{"id":16,"date":"2025-03-14T15:35:00","date_gmt":"2025-03-14T15:35:00","guid":{"rendered":""},"modified":"2026-04-27T11:24:18","modified_gmt":"2026-04-27T11:24:18","slug":"creatine-part-i","status":"publish","type":"post","link":"https:\/\/fitmia.fi\/?p=16","title":{"rendered":"Creatine Part I"},"content":{"rendered":"\n

 <\/p>\n\n\n\n

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<\/div>\n\n\n\n

Creatine is one of the most well-known and researched
\nsupplements on the market. I believe it was around 1997 when the product first
\narrived in Finland, and I quickly ended up trying it myself. Creatine can be
\nused in cycles or continuously, and everyone can find a method of use that
\nsuits them if they experience benefits from it.<\/o:p><\/span><\/p>\n\n\n\n

From my personal experience, I\u2019ve found that using it
\nfor 3-4 months at a time, twice a year, works best for me. As a
\nvegetarian\/vegan, this may partly explain why creatine supplementation has had
\na noticeably positive impact on my training results. Research has shown that
\nvegetarians tend to have lower creatine levels in their muscles and seem to
\nrespond better to creatine supplementation (Burke, 2003). This makes sense
\nsince dietary creatine comes exclusively from animal products.<\/o:p><\/span><\/p>\n\n\n\n

Interestingly, recent discussions have included
\nobservations about creatine’s effects on cognitive function. However, I
\npersonally haven\u2019t noticed any effects in that regard\u2014though I certainly
\nwouldn\u2019t have minded! <\/span>\ud83d\ude06<\/span> In
\nresearch studies, not all participants have shown increased brain creatine
\nlevels, even when dosage, administration method, product type, and timing were
\nstandardized. Perhaps for me, creatine only works below the brain level?<\/o:p><\/span><\/p>\n\n\n\n

In recent years, researchers have also started
\nexploring creatine\u2019s potential effects on brain function. In these writings, my
\nprimary focus will be on creatine\u2019s impact on muscle growth, strength, and
\ncognitive factors, but I\u2019ll also cover general observations about its use.
\nFinally, I will outline the researched dosage protocols and recommendations for
\ncreatine supplementation. However, in this first section, I will focus on
\ngeneral aspects and cognitive findings related to creatine.<\/o:p><\/span><\/p>\n\n\n\n

Creatine has traditionally been associated with energy
\nsupply, particularly in short-duration, high-intensity efforts. This assumption
\nis based on the use of aerobic and anaerobic energy during performance. ATP
\n(adenosine triphosphate) is the molecule in which energy is stored. It is
\npresent in all cells, including muscle cells. In order to initiate and sustain
\nmuscle contraction, ATP must be continuously regenerated. This process occurs
\nin three ways: through creatine phosphate (CP), anaerobic glycolysis, and
\naerobic glycolysis (oxidative system).<\/o:p><\/span><\/p>\n\n\n\n

Every cell contains a small amount of CP, and when it
\ndonates a phosphate group to ADP (adenosine diphosphate), ATP is formed. The
\nimmediate energy source for muscle activity is ATP, which lasts only a few
\nseconds. CP can provide energy for about 10 seconds (ACSM\u2019s Resources for the
\nExercise Physiologist, Komi, 2003). Additionally, creatine plays a role in
\nenergy transport from mitochondria (the cell\u2019s “powerhouse,” where
\nATP is produced) to the cytoplasm, helping maintain ATP balance during high
\nenergy demand. This prevents muscle fatigue by keeping ADP levels low and
\nreducing calcium leakage (Ca\u00b2\u207a) from the sarcoplasmic reticulum (Sahlin, 2011;
\nWallimann, 1977 & 1992).<\/o:p><\/span><\/p>\n\n\n\n

If the performance continues beyond this point,
\nanaerobic glycolysis is utilized as an energy source. This process requires
\ncarbohydrates\u2014glucose and glycogen stored in muscles\u2014which are broken down to
\nform ATP through phosphorylation (attachment of a phosphate group, PO\u2084\u00b3\u207b, to a
\nmolecule). This energy supply lasts for approximately 90 seconds. Longer
\nefforts require energy through the oxidative system, which involves two
\npathways: the Krebs cycle and the electron transport chain. Here, energy is
\nderived from fats, carbohydrates, and to a limited extent, proteins. During
\nexercise, anaerobic and aerobic systems work together to generate ATP for
\nenergy (ACSM\u2019s Resources for the Exercise Physiologist, Komi, 2003). This means
\nthat CP supplementation could be particularly beneficial for short bursts of
\nactivity lasting under 10 seconds. Research has also been conducted on creatine
\nuse in endurance sports, which I will discuss later.<\/o:p><\/span><\/p>\n\n\n\n

