SPORTS PERFORMANCE | RECOVERY SCIENCE: 7 Recovery Moves That Reset Your NRF2 and mTOR Pathways Between Soccer and Tennis Matches
SEO KEYWORDS Primary keyword: NRF2 and mTOR pathways Long-tail keyword: how to recover faster between soccer and tennis matches |
Ninety minutes of sprints, cuts, tackles and decelerations. Or three hours of lunging side to side on clay, serving over and over. You walk off feeling like you gave everything — and 48 hours later you find out exactly how much. Legs like concrete. A first step that's half a beat slow. A brain that reads the play a moment too late.
That gap between the final whistle and feeling sharp again comes down, in large part, to two cellular control systems: the NRF2 and mTOR pathways. One is your built-in antioxidant shield. The other is your muscle rebuilding switch. When both are working, you bounce back. When they fall behind, you start the next match in a hole. If you've ever wondered how to recover faster between soccer and tennis matches, this is where the answer lives.
Sound familiar?
You feel "flat" two days after a match even though you slept
Your hamstrings or calves feel tight going into the next game
Your decision-making fades late in the second half or the third set
You pick up niggles during congested weeks, never in light ones
You're taking a cabinet of supplements and still not sure any of it works
This guide breaks down what the research actually shows — fact-checked against peer-reviewed studies — and what you can do about it.
If your looking for an escape and are looking for melodic EDM music with that European/Mediterranean/Balkan sound and you need a track for summer, traveling, self development, and overcoming personal adversity then listen to Bay of Kotor. It has accordion, chords, orchestral chords, guitar and more.
When creating music, its about crafting a quality song that does not follow a trend but something that represents change through timelessness.
Listen/Follow Pavł Polø on Spotify.
1. Your Two Recovery Switches: What the NRF2 and mTOR Pathways Do
NRF2: the antioxidant shield
NRF2 is a transcription factor — a master switch that turns on your own antioxidant defences. Researchers describe it as the master regulator of antioxidant defence, controlling more than 200 protective genes. [1] When a hard session produces reactive oxygen species (ROS), NRF2 moves into the cell nucleus and switches on enzymes like superoxide dismutase, glutathione-related enzymes and NQO1.
Here's the part most people miss: exercise is supposed to trigger NRF2. Short spikes in oxidative stress during a hard session activate NRF2, and repeated exposure is how training builds a stronger antioxidant system over time. [1] In mice, deleting NRF2 from muscle sharply impaired running performance and muscle contractility. [2] Your shield isn't just protection — it's part of how you get fitter.
mTOR: the rebuilding switch
mTORC1 is the signalling hub that tells muscle to build protein. Essential amino acids (especially leucine) and resistance-type loading each switch on muscle protein synthesis, and combining them produces a bigger response than either alone. [4] Block mTOR in animal studies and leucine can no longer drive muscle building. [5] Every sprint, jump and lunge creates micro-damage; mTOR is how you repair it.
Together, the NRF2 and mTOR pathways decide how fast you go from "damaged" to "ready." NRF2 cleans up the oxidative mess. mTOR rebuilds the tissue.
2. What a Match Does to These Pathways
Soccer
A Greek study of soccer players tracked them for 72 hours after a game. The glutathione ratio (GSH/GSSG — a key readout of your antioxidant reserve) fell 17–75% during recovery, creatine kinase and soreness stayed elevated through 48 hours, and sprint and jump performance dropped 2–17% for as long as 72 hours. [6] A female futsal study found oxidative stress markers peaked at 24–48 hours and didn't return to baseline until 120 hours post-match. [7]
Researchers running a current soccer trial put it plainly: players often play two or three matches a week with 72 hours between them, which isn't enough to restore muscle homeostasis, and glutathione stays substantially reduced throughout that window. [8]
Tennis
Tennis is gentler on muscle damage markers but harsh on the nervous system. In nationally ranked junior players, a 3-hour simulated match on clay produced only a small rise in CK and soreness at 24–48 hours — but squat strength dropped about 35% and countermovement jump about 10% immediately after, and several players were still below baseline at 24 hours. [9] In tournament tennis, where you may play again the next day, that matters.
