Consider a series of metabolic events during fasting. Within a few days after a fast begins, nitrogen excretion accelerates to a higher‑than‑normal level. After a few weeks, the rate of nitrogen excretion falls to a lower level and continues at this low rate. However, after the fat stores have been depleted, nitrogen excretion rises to a high level. Identify the process that triggers the initial surge of nitrogen excretion. depletion of fatty acid stores depletion of glycogen stores nucleic acid breakdown liver damage Identify the process responsible for the fall in nitrogen excretion after several weeks of fasting. nucleic acid synthesis protein synthesis fatty acid breakdown glycogen breakdown

A series of events occur, in prolonged fasting; the body undergoes changes and adaptations of its metabolism to continue to meet energy needs and maintain vital functions, despite not receiving food

These changes are divided into three phases according to the elapsed days of fasting and according to the metabolic processes involved.

First phase: main consumption of reserve carbohydrates.

Second phase: main consumption of fats.

Third phase: serious consumption of proteins.

Explanation:

If the fast is prolonged in time, the metabolic processes change in their qualitative and quantitative characteristics, so that the energy products consumed (glucose, free fatty acids and ketone bodies) are modified, their oxidation decreases globally and after the initial depletion of hepatic and muscular glycogen and protein catabolism, the main source of glucose is the liver through gluconeogenesis. The substrates initially come from protein catabolism and lipolysis, but later protein destruction slows down, maximizing lipolysis.

Between the first phase and the second phase of the fast some muscle proteins are lost but not excessively, even with fasts of two or three weeks.

After about 2 weeks of fasting, up to two-thirds of the energy the brain needs is obtained from ketone bodies. These ketone bodies are the breakdown products of fats and are responsible for the typical ketone breath reminiscent of the smell of acid apples; urine also smells like ketone.

In this phase, damage begins to occur in some important organs such as the liver and kidneys. Starting the first week of fasting, acidosis affects the heart's function of the circulation and the brain.

In the third phase of the prolonged fast it happens from 3 weeks, that is, about twenty days without food, although it varies according to the constitution of each person. A peak of muscle protein consumption occurs and a great loss of weight begins to be perceived with great weakness. Edema occurs and albumin concentration in the blood is altered, as a sign of the self-digestion of muscle proteins.

From approximately 30 days of fasting, the state of malnutrition severely affects all body systems. After forty or fifty days the deterioration is noticeable due to physical wear, the person loses his mobility and suffers from unconsciousness. Finally, starvation death can occur from cardiorespiratory arrest or from lack of blood supply to the brain.

When one enters into very long fasts, he begins to expend the energy of the energy reserves coming from the ingestion of carbohydrates, therefore from the glycogen that is in reserve form in the muscles and liver.

Once this reserve is depleted, the decrease in body weight begins but due to the degradation of fatty acids or fatty / adipose tissue, thus generating an increase in body ketones and metabolic ketoacidosis (which is considered a great risk for the central nervous system ). When the fat energy reserves run out, if fasting continues, the next energy source will be all protein compounds, and it is for this reason that by disintegrating proteins and breaking them down, levels of nitrogen and ammonia increase (there are scientific studies that even support that the own muscular mass is consumed in extreme cases).

This triggers an increase in heart rate, demanding more energy not only metabolic but also heart. Many essential enzymes that are proteins are used as a reserve source and it is this that leads...

The increase in uric acid in extreme cases is also present, that is why some specialists associate the disease "gout" with long-term fasting.

Explanation:

In summary, the processes that take place as a result of fasting, would have the following chronology:

- First 24-48h: Consumption of circulating and stored glucose. Decreased glycemia and insulin, increased glucagon, initiation of hepatic neoglycogenesis, with muscle proteolysis and mobilization of triglycerides in adipose tissue that will be broken down by lipolysis, the glycerol obtained is processed when introduced as a substrate for glycolysis and fatty acids undergo its successive fragmentation into cc acetyl (mitochondrial beta oxidation) suitable for introduction into the Krebs cycle in the same way as acetyl from glycolysis or some amino acids.

- From the third day: the Krebs cycle (main source of ATP) is slowed down due to the lack of the oxalacetate that is being used for neoglycogenesis in order to not lack glucose to the brain, there is a main consumption of lipids. Acetyls that cannot be used in the Krebs cycle are exported to the blood from the liver as acetoacetate (2-acetyl or 4-carbon chain) to meet the energy needs of the myocardium and 1/3 of the brain's needs. Duration 40 days for a man of 70 Kg and 1.70 m tall. Proteins are consumed in the first days for neoglycogenesis, then they try to save, by using this alternative acetoacetate consumption, to avoid the deterioration that comes from basing the energy supply on the use of high-value proteins.

. The brain begins to use ketone bodies (acetoacetate) to fully adapt to the weeks of fasting and thus save protein.

- Last stage where the reserves have been exhausted and the essential proteins for life are consumed, with the risk that this entails. The brain has already adapted to the consumption of ketone bodies, but as these are insufficient, it requires protein-consuming neoglycogenesis.

 Everything described for fasting in a previously healthy person takes on special importance in the patient, who by multiple mechanisms may have limited nutrient supply. It may also have its metabolic demands modified with respect to a baseline situation and the possible corrective mechanisms for the normal functioning of the energy obtaining processes and the essential biological synthesis may be hindered according to its pathology.

 The consequence of all this is that we must maintain special attention to nutritional needs during illness, especially when it is prolonged. It is not uncommon that absorbed in the diagnostic process and treatment of fundamental pathology, we neglect nutritional care, thereby compromising the final results, which is what ultimately matters.

both anaerobic and aerobic respiration use glucose (or other carbohydrates), proteins and lipids to produce atp and nadh. cell uses those energy molecules, obtained from food and   breaks them down during the chemical reactions of respiration. in anaerobic respiration, nadh is regenerated to nad+ by enzymes lactate dehydrogenase (lactate is produced, e.g. in muscle cells) or by alcohol dehydrogenase where ethanol is produced (alcohol fermentation), while in aerobic respiration, electrons from nadh are deposited in the mitochondria to regenerate nad+ (electron transport chain. anaerobic respiration produces 2 atp per molecule of glucose compared to aerobic respiration where about 38 atp molecules are produced.

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