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Noninvasive Blood Gas Sensing with Electrodes
Published in Robert B. Northrop, Non-Invasive Instrumentation and Measurement in Medical Diagnosis, 2017
Also considered in this chapter is the NI, transcutaneous measurement of pCO2 in the peripheral blood, tcpCO2. High blood tcpCO2 is a sign of metabolic acidosis, which can have several causes, including damaged alveoli in the lungs. (Damaged alveoli will also give low tcpO2 readings.) Normal blood pH is ∼7.4. If the pH decreases for any reason, the rate of breathing increases automatically to exhale CO2 at a greater rate, and the kidneys also compensate for elevated acidity in the extracellular fluid by actively excreting hydrogen ions at an increased rate. Thus another cause of high pCO2 can be kidney failure, in which the tubular epithelial cells actively transport H+ ions from their interiors into the collecting tubes for excretion in urine at a reduced rate. Low blood flow to the kidneys, or damaged tubular cells can decrease this normal mechanism for blood pH regulation. High pCO2 can occur normally in exercise, but it drops in minutes due to increased breathing effort and H+ elimination by the kidneys. Acidosis can also result from gluconeogenesis in diabetes mellitus. Here, low-intracellular glucose concentration causes liver cells to break down fatty acids to acetoacetic acid and acetyl-Co-A. Acetyl-Co-A is used as an energy source, and acetoacetic acid enters the blood, causing the pH to fall. Even though CO2 is not involved directly, the lower pH causes the ratio of pCO2 to [ HCO3−] to increase. Loss of intestinal bicarbonate in severe diarrhea can also cause acidosis, and an elevated pCO2 to [ HCO3−] ratio (Guyton 1991, Chapter 30).
Metabolic load comparison between the quarters of a game in elite male basketball players using sport metabolomics
Published in European Journal of Sport Science, 2021
Kayvan Khoramipour, Abbas Ali Gaeini, Elham Shirzad, Kambiz Gilany, Saeed Chashniam, Øyvind Sandbakk
In the second quarter, Valine and Lucien were decreased, whereas Alanine, Glycerol, AcetoAcetic Acid, Acetone, Succinic Acid, Citric Acid, Acetate, and Taurine were increased. Since no previous study has assessed these metabolites in sport, we discuss these metabolic changes in response to previous studies examining bouts of exercise training. Increased Alanine in the second quarter indicates an increased transfer of BCAAs induced Ammonia to the liver (Mougios, 2019), a process called Alanine cycle (Mougios, 2019), which can be considered as a justification for increased Alanine. In addition, glucose reduction and Epinephrine, Glucagon, Growth Hormone and Cortical enhancement can stimulate Alanine Amino transferase converting Pyruvate to Alanine which is Gluconeogenesis precursor and therefore can increase Gluconeogenesis (Daskalaki et al., 2015). Also, several previous studies reported increased Alanine after acute bouts of exercise (Berton et al., 2017; Enea et al., 2010; Hoffman, 2017; Kirwan, Coffey, Niere, Hawley, & Adams, 2009; Netzer et al., 2011; Peake et al., 2014; Pechlivanis et al., 2010; Pechlivanis et al., 2015; Ra et al., 2014; Zafeiridis et al., 2016), which indicates an increase BCAAs metabolism and Gluconeogenesis. Furthermore, Pitti et al. (2019) detected significant changes in aromatic amino acid levels in a soccer game using salivary metabolomics, which was in line with that observed using blood analyses. The increased Glycerol during the second quarter represents an increase in both Gluconeogenesis (as a Gluconeogenesis precursor) and Lipolysis (as a byproduct of 3-acyl glycerol breakdown), which are pathways activated because of glycogen depletion (Mougios, 2019). This is supported by increases of the two ketone bodies, AcetoAcetic Acid and Acetone, most likely due to Glycogen depletion in the second quarter (Evans et al., 2017).