AUTHOR]

Cardiopulmonary bypass (CPB) contributes to the secretion of anti-inflammatory cytokines that mediate the inflammatory response observed during open heart surgery. In addition to many factors, type of anesthesia management affects immune response and central nervous system in cardiac surgery. The aim of this study was to assess the effect of propofol versus desflurane anesthesia on systemic immune modulation and central nervous system on patients undergoing coronary artery bypass grafting. Forty patients undergoing elective coronary artery bypass graft surgery with CPB were included in this prospective randomized study. Patients were allocated to receive propofol ( n = 20) or desflurane ( n = 20) for maintenance of anesthesia. The blood samples for IL-6, IL-8, TNF-α, and S100β were drawn just prior to the operation before the induction of anesthesia, second before cardiopulmonary bypass, third after CPB, fourth 4 h postoperatively at the ICU. Major finding in our study is that S100β levels were lower in propofol group when compared to desflurane anesthesia. And also immune reaction was less in patients exposed to desflurane anesthesia when compared to propofol anesthesia as indicated by lower plasma concentrations of IL-8 and IL-6. Propofol is more preferable in terms of S100β for anesthetic management for CABG. [ABSTRACT FROM AUTHOR]

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Reactive oxygen species induce formation of 15-F2t-isoprostane (15-F2t-IsoP), a specific marker of in vivo lipid peroxidation, which is increased after myocardial ischemia and during the subsequent reperfusion. 15-F2tIsoP possesses potent bioactivity under pathophysiological conditions. However, it remains unknown whether 15-F2t-IsoP, by itself, can influence myocardial ischemia-reperfusion injury (IRI). Adult rat hearts were perfused by the Langendorff technique with Krebs-Henseleit (KH) solution at a constant flow rate of 10 ml/min. 15-F2tIsoP (100 nM), SQ-29548 (1 µM, SQ), a thromboxane receptor antagonist that can abolish the vasoconstrictor effect of 15-F2t-IsoP, 15-F2t-IsoP + SQ in KH, or KH alone (vehicle control) was applied for 10 min before induction of 40 min of global ischemia followed by 60 min of reperfusion. During ischemia, saline (control), 15-F2t-IsoP, 15-F2t-IsoP + SQ, or SQ in saline was perfused through the aorta at 60 µl/min. 15-F2t-IsoP, 15-F2t-IsoP + SQ, or SQ in KH was infused during the first 15 min of reperfusion. Coronary effluent endothelin-1 concentrations were significantly higher in the group treated with 15-F2t-IsoP than in the control group during ischemia and also in the later phase of reperfusion (P < 0.05). Infusion of 15-F2t-IsoP increased release of cardiac-specific creatine kinase, reduced cardiac contractility during reperfusion, and increased myocardial infarct size relative to the control group. SQ abolished the deleterious effects of 15-F2t-IsoP. 15-F2t-IsoP exacerbates myocardial IRI and may, therefore, act as a mediator of IRI. 15-F2t-IsoP-induced endothelin-1 production during cardiac reperfusion may represent a mechanism underlying the deleterious actions of 15-F2t-IsoP. [ABSTRACT FROM AUTHOR]

Elevated levels of gut leakage markers have been shown after strenuous exercise in healthy individuals. Any association between a temporary increase in these markers and the presence of coronary artery disease (CAD) is unknown. We therefore aimed to explore circulating gut leakage markers in response to a bout of strenuous exercise in patients with symptoms of CAD. Patients referred to exercise stress testing due to symptoms of CAD were included (n = 287). A maximal exercise ECG stress test was performed and venous blood samples were drawn at rest and within five minutes after, for analysis of soluble cluster of differentiation 14 (sCD14), lipopolysaccharide-binding protein (LBP), intestinal fatty-acid binding protein (I-FABP), lipopolysaccharide (LPS) and gene expression of toll-like receptor 4 (TLR4) in circulating leukocytes. Patients then underwent coronary angiography. LPS, LBP and sCD14 increased significantly after strenuous exercise in patients with symptoms of CAD, suggesting that even short bouts of vigorous exercise are associated with gut leakage. The gene expression of TLR4 decreased significantly after exercise, possibly as a negative feedback to the increase in LPS. There were no differences in exercise-induced changes between the groups of CAD, suggesting gut leakage to be independent of the presence of CAD. [ABSTRACT FROM AUTHOR]

