Our Research

This paper demonstrates that exercise-induced sweating causes substantial sweat-facilitated amino acid loss (SFLAA), which threatens plasma homeostasis and triggers skeletal muscle proteolysis. It maps sweat kinetics to show that initial amino acid leaching from skin surfaces diminishes after 35 minutes, giving way to true eccrine clearance.

Finally, utilizing principal component analysis, the study phenotypically stratifies athletes into Low, Intermediate, and High SFLAA clusters. This identifies high-excretors who lose up to 22.8 mmol/h of amino acids, establishing a clinical rationale for targeted free-form amino acid supplementation.

This paper establishes a predictive amino acid turnover paradigm that calculates net daily nitrogen balances across specific amino acids under distinct physiological states. By integrating real-world excretion rates, it demonstrates that routine exertion drives negative balances for histidine, serine, glycine, and ornithine, particularly scaling with higher body masses.

Crucially, it models localised metabolic bottlenecks—showing how fasted exercise forces skeletal muscle catabolism, while acute infectious challenges selectively drain tyrosine, threonine, and valine for IgG synthesis. This provides a strong clinical rationale for low-dose, targeted amino acid replenishment.

This paper establishes that eccrine sweat is a physiologically "constructed fluid" where free amino acids and potassium actively drive the ductal resorption of sodium and chloride. By tracking sweat composition across prolonged exercise, it demonstrates a strong inverse relationship between certain amino acids and sodium and chloride.

• As cellular reservoirs of amino acids and potassium deplete over time, the duct's capacity to reclaim sodium and chloride declines, causing sweat concentrations of these key electrolytes to rise significantly.
• In other words, sodium and chloride are lost at faster rates as amino acids and potassium reserves become diminished.

Ultimately, it highlights the operational role of the ASCT-1 co-transporter in exchanging sodium for neutral amino acids, indicating that standard electrolyte rehydration is insufficient without amino acid replenishment.

This article introduces the framework of High-Demand Amino Acids (HDAAs)—histidine, serine, glycine, lysine, ornithine, and aspartic acid—and models their accelerated depletion during exercise, trauma, or infection.

• It demonstrates that because the body lacks amino acid storage reservoirs, these rapidly cleared deficits trigger muscle proteolysis to sustain vital metabolic and structural systems.

Finally, it establishes a clinical rationale for targeted, free-form HDAA supplementation to bypass post-exertion gastrointestinal digestive delays, suppress the catabolic response, and preserve skeletal muscle mass.

This article demonstrates how metabolic stress from exercise or infection drives severe musculoskeletal wasting by outpacing dietary protein intake. It phenotypically stratifies individuals, showing that high-excretor types drain their entire circulating plasma amino acid reservoir via sweat every 17 minutes.

Crucially, the study reveals a destructive metabolic feedback loop: breaking down skeletal muscle to replenish these localized High-Demand Amino Acid (HDAA) deficits inadvertently releases lower-demand amino acids, forcing secondary, irreversible branched-chain amino acid (BCAA) wasting.

It establishes a clinical model for targeted free-form HDAA therapy to protect lean mass.

This article establishes the metabolic indispensability of glycine and histidine during high-stress states, demonstrating how structural repair and cellular energy systems are limited by endogenous synthesis bottlenecks. It outlines that glycine production is strictly capped by tetrahydrofolate methylation requirements, failing to meet the massive skeletal demands of collagen, elastin, and keratin matrices.

Furthermore, it connects chronic deficits in these High-Demand Amino Acids (HDAAs) to impaired erythropoiesis and cytochrome-driven oxidative phosphorylation, providing a biochemical blueprint for targeted free-form supplementation to prevent clinical fatigue and downregulate muscle-wasting pathways.

This article exposes a critical flaw in conventional hydration strategies by quantifying that one hour of sweating drains a staggering 343% of the body's total circulating High-Demand Amino Acids (HDAAs).

Driven by active ductal ion-exchange mechanisms that sacrifice amino acids to resorb sodium, this rapid clearance empties plasma nutrient pools. Because standard electrolyte drinks fail to replace this nitrogen loss, the body is forced into immediate skeletal muscle catabolism to preserve homeostasis.

The study establishes a clinical rationale for combined HDAA and electrolyte rehydration to protect muscle integrity.

This article applies Bruce Ames’ Triage Theory to aging, demonstrating how nutrient scarcity forces the body to prioritize short-term survival over long-term cellular maintenance. It identifies a key catabolic triad driving sarcopenia—inactivity, low intake, and declining digestive efficiency—which severely limits amino acid absorption.

Crucially, the study illustrates how standard high-protein diets risk inducing harmful aminoaciduria in patients with renal limitations.

Ultimately, it provides evidence that targeted free-form High-Demand Amino Acid (HDAA) replenishment safely stimulates muscle protein synthesis and preserves skeletal lean mass without overloading renal nitrogen pathways.