2005 gj sentinel front page pictures7/7/2023 Hence, the entirety of liver glycogen would be consumed in about 15 minutes as there is no glucose release from glycogen in muscle cells because of the lack of glucose-6 phosphatase. As a matter of fact, 300 ml/minute oxygen consumption (VO 2 = 13.4 mmol O 2) represents an ATP turnover of approximately 80 mmol/minute, which costs about 1.6 mmol/minute (0.3 g) of glucose when oxidized and 40 mmol/minute (7.2 g) when metabolized anaerobically. However, anaerobic ATP supply from a glycolytic anaerobic source is limited in terms of its sustained rate of ATP production, except for a very acute and short muscle contraction. ATP turnover is controlled by pH : acidosis decreases ATP turnover and oxygen demand, representing an adapted or deleterious event depending on how deep, how long and how reversible.Īlthough there is no doubt about the fact that a change in lactate metabolism is linked to energy imbalance, the complete picture of the mechanisms involved in lactate regulation, which represents just a piece of a very complex puzzle, triggering or inducing an adaptive response is not completely clear as yet. The first indicates a potential deficit in oxidation (oxygen or oxidative capacity), the second shortage in energy and the third, which is closely linked to these parameters, could be viewed as a metabolic tool allowing the exact matching between them. Lactate metabolism is intimately linked to the three major potentials of living systems, all strictly related to energy metabolism: redox potential ((NADH, H+)/NAD+) phosphate potential (ATP/(ADP × Pi)) and hydrogen potential or pH (6.1 + log(HCO3-/0.03 × PaCO2)). Because these two parameters are not routinely assessed at the bedside, however, the pathophysiological view is mostly based on lactate concentration only, which may represent a sometimes hazardous shortcut. In fact, as for any metabolite, lactate concentration depends on the ratio between production and consumption. Thus, it should be noted that a decrease in lactate might imply 'a correction' of the initial disorder but also an exhaustion of the precursor (glucose) or a destruction of tissues. Therefore, in ischemic tissues, which don't have a sustained supply of blood glucose, a substantial amount of lactate can be released as long as glucose is present in the interstitial fluid or in the cells (glycogen). Moreover, as indicated by the authors, lactate production requires a complete glycolytic pathway, that is, an intact cell with sufficient glucose supply or glycogen storage. Indeed, whatever the cause of derangement and the metabolic environment, any rise in blood lactate indicates an attempt by the body to adapt to an unusual energetic situation, which may affect redox state, phosphate potential or pH. This proposal seems absolutely correct and very close to what has been already proposed regarding oxygen consumption (VO 2), but with a simple bedside parameter of metabolic integration. In this context, these authors propose to take the decrease in blood lactate following a therapeutic challenge as a major indicator of the efficacy of such treatment. propose, in a review-hypothesis paper in this issue of Critical Care, to regard lactate increase in the intensive care unit as a marker of a metabolic adaptation requiring a therapeutic aid ("possibly indicating that 'there is still room' to boost fast intervention") rather than a sign of irreversible end-stage energy failure. īased on their broad experience in the management of the profound metabolic derangements observed in critical illnesses, associated with some experimental data, Valenza et al. Above all, it is an indispensable soldier that actively acts as a major intermediate involved in the vast cellular and organ energy interplay, allowing the body to cope with a wide range of metabolic disorders (for example, exercise, hypoxia, ischemia, severe sepsis, shock). It is probably a trustworthy sentinel because it sensitively indicates that fire is potentially in the house and numerous works have already shown a good relationship between lactate level and outcome. Lactate is certainly not a pyromaniac: it is not toxic and possesses no harmful effect per se.
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