Amino acid supplementation accelerates resolution of exercise-induced phagocyte infiltration in human skeletal muscle.

Resistance exercise increased MPO-positive cell infiltration and oxidative DNA damage in skeletal muscle at 24 hours post-exercise.

• MPO+ cell infiltration increased by +161% at 24 h post-exercise (p = 0.02) in the placebo condition.
• 8-hydroxy-2-deoxyguanosine (8-OHdG) levels increased by +66% at 24 h post-exercise (p = 0.02).
• Study used a randomized, double-blind, placebo-controlled crossover design in 10 young men (22 ± 2.8 years).
• Biopsies of the vastus lateralis muscle were collected at baseline, immediately after exercise (0 h), and 24 h post-exercise.

Amino acid supplementation accelerated MPO-positive cell infiltration to immediately post-exercise, with the response diminishing by 24 hours.

• Under amino acid supplementation, MPO+ cell infiltration peaked at 0 h post-exercise (+100%, p = 0.03).
• By 24 h post-exercise under amino acid supplementation, MPO+ cell infiltration was only +53% and did not reach statistical significance (p = 0.06).
• In contrast, placebo showed peak MPO+ infiltration at 24 h (+161%, p = 0.02), indicating a delayed inflammatory response.
• Participants consumed either 15 g amino acids or an isocaloric placebo before resistance exercise.

MPO-positive infiltrating cells exhibited markedly higher mitochondrial density and integrated with injured regions of adjacent myofibers showing lower mitochondria.

• Immunofluorescence co-staining using TOM20 labeling revealed higher mitochondrial density in MPO+ cells.
• MPO+ cells were found integrated with the injured regions of adjacent myofibers that showed lower mitochondrial content.
• Other infiltrating MPO-negative cells also contributed mitochondria to exercised muscle tissue.
• These observations suggest that infiltrating bone marrow-derived cells contribute to mitochondrial gains in damaged muscle.

Overall mitochondrial content in skeletal muscle approximately doubled during 24-hour recovery following exercise, independent of supplementation condition.

• There was an overall ~2-fold increase in mitochondrial content during 24-h recovery (p < 0.001).
• This increase was similar under both amino acid supplementation and placebo conditions.
• The mitochondrial gains were associated with infiltration of both MPO-positive and MPO-negative bone marrow-derived cells.

Cellular senescence marker p16Ink4a mRNA decreased after exercise, with an earlier reduction observed under amino acid supplementation.

• p16Ink4a mRNA decreased by 58% at 24 h post-exercise overall.
• Under amino acid treatment, an earlier reduction was observed at 0 h post-exercise (-49%, p = 0.05).
• p16Ink4a serves as a cellular senescence marker in this context.
• The earlier reduction under amino acid treatment is consistent with accelerated resolution of the inflammatory response.

The study design was a randomized, double-blind, placebo-controlled crossover trial examining the effects of pre-exercise amino acid supplementation on skeletal muscle inflammation.

• Ten young men with a mean age of 22 ± 2.8 years participated.
• Participants consumed either 15 g amino acids or an isocaloric placebo before resistance exercise.
• Muscle biopsies were taken from the vastus lateralis at baseline, immediately post-exercise (0 h), and 24 h post-exercise.
• Outcome measures included MPO+ cell counts, 8-OHdG levels, mitochondrial content (TOM20), and p16Ink4a mRNA expression.