(1) Purpose: Performing strenuous exercises negatively impacts the immune and gastrointestinal systems. These alterations cause transient immunodepression, increasing the risk of minor infections, especially in the upper respiratory tract. Recent studies have shown that supplementation of probiotics confers benefits to athletes. Therefore, the objective of the current study was to verify the effects of probiotic supplementation on cytokine production by monocytes and infections in the upper respiratory tract after an acute strenuous exercise. (2) Methods: Fourteen healthy male marathon runners received either 5 billion colony forming units (CFU) of a multi-strain probiotic, consisting of 1 billion CFU of each of Lactobacillus acidophilus LB-G80, Lactobacillus paracasei LPc-G110, Lactococcus subp. lactis LLL-G25, Bifidobacterium animalis subp. lactis BL-G101, and Bifidobacterium bifidum BB-G90, or a placebo for 30 days before a marathon. Plasma cytokines, salivary parameters, glucose, and glutamine were measured at baseline, 24 h before, immediately after, and 1 h after the race. Subjects self-reported upper respiratory tract infection (URTI) using the Wisconsin Upper Respiratory Symptom Survey (WURSS—21). The statistical analyses comprised the general linear model (GLM) test followed by the Tukey post hoc and Student's t-test with p < 0.05. (3) Results: URTI symptoms were significantly lower in the probiotic group compared to placebo. The IL-2 and IL-4 plasma cytokines were lower 24 h before exercise, while the other cytokines showed no significant differences. A lower level of IL-6 produced by monocytes was verified immediately after the race and higher IL-10 at 1 h post. No differences were observed in salivary parameters. Conclusion: Despite the low number of marathoners participating in the study, probiotic supplementation suggests its capability to preserve the functionality of monocytes and mitigate the incidence of URTI. [ABSTRACT FROM AUTHOR]

The main objective of this research was to carry out an experimental study, triple-blind, on the possible immunophysiological effects of a nutritional supplement (synbiotic, Gasteel Plus®, Heel España S.A.U.), containing a mixture of probiotic strains, such as Bifidobacterium lactis CBP-001010, Lactobacillus rhamnosus CNCM I-4036, and Bifidobacterium longum ES1, as well as the prebiotic fructooligosaccharides, on both professional athletes and sedentary people. The effects on some inflammatory/immune (IL-1β, IL-10, and immunoglobulin A) and stress (epinephrine, norepinephrine, dopamine, serotonin, corticotropin-releasing hormone (CRH), Adrenocorticotropic hormone (ACTH), and cortisol) biomarkers were evaluated, determined by flow cytometer and ELISA. The effects on metabolic profile and physical activity, as well as on various parameters that could affect physical and mental health, were also evaluated via the use of accelerometry and validated questionnaires. The participants were professional soccer players in the Second Division B of the Spanish League and sedentary students of the same sex and age range. Both study groups were randomly divided into two groups: a control group—administered with placebo, and an experimental group—administered with the synbiotic. Each participant was evaluated at baseline, as well as after the intervention, which lasted one month. Only in the athlete group did the synbiotic intervention clearly improve objective physical activity and sleep quality, as well as perceived general health, stress, and anxiety levels. Furthermore, the synbiotic induced an immunophysiological bioregulatory effect, depending on the basal situation of each experimental group, particularly in the systemic levels of IL-1β (increased significantly only in the sedentary group), CRH (decreased significantly only in the sedentary group), and dopamine (increased significantly only in the athlete group). There were no significant differences between groups in the levels of immunoglobulin A or in the metabolic profile as a result of the intervention. It is concluded that synbiotic nutritional supplements can improve anxiety, stress, and sleep quality, particularly in sportspeople, which appears to be linked to an improved immuno-neuroendocrine response in which IL-1β, CRH, and dopamine are clearly involved. [ABSTRACT FROM AUTHOR]