Regulate Energy — glycation and chronic exposure
What this tells you about fuel regulation
- A1c is a 90-day average of glycemic exposure — but the deeper story is glycation accumulating in slow-turnover tissues: nerves, cartilage, vascular walls.
- Performance losses and recovery deficits show up before diagnostic thresholds are crossed.
- A rising A1c is an early indicator that fuel regulation is strained — and it responds to changes in nutrition structure and consistency.
If soreness lingers, recovery stalls, and output fades early — don't assume it's programming. It may be chronic fuel exposure showing up first as performance loss.
What matters for coaching
Reduce added sugar and liquid sugar exposure. Anchor protein so appetite has structure. Fit carbohydrate dose and timing to current capacity. Re-test under the same conditions.
The iceberg beneath "normal" blood sugar numbers
Sugar doesn't just float through the blood and disappear. It binds. It sticks to proteins, lipids, and DNA — warping structure and function. Once a molecule is glycated, there is no undoing it. The only fix is turnover: breaking down damaged tissue and rebuilding new.
Fast-turnover tissues can recover. Slow-turnover tissues — nerves, cartilage, vascular walls, connective tissue — carry the burden for years. This is why a person can be told they are "fine" while performance and recovery quietly erode.
A1c is the fingerprint of that chemistry — the share of hemoglobin bonded with glucose over roughly 90 days. Clinically, anything below 5.7% is considered normal. In coaching, we target closer to 5.0–5.4%, because that range reflects cleaner fuel regulation and lower chronic glycemic exposure. The Radar treats that as the coach target — 5.4% scores 85 for a forty-year-old, high in the Well band and just short of Fit — with 5.0 and under reading Fit, the cleanest reading of all.
Each blood sugar spike adds another microscopic layer of glycation the body has to repair. At 5.7, medicine calls it prediabetes. At 6.5, diabetes — usually confirmed with a repeat test. But glycation begins long before those diagnostic lines are drawn — and coaches live upstream of disease.
High-fructose foods — soda, juice, sauces — elevate methylglyoxal, a highly reactive byproduct that rapidly crosslinks proteins in slow-turnover tissues like collagen and neurons. That damage doesn't show up in a standard lab panel. We suspect it shows up in the gym — stiffness, lingering soreness, recovery that doesn't match training age — but soreness alone doesn't prove it. It's a reason to look at the numbers, not a diagnosis.
A coach who understands glycation watches for what a lab panel won't flag: performance loss as a possible early sign of chronic metabolic strain. The iceberg isn't inevitable. It builds with poor fuel regulation and melts when the inputs change.
References+
- WHO 2011 — Use of Glycated Haemoglobin (HbA1c)
- Singh 2014 — Advanced Glycation End Products
- Gugliucci 2025 — Fructose-Methylglyoxal-AMPK
- Lustig 2023 — "Alcohol without the buzz"
Recover From Stress — oxidative stress and the dose-response line
What this tells you about stress recovery
- Reactive oxygen species are metabolic exhaust — unavoidable — and dose determines whether they signal adaptation or cause damage.
- Too little stress produces no adaptive signal. Too much, too long, produces breakdown disguised as effort.
- You can't lab-test ROS directly, but you see the fingerprints in recovery speed, inflammatory markers, and cardiovascular regulation.
What matters for coaching
Coach intensity like a dosage — dose it like medicine, not like punishment. If blood pressure is rising and resting heart rate is climbing, the stress load is not being resolved. Adjust volume, protect sleep, address the obvious leaks.
The link between oxidative stress, adaptation, and performance
Cambridge, MA, 2025
At the end of day one at the MetFix Training Development Conference, I found myself at dinner with Bob Kaplan, Tomás Duraj, and Derek Lee. Thomás and Derek work for Dr. Thomas Seyfried's world renowned cancer research lab at Boston College. Bob is Head of Research at MetFix. Earlier, they had presented on mitochondrial dysfunction in cancer, connecting the dots between reactive oxygen species (ROS), mitochondrial damage, and cancer progression.