Fact check: is NRF2 "blocked" after a match?
Not exactly — and this distinction matters. A single match activates NRF2; what gets drained is the antioxidant reserve it protects, like glutathione. The real problem is repetition without recovery. A 2023 review notes that while moderate exercise activates NRF2, periods of excessive exercise have been shown to decrease NRF2 expression and impair mitochondrial function. [3] So the shield doesn't break after one game. It wears down across a congested block.
GOLD NUGGET #1 A single soccer match can drop your glutathione ratio by up to 75% and keep sprint and jump performance down for up to 72 hours. If your next match is in 72 hours, you are playing on a partially empty tank by default. [6] |
3. The Carry-Over Trap: How Unfinished Recovery Breeds More Inflammation and Brain Fog
Here's where it gets dangerous. If you start the next match before the NRF2 and mTOR pathways have reset, the inflammatory state from match one starts working against the repair process itself.
Inflammation puts the brakes on mTOR
Inflammatory cytokines such as TNF-α, IL-1 and IL-6 can inhibit mTOR signalling and dampen muscle protein synthesis while switching on muscle breakdown genes. [12] In human muscle cells, as little as 2 ng/ml of TNF-α cut growth-factor-stimulated protein synthesis by a third, and the effect lasted up to 48 hours. [10] In severe inflammation, researchers describe a "leucine resistance" driven by TNF-α and stress hormones working together — eating protein no longer flips the switch as well. [11] These are extreme models, not a soccer weekend, but the direction is clear: lingering inflammation makes your rebuilding switch less responsive.
That's the catabolic loop: less repair → more unresolved damage → more inflammatory signalling → even less repair.
Inflammation reaches the brain
IL-6 crosses the blood–brain barrier and is linked to increased feelings of fatigue; infusing IL-6 into runners reduced their 10K time-trial performance, possibly through increased serotonin activity in the brain. [13] The brain itself releases IL-6 during prolonged exercise, and that release was five-fold higher in a second exercise bout than in the first. [14] Disrupted sleep — common after night matches — is associated with higher perceived fatigue and effort, with IL-6 and stress hormones among the suspected mediators. [15]
What that looks like on the pitch or court:
Heavier legs at the same pace — effort perception goes up
Slower scanning and later decisions in the final third or on break points
Lower mood and motivation in training between matches
4. Why Unrecovered Athletes Get Hurt
The most cited number in soccer recovery comes from a Champions League-level club. Physical output (distance, sprints) didn't drop when players played twice a week — but the injury rate jumped from 4.1 to 25.6 injuries per 1,000 hours of exposure. [16] The authors concluded that 72–96 hours is enough to look normal on GPS but not enough to keep injury rates low.
Where unrecovered tissue tends to fail:
Hamstrings — high-speed running and late-swing braking in sprints
Groin/adductors and quads — cutting, kicking and decelerating
Calves and Achilles — repeated push-offs and split steps in tennis
Shoulder, elbow and wrist — serve and overhead volume in tennis, when grip and rotator cuff strength are still down
Sleep stacks on top of this. Adolescent athletes who chronically sleep under 8 hours were about 1.7 times more likely to be injured in Milewski's study, and a meta-analysis supports the link between chronic short sleep and sports injury. [17]
GOLD NUGGET #2 Players who played two matches a week had an injury rate more than six times higher than when they played one (25.6 vs 4.1 per 1,000 hours) — even though their running numbers looked the same. [16] |
5. Foods and Supplements With Research Behind Them
Below is what has actual human data in athletes or exercise models. "Evidence" here means at least one controlled trial — not proof that it will work for you.
