By Dr. Greg Fors
Chief Science Officer, BioSpec Nutritionals
This article is Part 2 of our discussion of aging muscle. Read “The Aging Muscle Is Losing More Than Protein” for the first part of the series.
For years, people who exercise have been warned about taking antioxidants.
The argument goes something like this:
Exercise produces free radicals. Those free radicals help signal the muscle to adapt. Therefore, taking antioxidants might block the signal and interfere with muscle development.
There is some science behind that idea.
But I believe we have taken a legitimate physiological observation and stretched it much too far, especially when we apply studies involving young, healthy athletes to people in their 40s, 50s, 60s, 70s, and beyond.
After more than 40 years in clinical practice, I look at the problem differently.
The question is not whether we should completely eliminate free radicals.
We shouldn’t.
The question is:
Can we preserve the short-lived oxidative signal created by exercise while protecting muscle from the chronic oxidative and nitrative damage occurring during the other 23 hours of the day?
I believe that is the much more important question.
I like to explain oxidative stress as cellular rust.
Oxidative stress is like rust caused by excessive oxygen-based reactive molecules.
Nitrative stress is related but potentially even more damaging.
Think of nitrative stress as a harsher chemical rust caused by reactive nitrogen chemistry.
Exercise deliberately creates a temporary increase in reactive molecules.
That is normal.
Those molecules participate in signaling pathways that tell the cell:
We just worked hard. Adapt. Build. Become stronger.
That is hormesis, a small, temporary stress that makes the body stronger.
But there is an enormous difference between lighting a controlled fire for an hour and having your house smoldering 24 hours a day!
I believe that distinction has been lost in much of the discussion about antioxidants.
Exercise is a controlled biological stimulus: generate the signal, respond to the signal, resolve the stress, recover, and adapt.
Here is one of the most important points in this entire discussion.
A well-trained person generally develops a stronger endogenous antioxidant-defense system.
Training can increase or improve systems involving:
Yet the next time that trained person exercises intensely, the muscle still generates a temporary increase in reactive oxygen and nitrogen chemistry.
Think about that.
Having strong antioxidant defenses does not prevent exercise redox signaling.
If it did, training would eventually defeat itself.
As athletes became better conditioned and developed stronger endogenous antioxidant defenses, those defenses would increasingly prevent the oxidative signal required for further adaptation.
That isn’t what happens.
Instead, training appears to make the body better at controlling the oxidative burst and returning the cell toward homeostasis after the signal has done its job.
That is precisely what I want for an aging or any patient.
I don’t want to eliminate the oxidative pulse.
I want to restore the ability to resolve it.
That may be one of the most important distinctions in healthy aging.
Exercise-generated reactive oxygen species activate redox-sensitive pathways, including Nrf2.
Nrf2 is fascinating because it helps turn on many of the body’s own cellular-defense systems.
Exercise creates an oxidative signal.
The cell detects that signal.
Nrf2 responds.
The body increases its own protective machinery.
Then the system moves back toward balance.
In simplified form:
Exercise → temporary ROS pulse → redox signaling/Nrf2 → stronger endogenous defenses → return toward homeostasis.
This is a beautifully regulated biological system.
The objective is not:
Exercise → ROS → eliminate every ROS molecule.
That would make little physiological sense.
The objective is:
Generate the signal. Respond to the signal. Resolve the stress. Recover. Become stronger.
This is more than theory.
Researchers have given people vitamin C before exercise and then measured oxidative-stress responses.
Vitamin C can decrease the magnitude of some oxidative markers.
But exercise still produces an oxidative response.
In one human study, subjects taking 1,000 mg of vitamin C per day still experienced an exercise-associated increase in oxidative-stress markers. The magnitude was modified; the exercise response was not magically erased.
Other work has shown something equally interesting:
People beginning with poor vitamin C or glutathione status appear to respond differently to antioxidant supplementation than people who already have adequate antioxidant defenses.
That makes biological sense.
Baseline matters.
Giving antioxidant support to someone already in excellent redox balance is not necessarily equivalent to giving it to an older person whose glutathione is depleted and whose resting oxidative burden is elevated.
Much of the exercise-antioxidant debate has been driven by studies involving relatively young, metabolically healthy people.
But that is not the person who concerns me most when we talk about sarcopenia.
Consider the modern 55-year-old.
He or she may have:
All of these factors do not affect everyone equally, but the larger point is difficult to ignore:
Modern aging frequently occurs in a biological environment very different from that of the healthy 22-year-old athlete used in an exercise laboratory.
Many of my patients are not starting at normal oxidative balance.
They may already be carrying a substantial inflammatory and oxidative burden before they ever pick up a dumbbell.
That changes the clinical question completely.