Creatine is generally well tolerated, with minimal
\nknown side effects. The most commonly reported side effect is water retention.
\nThis also ties into concerns about kidney function in relation to creatine use.
\nBut first, let\u2019s address water retention\u2026<\/o:p><\/span><\/p>\n\n\n\n

Creatine is an osmotically active substance, meaning
\nthat an increase in body creatine levels can theoretically lead to water
\nretention. Creatine is transported into muscles from the bloodstream via a
\nsodium-dependent creatine transporter (Wyss, 2000). This process occurs
\nalongside sodium, and water moves into the muscles to maintain intracellular
\nosmolality (solute concentration). However, significant changes in
\nintracellular sodium concentration due to creatine supplementation are
\nunlikely, given the function of sodium-potassium pumps (Francaux, 2006).<\/o:p><\/span><\/p>\n\n\n\n

It appears that the most common side effect of
\ncreatine supplementation is water retention, particularly in the initial phase
\nof use. Studies have shown an increase in total body water and extracellular
\nfluid after three days of creatine supplementation (Rosene, 2015).
\nIntracellular water content also increases in the early phase (Ziegenfuss,
\n1998).<\/o:p><\/span><\/p>\n\n\n\n

<\/p>\n\n\n\n

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There is extensive research on exercise training and
\ncreatine supplementation (with study durations ranging from 5 to 10 weeks).
\nMost studies have not observed an increase in total body water. One study
\ninvolved men performing resistance training while taking creatine at 0.3 g per
\nkg of lean body mass per day for 7 days (approximately 20 g\/day). This was
\nfollowed by a maintenance dose of 0.075 g per kg of lean body mass per day for
\n28 days (about 5 g\/day). No significant changes were observed in intracellular,
\nextracellular, or total body water (Andre, 2016). Another study used a creatine
\nsupplementation protocol of 20 g\/day for seven days, followed by 5 g\/day for 21
\ndays, with similar results (Jagim, 2012).<\/span><\/p>\n\n\n\n

When creatine was given to men and women at a dose of
\n0.03 g\/kg\/day for six weeks, no significant increase in total body water was
\nobserved (Rawson, 2011). From my own experience, I always retain about 2-4 kg
\nof water during the first week of creatine use, but this stabilizes over time.
\nHowever, whenever I stop using creatine, my weight drops again\u2014despite what
\nthese studies suggest.<\/o:p><\/span><\/p>\n\n\n\n

On the other hand, Ribeiro et al. (2020) examined the
\ncombined effects of creatine supplementation and resistance training over an
\neight-week period and found a significant increase in total body water (+7.0%)
\nand intracellular fluid (+9.2%) compared to the placebo group. In both groups,
\nextracellular fluid increased similarly (creatine group: 1.2% vs. placebo
\ngroup: 0.6%). However, the ratio of skeletal muscle mass to intracellular fluid
\nremained the same in both groups. Intracellular fluid plays an important role
\nas an intracellular signal for protein synthesis, which in turn promotes muscle
\ngrowth over time (Safdar, 2008). This has often been cited as evidence that
\nwhile creatine increases fluid levels, it also activates muscle hypertrophy.<\/o:p><\/span><\/p>\n\n\n\n

Now, onto the kidneys… In skeletal muscle, both
\ncreatine and phosphocreatine (PCr) degrade non-enzymatically into creatinine,
\nwhich enters the bloodstream and is eventually excreted in urine (Wyss, 2000).
\nHealthy kidneys filter creatinine from the blood into the urine; otherwise,
\ncreatinine would accumulate in the bloodstream. Therefore, blood creatinine
\nlevels can be used as a marker of kidney function. However, blood creatinine
\nlevels are also linked to muscle mass as well as dietary intake of creatine and
\ncreatinine itself. For example, men typically have higher blood creatinine
\nlevels than women due to their greater muscle mass (Hultman, 1996). When taking
\ncreatine supplements or consuming creatine-rich foods like meat, both blood and
\nurinary creatinine levels may temporarily rise. During creatine
\nsupplementation, urinary creatine levels can become extremely high (>10
\ng\/day), even though creatine is typically absent from urine (Rawson, 2002).<\/o:p><\/span><\/p>\n\n\n\n

