MUSCLES FOR HEALTH, NOT FOR MEDALS
Why we need to do this now
Not next year. Not when the time comes—NOW!
To parents (and those who decide):
This text is for you.
If you think, “Everything is normal with my kids” because all the kids in your class look alike, you might be letting your guard down.
Not just one parent, but an entire society. A society that fails to see what is invisible, what the education and healthcare systems fail to see— insulin resistance (IR), which develops even in children.
Which begins silently, with symptoms that no one sees.
And that's exactly why we need to do it now: build muscle as a wall against insulin resistance, before the consequences of insulin resistance become permanent.
SSM — School Dream Gym (strength and health lesson at school, 2–3 times a week).
MSSM — Intergenerational School Dream Gym (same room after the bell: parents and seniors).
IR — insulin resistance: tissues “don’t listen” to insulin; more and more of it is needed to achieve the same effect after a meal.
T2D — Type 2 diabetes.
Starter dictionary of abbreviations (full names on first use):
WAT — white adipose tissue.
TAG — triacylglycerols (a form of fat storage in adipocytes).
FFA — free fatty acids circulating in the blood.
NO — nitric oxide (signal “open vessel”, key to microcirculation).
ATBF — adipose tissue blood flow.
FMD — flow-mediated dilation; an index of endothelial efficiency.
GLP-1 — incretin drugs in the treatment of obesity/diabetes (here: “rails” = strength + protein).
PHH — perfusion-hypoxia hypothesis: poorer perfusion → microhypoxia → tissue remodeling and metabolic loop.
1) A story that begins early (and invisibly)
If you are a parent, this story is about you and your child.
Imagine a typical morning. The alarm goes off and your child asks for "five more minutes." At school, they somehow "fly through" the first few lessons, but during the second break, that familiar feeling appears: a sudden craving for something sweet, a yawn, a drop in patience. In PE, they feel a "tick in the side," their stomach tightens, their head feels heavier. Test results? "Normal." And this is where the story usually goes untold.
This isn't a story about "weak willpower." It's a story about weak muscles, a weak last mile of blood , and insulin resistance (IR) —the main antagonist of this article. IR isn't a disease that will last forever. It's a silent habit of the body, requiring more and more insulin for the same meal. The more often this happens, the more the "valve" in fat tissue becomes set to "store," and the blood vessels must contend with the excess sugar (glucose) in the circulatory system because the body's glucose stores (muscles and liver) refuse to accept and store glucose.
The School Dream Gym (SSM) exists to build a wall against IR during the most vulnerable period—childhood and adolescence. This is when we need to teach muscles to work in a way that opens microvessels, takes on a portion of food, and gives the child peace of mind: fewer cravings for sweets, more patience, easier mornings.
The School Dream Gym (SSM) isn't a "medal-winning sport." It's about daily circulatory and energy health.
Mornings "on the third alarm clock" and evenings "sudden spikes" of energy.
"Sweet hunger" in the second break; after the sweet one — fast descents.
Avoiding exercise not out of laziness, but out of a sense of effort without reward.
It's harder to be patient when studying in the afternoon; it's easier to get tense.
In PE, "stinging", heavy breathing, reluctance to be compared.
1a) How do I know that my child may be starting IR? (home signals)
Individually, these signals are not decisive, but when they form a pattern, it is precisely this silence in which IR increases.
2) What do muscles really do?
Think of a city after rain. The major arteries are passable, but the narrow residential streets determine whether you get home. It's the same in the body: the large vessels are the highways, but life happens in the smallest streets— the microvessels.
When muscles work, they activate the green wave: vessels open more easily, blood reaches the areas of need more quickly, and energy from a meal is transferred to the muscles and liver without being forced through. Some of the sugar "letting" into the muscles happens even without any additional assistance, because the contraction itself opens the doors to the cells. At the same time, muscles order fat fuel —free fatty acids—so the fat stores (fat cells) don't have to hold everything "forever and ever."
For IR, it's like letting the air out of a balloon: less insulin is needed after a meal, and the fat storage finally hears the message "it's okay to release fat" stored in fat cells. The child feels this tangible: fewer pangs of "sweet cravings," a calmer head in class, easier sleep. Parents see fewer sudden energy dips, and teachers see more patience in the classroom.
Imagine two worlds.
World A—"more exercise" without purpose. Children run around once or twice a week. There's fun, sweat, and laughter. But muscles remain small, microvessels sleepy, and after a meal, you have to push yourself a lot. More insulin circulates in the background. The fat stores hear this as a command: store it —which means the IR increases.
World B—"strength and muscle mass" with a goal. Two or three short blocks per week of strength and muscle mass building teach the muscles to absorb food and open micro-alveoli. With each week , the "pressure" on insulin after a meal decreases. The fat storage begins to hear: " It's okay to give back "—meaning, the IR weakens.
3) Why do we say muscle strength and mass and not just “more movement”?