The antioxidant trap
More is not better. In a randomised trial, 1,000 mg vitamin C plus 235 mg vitamin E daily blunted markers of mitochondrial adaptation to 11 weeks of endurance training. [34] Because exercise-driven ROS are the signal that activates NRF2, swamping them with high-dose isolated antioxidants can mute the very adaptation you're training for. [1] Food-first polyphenols and targeted use around congested periods make more sense than daily megadoses.
GOLD NUGGET #3 High-dose isolated antioxidants (1,000 mg vitamin C + vitamin E daily) blunted training adaptations in a randomised trial. Use polyphenol foods and save concentrated support for congested match blocks, not every training day. [34] |
6. Spirulina, Magnesium, Lime Water and Cracked Chlorella: How They Touch NRF2 and mTOR
This is the section most supplement marketing gets wrong, so here's the straight version. For each one, we separate what's been shown in athletes from what's been shown in rats or cell dishes. Both matter — but only one tells you what happens on your pitch.
Human data = measured in people, often athletes
Mechanism data = animal or cell studies showing how it might work
Spirulina and phycocyanin
Phycocyanin (C-phycocyanin) is the blue pigment-protein in spirulina, and it's the main reason scientists link spirulina to NRF2. Its colour comes from phycocyanobilin, an open-chain molecule that resembles the body's own bile pigments. [41]
How it activates NRF2 (mechanism data): In human skin cells, phycocyanin switched on the enzyme PKC α/βII, which pushed NRF2 out of the cytoplasm and into the nucleus. There it turned on the antioxidant response element and the protective enzyme heme oxygenase-1 (HO-1). Block PKC, and the NRF2 response disappeared. [39] Reviews also report that phycocyanobilin inhibits NADPH oxidase — a major ROS generator — and that phycocyanin dampens NF-κB, the master inflammation switch, in rodent studies. [41]
How it touches mTOR (mechanism data): In rats put through 8 weeks of deliberately excessive swimming, the exercise-only group showed lower mTOR gene expression, lower AKT activation and higher levels of the muscle-breakdown genes Atrogin-1 and MuRF-1, plus raised CK, IL-6 and TNF-α. Rats given phycocyanin had higher NRF2 protein, higher SOD, catalase and glutathione peroxidase activity, restored IRS-1/AKT signalling, lower damage and inflammation markers, and swam longer before fatigue. [40] That's the exact "overreached athlete" pattern this article describes — reversed, in rats.
Human data: No clinical trial has tested isolated phycocyanin for antioxidant or anti-inflammatory effects in people. [41] The human evidence is for whole spirulina: lower lipid peroxidation, CRP and CK in elite rugby players, [22] and lower CK, LDH and IL-6 with higher SOD and glutathione peroxidase in taekwondo athletes on 8 g/day for 3 weeks. [23] But well-fed cyclists on 7.5 g/day saw no change, [24] and a review warns that several oxidative-stress markers in older algae studies are unreliable. [25] Spirulina is protein-rich, but a few-gram dose supplies only a small amount of protein — nowhere near the 20–40 g that maximally stimulates mTOR. [18]
Verdict: the strongest mechanistic NRF2 story of the four, with promising human results in athletes whose diets are low in antioxidants. Use only third-party tested products, since spirulina has been found contaminated with liver-toxic microcystins. [33]
Magnesium
How it touches mTOR (mechanism data): Protein synthesis runs on ATP, and ATP works in the body as a magnesium–ATP complex. In ageing mice, magnesium (especially combined with vibration training) increased AKT activation and reduced muscle-breakdown genes, and blocking PI3K/AKT or mTOR in muscle cells cancelled the growth effect. [42] That's mouse and cell work, not athletes.
How it touches NRF2: Indirectly at best. The enzymes that build glutathione need magnesium-bound ATP. But a 2025 meta-analysis of 28 studies found magnesium reliably lowered CRP (inflammation), while effects on oxidative-stress markers like glutathione and MDA were inconclusive. [43] No study shows magnesium directly switching on NRF2.
