What Is the Krebs Cycle? (Citric Acid Cycle Explained)

The Krebs cycle is the chemical heart of how your cells turn food into usable energy. It runs inside your mitochondria millions of times a second, and understanding it makes almost everything else about cellular energy and healthy aging click into place.

What is the Krebs cycle?

The Krebs cycle — also called the citric acid cycle or the tricarboxylic acid (TCA) cycle — is a closed loop of eight enzyme-driven chemical reactions that takes place inside the mitochondria, the energy-producing compartments found in nearly every cell in your body. It was mapped out by biochemist Hans Krebs in 1937, work that later earned him a Nobel Prize, and it remains one of the most thoroughly understood pathways in all of biology.

Its job is deceptively simple to state: it takes the carbon fragments left over after your body breaks down carbohydrates, fats, and proteins, and it strips high-energy electrons off those fragments. Those electrons are the real prize. They get loaded onto two carrier molecules — NADH and FADH2 — which then shuttle them to the next stage of energy production. In other words, the Krebs cycle itself makes very little finished energy. Instead, it acts as a kind of preparation line, extracting the raw electrical potential that the rest of the mitochondrion will convert into fuel.

Where it sits in the bigger energy picture

To see why the Krebs cycle matters, it helps to zoom out to the three-stage process your body uses to make ATP, the molecule that powers essentially everything a cell does.

First comes glycolysis, which happens in the fluid of the cell (not the mitochondria). Here a molecule of glucose is split into two molecules of pyruvate, releasing a small amount of energy. Pyruvate is then ferried into the mitochondrial matrix — the gel-like interior of the mitochondrion — where an enzyme complex converts it into a two-carbon molecule called acetyl-CoA. Fats and certain amino acids can also be broken down into acetyl-CoA, which is why this molecule is often described as the common currency of fuel metabolism.

Acetyl-CoA is the actual input to the Krebs cycle. When it enters, it joins with a four-carbon molecule called oxaloacetate to form citrate (hence "citric acid cycle"). Over the next seven reactions, the cycle gradually rearranges and oxidizes this citrate, releasing two molecules of carbon dioxide (which you exhale), regenerating oxaloacetate so the loop can begin again, and — crucially — capturing electrons as NADH and FADH2. Per turn of the cycle, it typically yields three NADH, one FADH2, and one molecule of GTP (a close cousin of ATP). Because each glucose produces two acetyl-CoA, the cycle turns twice for every glucose molecule.

The electrons captured here then feed into the electron transport chain, where oxidative phosphorylation finally produces the bulk of your ATP. This is the stage that actually consumes the oxygen you breathe. So the Krebs cycle is the middle act of cellular respiration: glycolysis sets it up, the Krebs cycle extracts the electrons, and the electron transport chain cashes them in.

The eight steps, in plain language

You do not need to memorize the enzymes to grasp the logic. Here is the cycle as a story rather than a diagram.

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Acetyl-CoA (two carbons) combines with oxaloacetate (four carbons) to make citrate (six carbons). Citrate is then rearranged into a nearly identical molecule, isocitrate, which is better positioned for the oxidation steps that follow.

The first energy-releasing steps

Isocitrate is oxidized, releasing a molecule of carbon dioxide and generating the cycle's first NADH. The resulting five-carbon molecule is oxidized again, releasing a second carbon dioxide and a second NADH, and producing a four-carbon compound bound to CoA. These two steps are where most of the carbon you "burn" actually leaves as exhaled CO2.

Harvesting the rest

The remaining reactions regenerate oxaloacetate while producing one molecule of GTP (which can be converted to ATP), one FADH2, and a third NADH. With oxaloacetate restored, the cycle is ready to accept the next acetyl-CoA, and the loop closes. Nothing is wasted: the four-carbon backbone is recycled indefinitely, which is why a small pool of intermediates can process an enormous throughput of fuel.

Why the Krebs cycle is central to healthy aging

Here is the connection that makes this pathway more than a textbook curiosity. The Krebs cycle and the electron transport chain run on the same mitochondrial hardware. When mitochondria become fewer in number, damaged, or less efficient — a well-documented feature of aging and inactivity — the whole energy pipeline slows. Fuel still enters, but fewer usable electrons get converted into ATP, and more escape as reactive byproducts that can contribute to oxidative stress.

Researchers describe a decline in mitochondrial function with age, and it tends to show up first in tissues with high energy demands, such as muscle. This is part of why energy, endurance, and recovery can feel harder to come by over time even when the Krebs cycle itself is working exactly as designed — the problem is often not the recipe, but the number and quality of the kitchens running it.

This is where quality-control processes come in. Cells continuously renew their mitochondrial population through a housekeeping process called mitophagy, which clears out worn, underperforming mitochondria so that the remaining pool stays efficient. Supporting that renewal is the mechanism behind urolithin A, the compound SOMA HEALTH is built around.

How urolithin A fits in

Urolithin A is a postbiotic — a compound your gut bacteria produce from ellagitannins found in foods like pomegranates and walnuts. In foundational preclinical research (Ryu et al., 2016, Nature Medicine), urolithin A was shown to stimulate mitophagy and improve muscle function in rodents and extend lifespan in the worm C. elegans. That work is on animals and cells, not proof in humans, but it established the mechanism. In humans, a first-in-human trial (Andreux et al., 2019, Nature Metabolism) found urolithin A was safe and well tolerated up to 1,000 mg/day and produced a mitochondrial gene-expression signature in older adults. Later randomized human trials (Singh et al., 2022, Cell Reports Medicine; Liu/D'Amico et al., 2022, JAMA Network Open) reported benefits for muscle strength, endurance, and exercise performance over roughly four months. A 2025 randomized placebo-controlled trial in Nature Aging reported support for immune-cell mitochondrial health in midlife adults.

Importantly, urolithin A does not change the chemistry of the Krebs cycle. What the research suggests it supports is the upstream condition the cycle depends on: a cleaner, more functional pool of mitochondria to run it. You can read the full evidence base, with human and preclinical studies separated, on our clinical studies page.

Common misconceptions

A few myths are worth clearing up. First, the Krebs cycle does not "produce most of your energy" — it produces only a small amount directly. Its real contribution is the electrons it hands off. Second, it is not exclusively a carbohydrate pathway; fats and proteins feed in through acetyl-CoA and other intermediates, which is why your body can keep making energy during fasting or on a low-carbohydrate diet. Third, the cycle is not a one-way assembly line that can be "sped up" by willpower or by a single nutrient; its pace is governed by the cell's energy demand and the availability of oxygen and electron carriers downstream.

Supporting your mitochondria day to day

If the Krebs cycle is the engine's combustion chamber, then the number and condition of your mitochondria are the number and condition of the engines. The best-supported lever for building more and better mitochondria is exercise, especially a mix of endurance and resistance training, which signals the cell to make new mitochondria. Adequate protein, sleep, and managing chronic stress all play supporting roles. For people looking to add a studied compound to that foundation, urolithin A is among the most rigorously researched options for mitochondrial support.

*These statements have not been evaluated by the Food and Drug Administration. This product is not intended to diagnose, treat, cure, or prevent any disease. This guide is educational and is not a substitute for advice from a qualified healthcare provider.