Low Carb Diet,FFAs, High Free Tryptophan, Serotonin ,fatigue

paymanz

Member
Joined
Jan 6, 2015
Messages
2,693
Also the question of "does a high fat meal increase free fatty acid levels?"
The answer is yes!it does.

Low-Carbohydrate-High-Fat Diet: Can it Help Exercise Performance?


Low-carbohydrate-high-fat (LCHF) diets have been used as a means of weight loss and control of symptoms in several clinical conditions. There is emerging evidence that the metabolic changes induced by LCHF diets enhance endurance performance. The aims of this review are to examine the evidence of LCHF diets in improving various aspects of athletic performance. Long-term LCHF dietary intake may help control body weight and fat mass while maintaining lean body mass in athletes in weight-sensitive sports. LCHF-adapted endurance athletes can reach the maximal fat oxidation rate of approximately 1.5 g/min, with a lower carbohydrate oxidation rate and similar muscle glycogen content and a resynthesis rate compared to their counterparts consuming high-carbohydrate-low-fat (HCLF) diets. The elevated fat oxidation rate and glycogen sparing effect may improve performance in ultra-endurance events. These metabolic changes may also prevent the decline in performance in later stages of repeated high-intensity movements, in which the aerobic metabolism becomes more important. However, elevated blood concentrations of non-esterified fatty acids and ammonia during exercise after LCHF diets may lead to early development of central fatigue. It appears that at least several months of adaptation to a LCHF diet are required for the metabolic changes and restoration of muscle glycogen to occur. Further investigations on LCHF diets are needed regarding (1) performance after weight loss in weight-categorized sports; (2) repeated high-intensity exercise performance; (3) development of central fatigue during endurance events; (4) perceptual-motor performance during prolonged intermittent sports; and (5) ideal dietary fatty acid compositions.

.....

The increased rate of fat oxidation during exercise after adaptation to a LCHF diet is likely to increase brain uptake of free tryptophan. This is the consequence of increased competition for binding to albumin by rising concentrations of NEFA. Free tryptophan is the precursor of serotonin (5-hydroxytryptamine), a brain neurotransmitter associated with the feeling of lethargy and tiredness that may contribute to the loss of central drive and motivation (Davis and Bailey, 1997). Increased brain uptake of free tryptophan has been reported to favor cerebral serotonin synthesis and contribute to central fatigue (Pardridge, 1998).

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Exercise, Serum Free Tryptophan, and Central Fatigue

Abstract
Brain tryptophan (TRP) concentrations and serotonin (5HT) synthesis and release increase during running. This increase in 5HT function may promote central fatigue and contribute to suboptimal physical performance. The rise in brain TRP is reputed to result from exercise-induced elevations in serum nonesterified fatty acid (NEFA) concentrations, which dissociate TRP from albumin in blood and increase the serum free TRP pool. But, as discussed in this article, ample evidence exists that the serum free TRP pool does not control brain TRP uptake. The clearest data are dietary, but pharmacologic data in exercising rats also support this conclusion. Changes in the serum levels of amino acids that compete with TRP for brain uptake appear also not to explain the rise in brain TRP. The mechanism is therefore not presently known. The link between the rise in brain TRP and 5HT synthesis/release is not simple: a rise in brain TRP stimulates 5HT synthesis/release in actively firing neurons. Hence, during exercise, only 5HT neurons that are firing should increase 5HT production/release when brain TRP rises. It is not known which 5HT neurons fire during exercise; the 5HT neurons that respond to exercise-induced increases in brain TRP are therefore not known. Hence, it is not possible to conclude which 5HT neurons contribute to the generation of central fatigue. Because some 5HT neurons control specific functions important to physical performance (e.g., respiration), the current understanding of 5HT neuronal function in central fatigue might benefit from the study of specific 5HT pathways during exercise.

.....


The 45% fat meal raised serum NEFA and produced a 2-fold rise in serum free TRP concentrations (compared with values in fasting rats or rats ingesting the 0% fat meal)


Tryptophan, serotonin, and aging
The fatigue produced by “over-training” is probably produced by a tryptophan and serotonin overload, resulting from catabolism of muscle proteins and stress-induced increases in serotonin. Muscle catabolism also releases a large amount of cysteine, and cysteine, methionine, and tryptophan suppress thyroid function (Carvalho, et al., 2000). Stress also liberates free fatty acids from storage, and these fatty acids increase the uptake of tryptophan into the brain, increasing the formation of serotonin. Since serotonin increases ACTH and cortisol secretion, the catabolic state tends to be self-perpetuating. This process is probably a factor influencing the rate of aging, and contributing to the physiological peculiarities of aging and depression.