Although more than 95% of the body’s creatine is
\nstored in skeletal muscle, the brain is also a highly metabolic tissue,
\naccounting for up to 20% of the body’s total energy consumption (Gualano, 2009;
\nTurner, 2015). As such, creatine may serve as an important energy source for
\nthe central nervous system (Sahlin, 2011; Wallimann, 1977 & 1992). However,
\ncreatine is synthesized outside of muscle tissue, primarily in the liver,
\npancreas, and kidneys. From these sources, as well as from dietary intake, creatine
\nenters the bloodstream and is transported to muscles via a transporter protein.
\nWhile skeletal muscles cannot synthesize creatine themselves, the brain does
\nhave this ability (Andres, 2008; Braissant, 2017). This has led to the
\nassumption that the brain may be more resistant to external creatine
\nabsorption. Instead, the brain likely relies on endogenous creatine synthesis
\nuntil a disturbance affects its creatine balance. Such disturbances may include
\nintense exercise or sleep deprivation, while chronic disruptions include
\ntraumatic brain injury, aging, Alzheimer’s disease, and depression.<\/o:p><\/span><\/p>\n\n\n\n

Creatine may reduce the formation of reactive oxygen
\nspecies (e.g., free radicals) either by transporting ATP to the mitochondria or
\nby directly scavenging free radicals in the extracellular environment (Sestili,
\n2011). These direct and indirect antioxidant effects may provide benefits in
\nthe treatment of neurodegenerative diseases (Beal, 2011). Creatine deficiency
\nsyndromes, where brain creatine levels are low, manifest as cognitive and
\ndevelopmental disorders (e.g., intellectual disability, learning difficulties,
\nautism, and epileptic seizures), which may be alleviated, at least partially,
\nwith creatine supplementation (Kaldis, 1996; Salomons, 2003; Stockler, 1994
\n& 2007).<\/o:p><\/span><\/p>\n\n\n\n

Creatine metabolism may also influence cognitive
\nprocesses by supporting ATP balance in situations where brain ATP production is
\naccelerated or disrupted. Such situations include complex cognitive tasks,
\nhypoxia (oxygen deprivation), sleep deprivation, and certain neurological
\nconditions (Dolan, 2019; Benton, 2010; McMorris, 2007). Creatine
\nsupplementation may also be beneficial in recovery from mild traumatic brain
\ninjury by supporting the brain\u2019s energy needs. Several literature reviews have
\nexamined the effects of creatine on brain creatine levels, cognitive function,
\nand mild traumatic brain injury (Dolan, 2019; Rae, 2015; Avgerinos, 2018).<\/o:p><\/span><\/p>\n\n\n\n

Sleep deprivation is known to affect brain energy
\nproduction, and evidence suggests that creatine supplementation may enhance
\ncognitive performance under sleep-deprived conditions compared to a placebo.
\nHowever, only two studies have specifically investigated cognitive performance
\nfollowing sleep deprivation, both of which included mild to moderate physical
\nactivity (Hammett, 2010; Ling, 2009). For instance, after 24 hours of sleep
\ndeprivation, creatine supplementation reduced performance deterioration in tasks
\ninvolving random movement generation, choice reaction time, balance, and mood
\n(Ling, 2009). Additionally, in a similar study conducted by the same research
\ngroup, creatine supplementation mitigated sleep deprivation-induced impairments
\nin complex cognitive functions (Hammett, 2010).<\/o:p><\/span><\/p>\n\n\n\n

As is often the case, not all studies have found
\ncognitive benefits from creatine supplementation (Nemets, 2013; Alves, 2013;
\nRawson, 2008; Merege-Filho, 2017). Studies on Huntington’s disease, multiple
\nsclerosis (MS), amyotrophic lateral sclerosis (ALS), Parkinson\u2019s disease, and
\nDuchenne muscular dystrophy have generally not shown significant effects from
\ncreatine supplementation.<\/o:p><\/span><\/p>\n\n\n\n