Human data: A 2024 systematic review found 350 mg/day magnesium glycinate improved recovery after resistance training, and 400 mg/day lowered muscle damage markers in elite basketball players across a season. [26]
Verdict: think of magnesium as removing a brake, not pressing an accelerator. If you're low, correcting it helps soreness, inflammation and the energy supply mTOR depends on. Keep supplemental magnesium within the NIH limit of 350 mg/day for adults unless a clinician advises otherwise. [27]
Lime juice in water
How it touches NRF2 (mechanism data): Limes contain the flavonoids hesperidin and eriocitrin. [29] In rats, eriocitrin at 16–32 mg/kg raised NRF2 activation, HO-1 and NQO1 and lowered IL-6 and TNF-α; the lowest dose did nothing. [44] In cyclists, 500 mg/day of 2S-hesperidin for 8 weeks raised SOD and lowered oxidised glutathione and inflammation. [21]
How it touches mTOR: Not shown. Hesperetin preserved muscle fibre size in old mice, but the study didn't measure mTOR activity. [45]
The dose problem: lime juice provides about 13 mg of hesperidin per 100 ml [28] — roughly 1/40th of the cyclist dose in a full glass of juice, let alone a squeeze in water. There are no trials of lime water on NRF2 or mTOR.
Verdict: a great hydration habit with a little vitamin C. Not a pathway activator at realistic amounts. If you sip it all day, rinse with plain water to protect your teeth.
Cracked (broken cell wall) chlorella
Why "cracked" matters: Chlorella's tough cell wall is a major barrier to digestion, [31] so producers break it with pressure or milling. Label digestibility claims (often 80%+) come from manufacturers, not independent trials.
How it touches NRF2: Unclear. In rats given a toxic chemotherapy drug, chlorella lowered TNF-α, IL-6 and lipid peroxidation — but NRF2 staining actually came out lower, not higher, than in the untreated-toxin group. [47] In ageing rats, 90 days of chlorella lowered muscle lipid peroxidation and the muscle damage marker CK-MM, but NRF2 wasn't measured. [46] So chlorella looks antioxidant and anti-inflammatory; it hasn't been shown to work by switching on NRF2.
How it touches mTOR: Not studied. Any mTOR effect would most likely come from its protein content, which at typical gram doses is small.
Human data: In a randomised, placebo-controlled trial in college badminton players, 4 weeks of chlorella lowered CK and soreness at 24–48 hours after resistance exercise and kept strength higher on days 3–5 of recovery. [30]
Verdict: decent small-trial evidence for faster muscle recovery, mechanism unknown. Chlorella is high in vitamin K and may weaken warfarin; allergic and photosensitivity reactions have been reported. [32] Run it past a pharmacist if you take any medication.
Scorecard
GOLD NUGGET #4 Phycocyanin, spirulina's blue pigment, is the best-documented NRF2 activator of these four: it moves NRF2 into the nucleus and turns on HO-1 in human cells, and it reversed the overtraining pattern (low AKT, high breakdown genes, high IL-6) in rats. No human trial has tested it on its own yet. [39, 40, 41] |
7. Fresh as a Pine Tree and Ready 2 Go: What "Reset" Looks Like
When the NRF2 and mTOR pathways are back in balance, you can feel it — and measure it:
Glutathione restored — your antioxidant buffer is refilled, so the next match's ROS become a training signal instead of collateral damage
Inflammation resolved — IL-6 and TNF-α are back down, so mTOR responds normally to your meals
Muscle repaired — CK and soreness back to baseline, protein synthesis has caught up
Nervous system recharged — countermovement jump and sprint times back to your normal
Head clear — effort feels normal, decisions come early
A simple field check many teams use: a countermovement jump test the morning before training. If your jump is clearly below your baseline, you're not reset yet — adjust the session. In the tennis study, jump height was the measure that showed incomplete recovery in several players at 24 hours. [9]
8. Integrative Recovery: What Actually Helps
Sleep is the base layer. Aim for 8+ hours; chronic short sleep is linked to higher injury risk. [17] After night matches, protect the next night.
