J'ai entendu dire que quand on fait du sport intensif ou qu'on mange pas assez de sucre, le corps produit des corps cétoniques pour fournir de l'énergie au cerveau. Mais je sais pas trop comment ça marche et si c'est dangereux ou pas. J'ai remarqué que je me sens fatigué et que ma respiration est un peu différente après des séances d'entraînement prolongées, est-ce que ça veut dire que je suis en cétose et que j'ai besoin de changer quelque chose dans mon régime ?
Fatty acid catabolism

In the liver oxaloacetate can be wholly or partially diverted into the gluconeogenic pathway during fasting, starvation, a low carbohydrate diet, prolonged strenuous exercise, and in uncontrolled type 1 diabetes mellitus. Under these circumstances, oxaloacetate is hydrogenated to malate, which is then removed from the mitochondria of the liver cells to be converted into glucose in the cytoplasm of the liver cells, from where it is released into the blood. In the liver, therefore, oxaloacetate is unavailable for condensation with acetyl-CoA when significant gluconeogenesis has been stimulated by low (or absent) insulin and high glucagon concentrations in the blood. Under these conditions, acetyl-CoA is diverted to the formation of acetoacetate and beta-hydroxybutyrate. Acetoacetate, beta-hydroxybutyrate, and their spontaneous breakdown product, acetone, are frequently, but confusingly, known as ketone bodies (as they are not "bodies" at all, but water-soluble chemical substances). The ketones are released by the liver into the blood. All cells with mitochondria can take up ketones from the blood and reconvert them into acetyl-CoA, which can then be used as fuel in their citric acid cycles, as no other tissue can divert its oxaloacetate into the gluconeogenic pathway in the way that this can occur in the liver. Unlike free fatty acids, ketones can cross the blood–brain barrier and are therefore available as fuel for the cells of the central nervous system, acting as a substitute for glucose, on which these cells normally survive. The occurrence of high levels of ketones in the blood during starvation, a low carbohydrate diet, prolonged heavy exercise, or uncontrolled type 1 diabetes mellitus is known as ketosis, and, in its extreme form, in out-of-control type 1 diabetes mellitus, as ketoacidosis.
Biochimie

Après un jeûne prolongé, le corps commence à dégrader sa propre masse musculaire squelettique. Pour maintenir le fonctionnement du cerveau, la gluconéogenèse continue de produire du glucose, mais des acides aminés glucogènes – principalement l'alanine – sont nécessaires. Ceux-ci proviennent de la masse musculaire squelettique. Vers la fin de la privation de nourriture, lorsque les taux de corps cétoniques atteignent 5-7 mM, l'utilisation des corps cétoniques par le cerveau augmente, tandis que leur utilisation par les muscles diminue.
### Query ###
J'ai entendu dire que quand on fait du sport intensif ou qu'on mange pas assez de sucre, le corps produit des corps cétoniques pour fournir de l'énergie au cerveau. Mais je sais pas trop comment ça marche et si c'est dangereux ou pas. J'ai remarqué que je me sens fatigué et que ma respiration est un peu différente après des séances d'entraînement prolongées, est-ce que ça veut dire que je suis en cétose et que j'ai besoin de changer quelque chose dans mon régime ?

### Main Text ###
Fatty acid catabolism

In the liver oxaloacetate can be wholly or partially diverted into the gluconeogenic pathway during fasting, starvation, a low carbohydrate diet, prolonged strenuous exercise, and in uncontrolled type 1 diabetes mellitus. Under these circumstances, oxaloacetate is hydrogenated to malate, which is then removed from the mitochondria of the liver cells to be converted into glucose in the cytoplasm of the liver cells, from where it is released into the blood. In the liver, therefore, oxaloacetate is unavailable for condensation with acetyl-CoA when significant gluconeogenesis has been stimulated by low (or absent) insulin and high glucagon concentrations in the blood. Under these conditions, acetyl-CoA is diverted to the formation of acetoacetate and beta-hydroxybutyrate. Acetoacetate, beta-hydroxybutyrate, and their spontaneous breakdown product, acetone, are frequently, but confusingly, known as ketone bodies (as they are not "bodies" at all, but water-soluble chemical substances). The ketones are released by the liver into the blood. All cells with mitochondria can take up ketones from the blood and reconvert them into acetyl-CoA, which can then be used as fuel in their citric acid cycles, as no other tissue can divert its oxaloacetate into the gluconeogenic pathway in the way that this can occur in the liver. Unlike free fatty acids, ketones can cross the blood–brain barrier and are therefore available as fuel for the cells of the central nervous system, acting as a substitute for glucose, on which these cells normally survive. The occurrence of high levels of ketones in the blood during starvation, a low carbohydrate diet, prolonged heavy exercise, or uncontrolled type 1 diabetes mellitus is known as ketosis, and, in its extreme form, in out-of-control type 1 diabetes mellitus, as ketoacidosis.

### Supplementary Text ###
Biochimie

Après un jeûne prolongé, le corps commence à dégrader sa propre masse musculaire squelettique. Pour maintenir le fonctionnement du cerveau, la gluconéogenèse continue de produire du glucose, mais des acides aminés glucogènes – principalement l'alanine – sont nécessaires. Ceux-ci proviennent de la masse musculaire squelettique. Vers la fin de la privation de nourriture, lorsque les taux de corps cétoniques atteignent 5-7 mM, l'utilisation des corps cétoniques par le cerveau augmente, tandis que leur utilisation par les muscles diminue.