This is a qualitative difference, not a quantitative one. It's not about "more minutes of movement." It's about a different kind of stimulus: one that builds a perfectly functioning organ of perfusion—muscles—and stops IR already in childhood. Therefore, SSM doesn't compete with PE. SSM accomplishes what PE—by its nature of games and play—doesn't have to do.
A parent's micro-story: "My son always said that running was tiring for him, 'without any sense.' After 8 weeks of SSM, he said for the first time: 'Mom, I feel the city opening up inside me.' He stopped asking for a candy bar during the second break. That was a signal to me that we were starting to overcome the IR."
4) Fatty Acids in Children and Adolescents - What's Really Happening Early
Why do we do this now, and not "someday"? Because the fat storage facility learns from our daily lives. If for years it only hears "store it," it becomes hard and silent. What might have been released from the fat storage facility after the Strength and Health lesson stays for months—and boosts the IR.
Fat storage isn't "cotton wool." It's living tissue with vessels. When a lot of food flows into the circulatory system and a frequent "strong stimulus" (insulin) is required, the valve in the fat cells switches to "store" mode. Temporarily, that's good. Permanently, that's bad.
ATBF is weakening - streets too narrow for this traffic.
Microhypoxia and fibrosis occur in fat cells - the tissue "scars" and does not obey the "give back" command.
“Old” TAGs accumulate in fat cells—not because they are old, but because the metabolism has been switched to store rather than release.
SSM is key when applied early: muscle contraction increases blood flow, triggers demand for FFAs, and "unfreezes" fat stores. Less insulin is needed after a meal, and between meals, it's easier to switch the metabolism to "fat burning."
The insulin resistance of muscle cells stops increasing and begins to decrease.
This is the wheel that begins to turn in silence - from IR:
Weak muscles → few “open vessels” signals.
Poorer perfusion → more "pushing" (insulin) is needed after a meal — IR increases.
High insulin → the warehouse hears: "put it aside, don't give it away."
Microhypoxia, fibrosis, “old TAG” → warehouse hardens, which drives IR.
Even worse perfusion → the circle closes.
5) PHH: Perfusion ⇄ Hypoxia ⇄ Fat Retention loop (core of the problem)
Where to stick the stick in the spokes? In the muscles—now. Muscle strength and mass open blood vessels, calm insulin after a meal, and restore "movement" in the warehouse. That's why we say: either now, at school, or later—but then it will be increasingly difficult.
6) Why school and now
The window of life: during puberty, IR increases naturally—like a tidal wave. If muscle is lacking, the wave floods in. If muscle is built, the wave passes, and we are left standing on "dry land."
School is the only place where we can reach all children equally. Two or three short Strength and Health lessons a week don't require stadiums or new buildings. They require adult consent, to put it bluntly: the most important work a student's body does at school is building strength and muscle mass for life.
Understanding what strength and muscle mass mean for people of all ages means that after the bell rings, SSM transforms into MSSM and makes it a family habit. It's no longer a fad. It's a public health infrastructure.
For children, adolescents and adults, the elderly and seniors.
PE is necessary: it teaches cooperation, joy, and gets the pulse going.
But it rarely builds muscle as an efficient perfusion organ, supplying blood to all the cells of the body.
Games and races are a "broad brush" - they paint the background brilliantly, but they do not sculpt what determines the fate of the meal: the mass and strength of the muscles that open the microvessels and absorb the energy from the plate.
6a) Why PE alone is not enough (with respect to PE)
SSM isn't a competition—it's a missing piece against a finished backdrop. Together, they form a whole.
6b) If not now - the trajectory we see up close
Ages 10–12: "Sweet hunger" during the second break, less and less desire to move. Lack of muscle mass = more "pushing" after meals.
Ages 13–16: Natural IR rises during puberty. Without SSM, the wave washes over: belly fat, shame, avoiding PE. Fat stores learn to "store" mode.
Ages 17–25: "Continuous rehearsals starting tomorrow." Fatigue becomes a habit. The "city" of blood vessels runs on red lights.
Age 25+: Results are "still normal," but the body pays dearly for every effort. Muscle recovery is still possible —just more difficult and less common. Every year without a habit closes another door.
The consequences that aren't discussed: more sick leave, poorer sleep and working memory, and then—a late medical bill. That's not scaremongering. It's a bill with interest that you can stop today.
That's why we need to do this now so that every student in the education system has access to strength and muscle-building training.
The short answer: theoretically, you can "get results" despite having small and weak muscles, but this is a fragile and usually unsustainable solution.
Muscles are the main sink for glucose after a meal.
Low MASS = low "sink" capacity; low STRENGTH = weak hemodynamic stimulus and less frequent activation of insulin-independent GLUT4 translocation during contraction. The daily effect: the same meal costs the body more insulin, energy is pushed through the blood more frequently, and the "last mile of blood" (microcirculation) doesn't learn to function. Over time, energy fluctuations and sweet cravings increase.