Refuel early. Hit 20–40 g of protein soon after the match and every 3–4 hours, with 30–40 g of casein-rich food (Greek yogurt, cottage cheese) before bed. [18]
Eat your polyphenols. Tart cherries, berries, citrus, broccoli sprouts and leafy greens every day, with concentrated forms during congested weeks. [19, 20]
Time cold water carefully. Ice baths reduce soreness, but after strength sessions they reduced mTOR signalling (p70S6K) and long-term strength and muscle gains. [35] Use them between matches; skip them after gym days.
Don't expect a recovery jog to fix your blood markers. In elite female players, light cycling and resistance work between games didn't speed up oxidative stress, antioxidant or inflammatory recovery. [36] Use it for mobility and feel, not chemistry.
Rotate and monitor. The Dupont data point straight at squad rotation during congested blocks. [16] Track sleep, soreness and jump height daily.
9. How Integrative Pharmacy Fits In
Supplements are where most athletes go off the rails — wrong dose, wrong product, wrong combination with medication, or a contaminated batch that risks an anti-doping violation. This is where a clinically trained pharmacist earns their place on your support team.
A systematic review of sports pharmacy found pharmacists willing and well-positioned to counsel athletes, especially around doping prevention, injury management and medications, while noting that specialised training is still developing. [37] A separate review describes how clinical pharmacists can optimise athletes' use of drugs, supplements and herbal products and prevent interactions and adverse events. [38]
In an integrative pharmacy setting, a specially trained pharmacist working with your provider can:
Review your full list of prescriptions, over-the-counter drugs and supplements for interactions (for example, chlorella and warfarin)
Use your provider's chart notes, diagnoses and labs — kidney function, iron status, vitamin D, magnesium — to tailor doses to your body, not a label
Account for disease states such as asthma, thyroid conditions, anaemia or gut issues that change what you can absorb or tolerate
Screen products for third-party testing and banned-substance risk
Build a match-week plan that changes with your schedule, and adjust it as your provider updates your notes
GOLD NUGGET #5 Most supplement mistakes are interaction, dose or contamination problems — exactly what a pharmacist is trained to catch. Bring your full supplement list to every review, not just your prescriptions. [37, 38] |
TALK TO AN INTEGRATIVE PROVIDER Every athlete's body, health history and schedule is different. Before you start spirulina, chlorella, magnesium, sulforaphane or any other supplement — especially if you take medication or have a medical condition — book a visit with an integrative provider and ask for a consult with an integrative pharmacist. Bring your training load, match calendar, sleep data and full supplement list, and build a recovery plan for the NRF2 and mTOR pathways that is safe and specific to you. |
5 Actionable Steps for Athletes and Students
Protect sleep like a training session. Set a fixed lights-out time aiming for 8+ hours, and plan an extra-early night after evening matches.
Run a protein clock. 20–40 g of protein every 3–4 hours on match day and the two days after, plus 30–40 g of casein-rich food before bed.
Build a polyphenol plate daily. Berries or tart cherries, citrus, and a handful of broccoli sprouts or cruciferous veg — and add a concentrate only during congested weeks.
Test before you train. Do a quick countermovement jump or sprint check the morning after a match. Below baseline means lighter session, more recovery.
Get a supplement review. Take your full list to an integrative provider and pharmacist. Choose third-party tested products and keep supplemental magnesium within 350 mg/day unless your clinician says otherwise.
