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Nonhematological Manifestations of Iron Deficiency
Published in Bo Lönnerdal, Iron Metabolism in Infants, 2020
It is not known whether these changes brought about by 4 d of iron therapy has a counterpart in man. However, in a recent report, the effect of 2 weeks of iron therapy on exercise performance and exercise-induced lactate production was measured in trained athletes. All the performance parameters measured on a bicycle ergometer were unchanged after iron therapy, but blood lactate levels at maximum exercise decreased significantly from 10.3 to 8.4 mM in the iron-deficient women following therapy (p <0.03). These observations suggest that muscles call on anaerobic metabolism for energy needs with greater lactate production.58 Another series of studies also suggests that the low hemoglobin level is not the major deficit in chronic iron deficiency.15 When iron-deficient subjects were given an i.v. injection of iron dextran, work performance improved slightly more rapidly than the rise in hemoglobin, suggesting that iron had an effect not only related to relief of anemia. Further studies of work performance are needed to provide clear understanding of tissue iron deficiency and work performance in man.
The respiratory system and exercise
Published in John W. Dickinson, James H. Hull, Complete Guide to Respiratory Care in Athletes, 2020
As exercise intensity increases aerobic metabolism must be supplemented by anaerobic metabolism. This anaerobic metabolism produces lactic acid which must be buffered by the bicarbonate system. This buffering process produces additional carbon dioxide to that of aerobic metabolism and hence ventilation increases further. Although this has been the standard explanation for the additional carbon dioxide produced during exercise, there is some contention within the literature, a summary of which can be found in sources within the additional reading list (see below). As exercise intensity continues to increase there is a point whereby there is insufficient buffering of lactic acid and the concentration of hydrogen ions increases. At this point the increase in hydrogen ions is detected by the peripheral chemoreceptors in the carotid bodies and these now takes over control of ventilation.
Carbohydrates
Published in Geoffrey P. Webb, Nutrition, 2019
Lactic acid is the end product of anaerobic metabolism in mammalian cells and anaerobic energy production is only possible from carbohydrate substrate. Red blood cells do not have mitochondria and thus they metabolise glucose only as far as pyruvic acid and lactic acid. During heavy exercise, the oxygen supply to a muscle limits aerobic metabolism and so the muscles will generate some ATP anaerobically and produce lactic acid as a by-product. Accumulation of lactic acid is one factor responsible for the fatigue of exercising muscles. Note also that in thiamin deficiency (beriberi) there is effectively a partial block in the metabolism of carbohydrate beyond pyruvic acid because the conversion of pyruvic acid to acetyl coenzyme A requires a coenzyme, thiamin pyrophosphate, which is derived from thiamin. Lactic acid and pyruvic acid therefore also accumulate in victims of beriberi because of this metabolic block.
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
Interval aerobic exercise in individuals with advanced interstitial lung disease: a feasibility study
Published in Physiotherapy Theory and Practice, 2021
Lisa Wickerson, Dina Brooks, John Granton, W. Darlene Reid, Dmitry Rozenberg, Lianne G. Singer, Sunita Mathur
There was also a trend toward lower blood lactate accumulation during interval exercise. Exercise performed at a high intensity (e.g. > 85% VO2peak) relies on anaerobic metabolism due to depletion of intramuscular phosphocreatine and myoglobin oxygen stores, leading to accumulation of blood lactate, which is a metabolic byproduct of glycolysis (Billat, 2001). The interspersed rest intervals during interval exercise decrease muscle oxygen consumption, and can assist in re-phosphorylation of phosphocreatine, reloading myoglobin oxygen stores and facilitating lactate removal (Astrand and Rodahl, 1986; Billat, 2001). Less blood lactate accumulation during interval training has been shown to reduce ventilatory demand in COPD and diminish symptoms of dyspnea and leg discomfort (Beauchamp et al, 2010; Kortianou et al, 2010; Vogiatzis et al, 2005). The participants in this study also reported less leg fatigue after interval exercise. Lower leg fatigue and blood lactate elevation may permit a longer duration of exercise training and greater physiological muscle adaptations. One study evaluated how long people with severe COPD could tolerate high intensity exercise by comparing two symptom-limited exercise tests: a constant load exercise test at 80% Wpeak and an interval exercise test of alternating 30 seconds of 100% Wpeak: unloaded cycling (Vogiatzis et al, 2004). Participants were able to exercise longer during interval cycling compared to constant load cycling, and demonstrated lower metabolic and ventilatory responses during interval exercise (Vogiatzis et al, 2004).
Spaceflight-Associated Neuro-ocular Syndrome (SANS): a review of proposed mechanisms and analogs
Published in Expert Review of Ophthalmology, 2020
Peter Wojcik, Shehzad Batliwala, Tyler Rowsey, Laura A. Galdamez, Andrew G. Lee
CSF, lymphatic and vascular stasis can create a local ischemia, impairing perfusion, and delivery of necessary metabolites [36]. Impaired nutrient delivery shifts cells toward anaerobic metabolism and hydrogen ion accumulation. The hydrogen ions cause vasodilation of the choroidal vasculature which can compress the RPE capillaries leading to local ischemic changes that may explain the observed retinal nerve fiber layer infarcts described in SANS, according to Galdamez et al. [37,38]. Local ischemia also leads to a failure of energy-dependent cellular transport mechanisms, creating an accumulation of organelles and axoplasmic flow stasis. Kramer et al. hypothesized that stasis and ischemia could create a buildup of metabolic by-products (e.g., TNFa, metalloproteinases, and endothelin), which have been implicated in glaucoma, putting astronauts potentially at risk for nerve damage after LDSF [24].