Numerous studies have attributed the decrease in force production of skeletal muscle during exercise to a increase in lactate concentration ([lactate]). This notion is based on the high negative correlation between plasma lactate and force during fatigue and recovery. These experiments attempted to determine if lactate directly effects force production in skeletal muscle. Mouse extensor digitorum longus muscles (EDL) were isolated and incubated in a buffered Ringers solution at a pH 7.2 and exposed at three minute intervals to a final concentration of 10, 20, 30, 50mM lactate. At 21° C, tetanic force production (Po, 250ms, 110Hz) decreased to 99.3 ± 1.0, 97.1 ± 1.2, 94.9 ± 1.1* and 93.1 ± 1.3*% of initial and the rate of force development (+dP/dt) was reduced to 99.4 ± 0.7, 96.8 ± 0.5, 93.5 ± 0.6*, and 89.3 ± 1.2*% of initial (*p<0.05 vs untreated muscles). At 37° C the effects of lactate were augmented. Po was reduced to 89.7 ± 1.1, 81.0 ± 2.4, 73 ± 3.9*, and 61.6 ± 5.4*% and +dP/dt was reduced to 79.4 ± 1.8*, 65.9 ± 2.8*, 55.4 ± 4.0*, and 44.3 ± 5.0*% of initial (*p<0.05 vs control muscles). The next phase was to determine if the changes in Po and +dP/dt were due to alterations in the sacroplasmic reticulum (SR) Ca2+ exchange. The SR of EDL homogenates were actively loaded with Ca2+ and release was initiated by 25 mM AgNO3. The rate of Ca2+ release was significantly reduced by 31% (2.48 ± 1.21 vs 1.72 ± 0.24 mmol·mg-1·min-1) in the presence of 25 mM lactate. These results indicate that exposure to increased [lactate], independent of the H+, decreases force production of whole muscle, effects that are greater at 37° C than 21° C. Also increased lactate reduces the rate of SR Ca2+ release. These results suggest that lactate depresses whole muscle force production by altering Ca2+ release of the SR. They also support the idea that increased lactate concentrations disrupt normal muscle function leading to the development of fatigue. / Master of Science

Postendoscopic retrograde cholangiopancreatography pancreatitis (PEP) is the most common complication of endoscopic retrograde cholangiopancreatography pancreatitis (ERCP). No randomized controlled trial (RCT) has compared the efficacy of the American Society of Gastrointestinal Endoscopy and European Society of Gastrointestinal Endoscopy recommended interventions for PEP prevention. We assessed the effectiveness of these interventions using network meta-Analysis. PubMed, EMBASE, and Cochrane databases were searched to identify RCTs investigating guideline-recommended interventions and their combinations [rectal nonsteroidal anti-inflammatory drugs (NSAIDs): indomethacin or diclofenac, pancreatic stent (PS), aggressive hydration (AH), sublingual nitrate) for PEP prevention. We performed direct and Bayesian network meta-Analysis, and the surface under the cumulative ranking curve to rank interventions. Subgroup network meta-Analysis for high-risk populations was also performed. We identified a total of 38 RCTs with 10 different interventions. Each intervention was protective against PEP on direct and network meta-Analysis compared with controls. Except AH+diclofenac and NSAIDs+ sublingual nitrate, AH+indomethacin was associated with a significant reduction in risk of PEP compared with PS [odds ratio (OR), 0.09; credible interval (CrI), 0.003-0.71], indomethcin+PS (OR, 0.09; CrI, 0.003-0.85), diclofenac (OR, 0.09; CrI, 0.003-0.65), AH (OR, 0.09; CrI, 0.003-0.65), sublingual nitrate (OR, 0.07; CrI, 0.002-0.63), and indomethacin (OR, 0.06; CrI, 0.002-0.43). AH with either rectal NSAIDs or sublingual nitrate had similar efficacy. AH+indomethacin was the best intervention for preventing PEP with 95.3% probability of being ranked first. For high-risk patients, although the efficacy of PS and indomethacin were comparable, PS had an 80.8% probability of being ranked first. AH+indomethacin seems the best intervention for preventing PEP. For high-risk patients, PS seems the most effective strategy. The potential of combination of interventions need to be explored further.

A Research Report submitted to the Faculty of Medicine, University of the Witwatersrand, Johannesburg in partial fulfilment for the degree of M.Sc.(Med) / During a typical swimming training session, the volume of fluid lost via sweat is not evident which may contribute to a swimmer not replacing fluid loss effectively. This study investigates fluid balance during a typical swim training session. The physiological responses measured included fluid loss, fluid gain and plasma lactate concentrations / IT2018

Sodium lactate and acetic acid derivatives were evaluated for their effects on color retention, microbial growth (TPC), oxidation (TBARS), and sensory attributes of hot-boned pork sausage patties that were stored under retail store display conditions over time. Treatments included: (a) 2.5% sodium lactate 60% solids (L), (b) 2.5% buffered vinegar pH 6.5-8.0 (V), (c) 2.5% sodium lactate and vinegar 52/48% mixture (LV), (d) control with 0.02% BHA/BHT (C), and (e) negative control without additives (NC). Overall acceptability of day 17 LV and L treatments were not different (P>0.05) from day 14 treatments. These results revealed that the L and LV sausage patties retained sensory acceptability and microbial quality from day 14 through day 17 as opposed to other treatments. Additionally, sausage patties with 2.5% LV maintained color (redness) and overall acceptability throughout 17 days of shelf-life when held in retail conditions, when compared to other treatments.