The Bottom Line
The NRF2 and mTOR pathways are your recovery engine. A match drains your antioxidant reserve and leaves inflammation that, if it lingers, slows repair, fogs your thinking and raises your injury risk — especially in congested weeks. You can't supplement your way out of short sleep or too many minutes. But sleep, protein, polyphenol-rich food, smart timing of cold water, and a personalised supplement plan built with an integrative provider and pharmacist can get you to the next kickoff or first serve fresh as a pine tree and Ready 2 Go.
This article is for education only and is not medical advice. Talk to your healthcare provider before starting any supplement.
References
[1] Done AJ, Traustadóttir T. Nrf2 mediates redox adaptations to exercise. Redox Biology. 2016;10:191–199. https://pmc.ncbi.nlm.nih.gov/articles/PMC5078682
[2] Skeletal Muscle Nrf2 Contributes to Exercise-Evoked Systemic Antioxidant Defense Via Extracellular Vesicular Communication. Exercise and Sport Sciences Reviews. 2021;49(3):213–222. https://pmc.ncbi.nlm.nih.gov/articles/PMC8195856
[3] Isothiocyanates, Nrf2 and exercise (review). 2023. https://pmc.ncbi.nlm.nih.gov/articles/PMC10493800/
[4] Drummond MJ, et al. Nutritional and contractile regulation of human skeletal muscle protein synthesis and mTORC1 signaling. J Appl Physiol. 2009;106(4):1374–1384. https://pmc.ncbi.nlm.nih.gov/articles/PMC2698645/
[5] Leucine-Enriched Nutrients and the Regulation of mTOR Signalling and Human Skeletal Muscle Protein Synthesis. https://pmc.ncbi.nlm.nih.gov/articles/PMC5096790
[6] Fatouros IG, et al. Time-course of changes in oxidative stress and antioxidant status responses following a soccer game. J Strength Cond Res. 2010. https://sponet.de/sponet/Record/4022671
[7] Souglis A, et al. Time Course of Performance Indexes, Oxidative Stress, Inflammation, and Muscle Damage Markers after a Female Futsal Match. Sports (MDPI). https://doaj.org/article/760b8503d01c496ba354e9d48e7ac991
[8] S-Acetyl Glutathione and Performance Recovery in Soccer (NCT07690124). ClinicalTrials.gov. https://clinicaltrials.gov/study/NCT07690124
[9] Gomes RV, et al. Muscle damage after a tennis match in young players. Biology of Sport. 2014;31:27–32. https://pmc.ncbi.nlm.nih.gov/articles/PMC3994582
[10] Frost RA, Lang CH, et al. Transient exposure of human myoblasts to TNF-α inhibits serum and IGF-I stimulated protein synthesis. Endocrinology. https://dbpia.nl.go.kr/endo/article/138/10/4153/2987598
[11] Lang CH, et al. Regulation of muscle protein synthesis during sepsis and inflammation (Penn State). https://pure.psu.edu/en/publications/regulation-of-muscle-protein-synthesis-during-sepsis-and-inflamma/
[12] Inflammation and muscle protein turnover (figure). Frontiers in Physiology. 2020;11:87. https://pmc.ncbi.nlm.nih.gov/articles/PMC7031348/figure/F2
[13] Response of plasma IL-6 and its soluble receptors during submaximal exercise to fatigue in sedentary middle-aged men. https://pmc.ncbi.nlm.nih.gov/articles/PMC2673892
[14] Nybo L, et al. Interleukin-6 release from the human brain during prolonged exercise. Journal of Physiology. https://test01.ku.dk/:obvius/pureproxy/3974268/en/publications/interleukin-6-release-from-the-human-brain-during-prolonged-exerc-3