There is experimental research showing that certain chemical exposures can increase oxidative stress.
There is also experimental literature reporting oxidative effects from some radiofrequency electromagnetic-field exposures.
That research is interesting and deserves continued investigation, especially in individuals with high baseline oxidative stress or genetically low endogenous antioxidant production.
What we can say with much greater confidence is that metabolic disease, chronic inflammation, obesity, smoking, air pollution, poor nutrition, mitochondrial dysfunction, and aging itself can increase oxidative burden.
And modern humans can encounter many of those simultaneously.
That is enough reason for me to care deeply about maintaining redox balance.
Picture oxidative stress as a graph.
A metabolically healthy person begins down here:
LOW BASELINE OXIDATIVE STRESS → EXERCISE SPIKE IN OXIDATIVE STRESS ↑ → RECOVERY → RETURN TO LOW BASELINE OXIDATIVE STRESS
The spike is temporary.
It sends a signal.
The body’s antioxidant machinery responds.
Homeostasis returns.
Now imagine someone with metabolic disease and chronic inflammation:
HIGH BASELINE OXIDATIVE STRESS → EXERCISE SPIKE OXIDATIVE STRESS ↑ → INCOMPLETE RECOVERY → HIGH BASELINE OXIDATIVE STRESS
That is an entirely different cellular environment.
My goal with nutrition, metabolic therapy, exercise, and targeted supplementation is not to flatten the exercise spike.
My goal is to bring down the pathological baseline and improve recovery after the spike.
That is redox medicine.
The key clinical distinction is not whether an exercise-related spike occurs. It is whether the body can recover and return toward a healthier baseline.
Why does any of this matter for sarcopenia? Because muscle does not simply need protein.
Muscle needs functioning mitochondria. Muscle needs ATP. Muscle needs insulin sensitivity. Muscle needs healthy cell membranes. Muscle needs intact signaling.
And muscle needs functioning satellite cells capable of helping repair damaged muscle fibers.
Chronic oxidative and nitrative stress can interfere with several of those systems. As mitochondria become damaged, they can become part of a vicious cycle:
Mitochondrial dysfunction → excessive oxidative stress → inflammation → further mitochondrial damage → impaired muscle function → inactivity → additional mitochondrial decline.
This is one reason I believe mitochondrial health belongs at the center of the sarcopenia discussion.
Recent research makes this even more interesting. Muscle contains satellite cells: specialized stem cells that participate in muscle repair and regeneration.
One of the important signals activating these cells is hepatocyte growth factor, or HGF. I like to describe HGF as a key.
Its receptor, c-Met, is the lock. When HGF connects with c-Met, it helps tell the satellite cell:
Wake up. We have muscle to repair.
Researchers have now demonstrated that HGF can become nitrated.
Remember our analogy:
Oxidative stress is cellular rust. Nitrative stress is harsher nitrogen-based rust. Nitration can alter HGF and impair its ability to communicate effectively with the muscle-repair system.
Suddenly the antioxidant discussion becomes much larger than whether we might suppress a few signaling molecules immediately after exercise.
I am also concerned about protecting the repair machinery itself.
R-alpha-lipoic acid sits in an interesting position in this discussion. It participates in mitochondrial metabolism while also influencing redox biology.
I am not proposing that taking R-lipoic acid has been proven to prevent HGF nitration or prevent human sarcopenia. The argument is broader.
If excessive oxidative and nitrative stress contributes to mitochondrial dysfunction and damages proteins involved in muscle repair, then maintaining a healthier redox environment becomes biologically important.
That is where R-lipoic acid becomes interesting to me.
N-acetylcysteine, or NAC, supplies cysteine that the body can use to manufacture glutathione.
Glutathione is not simply another antioxidant pill floating through the bloodstream. It is one of the body’s major endogenous redox-control systems.
That distinction matters.
Human research using glycine plus NAC: GlyNAC: in older adults has reported improvements in glutathione deficiency, oxidative stress, mitochondrial dysfunction, inflammation, insulin resistance, exercise capacity, gait speed, and muscle strength.
Again, look at the larger message:
Improving endogenous antioxidant capacity did not make these older people physically weaker. Their physical function actually improved.
This brings us to one of the simplest questions patients ask me:
Should I worry that taking vitamin C will interfere with maintaining my muscle?
At reasonable supplemental doses, I don’t think the current evidence justifies that fear.
Several studies have raised legitimate questions about very high-dose combinations of vitamin C and vitamin E in particular populations.
But the results are inconsistent. Some studies found alterations in molecular signaling without meaningful suppression of muscle growth.
And now we have something particularly important. Researchers recently studied 60 women between 60 and 75 years old who already had sarcopenia.
Everyone resistance trained.
One group received placebo.