Malnutrition, and specifically protein deficiency, produces an inflammatory state that involves extreme serotonin dominance. Stress or malnutrition prenatally or in infancy leads to extreme serotonin dominance in adulthood. Other functions of tryptophan are reduced, as more of it is turned into serotonin.

Decreasing tryptophan or decreasing serotonin improves learning and alertness, while increased serotonin impairs learning.

Some researches believe free tryptophan may not affect brain level of the amino acid.

But even with that , you still have it in prepheral level to increase prepheral level of serotonine.
 
Last edited:

Jackrabbit

Member
Joined
Jun 29, 2018
Messages
172
Also the question of "does a high fat meal increase free fatty acid levels?"
The answer is yes!it does.

Low-Carbohydrate-High-Fat Diet: Can it Help Exercise Performance?


Low-carbohydrate-high-fat (LCHF) diets have been used as a means of weight loss and control of symptoms in several clinical conditions. There is emerging evidence that the metabolic changes induced by LCHF diets enhance endurance performance. The aims of this review are to examine the evidence of LCHF diets in improving various aspects of athletic performance. Long-term LCHF dietary intake may help control body weight and fat mass while maintaining lean body mass in athletes in weight-sensitive sports. LCHF-adapted endurance athletes can reach the maximal fat oxidation rate of approximately 1.5 g/min, with a lower carbohydrate oxidation rate and similar muscle glycogen content and a resynthesis rate compared to their counterparts consuming high-carbohydrate-low-fat (HCLF) diets. The elevated fat oxidation rate and glycogen sparing effect may improve performance in ultra-endurance events. These metabolic changes may also prevent the decline in performance in later stages of repeated high-intensity movements, in which the aerobic metabolism becomes more important. However, elevated blood concentrations of non-esterified fatty acids and ammonia during exercise after LCHF diets may lead to early development of central fatigue. It appears that at least several months of adaptation to a LCHF diet are required for the metabolic changes and restoration of muscle glycogen to occur. Further investigations on LCHF diets are needed regarding (1) performance after weight loss in weight-categorized sports; (2) repeated high-intensity exercise performance; (3) development of central fatigue during endurance events; (4) perceptual-motor performance during prolonged intermittent sports; and (5) ideal dietary fatty acid compositions.

.....

The increased rate of fat oxidation during exercise after adaptation to a LCHF diet is likely to increase brain uptake of free tryptophan. This is the consequence of increased competition for binding to albumin by rising concentrations of NEFA. Free tryptophan is the precursor of serotonin (5-hydroxytryptamine), a brain neurotransmitter associated with the feeling of lethargy and tiredness that may contribute to the loss of central drive and motivation (Davis and Bailey, 1997). Increased brain uptake of free tryptophan has been reported to favor cerebral serotonin synthesis and contribute to central fatigue (Pardridge, 1998).

View attachment 6666

Exercise, Serum Free Tryptophan, and Central Fatigue

Abstract
Brain tryptophan (TRP) concentrations and serotonin (5HT) synthesis and release increase during running. This increase in 5HT function may promote central fatigue and contribute to suboptimal physical performance. The rise in brain TRP is reputed to result from exercise-induced elevations in serum nonesterified fatty acid (NEFA) concentrations, which dissociate TRP from albumin in blood and increase the serum free TRP pool. But, as discussed in this article, ample evidence exists that the serum free TRP pool does not control brain TRP uptake. The clearest data are dietary, but pharmacologic data in exercising rats also support this conclusion. Changes in the serum levels of amino acids that compete with TRP for brain uptake appear also not to explain the rise in brain TRP. The mechanism is therefore not presently known. The link between the rise in brain TRP and 5HT synthesis/release is not simple: a rise in brain TRP stimulates 5HT synthesis/release in actively firing neurons. Hence, during exercise, only 5HT neurons that are firing should increase 5HT production/release when brain TRP rises. It is not known which 5HT neurons fire during exercise; the 5HT neurons that respond to exercise-induced increases in brain TRP are therefore not known. Hence, it is not possible to conclude which 5HT neurons contribute to the generation of central fatigue. Because some 5HT neurons control specific functions important to physical performance (e.g., respiration), the current understanding of 5HT neuronal function in central fatigue might benefit from the study of specific 5HT pathways during exercise.

.....


The 45% fat meal raised serum NEFA and produced a 2-fold rise in serum free TRP concentrations (compared with values in fasting rats or rats ingesting the 0% fat meal)


Tryptophan, serotonin, and aging


Some researches believe free tryptophan may not affect brain level of the amino acid.

But even with that , you still have it in prepheral level to increase prepheral level of serotonine.

All these people who think the high protein/fat diet is the answer and consider bacon to be super healthy! It’s al fat and protein, therefore good. I feel bad for these people in twenty years!
 
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