Creatine supplementation may be beneficial in the
\ntreatment of various forms of depression (Hellem, 2015; Kious, 2019; Kondo,
\n2009; Lyoo, 2012; Roitman, 2007; Toniolo, 2017; Toniolo, 2018). Additionally,
\nsome evidence suggests benefits in managing and protecting against concussions
\nand traumatic brain injuries (Forbes et al., 2022).<\/o:p><\/span><\/p>\n\n\n\n

A systematic review by Prokopidis et al. (2023)
\nsummarized findings indicating that creatine supplementation improved memory
\nperformance in healthy individuals, particularly in older adults (66\u201376 years
\nold). The studies included in the review were of moderate quality, despite
\nbeing carefully selected. This pattern seems to apply to many studies in the
\nfield.<\/o:p><\/span><\/p>\n\n\n\n

Overall, there is some evidence suggesting that
\ncreatine supplementation may enhance cognitive function. These effects appear
\nto be more pronounced under conditions of increased brain energy demand, such
\nas sleep deprivation (Forbes et al., 2022). However, variability among studies
\nmakes direct comparisons challenging. Study populations differ, supplementation
\nprotocols vary (ranging from 2\u201320 g\/day), and different brain regions have been
\nexamined using various methods. Additionally, brain phosphocreatine levels have
\nbeen measured using different techniques, and different methods have been used
\nto assess memory function. As a result, the optimal dosage for maximizing brain
\ncreatine absorption remains unclear and warrants further investigation. Current
\nevidence suggests that creatine monohydrate supplementation increases brain
\ncreatine levels, but to a lesser extent than in skeletal muscle under similar
\nsupplementation protocols.<\/span><\/p>\n\n\n

<\/div>

Mia<\/p><\/div><\/div>\n\n

Olen Terveystieteiden ja liikuntatieteiden maisteri, fysioterapeutti ja urheiluhieroja. Ty\u00f6skentelen v\u00e4it\u00f6skirjatutkijana sek\u00e4 tutkimusavustajana, ja toteutan lis\u00e4ksi valmennuksia ja luentoja. Minulla on my\u00f6s pitk\u00e4 kokemus liikunta-ja kuntoutusalan opetusty\u00f6st\u00e4.\r\nTutkimukseni keskittyy aivojen ja liikunnan vuorovaikutukseen sek\u00e4 menetelmiin, joilla voidaan kehitt\u00e4\u00e4 toimintakyky\u00e4. Olen erityisen kiinnostunut lihastoiminnasta, voimantuotosta ja motorisesta suorituskyvyst\u00e4 biomekaniikan ja neurofysiologian n\u00e4k\u00f6kulmasta.\r\nHy\u00f6dynn\u00e4n ty\u00f6ss\u00e4ni muun muassa EMG:t\u00e4, TMS:\u00e4\u00e4 sek\u00e4 toiminnallisia suorituskykytestej\u00e4 neuromuskulaarisen toiminnan tutkimiseen.\r\n\r\n\r\nI am MSc (Health Sciences & Sport Sciences), \r\nPhysiotherapist, sports massage therapist, and doctoral researcher. I currently work as a research assistant while also providing coaching and delivering lectures. I have extensive experience in teaching within the field of exercise and health sciences.\r\nMy research focuses on the interaction between the brain and physical exercise, as well as methods to enhance functional capacity. I am particularly interested in muscle function, strength production, and motor performance from a neurophysiological and biomechanical perspective.\r\nI utilize methods such as electromyography (EMG), transcranial magnetic stimulation (TMS), and functional performance testing to study neuromuscular function.<\/div>\n\n\n


<\/span><\/p>\n\n\n\n

Photo 1 by Milad Fakurian on Unsplash<\/span>
\n<\/span>https:\/\/unsplash.com\/photos\/blue-and-green-peacock-feather-58Z17lnVS4U<\/span><\/a><\/span><\/o:p><\/span><\/span><\/p>\n\n\n\n

Photo 2 by Aleksander Saks on Unsplash<\/span>
\n<\/span>https:\/\/unsplash.com\/photos\/a-bottle-of-creatine-next-to-a-spoon-on-a-table-lVZGEyL_j40<\/span><\/a><\/span><\/span><\/o:p><\/span><\/p>\n\n\n\n


