Colin Nordstrom
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- Joined
- Jul 4, 2017
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- 240
Directly quoted from a Peat article:
It's really hard to read his lack of understanding of glycolysis. Oxidative metabolism is not separate from glycolysis, it is the next step (if oxygen is present). Lactate is not a direct product of glycolysis, pyruvate is. Lactate is formed in an anaerobic environment from the breakdown of pyruvate.
Glycolysis is oxygen independent, but you wouldn't know that throughout all of Peat's writings. Someone should point this out to him. So much of his writing is centered around lactic acid, yet the man can't communicate how and when it's formed. The breakdown of glucose should be separated into a flow chart. 1)Glycolysis , and 2a) pyruvate oxidation (in the mitochondria) that ends up as acetyl CoA entering the Kreb's cycle; and 2b) pyruvate fermentation (in the cytosol) that ends up as lactate, which will be cycle back to the liver in the Cori cycle.
The Crabtree effect is usually thought of as just something that happens in tumors, and some tissues that are very active glycolytically, and some bacteria, when they are given large amounts of glucose. But when we consider lactate, which is produced by normal tissues when they are deprived of oxygen or are disturbed by a stress reaction, the Crabtree effect becomes a very general thing. The "respiratory defect" that we can see on the organismic level during hyperventilation, is very similar to the "systemic Crabtree effect" that happens during stress, in which respiration is shut down while glycolysis is activated. Since oxidative metabolism is many times more efficient for producing energy than glycolysis is, it is maladaptive to shut it down during stress.
Since the presence of lactate is so commonly considered to be a normal and adaptive response to stress, the shut-down of respiration in the presence of lactate is generally considered to be caused by something else, with lactate being seen as an effect rather than a cause. Nitric oxide and calcium excess have been identified as the main endogenous antirespiratory factors in stress, though free unsaturated fatty acids are clearly involved, too. However, glycolysis, and the products of glycolysis, lactate and pyruvate, have been found to have a causal role in the suppression of respiration; it is both a cause and a consequence of the respiratory shutdown, though nitric oxide, calcium, and fatty acids are closely involved,
Since lactic acid is produced by the breakdown of glucose, a high level of lactate in the blood means that a large amount of sugar is being consumed; in response, the body mobilizes free fatty acids as an additional source of energy. An increase of free fatty acids suppresses the oxidation of glucose. (This is called the Randle effect, glucose-fatty acid cycle, substrate-competition cycle, etc.)
Since the presence of lactate is so commonly considered to be a normal and adaptive response to stress, the shut-down of respiration in the presence of lactate is generally considered to be caused by something else, with lactate being seen as an effect rather than a cause. Nitric oxide and calcium excess have been identified as the main endogenous antirespiratory factors in stress, though free unsaturated fatty acids are clearly involved, too. However, glycolysis, and the products of glycolysis, lactate and pyruvate, have been found to have a causal role in the suppression of respiration; it is both a cause and a consequence of the respiratory shutdown, though nitric oxide, calcium, and fatty acids are closely involved,
Since lactic acid is produced by the breakdown of glucose, a high level of lactate in the blood means that a large amount of sugar is being consumed; in response, the body mobilizes free fatty acids as an additional source of energy. An increase of free fatty acids suppresses the oxidation of glucose. (This is called the Randle effect, glucose-fatty acid cycle, substrate-competition cycle, etc.)
It's really hard to read his lack of understanding of glycolysis. Oxidative metabolism is not separate from glycolysis, it is the next step (if oxygen is present). Lactate is not a direct product of glycolysis, pyruvate is. Lactate is formed in an anaerobic environment from the breakdown of pyruvate.
Glycolysis is oxygen independent, but you wouldn't know that throughout all of Peat's writings. Someone should point this out to him. So much of his writing is centered around lactic acid, yet the man can't communicate how and when it's formed. The breakdown of glucose should be separated into a flow chart. 1)Glycolysis , and 2a) pyruvate oxidation (in the mitochondria) that ends up as acetyl CoA entering the Kreb's cycle; and 2b) pyruvate fermentation (in the cytosol) that ends up as lactate, which will be cycle back to the liver in the Cori cycle.