Puberty: physiologically, insulin sensitivity decreases; without a "muscle buffer," the scales can easily tip towards insulin resistance.
7) Can you have low STRENGTH and MASS and have a normal metabolism?
Exceptions (why it's fragile): Someone very lean, with minimal visceral fat, high endurance/NEAT activity, excellent sleep, and no caloric surplus can "stick to the norm" as long as each of these building blocks fits perfectly. This is a narrow margin of safety and is not a strategy for the student population.
Practical conclusion: we are building a duo of STRENGTH + MASS.
More muscle = greater vascular surface area and greater glucose "sink".
Greater force = greater flow (shear), endothelial stimulus and more frequent GLUT4 activation without the help of insulin.
Together, they lower the “insulin cost” of meals, stabilize energy, and reduce sweet cravings.
This isn't a "medal sport" - it's metabolic engineering implemented lesson by lesson.
What can temporarily “mask” low muscle tone (why it’s fragile):
very low visceral fat,
high NEAT/CRF (lots of exercise despite no strength training),
no caloric surpluses and rare glucose "overloads",
great sleep and low stress,
young age (short "metabolic experience").
Call to Action
You are the deciding vote.
Ask the principal for regular Strength and Health lessons for your children at the School Dream Gym (SSM) and an open room after the bell ( MSSM ). Ask: when do we start to stop insulin resistance in our classroom?
For those interested: keep a small energy diary at home (2 sentences a day: "How much energy did I have in the afternoon?" "Did I crave sweets?") — it's a great map of progress.
Parents
Directors
Include 2–3 Strength and Health lessons per week.
Start piloting for 6–12 months, measure IR KPIs (relative strength/grip, HRR-1', WHtR, optional glycemia).
If after a semester the class sleeps better, craves sweets less and the heart rate returns faster - scale it for all students in the school.
Let's call it what it is: muscles + education are the cheapest barrier against insulin resistance (IR) and type 2 diabetes (T2D).
The NFZ/regional budgets will feel this sooner than you think.
Local governments and the state
Why do we need to do this now?
Because children don't have "later." If we don't teach them today, they'll leave school not only feeling drained but also without the knowledge that stopping insulin resistance is their daily health insurance.
A parent who knows changes the lesson plan.
Evidence checkpoint (6 short theses with links)
IR begins early; it increases physiologically during puberty – therefore, school is the decisive window. [1–3]
Hypoxia and adipose tissue fibrosis impair lipolysis and promote lipid retention; ATBF in the IR is impaired.[4–7]
Fat turnover in adipocytes slows down in obesity – “old” TAGs remain stored for months to years. [8–10]
Strength training and exercise improve endothelial/microcirculation (FMD) and metabolic sensitivity also in adolescents.[11–13]
Strength-training classes for adolescents can improve indicators of insulin resistance.[12]
Pharmacology (e.g., GLP-1) can reduce mass, but without muscle protection we risk losing lean mass; strength + protein are safety nets.[14–15]
Bibliography
1. Jeffery AN, Metcalf BS, Voss LD, Wilkin TJ. Insulin resistance rises before the onset of puberty: the EarlyBird study. Diabetology. 2008;51(10):2039–46.
2. DeFronzo RA. From the triumvirate to the ominous octet. Diabetes. 2009;58(4):773–95.
3. Taylor R. Pathogenesis of type 2 diabetes: the twin-cycle hypothesis. Diabetology. 2008;51(10):1781–9.
4. Trayhurn P. Hypoxia and adipose tissue function and dysfunction. Physiol Rev. 2013; 93:1–21.
5. Karpe F, Fielding BA, et al. Impaired postprandial adipose tissue blood flow in insulin resistance. Diabetes. 2002; 51:2467–73.
6. Karpe F, Frayn KN. The nicotinic acid story. Int J Obes. 2004;28 Suppl 4: S50–S54.
7. Ye J. Emerging role of adipose tissue hypoxia in obesity and insulin resistance. Int J Obes. 2009; 33:54–66.
8. Spalding KL, et al. Dynamics of fat cell turnover in humans. Nature. 2008; 453:783–7.
9. Arner P, Spalding KL. Fat cell turnover in humans. BBCRC. 2010;396(1):101–4.
10. Spalding KL, et al. The effect of fat mass on lipid turnover in human adipose tissue. Nat Commun. 2017; 8:15253.
11. Montero D, et al. Exercise training and endothelial function in youth. Am J Physiol Heart Circ Physiol. 2014;307:H1469–H1473.
12. Shaibi GQ, et al. Resistance training and insulin sensitivity in overweight Latino adolescent males. Med Sci Sports Exerc. 2006;38(7):1208–15.
13. Early K.S., et al. Exercise effects on flow-mediated dilation. SportsMed. 2017; 47:1315–27.
14. Wilding JPH, et al. Once-weekly semaglutide in adults with overweight or obesity (STEP). N Engl J Med. 2021; 384:989–1002.