<\/span><\/p>\n\n\n\n

References: <\/span><\/p>\n\n\n\n

<\/p>\n\n\n\n

Alves CRR, Filho CAAM, Benatti FB, Brucki SMD, Pereira
\nRMR, Pinto ALDS, Lima FR, Roschel H & Gualano B (2013): Creatine
\nSupplementation Associated or Not with Strength Training upon Emotional and
\nCognitive Measures in Older Women: A Randomized Double-Blind Study<\/o:p><\/span><\/span><\/p>\n\n\n\n

American
\nCollege of Sports Medicine. ACSM\u00b4s Resources for the
\nExercise Physiologist<\/a>. 3rd<\/sup> Edition. Philadelphia (PA): Wolters
\nKluwer; 2022<\/o:p><\/span><\/span><\/p>\n\n\n\n

Andre TL, Gann JJ, McKinley-Barnard SK, Willoughby DS (2016):
\nEffects of five weeks of resistance training and relatively-dosed creatine
\nmonohydrate supplementation on body composition and muscle strength and
\nwhole-body creatine metabolism in resistance-trained males<\/o:p><\/span><\/span><\/p>\n\n\n\n

Andres RH, Ducray AD, Schlattner U, Wallimann T &
\nWidmer HR (2008): Functions and effects of creatine in the central nervous
\nsystem <\/o:p><\/a><\/span><\/span><\/p>\n\n\n\n

Avgerinos<\/span><\/a><\/span> KI, Spyrou N, Bougioukas KI & Kapogiannis D (2018):
\nEffects of creatine supplementation on cognitive function of healthy
\nindividuals: A systematic review of randomized controlled trials<\/o:p><\/span><\/span><\/span><\/p>\n\n\n\n

Benton<\/span><\/span>
\nD & Donohoe R (2010): The influence of creatine supplementation on the
\ncognitive functioning of vegetarians and omnivores <\/o:p><\/span><\/span><\/p>\n\n\n\n

Beal MF (2011): Neuroprotective effects of creatine<\/o:p><\/span><\/span><\/p>\n\n\n\n

Burke DG, Chilibeck PD, Parise G, Candow DG, Mahoney D
\n& Tarnopolsky M (2003): Effect of creatine and weight training on muscle
\ncreatine and performance in vegetarians<\/o:p><\/span><\/span><\/p>\n\n\n\n

Braissant O, Bachmann C & Henry H (2007): Expression
\nand function of AGAT, GAMT and CT1 in the mammalian brain <\/o:p><\/span><\/span><\/p>\n\n\n\n

Dolan<\/span><\/a>
\nE, Gualano B & Rawson ES (2019): Beyond muscle: The effects of creatine
\nsupplementation on brain creatine, cognitive processing, and traumatic brain
\ninjury<\/o:p><\/span><\/span><\/p>\n\n\n\n

Francaux M & Poortmans JR. (2006): Side effects of
\ncreatine supplementation in athletes <\/o:p><\/a><\/span><\/span><\/p>\n\n\n\n

Gualano<\/span><\/span>
\nB, Artioli GG, Poortmans JR & Junior AHL (2009): Exploring the therapeutic
\nrole of creatine supplementation<\/o:p><\/span><\/span><\/p>\n\n\n\n

Hall M & Trojian TH (2013): Creatine
\nsupplementation<\/o:p><\/span><\/span><\/p>\n\n\n\n

Hammett ST, Wall MB, Edwards TC & Smith AT (2010):
\nDietary supplementation of creatine monohydrate reduces the human fMRI BOLD
\nsignal<\/o:p><\/span><\/span><\/p>\n\n\n\n

Hellem TL, Sung Y-H, Shi X-F, Pett MA, Latendresse G,
\nMorgan J, Huber RS, Kuykendall D, Lundberg KJ, Renshaw PF (2015): Creatine as a
\nNovel Treatment for Depression in Females Using Methamphetamine: A Pilot Study<\/o:p><\/span><\/span><\/p>\n\n\n\n

Hultman E, Soderlund K,
\nTimmons JA, Cederblad G & Greenhaff PL (1996): Muscle creatine loading in
\nmen<\/o:p><\/span><\/span><\/p>\n\n\n\n