Introduction. Exercise and head-out water immersion (HOI) have consistently reported an increase in central blood volume associated with the cephalad shift in blood volume. This causes an increase in left ventricular end diastolic volume and greater stroke volume during exercise compared to exercise in air at similar metabolic costs. In contrast, the metabolic response, specifically, blood lactate accumulation during exercise combined with HOI has yielded varying results depending on the mode of exercise. At present it appears that during exercise at similar metabolic costs, cycle ergometry exercise augments plasma lactate over treadmill running while HOI reduces the plasma lactate response to cycle ergometry exercise. The interaction between treadmill running and HOI appears less certain. Thus, we tested the hypothesis that running on a treadmill on land would result in a lesser accumulation of lactate than during HOI treadmill running. Methods. Eleven subjects' lactate thresholds were determined while running at a 0% grade at increasing speeds on a treadmill on land or during HOI on an underwater treadmill in a randomized cross-over design. Exercise tests were separated by a minimum of 3 days. Lactate concentrations were expressed in mM• kg-1 H2O after correcting for plasma solid concentration. During exercise changes in plasma volume were calculated from changes in hematocrit and hemoglobin. Lactate threshold was estimated from a log-log plot of lactate concentration (mM• kg-1 H2O) as a function of relative oxygen consumption (ml O2•min-1•kg-1 BW). Results. The energy cost and heart rate response to running at speeds between 5.5 and 7.5 mph was similar for land and HOI. During treadmill running on land, plasma volume decreased by 6.4 ± 4.0% at a speed of 7.5 mph. The decrease in plasma volume was significantly greater during HOI and averaged 18.7 ± 1.7% (p <0.05) at 7.5 mph. Plasma lactate was higher at any given treadmill speed ≥ 5.5 mph during HOI compared to land (p <0.05). Lactate threshold during HOI running (21.8 ± 1.6 mM• kg-1 H2O) was lower (p <0.05) than during running on the land treadmill (27.0 ± 1.6 mM• kg-1 H2O). Discussion. HOI running resulted in a consistent shift to the left (rise in plasma lactate occurred at a lower ) in the lactate threshold and elevated plasma lactate concentration at speeds between 5.5-7.5 mph despite similar metabolic and HR responses to the exercise.

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No / The increasing prevalence of chronic wounds has significant financial implications for nations with advanced healthcare provision. Although the diseases that predispose to hard-to-heal wounds are recognized, their etiology is less well understood, partly because practitioners in wound management lack specialized diagnostic support. Prognostic indicators for healing may be inherent to wound biochemistry but remain invisible under routine clinical investigation; lactate is an example of this. In this study, lactate concentration in exudate obtained from 20 patients undergoing wound management in hospital was variable but in some cases approached or exceeded 20 mM. In vitro viability studies indicated that fibroblasts and endothelial cells tolerated low levels of lactate (1-10 mM), but cell viability was severely compromised by high lactate concentrations (=20 mM). Scratched monolayer experiments revealed that cell migration was affected earlier than viability in response to increasing lactate dose, and this was shown by immunocytochemistry to be associated with cytoskeletal disruption. A prototype enzyme-based colorimetric assay for lactate generating a color change that was rapid in the context of clinical practise, and capable of functioning within a gel vehicle, was developed with point-of-care dipstick applications in mind. A randomized single-blinded trial involving 30 volunteers and using a color chart to calibrate the assay demonstrated that lactate concentration could be reliably estimated with 5 mM precision; this suggesting that "physiological" and "pathological" lactate concentration could be distinguished. The present data suggest that a dipstick-type colorimetric assay could comprise a viable diagnostic tool for identifying patients at-risk from high-wound lactate.

No / Expecting ambulance clinicians to dependably differentiate the life-threatening organ dysfunction caused by sepsis from an inflammatory response to a non-infectious aetiology, relying upon vital signs and a physical examination of the patient alone, must be considered unrealistic. Although lactate measurement has been integrated into numerous prehospital sepsis screening tools, it is not yet measured routinely within UK ambulance services. Research has generally focused on whether handheld point-of-care lactate measurement devices are as accurate as laboratory analysis of venous or arterial samples. The weight of literature has concluded negatively in relation to this. However, there is potential for handheld devices to be used independently to monitor trends in lactate elimination or accumulation to inform decisions on the efficacy of prehospital interventions, or simply to report categorical data in terms of whether lactate levels are elevated or not. This offers UK paramedics the opportunity to improve sepsis care through the enhanced assessment of risk and acuity, the identification of patients with cryptic shock, more aggressive fluid resuscitation and advanced notification to receiving units.

No / The aim of this review was to examine whether the measurement of lactate in capillary blood samples using point-of-care handheld analysers corresponds sufficiently closely with arterial and venous whole-blood samples analysed by hospital central laboratory or blood gas analyser to be used interchangeably. A systematic search, informed by focused inclusion/exclusion criteria, was performed using multiple databases up to October 2015. A total of 65 articles were considered to have potential relevance and were evaluated in full text, of which ultimately five articles met all inclusion/exclusion criteria, and a final four were selected after data extraction and quality appraisal. All four studies found a predominantly upward bias in the measurement of lactate in capillary samples tested using a handheld point-of-care device over arterial or venous samples tested by laboratory methods or blood gas analyser. In terms of correlation, there was consensus between the studies that the strength of association between the two methods of measurement was statistically significant. Three studies directly examined the extent of agreement between point-of-care capillary lactate measurements and those of laboratory or blood gas analyser reference determined to ±2 standard deviations; 95% confidence intervals, and report contextually broad limits of agreement, identifying a potential for both over triage and, to a lesser extent, under triage. The findings of the review do not support interchangeable use of handheld fingertip point-of-care lactate measurement with laboratory or blood gas analyser methods in the identification of sepsis.