What Insulin Resistance Actually Is, Without the Scary Graphics

The graphic you have seen is the problem

Search "what is insulin resistance" and you get some version of the same image: a cell with a locked door, a key that will not fit, and a caption about cells that have "stopped listening" to insulin. Sometimes there is a red arrow and a scary font.

That picture is not exactly wrong. It is just useless. It tells you a part broke and gives you nothing to do about it, which is why most people read it, feel vaguely alarmed, and close the tab.

I am Ravi Dewangan, CFL3, MS in Strength and Conditioning, and CrossFit Seminar Staff. I coach at Persistence Athletics in Belltown and I wrote the MetFix course, which is the free metabolic health series we teach here. This post is the explanation I open that course with, because once people have the right picture in their head the rest of the material stops feeling like memorization. Nothing here is medical advice, and I am not going to tell you what any number of yours means. Updated August 2026.

Table of Contents

• What insulin is actually doing after you eat
• The better framing: the cell is full, not deaf
• Why blood glucose can read normal for years
• The markers, and what a standard panel leaves out
• What movement does that a diet change alone does not
• How we talk about this at Persistence Athletics
• Frequently Asked Questions

What insulin is actually doing after you eat

You eat. Glucose shows up in the blood. Beta cells in the pancreas release insulin, mostly in response to carbohydrate and to a smaller degree protein.

Insulin is a message, and it says roughly three things at once:

1. To muscle and fat cells: bring glucose in. Cells do this by moving glucose transporters, the GLUT4 family, from inside the cell out to the cell surface where they can actually do the work. No transporters at the surface, no glucose entering.
2. To the liver: stop making glucose. The liver produces glucose between meals. Insulin is the signal that says the kitchen is closed for now.
3. To fat cells: hold what you have stored rather than releasing it. Fuel is arriving from outside, so there is no reason to pull it out of the tank.

That is the entire job. Insulin is a traffic signal for fuel, not a villain. Insulin resistance simply means that a given amount of that signal produces less of the usual response in those tissues.

The better framing: the cell is full, not deaf

Here is the framing I teach instead of the locked door.

Think of a warehouse with a loading dock. Insulin is the paperwork that says "sign for this delivery and put it away." The dock crew is not ignoring you out of spite. The aisles are full. There is nowhere to put another pallet. Declining the delivery is the reasonable thing to do, and the crew that signs for it anyway ends up with product stacked in the walkways.

That is closer to what appears to be happening inside a muscle or liver cell. Muscle glycogen storage is finite. When those stores stay topped up and fat also accumulates inside the muscle and liver cells themselves, one of the leading mechanistic accounts is that lipid signaling intermediates, species like diacylglycerol and ceramide, interfere with the insulin signaling cascade downstream of the receptor. The cell dials down its own response.

Read that as protection rather than malfunction. Forcing more glucose into a cell that has nowhere to put it is not a neutral act. The cell has to do something with it, and the handling has costs. Turning down the signal is the cell defending itself from a delivery it cannot store.

This matters because the two pictures point you in different directions. The broken-receiver picture suggests something needs fixing, and you have no obvious lever. The full-warehouse picture points at two levers that are actually yours: how much is arriving, and how much gets used or stored. Diet is mostly the first lever. Training is mostly the second. Most people only ever hear about the first.

Why blood glucose can read normal for years

This is the part that surprises people, and it is the single most useful thing in this post.

When cells respond less to insulin, the body does not simply let blood glucose drift up. The pancreas compensates. Beta cells release more insulin, and more insulin applied to a less responsive tissue can still get the job done. Blood glucose lands back in the usual range.

So the number on the lab report is normal. What produced that normal number is a system working considerably harder than it used to.

Picture two people with the same fasting glucose. One got there with a modest amount of insulin. The other got there with a great deal of it. The lab report cannot tell them apart, because the lab report measured the result and not the effort. That is the whole reason this condition tends to develop quietly. There is no symptom for "my pancreas is working overtime to keep this reading boring."

Two consequences follow. First, fasting insulin often starts moving well before fasting glucose does, because insulin is the thing being ramped up and glucose is the thing being defended. Second, glucose only starts to drift when the compensation stops keeping up, which can be years into the process. By the time the defended number moves, a lot has already happened.

I want to be careful here. This is a description of a general pattern, not a prediction about you. Where any individual sits, whether it matters clinically, and what to do about it are questions for a physician with your full history in front of them.

The markers, and what a standard panel leaves out

Given the above, the gap in a typical annual blood draw is easy to see.

What it measures	What it tells you	What it misses
Fasting glucose	The defended number, right now	Nothing about the effort behind it
HbA1c	Roughly the average glucose over about the past three months	Same limitation, longer window
Triglycerides and HDL	Part of the lipid picture, often shifts with this pattern	Indirect, many other inputs
Fasting insulin	The effort side of the equation	Usually not ordered by default

A standard metabolic panel and a lipid panel measure the defended numbers. Neither one measures insulin. Fasting insulin generally has to be requested specifically, and HOMA-IR, the common calculation people run, needs both fasting glucose and fasting insulin as inputs. Without the insulin value there is nothing to calculate.

