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Bioenergetics
Published in Michael H. Stone, Timothy J. Suchomel, W. Guy Hornsby, John P. Wagle, Aaron J. Cunanan, Strength and Conditioning in Sports, 2023
Michael H. Stone, Timothy J. Suchomel, W. Guy Hornsby, John P. Wagle, Aaron J. Cunanan
The production of lactic acid can accelerate for several reasons apart from insufficient oxygen. For example, during aerobic exercise, if the intensity is suddenly increased, as often occurs in long-distance races, then glycolysis will be accelerated because the aerobic system can be momentarily unable to keep up with the sarcoplasmic production of NADH+. As a result, during the initiation of exercise and during periods of increasing intensity, some lactic acid may be produced until the aerobic system “gears up” and accommodates the increased NADH+ production. Furthermore, a finding of a constant blood lactate concentration does not necessarily mean that no lactic acid is being produced; it may mean that a dynamic equilibrium has been established and production and removal are equal (33, 35). Blood lactate accumulation can be influenced by several factors. Basically, this means that production has to increase faster than clearance or clearance is reduced or both. For example, glycogenolysis acceleration can result from increased catecholamine concentrations and increases in type II muscle fibers recruitment (35, 224). These factors tend to increase with increasing intensity of exercise with clearance being reduced above approximately 65% of VO2max (117, 118).
Airway Management
Published in Ian Greaves, Keith Porter, Jeff Garner, Trauma Care Manual, 2021
Ian Greaves, Keith Porter, Jeff Garner
Cellular metabolism is oxygen dependent, and different organs have varying sensitivities to hypoxia. Generally, in a hypoxic environment there will be a temporary transition to anaerobic metabolism. This cannot be sustained, as the production of lactic acid creates a progressive metabolic acidosis impairing cellular function. Therefore, a trauma patient presenting with a high lactate and an acidosis is already significantly at risk having used up much of their reserves.8
Introduction to lactic acidemias
Published in William L. Nyhan, Georg F. Hoffmann, Aida I. Al-Aqeel, Bruce A. Barshop, Atlas of Inherited Metabolic Diseases, 2020
William L. Nyhan, Georg F. Hoffmann, Aida I. Al-Aqeel, Bruce A. Barshop
Lactate levels can be lowered in some patients by the administration of dichloroacetate (DCA), regardless of the cause [64–68]. It is not generally recommended in disorders of gluconeogenesis, because DCA can itself produce hypoglycemia. Its use has been employed experimentally in a variety of other lactic acidemic conditions. Dichloroacetate activates the PDHC by inhibiting PDH kinase. In vivo, this compound reduces concentrations of lactate, pyruvate, and alanine, and increases the percentage of the active form of PDHC in brain, liver, and muscle. It has been used to treat congenital lactic acidosis [67–69], and levels of lactic acid have been improved. Neurologic improvement has been elusive in most patients reported, but there have been some successes. Peripheral neuropathy can be expected to worsen with DCA, and some patients have developed peripheral neuropathy [69].
Impact of resistance training on muscle fatigue in type 2 diabetes mellitus patients during dynamic fatigue protocol
Published in Physiotherapy Theory and Practice, 2023
Surface electromyography (EMG) is an excellent method with benefits of real-time monitoring of muscle fatigue during the performance of defined work by measuring myoelectric activity (Cifrek, Medved, Tonković, and Ostojić, 2009). During fatigue, a decline in spectral parameters such as mean and median frequency (MF) and an increase in amplitude parameters such as root mean square (RMS) has been observed (Cifrek, Medved, Tonković, and Ostojić, 2009). Recently, a new highly sensitive spectral index of muscle fatigue (i.e. Dimitrov’s muscle fatigue index (FInsmk)) has been proposed which has shown good sensitivity and specificity to detect muscle fatigue during dynamic contractions (Arabadzhiev, Dimitrov, and Dimitrova, 2005; Dimitrova, Hogrel, Arabadzhiev, and Dimitrov, 2005). During exercise, when aerobic processes are not able to meet energy demands, there occurs a shift to anaerobic processes, end product of which is lactic acid. When lactate clearance is not equivalent to lactate production, lactic acidosis commences, and its level in the blood is commonly used as a biomarker for evaluating muscle fatigue (Gosker and Schols, 2008). Alterations in surface EMG indices of muscle fatigue and blood lactate responses during exercise have been observed in T2DM patients (Bhati, Singla, Masood, and Hussain, 2021).
Nutrition and vasoactive substances in the critically ill patient
Published in South African Journal of Clinical Nutrition, 2022
To emphasise, it is important to monitor haemodynamic stability in conjunction with vasoactive substance dose. Continuous monitoring of physiological parameters (also known as shock endpoints) signals improvement or worsening in tissue perfusion and oxygenation.8 Heart rate, blood pressure and urine output are considered basic endpoints, where a resolution of tachycardia, a mean arterial blood pressure (MAP) of >60–65 mmHg4 and a normal urine output may indicate an improvement.8,13 In the presence of anaerobic metabolism, increased lactic acid is produced.8 If the production of lactic acid exceeds the ability of the liver to excrete excess lactic acid, the serum lactate level will increase.8 The stabilisation or decrease4 of serum lactate levels will indicate an improvement; a lactate level of <2 mmol/l is considered normal.8 The arterial base deficit (calculated from pH, partial pressure of arterial oxygen tension and serum bicarbonate) reflects the use of bicarbonate to buffer acidosis.8 A reduction of base deficit reflects the successful restoration of tissue perfusion and oxygenation; a base deficit of −2 to 2 mmol/l is considered normal.8
The pharmacotherapeutic options in patients with catecholamine-resistant vasodilatory shock
Published in Expert Review of Clinical Pharmacology, 2022
Timothy E. Albertson, James A. Chenoweth, Justin C. Lewis, Janelle V. Pugashetti, Christian E. Sandrock, Brian M. Morrissey
A retrospective series of 223 patients with refractory vasodilatory shock, post-CPB vasoplegic shock found that those treated with MB demonstrated a 39.5% response rate (defined as ≥10% increase in MAP) with a non-statistically significant trend in survival in the responders [131]. A meta-analysis of five RCTs using MB in hypotensive patients reported significant MAP increases (weighted mean difference 6.93 mmHg, 95% CI 1.67–12.18, P = 0.01) [132]. Insignificant improvement in the overall mortality rate was seen with MB (16%, 14/88) as compared to the control group 23% (20/86) (OR = 0.65, 95% CI 0.21–2.08, P = 0.5). Another later meta-analysis of six RCTs with total 214 patients in refractory vasodilatory shock showed an improvement in MAP after MB as compared to control groups (mean difference MAP = 4.87 mmHg, 95% CI 2.61–7.13, P < 0.0001) [133]. Reductions in serum lactic acid levels were also found with MB versus control treatments (mean difference lactic acid = −1.06, 95% CI −1.98 to −0.14, P = 0.02). Similar to earlier studies, overall mortality was not significantly decreased (OR = 0.58, 95% CI 0.25–1.31, P = 0.19).