5 RESEARCH ARTICLES
Jooyoung Kim,1 and Dong Jun Sung ET AL
(1) Creatine is a widely used dietary supplement to improve exercise performance by reducing exercise-induced muscle damage.
(2) Many researchers have suggested creatine reduces muscle damage by decreasing the inflammatory response and oxidative stress, regulating calcium homeostasis, and activating satellite cells.
(3) However, the underlying mechanisms of creatine and muscle damage have not been clarified.
(4) This review discusses regulatory effects of creatine on muscle damage by compiling information collected from basic science and sports science research
Turner CE1, Byblow WD2, Gant N3.
(1) Impairment or interruption of oxygen supply compromises brain function and plays a role in neurological and neurodegenerative conditions
(2) Creatine is a naturally occurring compound involved in the buffering, transport, and regulation of cellular energy, with the potential to replenish cellular adenosine triphosphate without oxygen
(3) Creatine is also neuroprotective in vitro against anoxic/hypoxic damage
(4) Dietary creatine supplementation has been associated with improved symptoms in neurological disorders defined by impaired neural energy provision
(1) Here we investigate, for the first time in humans, the utility of creatine as a dietary supplement to protect against energetic insult
(2) Assess the influence of oral creatine on neurophysiological and neuropsychological function of healthy young adults during acute oxygen deprivation
(1) 15 healthy adults were supplemented with creatine and placebo treatments for 7 d, which increased brain creatine on average by 9.2%
(2) A hypoxic gas mixture (10% oxygen) was administered for 90 min, causing global oxygen deficit and impairing a range of neuropsychological processes
(1) Hypoxia-induced decrements in cognitive performance, specifically attentional capacity, were restored when participants were creatine supplemented, and corticomotor excitability increased
(2) A neuromodulatory effect of creatine via increased energy availability is presumed to be a contributing factor of the restoration, perhaps by supporting the maintenance of appropriate neuronal membrane potentials
(1) Dietary creatine monohydrate supplementation augments neural creatine, increases corticomotor excitability, and prevents the decline in attention that occurs during severe oxygen deficit
(2) This is the first demonstration of creatine’s utility as a neuroprotective supplement when cellular energy provision is compromised
Smith RN1, Agharkar AS1, Gonzales EB2.
(1) Creatine is an endogenous compound synthesized from arginine, glycine and methionine
(2) Sources: meat and fish, along with athlete supplement powders
(3) Since the majority of creatine is stored in skeletal muscle, dietary creatine supplementation has traditionally been important for athletes and bodybuilders to increase the power, strength, and mass of the skeletal muscle
(1) New research suggests it may be important in preventing or delaying onset of neurodegenerative diseases associated with aging
(2) On average, 30% of muscle mass is lost by age 80, while muscular weakness remains a vital cause for loss of independence
(3) In light of these new roles of creatine, the dietary supplement’s usage has been studied to determine its efficacy in treating congestive heart failure, gyrate atrophy, insulin insensitivity, cancer, and high cholesterol
AGING & THE BRAIN
(1) In relation to the brain, creatine has been shown to have antioxidant properties, reduce mental fatigue, protect the brain from neurotoxicity, and improve facets/components of neurological disorders like depression and bipolar disorder
(2) This has made creatine a leading candidate in the fight against age-related diseases, such as Parkinson’s, Huntington’s, ALS, long-term memory impairments associated with the progression of Alzheimer’s disease, and stroke
(3) In this review, we explore normal mechanisms by which creatine is produced and its necessary physiology, while paying special attention to the importance of creatine supplementation in improving diseases and disorders associated with brain aging and outlining clinical trials involving creatine to treat these diseases
Ellen Cristini de Freitas
– Evaluate effects of creatine (Cr) on oxidative stress and inflammation markers after acute repeated-sprint exercise
– 25 players under age 20 yrs were assigned to two groups:
(1) Cr supplemented
– supplementation was performed using Cr (0.3 g/kg) or placebo tablets for 7 d.
– Before and after 7 d of supplementation, the athletes performed two consecutive Running-based Anaerobic Sprint Tests (RAST).
– RAST consisted of six 35-m sprint runs at maximum speed with 10 sec rest between them.
– Blood samples were collected just prior to start of test (pre), just after the completion (0 h), and 1 h after completion.
– Cr inhibited the increase of inflammation markers TNF-α and CRP, but not oxidative stress markers, due to acute exercise
– Investigate the effects of an acute bout of resistance exercise (RE) on oxidative stress response and oxidative DNA damage in male athletes and whether supplementation with Cr could negate any observed differences.
– 27 resistance-trained men were randomly divided into a
(1) Cr supplementation group (the Cr group [21.6 ± 3.6 years], taking 4 × 5 g Cr monohydrate per day)
(2) or a placebo (PL) supplementation group (the PL group [21.2 ± 3.2 years], taking 4 × 5 g maltodextrin per day).
(2) A double-blind research design was employed for a 7-day supplementation period.
– Before and after the seventh day of supplementation, the subjects performed an RE protocol (7 sets of 4 exercises using 60-90 1 repetition maximum) in the flat pyramid loading pattern.
(1) Before the supplementation period, a significant increase in the urinary 8-OHdG excretion and plasma MDA levels was observed after RE.
(2) The Cr supplementation induces a significant increase in athletics performance
(3) It attenuated (reduced) the changes observed in the urinary 8-OHdG excretion and plasma MDA.
– Cr supplementation reduced oxidative DNA damage and lipid peroxidation induced by a single bout of RE.