Bob had suggested ROS could be beneficial, even necessary. I asked him to explain. He described ROS as part of fuel signaling and insulin sensitivity. Thomás and Derek jumped in: moderate ROS is essential — it signals adaptation. Too much, too long, and it's destructive. We were all aligned: ROS wasn't just about damage. It was about balance.
Somewhere in that conversation, I had a realization: ROS might be the cellular version of intensity. Just like in the gym, there's a red line. Push too little, nothing changes. Push too hard, you break. Find the edge? That's where adaptation lives.
Reactive oxygen species are small, unstable molecules your body makes every day — superoxide, hydrogen peroxide, hydroxyl radicals. At controlled levels, they're signals: telling cells to grow stronger, mitochondria to multiply, immune systems to sharpen. At uncontrolled levels, they're wrecking balls: oxidizing LDL, tearing DNA, inflaming neurons. This dual nature caused the person who coined the term to divide it: (1) oxidative eustress (physiological and essential) and (2) oxidative distress (excessive and toxic).
You can't walk into a diagnostic lab and get a neat ROS readout. They're too reactive, too fleeting. But you can see their shadow in the outcomes: improved work capacity, blood pressure improves, triglycerides drop, A1c normalizes, bones grow stronger, recovery speeds up.
Scaling isn't just about protecting joints or egos. It's protecting the cell. It's keeping ROS in the adaptive zone. ROS is the exhaust signal of human performance — the unseen byproduct that hints at whether the levers of food and training were pulled correctly.
References+
- Sies et al. (2017)
- Powers et al. (2011)
- Ristow et al. (2009)
- Seyfried & Shelton (2010)
Preserve Functionality — the mitochondrial engine
What this tells you about functionality
- Mitochondria are the engines that turn fuel into ATP. What coaches see as "fitness" is mitochondrial function expressed on the floor.
- Metabolic flexibility — the ability to burn the right fuel at the right time — determines whether the body can sustain capacity under repeated load or collapses early.
- Performance is often the first stress test of metabolic health. Coaches see engine problems before lab values cross diagnostic thresholds.
The athlete who keeps mechanics crisp under fatigue likely has more oxidative capacity. The athlete who redlines early may be metabolically inflexible — relying on glucose when they should be accessing fat.
What matters for coaching
Give the mitochondria a consistent adaptive signal: progressive loading, aerobic base, adequate recovery. Avoid chronic redline living. Mitochondria are trainable — give them a reason to expand and they will.
The engine behind human performance
I've seen it, and so have you. We coach the same workout all day. Some athletes thrive on the challenge, and others don't look as good. We second-guess ourselves: "Did I scale them right?" "Was that the right workout today?" But sometimes the answer is simpler. It's not the workout that needs a closer look, it's the athlete who is struggling. This is where mitochondria enter the conversation.
That is why at MetFix we claim, "We are the only commercial entity concerned with the care and feeding of mitochondria."
Capacity lives or dies inside the mitochondria. What we call fitness is really mitochondrial function expressed on the floor. Nearly every cell in your body is built around these engines. Each mitochondrion fires like a cylinder, turning the fuel you eat into ATP, the cell's universal energy currency.
Everything — fat, carbohydrate, and protein — gets broken down into acetyl-CoA, the molecule they burn to produce ATP. In metabolic terms, fat is the long, clean burn; carbohydrate is the fast, hot flame. Metabolic flexibility is the capacity to burn the right fuel at the right time. When mitochondria are efficient, fat supports the easy gears and glucose is reserved for speed. When they're limited, the engine runs too hot, too soon.
What we see as poor performance is often early metabolic disease. Long before fasting insulin climbs above 5 µIU/mL or the triglyceride-to-HDL ratio rises past 2.0, coaches can see the engine struggling on the gym floor. Adaptation is a fuel problem long before it's a fitness problem. They're trainable. Give them a consistent signal and they expand. Remove the signal and they retract. Coach the mitochondria, and you coach both performance and health.
References+
- San-Millán & Brooks (2018)
- Seyfried (Cancer as a metabolic disease)
- Coyle (1995) fat metabolism during exercise