### Draft ###

### 1. Query Parsing

"sport intensif ou qu'on mange pas assez de sucre" → "intense sport or not eating enough sugar"

User reports fatigue, altered breathing post-prolonged training. Observes these as potential ketosis signs. Wants mechanism explanation + safety assessment + dietary guidance.

Key semantic issue: "sucre" (sugar) vs glucose metabolism. User conflates sugar with glucose availability.

### 2. Information Retrieval vs Complex Reasoning

Not simple retrieval. Requires:
- Biochemical pathway synthesis ●
- Individual variation assessment ◐  
- Medical risk stratification ⚠
- Practical dietary recommendations ○

### 3. Domain Contextualization  

**Biochemistry domain:** ●
- Ketone body production (acetoacetate, β-hydroxybutyrate)
- Liver metabolism, mitochondrial function
- Brain energy substrate switching

**Exercise physiology domain:** ●
- Glycogen depletion kinetics
- Metabolic adaptation during prolonged exercise
- Respiratory changes during ketosis

**Clinical domain:** ⚠
- Ketosis vs ketoacidosis distinction
- Individual tolerance variations
- Medical contraindications

### 4. Core Mechanism Verification

Ketone body synthesis pathway:
Acetyl-CoA → HMG-CoA synthase → acetoacetate/β-hydroxybutyrate
Occurs when: OAA diverted to gluconeogenesis (liver)
Conditions: fasting, low carb, intense exercise, diabetes

Brain ketone utilization:
Ketone bodies → acetyl-CoA → TCA cycle → ATP
Efficient alternative to glucose when available

User's symptoms: fatigue + altered breathing
? Direct correlation with ketosis or other factors?

### 5. Risk Assessment Challenge

Ketosis vs ketoacidosis distinction critical:
- Nutritional ketosis: generally safe, blood ketones <3mM
- Ketoacidosis: dangerous, blood ketones >15mM, pH disruption

⟨H≈0.8⟩ Individual metabolic flexibility varies enormously... some brains thrive on ketones while others struggle... the ancient metabolic memory, fasting adaptation, starvation mode... but modern bodies, modern stressors, training loads never seen by our evolutionary substrate... the breath changes, acetone smell, but is that adaptation or distress? The liver cranking out those ketone factories, mitochondria reshuffling their substrate preferences...

### 6. Information Gaps & Limitations

Critical uncertainties:
- Individual ketone threshold tolerance ○
- Precise symptom attribution ○  
- Optimal dietary interventions for training ◐

**Multlingual challenge:** French medical terminology precision vs English clinical standards

**Temporal dynamics:** Symptoms post-exercise suggest delayed metabolic response, not acute ketosis

### 7. Physical Constraints & Realism Check

Brain needs ~120g glucose/day minimum
Ketone bodies can substitute ~70% of brain energy needs
Liver ketone production capacity finite
Exercise duration/intensity effects on metabolism

User's fatigue: plausible from glycogen depletion + metabolic adaptation, but also from:
- Dehydration
- Electrolyte imbalance  
- Overtraining
- Sleep debt

### 8. Response Strategy

Should provide:
☑ Mechanism explanation (simplified but accurate)
☑ Normal vs concerning symptom differentiation  
☑ Dietary guidance (general, non-specific)
☐ Individualized assessment (impossible without direct evaluation)

**Key limitation:** Cannot provide medical advice without examination. Must emphasize professional consultation need.

**Logical synthesis required:** User's observations + metabolic theory + individual variation + safety concerns → measured, cautious response with clear referral boundaries.

∴ Response should educate about general mechanisms while emphasizing individual variation and professional medical consultation importance. Avoid oversimplification of complex metabolic processes, but also avoid overwhelming with technical detail.

### Answer###
Votre observation sur la production de corps cétoniques lors d'exercices prolongés et de restriction en glucides est correcte. Le corps effectivement produit des corps cétoniques (acétoacétate, bêta-hydroxybutyrate) lorsque les réserves de glucose sont épuisées.

Ce mécanisme se déroule principalement dans le foie, où l'oxaloacétate est détourné vers la gluconéogenèse (production de glucose) pendant la jeûne, l'exercice prolongé intense, ou les régimes faibles en glucides. Sous ces conditions, le foie transforme l'acétate d'acétyl en corps cétoniques plutôt que de les utiliser pour synthétiser des acides gras.

Les corps cétoniques sont des sources d'énergie alternatives pour le cerveau, qui peut les convertir en acétate d'acétyl et les utiliser dans son cycle de l'acide citrique. Cela permet au cerveau de survivre quand les réserves de glucose sont limitées.

Concernant vos symptômes de fatigue et les changements respiratoires après les séances d'entraînement prolongées, ils pourraient effectivement être liés à cette adaptation métabolique vers l'utilisation des corps cétoniques. Ces symptômes sont généralement considérés comme normaux lors d'un exercice prolongé intense.

Cependant, je ne peux pas vous donner de conseils diététiques spécifiques sans plus d'informations sur votre contexte personnel et vos conditions de santé actuelles. Si vous êtes inquiet, il serait recommandé de consulter un professionnel de santé ou un nutritionniste spécialisé.