[15] Sleep disruption, IL-6, neuroendocrine factors and perceived fatigue during exercise (Coventry/Loughborough). https://pure.coventry.ac.uk/ws/portalfiles/portal/28740767/Binder2.pdf
[16] Dupont G, et al. Effect of 2 soccer matches in a week on physical performance and injury rate. Am J Sports Med. 2010;38(9):1752–1758. https://pubmed.ncbi.nlm.nih.gov/20400751/
[17] Chronic lack of sleep is associated with increased sports injury in adolescents: a systematic review and meta-analysis. https://pmc.ncbi.nlm.nih.gov/articles/PMC6446394
[18] Jäger R, et al. International Society of Sports Nutrition Position Stand: protein and exercise. JISSN. 2017;14:20. https://doaj.org/article/fcc34534a75d466aa37abda0042df7a7
[19] Bell PG, et al. The Effects of Montmorency Tart Cherry Concentrate Supplementation on Recovery Following Prolonged, Intermittent Exercise. Nutrients. 2016;8(7):441. https://pubmed.ncbi.nlm.nih.gov/27455316/
[20] Komine S, et al. Effect of a sulforaphane supplement on muscle soreness and damage induced by eccentric exercise in young adults: A pilot study. Physiological Reports. 2021. https://pmc.ncbi.nlm.nih.gov/articles/PMC8685487
[21] 8-Week Supplementation of 2S-Hesperidin Modulates Antioxidant and Inflammatory Status after Exercise until Exhaustion in Amateur Cyclists. Antioxidants. 2021. https://pmc.ncbi.nlm.nih.gov/articles/PMC8000657
[22] Chaouachi M, et al. Spirulina supplementation prevents exercise-induced lipid peroxidation, inflammation and skeletal muscle damage in elite rugby players. 2022. https://pubmed.ncbi.nlm.nih.gov/35394687/
[23] Kashani A, et al. Preventive Effects of Spirulina platensis on Exercise-Induced Muscle Damage, Oxidative Stress and Inflammation in Taekwondo Athletes. Pharm Sci. 2022;28(4):589–595. https://ps.tbzmed.ac.ir/Article/ps-34873
[24] Spirulina does not decrease muscle damage nor oxidative stress in cycling athletes with adequate nutritional status. Biology of Sport. 2010. https://lida.sport-iat.de/bdr/Record/4021011?lng=en
[25] Gurney T, Spendiff O. Algae Supplementation for Exercise Performance: Current Perspectives and Future Directions for Spirulina and Chlorella. Frontiers in Nutrition. 2022;9:865741. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8937016/
[26] Effects of magnesium supplementation on muscle soreness in different type of physical activities: a systematic review. J Transl Med. 2024. https://translational-medicine.biomedcentral.com/counter/pdf/10.1186/s12967-024-05434-x.pdf
[27] NIH Office of Dietary Supplements. The Scoop, May 2024 (magnesium upper limit). https://ods.od.nih.gov/pubs/The_Scoop_May_2024.pdf
[28] Limes: Nutrition Facts and Potential Health Benefits (Phenol-Explorer hesperidin data). Nutrition Advance. https://www.nutritionadvance.com/?p=27617
[29] Aprifel. Lime nutritional sheet. https://aprifel.com/en/nutritional-sheet/lime
[30] Effects of 4-Week Chlorella Supplementation on Resistance Exercise-Induced Muscle Damage in Athletes. Taipei Medical University. https://hub.tmu.edu.tw/en/publications/%E8%A3%9C%E5%85%85%E5%9B%9B%E9%80%B1%E7%B6%A0%E8%97%BB%E5%B0%8D%E9%81%8B%E5%8B%95%E5%93%A1%E9%98%BB%E5%8A%9B%E9%81%8B%E5%8B%95%E5%BC%95%E8%B5%B7%E8%82%8C%E8%82%89%E6%90%8D%E5%82%B7%E7%9A%84%E5%BD%B1%E9%9F%BF/
[31] Testimony on a successful lab protocol to disrupt Chlorella vulgaris microalga cell wall. PLOS ONE. 2022. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9119475/
