Insulin Is Not the Whole Blood Sugar Story

I love this short explanation. My family and I have been doing this for many years.

It's simple, it's easy, and you feel the benefits.

Take a walk!

By Dr. David Traster, DC, MS, DACNB

Co-owner, The Neurologic Wellness Institute

Boca Raton • Chicago • Waukesha • Wood Dale

Most people believe blood sugar is controlled by one thing.

Insulin.

You eat.

Your pancreas responds.

Glucose enters cells.

Balance is restored.

That story is tidy.

And incomplete.

Your muscles actually clear glucose in two distinct ways after a meal.

Most people regularly engage only one.

The consequence isn’t subtle.

It shows up as higher glucose peaks, longer recovery times, rising insulin demand, and—over years—metabolic strain that feels mysterious but isn’t.

The body isn’t failing.

It’s being underused.

The First Pathway: Insulin Does the Work Alone

When you remain seated after eating, glucose disposal depends almost entirely on pancreatic insulin signaling.

Insulin binds its receptor on muscle cells.

That signal travels through a well-studied intracellular cascade.

GLUT4 transporters move to the muscle cell membrane.

Glucose enters.

This pathway works.

But it has limits.

When muscle remains inactive:

• GLUT4 availability is constrained

• Glucose clearance is slower

• Post-meal glucose peaks are higher and last longer

• The pancreas must secrete more insulin to compensate

  
  

This is why prolonged sitting after meals reliably produces exaggerated post-prandial glucose and insulin responses—even in people who are otherwise “healthy.”

The system is doing its best.

But it’s operating with half its tools offline.

The Second Pathway: Muscle Contraction Changes the Rules

Something very different happens when you move after eating.

Not exercise.

Not training.

Not sweating.

Just movement.

When muscle contracts, it activates a second glucose-clearance pathway that runs in parallel to insulin, not downstream from it.

Muscle contraction itself:

• Triggers GLUT4 translocation through AMPK, calcium, and nitric-oxide signaling

• Allows glucose to enter muscle without waiting for insulin

• Accelerates glucose clearance from the bloodstream

Under the hood, the sequence is simple:

• Muscle contracts

• GLUT4 moves to the membrane

• Glucose enters directly

• Blood glucose falls faster

• Insulin demand drops

Insulin is still present.

But it no longer has to do all the work alone.

This pathway is not a backup.

It’s not a hack.

It’s not optional physiology.

It’s built in.

The Molecular Proof That These Are Separate Systems

This isn’t metaphor.

At the cellular level, these pathways are demonstrably distinct.

When researchers block insulin signaling, contraction-mediated glucose uptake continues.

When they block contraction signaling, insulin-mediated uptake continues.

Each pathway stands on its own.

Each can compensate for the other.

And when both are active, glucose clearance is additive.

Muscle contraction does not amplify insulin.

It adds capacity.

What Happens When This Physiology Is Used in Real Life

When this mechanism is tested in humans—not in athletes, not in training studies, but in everyday post-meal behavior—the results are consistent.

Interrupting prolonged sitting with short bouts of light movement:

• Lowers post-meal glucose peaks

• Reduces total insulin exposure

• Improves triglyceride handling

These effects occur:

• With walking, not workouts

• In healthy individuals and those with insulin resistance or type 2 diabetes

• Even when total calorie expenditure is matched

Which means the benefit is not driven by burning energy.

It’s driven by repeatedly activating contraction-mediated glucose uptake at the moment glucose enters the bloodstream.

Timing, not intensity, is doing the work.

Why This Matters More Than “Exercise”

Exercise is often framed as something you do to compensate.

Burn off what you ate.

Earn your meal.

Correct excess.

That framing is biologically wrong.

Post-meal movement doesn’t undo food.

It completes digestion.

It allows glucose to enter the tissue designed to store and use it most effectively—skeletal muscle—through a pathway evolution already built for that purpose.

Walking after meals doesn’t override insulin.

It doesn’t replace it.

It doesn’t suppress it.

It shares the load.

The Unifying Insight

Metabolic health doesn’t fail all at once.

It erodes quietly when one pathway is asked to do the work of two.

By engaging both insulin-dependent and contraction-mediated clearance at the same time:

• Glucose peaks are lower

• Clearance is faster

• The pancreas experiences less strain

• Metabolic control improves with minimal effort

This is not about discipline.

It’s not about optimization.

It’s not about earning food.

It’s about using the physiology you already have—at the moment it matters most.

Your muscles know how to help.

They just need to be invited into the conversation.

References

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2. Richter, E. A., Garetto, L. P., Goodman, M. N., & Ruderman, N. B. (2001). Muscle contraction and insulin regulate glucose transport via distinct signaling pathways. Journal of Biological Chemistry, 276(51), 47368–47375.

3. Hayashi, T., Hirshman, M. F., Kurth, E. J., Winder, W. W., & Goodyear, L. J. (1998). Evidence for 5′ AMP-activated protein kinase mediation of the effect of muscle contraction on glucose transport. Diabetes, 47(8), 1369–1373.

4. Holloszy, J. O. (2005). Exercise-induced increase in muscle insulin sensitivity. Journal of Applied Physiology, 99(1), 338–343.

5. Loh, R., Stamatakis, E., Folkerts, D., Allgrove, J. E., & Moir, H. J. (2019). Effects of interrupting prolonged sitting with physical activity breaks on postprandial metabolic responses. Sports Medicine, 49(7), 1025–1038.

6. Dempsey, P. C., Larsen, R. N., Sethi, P., Sacre, J. W., Straznicky, N. E., Cohen, N. D., & Dunstan, D. W. (2016). Benefits for glycaemic control with breaking up prolonged sitting. Diabetologia, 59(5), 964–972.

7. Thompson, D., Karpe, F., Lafontan, M., & Frayn, K. (2018). Physical activity and exercise in the regulation of human adipose tissue physiology. Sports Medicine, 48(4), 795–809.

8. DeFronzo, R. A., Ferrannini, E., Hendler, R., Felig, P., & Wahren, J. (1981). Regulation of splanchnic and peripheral glucose uptake by insulin and hyperglycemia. Journal of Clinical Investigation, 68(6), 1468–1474.

9. Richter, E. A., & Kiens, B. (2001). Muscle glucose uptake during exercise: How contraction opens another door. American Journal of Physiology-Endocrinology and Metabolism, 280(5), E765–E774.

10. Wasserman, D. H., Kang, L., Ayala, J. E., Fueger, P. T., & Lee-Young, R. S. (2011). The physiological regulation of glucose flux into muscle in vivo. Journal of Experimental Biology, 214(2), 254–262.