Jagim AR, Oliver JM, Sanchez A, Galvan E, Fluckey J,
\nRiechman S, Greenwood M, Kelly K, Meininger C, Rasmussen C, Kreider RB. (2012) A
\nbuffered form of creatine does not promote greater changes in muscle creatine
\ncontent, body composition, or training adaptations than creatine monohydrate<\/o:p><\/span><\/span><\/p>\n\n\n\n

Kaldis P, Hemmer W, Zanolla E, Holtzman D &
\nWallimann T (1996): \u2019Hot Spots\u2019 of Creatine Kinase Localization in Brain:
\nCerebellum, Hippocampus and Choroid Plexus<\/o:p><\/span><\/span><\/p>\n\n\n\n

Kious BM, Kondo DG
\n& Renshaw PF (2019): Creatine for the Treatment of Depression<\/span><\/span> <\/span><\/p>\n\n\n\n

Komi edited (2003): Strenth and power in sport. 2nd<\/sup>
\nedition. Blackwell Science Ltd.<\/o:p><\/span><\/span><\/p>\n\n\n\n

Kondo DG, Sung YH, Hellem TL, Fiedler KK, Shi X, Jeong
\nEK & Renshaw PF (2011): Open-label adjunctive creatine for female
\nadolescents with SSRI-resistant major depressive disorder: A 31-phosphorus
\nmagnetic resonance spectroscopy study <\/o:p><\/span><\/span><\/p>\n\n\n\n

Ling J, Kritikos M & Tiplady B (2009): Cognitive
\neffects of creatine ethyl ester supplementation <\/o:p><\/span><\/span><\/p>\n\n\n\n

Lyoo IK, Yoon S, Kim,
\nT-S, Hwang J, Kim JE, Won W, Bae S & Renshaw PF (2012): A Randomized,
\nDouble-Blind Placebo-Controlled Trial of Oral Creatine Monohydrate Augmentation
\nfor Enhanced Response to a Selective Serotonin Reuptake Inhibitor in Women with
\nMajor Depressive Disorder<\/span><\/span><\/p>\n\n\n\n

McMorris<\/span><\/a>
\nT, Mielcarz G, Harris RC, Swain JP (2007): Howard, A.N. Creatine
\nSupplementation and Cognitive Performance in Elderly Individuals<\/o:p><\/span><\/span><\/p>\n\n\n\n

Merege-Filho<\/span><\/a>
\nCAA, Otaduy MCG & De S\u00e1-Pinto AL, De Oliveira MO, Gon\u00e7alves LDS, Hayashi APT,
\nRoschel H, Pereira RMR, Silva CA, Brucki SMD, da Costa Leite C & Gualano B (2017):
\nDoes brain creatine content rely on exogenous creatine in healthy youth? A
\nproof-of-principle study<\/o:p><\/span><\/span><\/p>\n\n\n\n

Nemets B & Levine
\nJ (2013): A pilot dose-finding clinical trial of creatine monohydrate
\naugmentation to SSRIs\/SNRIs\/NASA antidepressant treatment in major depression<\/span><\/span><\/p>\n\n\n\n

Safdar A, Yardley NJ, Snow R, Melov S, &Tarnopolsky
\nMA (2008): Global and targeted gene expression and protein content in skeletal
\nmuscle of young men following short-term creatine monohydrate supplementation<\/o:p><\/span><\/span><\/p>\n\n\n\n

Sahlin K & Harris RC (2011): The creatine kinase
\nreaction: A simple reaction with functional complexity<\/o:p><\/span><\/span><\/p>\n\n\n\n

Salomons GS, Van Dooren SJM, Verhoeven NM, Marsden D,
\nSchwartz C, Cecil KM, Degrauw TJ & Jakobs C (2003) X-linked creatine
\ntransporter defect: An overview<\/o:p><\/span><\/span><\/p>\n\n\n\n

Sestili P, Martinelli C, Colombo E, Barbieri, E,
\nPotenza, L, Sartini S & Fimognari C. (2011) Creatine as an antioxidant<\/o:p><\/span><\/span><\/p>\n\n\n\n

Stockler S, Holzbach U, Hanefeld F, Marquardt I, Helms
\nG, Requart M, Hanicke W, Frahm J. (1994): Creatine Deficiency in the Brain: A
\nNew, Treatable Inborn Error of Metabolism<\/o:p><\/span><\/span><\/p>\n\n\n\n