So the reassuring panel is not lying. It is answering a narrower question than the one most people think they asked.

What I will not do is give you ranges. Reference intervals vary by lab, assays are not standardized across labs the way glucose assays are, and a single fasting value taken on a stressful morning after bad sleep is a snapshot. Bring the question to your doctor and ask what is worth measuring in your case.

What movement does that a diet change alone does not

Here is the mechanism that changed how I coach this.

Muscle can bring glucose in through two separate routes. One is the insulin route described above. The other is contraction itself. When a muscle contracts, calcium release and energy-sensing signals inside the cell move GLUT4 transporters to the surface without requiring insulin to ask.

Sit with that for a second. It means a contracting muscle can pull glucose out of the blood even when the insulin signal is struggling. The route that is compromised and the route that opens during exercise are not the same route.

That is why a ten or fifteen minute walk after a meal is worth more than its reputation suggests. It is not burning off the meal in any meaningful caloric sense. It is opening a second door on the largest single destination for post-meal glucose in the body, which is skeletal muscle.

Three practical implications follow from the mechanism:

• Frequency beats heroics. The improvement in insulin sensitivity after a session is real but temporary, measured in hours to a day or two rather than weeks. Three sessions spread across a week plus daily walking does more for this than one brutal weekend session.
• Strength training changes the warehouse, not just the traffic. Adding muscle over months adds storage capacity, and training raises the amount of GLUT4 the tissue has available. That is a slower lever than a post-meal walk and it compounds.
• The other 165 hours count. An hour in class three times a week is excellent. Ten hours a day in a chair is still ten hours a day in a chair. Both are true at once.

None of this replaces medical care, and none of it is a claim about outcomes. It is a description of a route your muscle already has.

How we talk about this at Persistence Athletics

Most of the people who ask me about this at the gym are Belltown desk workers, a lot of them engineers who walk the eight minutes over from Amazon for the 6:30 PM class. The usual version of the conversation starts with someone holding a phone with a lab result on it, saying their doctor said everything looked fine but something feels off.

My answer is always the same and it is deliberately boring. I am not qualified to interpret that result and I am not going to try. What I can do is explain what the panel measured and what it did not, so the person can go back and ask a better question. That is the entire job of the education side of what we do here.

On the training side, the coaching does not change much. It is group classes that contract a lot of muscle several times a week, enough protein to support the tissue you are building, which the protein timing article covers in more detail, and a walk after the meals you can manage it after. For members who want the food side structured properly, nutrition coaching is where that happens.

We also run a MetFix assessment at the gym for members who want a more thorough look at the metabolic picture. Jacque runs most of those, and she is better at that conversation than I am.

My own background and credentials are on my coach page if you want to know who is telling you this.

Frequently Asked Questions

What is insulin resistance in simple terms?

Insulin is the signal that tells muscle, liver, and fat cells to take glucose out of the blood and store it. Insulin resistance means the same amount of insulin produces less of that effect. The usual picture is a cell that has stopped listening. A more useful picture is a cell that is already full and is declining more fuel it has nowhere to put. Turning the signal down is self-protective in the short run, which is why it happens at all.

Can you have insulin resistance with normal blood sugar?

Yes, and this is common. When cells respond less to insulin, the pancreas can release more insulin to keep blood glucose in the usual range. As long as that compensation holds, a fasting glucose reading can look completely normal while the system is working much harder to produce that number. This is why fasting insulin often moves before fasting glucose does. Interpreting any individual result is a conversation for your physician, not a blog post.

Does a standard blood panel show insulin resistance?

Not directly. A standard metabolic panel measures fasting glucose, a lipid panel measures triglycerides and HDL, and HbA1c reflects average glucose over roughly the past three months. None of those measures insulin. Fasting insulin generally has to be requested separately. That is why a panel can look reassuring while the earlier part of the picture was never sampled. Ask your physician what is worth measuring in your case.

Does walking after meals help with insulin resistance?

Muscle contraction moves glucose transporters to the muscle cell surface through a route that does not require insulin. That means contracting muscle can pull glucose out of the blood even when the insulin signal is working poorly. A walk after a meal uses that route, which is why it is useful regardless of where someone is in the picture. It is a mechanism, not a treatment, and it does not replace medical care.

Is insulin sensitivity something that can change?

Insulin sensitivity is not a fixed trait. It shifts with sleep, illness, acute stress, activity, and how much storage capacity your muscle has. Short sleep alone reduces it measurably in controlled settings. How much any individual can change, how fast, and whether medication belongs in the plan are medical questions that depend on your history and labs. That conversation belongs with your doctor.

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Want the rest of it

This post is one idea out of the MetFix course, which is the free metabolic health series I wrote and teach. The course goes through the rest of it in short modules: what metabolic flexibility actually means, what mitochondria have to do with any of this, and how to read a nutrition claim without getting taken in by it. It is free and there is nothing to buy at the end of it.

Start the free course, or if you would rather see where you stand before committing to reading anything, there is a 2-minute score that takes about as long as it sounds.

If you want the training side too, your first class at Persistence Athletics in Belltown is free and scaled to wherever you are. Book a free class at 3025 1st Ave, Seattle, or call (206) 593-4236 if you would rather ask first.

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