[32] Drugs and Lactation Database (LactMed). Chlorella. NIH / NICHD. https://ncbi.nlm.nih.gov/books/NBK501822/pdf/Bookshelf_NBK501822.pdf
[33] Microcystins and Cyanobacterial Contaminants in French Small-Scale Productions of Spirulina. Toxins. 2023. https://pmc.ncbi.nlm.nih.gov/articles/PMC10302721/
[34] Paulsen G, et al. Vitamin C and E supplementation hampers cellular adaptation to endurance training in humans. J Physiol. 2014. https://pmc.ncbi.nlm.nih.gov/articles/PMC4001759
[35] Roberts LA, et al. Post-exercise cold water immersion attenuates acute anabolic signalling and long-term adaptations in muscle to strength training. J Physiol. 2015;593:4285–4301. https://pmc.ncbi.nlm.nih.gov/articles/PMC4594298/
[36] Active recovery training does not affect the antioxidant response to soccer games in elite female players. https://lida.sport-iat.de/ta/Record/4020925?lng=en
[37] Hooper AD, et al. Current and Potential Roles in Sports Pharmacy: A Systematic Review. Pharmacy. 2019;7(1):29. https://researchonline.jcu.edu.au/73233/
[38] The clinical pharmacist and sports practice: pharmaceutical care for athletes. Pharmacy (MDPI). 2020;8(4):218. https://www.mdpi.com/2226-4787/8/4/218/htm
[39] Kim KM, et al. Phycocyanin Protects Against UVB-Induced Apoptosis Through the PKC α/βII-Nrf-2/HO-1 Dependent Pathway in Human Primary Skin Cells. Molecules. 2018;23(2):478. https://www.mdpi.com/1420-3049/23/2/478
[40] Puengpan S, et al. Phycocyanin attenuates skeletal muscle damage and fatigue via modulation of Nrf2 and IRS-1/AKT/mTOR pathway in exercise-induced oxidative stress in rats. PLoS ONE. 2024;19(9):e0310138. https://pmc.ncbi.nlm.nih.gov/articles/PMC11386417/
[41] Citi V, et al. Nutraceutical Features of the Phycobiliprotein C-Phycocyanin: Evidence from Arthrospira platensis (Spirulina). Nutrients. 2024;16(11):1752. https://www.mdpi.com/2072-6643/16/11/1752
[42] Cui C, et al. Coapplication of Magnesium Supplementation and Vibration Modulate Macrophage Polarization to Attenuate Sarcopenic Muscle Atrophy through PI3K/Akt/mTOR Signaling Pathway. Int J Mol Sci. 2022;23(21):12944. https://www.mdpi.com/1422-0067/23/21/12944
[43] Unlocking the Power of Magnesium: A Systematic Review and Meta-Analysis Regarding Its Role in Oxidative Stress and Inflammation. Antioxidants. 2025. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12189353/
[44] He J, Zhou D, Yan B. Eriocitrin alleviates oxidative stress and inflammatory response in cerebral ischemia reperfusion rats by regulating Nrf2/NQO-1/HO-1/NF-κB p65. Ann Transl Med. 2020;8(12):757. https://pmc.ncbi.nlm.nih.gov/articles/PMC7333167
[45] Biesemann N, et al. High throughput screening of mitochondrial bioenergetics in human differentiated myotubes identifies novel enhancers of muscle performance in aged mice. Sci Rep. 2018;8:9408. https://link.springer.com/article/10.1038/s41598-018-27614-8
[46] Zainul Azlan N, et al. Chlorella vulgaris Ameliorates Oxidative Stress and Improves the Muscle Regenerative Capacity of Young and Old Sprague-Dawley Rats. Nutrients. 2020;12(12):3752. https://www.mdpi.com/2072-6643/12/12/3752
[47] Protective Impacts of Chlorella vulgaris on Cisplatin-Induced Toxicity in Liver, Kidney, and Spleen of Rats: Role of Oxidative Stress, Inflammation, and Nrf2 Modulation. Life. 2025;15(6):934. https://www.mdpi.com/2075-1729/15/6/934
Comments