The ISSN conference in June was a blast—a migration of protein scientists, coaches, supplement degenerates, and sleep-deprived PhDs surviving on hotel coffee while debating leucine thresholds before breakfast.

Exactly my kind of vacation.

Buried beneath the usual discussion of muscle protein synthesis and hypertrophy was something far stranger:

Essential amino acids may help preserve cognitive performance under stress.

Not merely muscle. Your brain.

Here is the wild part, dear reader: the human trial is not published yet.

There is no finished manuscript on PubMed, no polished PDF, and no abstract you can flash on social media after reading only the conclusion.

This is bleeding-edge conference data, hauled directly out of the scientific wilderness before reviewers have sharpened their tiny red pencils and begun fistfighting over commas.

You are getting it because I was sitting in the room.

Welcome to the Cognitive Wood Chipper

Arny Ferrando, PhD, from the University of Arkansas for Medical Sciences presented the work.

His group ran an eight-subject, three-condition crossover trial comparing essential amino acids,

EAAs plus tyrosine, and placebo. Each participant completed every condition, serving as their own control—a strong design feature when your entire sample could fit inside a conversion van. Only five participants had complete blood draws.

Participants received two supplement doses across roughly two hours before entering the Multi-Tasking Framework, a computer-based stress task designed to make the frontal cortex consider filing for workers’ compensation.

The screen demanded simultaneous arithmetic, Stroop-style color discrimination, target tracking, and memory retrieval for approximately 40 minutes. Mood, perceived workload, cognition, and reaction time were measured at baseline, after supplementation, and following the stressor.

One crucial detail: the slides did not state the gram dose used in this completed trial. Several upcoming studies use 20 grams of EAAs, but we cannot reverse-engineer that number into the finished pilot and call it fact. Stay tuned as I have a pretty good idea what was used that I reveal later on here.

The stress task worked exactly as intended. Frustration, mental fatigue, tension, anger, general fatigue, confusion, and reaction time deteriorated.

With EAAs aboard, that deterioration was blunted across the cluster. During the task, participants also reported lower mental demand, less frustration, and better perceived performance.

Reaction time interests me most because a stopwatch has no emotional investment in your supplement stack. It does not care about mercury was in retrograde yet again, your readiness score, or hotel eggs built from the same material used to insulate attics.

On the procedural reaction-time task, placebo deteriorated by roughly 28 milliseconds while the EAA condition remained near baseline.

The amino acids did not turn anyone into a neurological superhero. They appeared to help participants hold the line when stress tried to pry the machinery apart with a crowbar.

Memory, visual discrimination, and Go/No-Go performance leaned in the same direction.

However, the individual figures did not show statistical markers across every panel, so those findings should be treated as directional—not commandments delivered from Mount Anabolism.

Tyrosine Enters the Arena and Does... F -All Nothing

The researchers also added 10 grams of L-tyrosine on top of the EAAs.

This was not a decorative pinch hidden between 40 milligrams of lion’s mane and three molecules of unicorn eyelash. It was a dedicated condition using the same participants, stressor, and testing battery.

The result was no substantive advantage over EAAs alone.

That should make you lean forward because tyrosine is one of the reigning champions of acute-stress cognition research. Cold exposure, sleep loss, noise, and heavy cognitive demand are precisely where tyrosine has built its reputation.

Nearly every “focus” formula leans on it.

Here, piling tyrosine onto a complete EAA blend added exactly squat—not even a polite neurological golf clap.

Why Might Tyrosine Have Failed?

Nerd alert. Phenylalanine can become tyrosine. Tyrosine is converted into L-DOPA by tyrosine hydroxylase, after which L-DOPA can become dopamine and eventually norepinephrine.

Tyrosine hydroxylase is the rate-limiting enzyme in that sequence. Adding more precursor therefore does not guarantee greater output.

It is like hiring twelve bakers for a shop with one oven: everyone gets an apron, morale briefly improves, and the bread emerges at the same speed.

Then we have the doorway problem.

Several large neutral amino acids—including the BCAAs, phenylalanine, tyrosine, and tryptophan—use LAT1 to cross the blood-brain barrier.

Adding a massive slug of tyrosine does not construct another transporter. It may only create a longer biochemical queue at the same nightclub entrance.

Important caveat: the study did not test why tyrosine failed. Enzyme saturation and transporter competition are plausible explanations, not proven mechanisms. Selling a plausible pathway as demonstrated causation is how science communication wakes up face-down in a drainage ditch wearing somebody else’s pants. Or so I've heard.

The Blood Work Gets Interesting

Ferrando’s group collected blood at baseline and after supplementation.

Homovanillic acid increased. HVA is a major product of dopamine metabolism, so the result is consistent with increased dopamine turnover. The presentation described this as greater dopamine production.

That is fascinating, but peripheral HVA is not a surveillance camera aimed directly into the brain. It cannot establish where the turnover occurred or prove dopamine preserved reaction time.

Kynurenine decreased significantly by 120 minutes. Kynurenine belongs to a major tryptophan-catabolism pathway, and the presentation interpreted this as reduced serotonin production.

Again, the plumbing moved.

Nobody directly measured serotonin inside the brain.

Still, the pattern is difficult to ignore: a dopamine-related metabolite increased, kynurenine fell, and cognitive deterioration under stress was blunted.

