"Anything Meds Can Do, You Can Do Better" Part 3A of 12 - Insulin Resistance in the Muscles

The Diabetes Podcast — Insulin Resistance in the Muscles (Part 1 of 2)

In this episode, we dig into Insulin Resistance in the Muscles. This is Part 1 of a two-part deep dive.

We keep it real, simple, and helpful. If you want clear steps to lower blood sugar and feel better, you’re in the right place.

Episode Summary

• Insulin is a hormone. Think of it like a key. It opens your cells so sugar (glucose) can get in and be used for energy.
• When cells don’t respond well to insulin, that’s insulin resistance. Your body then makes more insulin to push sugar into cells. Over time, this is hard on your body and can raise weight.
• Insulin Resistance in the Muscles matters a lot. Your muscles take up about 80% of the sugar after you eat. When muscle cells resist insulin, blood sugar stays higher.
• Good news: exercise gives your muscles a second door for sugar that does not need insulin. Even a short walk after meals helps. The benefits can last up to 48 hours.

What You’ll Learn

• What insulin does in your body (in simple words)
• How high insulin makes fat loss harder
• What causes insulin resistance
• How to test insulin resistance (fasting insulin)
• Why muscle is the main player for blood sugar control
• How movement opens a second pathway for sugar to get into muscle
• Easy walking tips that lower blood sugar fast

Key Topics and Timestamps

• 00:00 — Welcome to The Diabetes Podcast
• 00:01 — Insulin 101: the “key and lock” idea
• 00:03 — Where sugar goes: energy now or stored as glycogen or fat
• 00:04 — High insulin = storage mode (harder to burn fat)
• 00:05 — Causes of insulin resistance: too much refined food, too little movement, visceral fat, poor sleep, stress
• 00:08 — How to test: fasting insulin; why doctors don’t always order it
• 00:11 — High insulin can be there 10–20 years before a diabetes diagnosis
• 00:13 — The ripple effect: triglycerides, VLDL, HDL, and blood vessel risk
• 00:16 — Visceral fat is active tissue; it sends signals and raises inflammation
• 00:17 — Big point: muscles handle ~80% of post-meal glucose
• 00:18 — The exercise “second door”: AMPK, GLUT4, and RAC1 (simple explainers)
• 00:21 — The 48-hour window after exercise; real client story
• 00:24 — Research highlights: 30-min brisk walk, 2–5 min movement, and 10 min after meals
• 00:27 — Part 2 teaser: meds for muscle insulin resistance and what to do next

Insulin, Made Simple

• Insulin is made by your pancreas.
• It helps sugar (from carbs like glucose, fructose, lactose) move from your blood into your cells.
• Cells use sugar for energy to breathe, move, and live.
• Sugar can also be stored in your liver and muscles as glycogen. Extra can be stored as fat.
• Insulin also tells your liver to stop making more sugar when you have enough.

When insulin is high for a long time, your body is in “storage mode.” That makes fat loss harder.

What Causes Insulin Resistance?

• Too much refined food (white bread, sweets, sugary drinks, ultra-processed snacks)
• Too little movement (a sedentary day)
• Visceral fat (fat around your belly and organs)
• Poor sleep and chronic stress (raises cortisol and lowers insulin sensitivity)

In short: too much energy in, not enough energy out, and stress on the system.

How Do I Know If I Have It?

You often can’t feel it. It’s happening at the cell level. You can ask your doctor for a fasting insulin test.

• Test: Fasting insulin (after 8–12 hours without food)
• A red flag: fasting insulin above about 10–12 micro-units per milliliter
• Why it’s not ordered a lot:
  • Not part of basic labs
  • Results can vary day-to-day (stress, sleep, exercise)
  • It’s a snapshot, not a 3-month average like A1C

Important: high insulin can be present 10–20 years before type 2 diabetes shows up on A1C or fasting glucose.

• Diabetes diagnosis criteria often include:
  • A1C ≥ 6.5%
  • Fasting glucose ≥ 126 mg/dL
  • Or a random glucose ≥ 200 mg/dL with symptoms

Catching insulin resistance early matters.

The Ripple Effect: Triglycerides, VLDL, and HDL

When insulin isn’t working well:

• Fat cells get “leaky” and release more free fatty acids.
• The liver turns these into triglycerides and sends them out in VLDL (very low-density lipoprotein) particles.
• VLDL are small and dense. They can slip into blood vessel walls and oxidize (like a rusty chair in the rain). That can start plaque problems.
• HDL (the “cleanup crew”) can get tossed off their normal job when triglycerides are high. This can lower their helpful action.

More visceral fat = more inflamm