Stockler S, Schutz PW & Salomons GS (2007): Cerebral
\ncreatine deficiency syndromes: Clinical aspects, treatment and pathophysiology<\/o:p><\/span><\/span><\/p>\n\n\n\n

Rae CD & Br\u00f6er S. (2015) Creatine as a booster for
\nhuman brain function. How might it work? <\/o:p><\/span><\/span><\/p>\n\n\n\n

Rawson ES, Clarkson PM,
\nPrice TB, Miles MP (2002): Differential response of muscle phosphocreatine to
\ncreatine supplementation in young and old subjects<\/o:p><\/span><\/span><\/p>\n\n\n\n

Rawson ES, Lieberman HR, Walsh TM, Zuber SM, Harhart JM
\n& Matthews TC (2008): Creatine supplementation does not improve cognitive
\nfunction in young adults<\/o:p><\/span><\/span><\/p>\n\n\n\n

Rawson ES, Stec MJ, Frederickson SJ, Miles MP (2011): Low-dose
\ncreatine supplementation enhances fatigue resistance in the absence of weight
\ngain<\/o:p><\/span><\/span><\/p>\n\n\n\n

Ribeiro AS, Avelar A, Kassiano W, Nunes JP, Schoenfeld
\nBJ, Aguiar AF, Trindade MCC, Silva AM, Sardinha LB, Cyrino ES (2020): Creatine
\nSupplementation Does Not Influence the Ratio Between Intracellular Water and
\nSkeletal Muscle Mass in Resistance-Trained Men<\/o:p><\/span><\/span><\/p>\n\n\n\n

Roitman S, Green T,
\nOsher Y, Karni N & Levine J: (2007) Creatine monohydrate in resistant
\ndepression: A preliminary study<\/span><\/span><\/p>\n\n\n\n

Roschel HB, Ostojic SM & Rawson
\nES (2021): Creatine Supplementation and Brain Health<\/span><\/span><\/p>\n\n\n\n

Rosene JM, Matthews TD, Mcbride KJ, Galla A, Haun M,
\nMcdonald K, Gagne N, Lea J, Kasen J, Farias C (2015): The effects of creatine
\nsupplementation on thermoregulation and isokinetic muscular performance
\nfollowing acute (3-day) supplementation<\/o:p><\/span><\/span><\/p>\n\n\n\n

Toniolo R, Fernandes F,
\nSilva M, Dias R & Lafer B (2017): Cognitive effects of creatine monohydrate
\nadjunctive therapy in patients with bipolar depression: Results from a
\nrandomized, double-blind, placebo-controlled trial<\/span><\/span><\/p>\n\n\n\n

Toniolo RA, Silva M & de Brito
\nFerreira Fernandes F, de Mello Siqueira Amaral JA, da Silva Dias R, Lafer BA(2018):
\nRandomized, double-blind, placebo-controlled, proof-of-concept trial of
\ncreatine monohydrate as adjunctive treatment for bipolar depression<\/span>
\n<\/o:p><\/span><\/span><\/p>\n\n\n\n

Turner CE, Byblow WD & Gant N (2015): Creatine
\nSupplementation Enhances Corticomotor Excitability and Cognitive Performance
\nduring Oxygen Deprivation<\/o:p><\/span><\/span><\/p>\n\n\n\n

Wallimann T, Turner DC & Eppenberger HM (1977): Localization
\nof creatine kinase isoenzymes in myofibrils. I. Chicken skeletal muscle<\/o:p><\/span><\/span><\/p>\n\n\n\n

Wallimann<\/span><\/a>
\nT, Wyss M, Brdiczka D, Nicolay K & Eppenberger HM (1992): Intracellular
\ncompartmentation, structure and function of creatine kinase isoenzymes in
\ntissues with high and fluctuating energy demands: The \u2018phosphocreatine circuit\u2019
\nfor cellular energy homeostasis<\/o:p><\/span><\/span><\/p>\n\n\n\n

Wyss M & Kaddurah-Daouk R (2000) Creatine and
\ncreatinine metabolism<\/o:p><\/span><\/span><\/p>\n\n\n\n

Ziegenfuss T, Lowery LM & Lemon P (1998) Acute
\nfluid volume changes in men during three days of creatine supplementation<\/span><\/o:p><\/span><\/p>\n\n\n\n

<\/span><\/p>\n\n\n\n

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