The other received 1,000 mg of vitamin C plus vitamin E daily.
The antioxidant group did not do worse. They actually experienced greater improvements in several measurements, including skeletal muscle mass index, arm lean mass, handgrip strength, and knee-extension strength. Oxidative-stress and inflammatory markers also improved.
That is extremely relevant. These weren’t 22-year-old athletes. These were older women who already had sarcopenia.
For the aging population I am concerned about, that study deserves considerable attention.
Based on the totality of this physiology and human evidence, I am comfortable using approximately 1,000 mg of vitamin C daily, commonly divided as 500 mg twice daily, as part of a broader nutritional program when appropriate.
I don’t view that as an attempt to eliminate exercise-generated ROS. It won’t.
Exercise is a powerful metabolic event. Working skeletal muscle will still generate a temporary redox signal.
What I am interested in is maintaining a healthier baseline and helping the body’s antioxidant network deal with excessive oxidative stress between those exercise signals. That is a completely different objective.
This same philosophy is behind Mito-Detox III.
It combines nutrients that address several parts of mitochondrial and redox physiology:
I don’t think of this as simply “taking antioxidants.” I think of it as supporting the machinery responsible for energy production, redox regulation, and cellular resilience.
And muscle is enormously dependent upon that machinery.
Mito-Detox III is a comprehensive mitochondrial and redox-support formula. Discuss supplement selection and dosing with a qualified healthcare professional.
There is one thing I want to make absolutely clear. Nothing I have discussed replaces resistance exercise.
Exercise provides the signal.
Protein supplies essential amino acids.
Vitamin D supports normal muscle physiology.
Metabolic health helps maintain insulin sensitivity.
Mitochondria provide the energy.
Satellite cells help provide the repair capacity.
And the antioxidant/redox system helps control the cellular environment in which all of this occurs.
This is not either/or physiology. It is an integrated system.
I think we have spent too much time worrying that supporting antioxidant defenses will somehow make aging muscle incapable of responding to exercise.
The concern came from legitimate research. But the sweeping conclusion went too far.
Having strong antioxidant defenses does not prevent exercise from producing an oxidative signal.
Trained people themselves demonstrate this beautifully. Training strengthens endogenous antioxidant defenses.
Yet trained muscle continues to generate transient ROS during subsequent exercise and continues to adapt. The body is designed for this.
Exercise creates the signal.
Antioxidant systems shape the signal.
Recovery resolves the signal.
Chronic oxidative stress is what we don’t want.
That is the distinction.
I don’t want zero oxidative stress.
That would neither be possible nor desirable.
I want:
And then I want the patient to exercise again.
That is the cycle of adaptation.
Not:
Suppress every free radical.
But:
Generate the appropriate signal, respond to it, resolve it, repair the tissue, and become stronger.
I believe the antioxidant-and-exercise discussion needs to mature.
A temporary oxidative burst is part of healthy exercise physiology.
Chronic oxidative and nitrative stress is part of aging and disease physiology.
Those are not the same thing.
For an aging individual concerned about maintaining muscle, I see little reason to fear reasonable antioxidant and mitochondrial support such as approximately 1,000 mg of vitamin C daily and a comprehensive mitochondrial formula such as Mito-Detox III, when used as part of a program built around resistance exercise, appropriate protein intake, vitamin D sufficiency, metabolic health, and control of chronic inflammation.
The purpose isn’t to extinguish the exercise signal.
The purpose is to keep the cellular environment healthy enough to hear that signal. This may be the most important sentence in this entire discussion.
Because preserving muscle as we age requires more than protein.
It requires a muscle cell capable of producing energy.
A mitochondrion capable of doing its job.
A satellite cell capable of repairing tissue.
An HGF signal capable of reaching that satellite cell.
And a redox environment healthy enough to allow the entire system to work.
Protect the signal. Protect the mitochondria. Protect the muscle.
This article is for educational purposes only and is not intended to diagnose, treat, cure, or prevent any disease or medical condition. It is not a substitute for personalized medical advice, diagnosis, or treatment from a qualified healthcare professional.
Always consult your physician or another appropriately licensed healthcare practitioner before starting an exercise program, changing your diet, or using any dietary supplement. Do not delay, discontinue, or modify prescribed medical care based on information in this article. Dietary supplements may not be appropriate for every individual, may interact with medications or medical conditions, and should be used under professional guidance. Statements regarding dietary supplements have not been evaluated by the U.S. Food and Drug Administration unless specifically stated otherwise. BioSpec Nutritionals products are not intended to diagnose, treat, cure, or prevent any disease.
If you experience severe muscle weakness, chest pain, shortness of breath, fainting, sudden loss of function, severe pain, or another urgent symptom, seek immediate medical attention.
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