The pieces fit neatly enough to make a scientist lean forward, but not tightly enough for a supplement salesman in a rented lab coat to declare victory. The metabolite slides explicitly labeled HVA as increasing and kynurenine as decreasing after EAA ingestion.

The Rats Also Lifted

The presentation included a published mouse study by Binman and colleagues.

Male mice completed resistance training, with one group exposed to volume overload plus EAA supplementation. Researchers then examined behavior and hippocampal tissue.

The EAA-supplemented overtraining group made more open-arm entries in the elevated plus maze, interpreted as reduced anxiety-like behavior.

Hippocampal TrkB expression increased; TrkB is the receptor for BDNF and participates in synaptic plasticity and memory formation. Hippocampal 5-HT1A receptor expression also rose, a finding associated with spatial memory and anxiety regulation under stress.

Rodents are not people. They do not have mortgages, inboxes, or training partners who redesign the program after watching half a podcast while driving.

Nevertheless, the animal results provide a mechanistically coherent foundation beneath the human pilot. That is more scientific scaffolding than most supplements assemble in a decade.

Where the Wheels Could Leave the Vehicle

This was an eight-subject pilot, with complete blood draws from only five. The crossover design improves control, but it cannot repeal mathematics.

Effects found in tiny samples may shrink, mutate, or evaporate when the study becomes large enough to require more than one pizza.

The human trial is also unpublished and has not survived peer review. Individual performance figures lacked significance markers, the demographic breakdown was limited, and the completed-trial dose was not shown.

The clean replacement for the repetitive section is:

This was a small crossover pilot from one laboratory, presented at one conference. The signal is fascinating; the evidence remains preliminary but still super cool.

A conference presentation is a promissory note, not a receipt. Results can change during peer review, lose sparkle when the full statistics appear, or vanish into the swamp where abandoned graduate projects and exercise gadgets from 2014 go to die.

How I Am Using It

The great part is that you can test this yourself and find out.
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My current setup is 16 grams of free-form EAAs before morning cardio, usually 20–30 minutes before starting.

That is my dose and timing—not the study protocol. Their participants received two doses across roughly two hours. My single serving is built around practical mornings rather than an attempt to replicate a controlled experiment beside the coffee maker while wearing sweatpants. And I may have talked to said researchers off the record too.

Acute aerobic exercise can temporarily sharpen aspects of cognition through changes in arousal, catecholamines, cerebral blood flow, and neurotrophic signaling. The conference data suggest EAAs may help preserve performance when cognitive demand arrives carrying a tire iron.

There is also the muscle side. Fasted cardio creates training-related signaling when circulating amino acid availability may be relatively low. That is a foreman starting the machinery, unfolding the blueprints, and discovering nobody ordered lumber.

Free-form EAAs provide all nine essential amino acids without leaving breakfast in your stomach like a wet cinder block.

This gives me (and potentially you) potential cognitive support, anabolic substrate, and convenient pre-cardio nutrition.

What I Use

I use Kion Aminos.

They are free-form, contain all nine essential amino acids, are leucine-forward, and taste good. More importantly, they avoid the incomplete-amino-acid circus where someone hands you a signaling molecule and pretends the construction materials are optional.

Full disclosure: I am a Kion affiliate.

Purchasing through my link may earn me a few bucks at no additional cost to you. I am also not pretending I discovered the product inside a glowing cave after a kiteboarding vision quest involving a shirtless shaman named Craig. Hi Craig.

I use it because it fits the physiology:

Signal plus substrate. Switch plus lumber. Foreman plus crew.

Grab Kion Aminos here:

​getkion.com/drmike​

The Takeaway

Leucine matters, but complete EAAs provide the entire substrate package.

Flipping the anabolic switch without supplying the other essentials resembles slamming the accelerator while your car sits on concrete blocks. There will be noise, but nothing useful is going anywhere.

Based on the ISSN presentation, your brain may require the whole crew too.

This is bleeding-edge conference intel: mechanistically interesting, experimentally incomplete, and delivered before the ink exists.

That is exactly where the fun starts.

Much love and full-rep anabolism,

Dr Mike

PS — The research pipeline gets stranger. One upcoming trial will compare EAAs with modafinil in C-130 pilots performing simulated night missions after four hours of sleep. Another will examine visual processing in professional fighters, while a placebo-controlled cognition study using 20 grams of EAAs is scheduled for fall 2026.

Test it out for yourself!

Grab Kion Aminos here:

​getkion.com/drmike​

Nerd Fuel

Ferrando, A. A. (2026, June). Essential amino acids and cognition. Presentation delivered at the International Society of Sports Nutrition Annual Conference. University of Arkansas for Medical Sciences. Unpublished human pilot data.

Binman, L., Ben-Zeev, T., Harris, A., Levi, C., Weissman, I., Church, D. D., Ferrando, A. A., & Hoffman, J. R. (2025). The effects of essential amino acid supplementation on hippocampal neurotrophin, dopaminergic and serotonergic changes in an overtraining mouse model. Nutrients, 17(18), 2957.

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Mike T Nelson CISSN, CSCS, MSME, PhD
Associate Professor, Carrick Institute
Owner, Extreme Human Performance, LLC
Editorial Board Member, STRONG Fitness Mag

Mike T Nelson is a PhD and not a physician or registered dietitian. The contents of this email should not be taken as medical advice. It is not intended to diagnose, treat, cure, or prevent any health problem - nor is it intended to replace the advice of a physician. Always consult your physician or qualified health professional on any matters regarding your health.