phosphocreatine helps to maintains muscular performance. This appears to be an early benefit. The question is does this help in prolonged performance requirements.
Loading dose of creatine, 20 grams/day, over 5-6 days increases total muscle creatine levels. This has been shown to improve athletic performance. The phosphocreatine in Type II muscle fibers are particularly increased. This can be maintained at 2 grams/day.
the energy supplied to rephosphorylate
adenosine diphosphate (ADP) to adenosine triphosphate (ATP) during and following intense
exercise is largely dependent on the amount of phosphocreatine (PCr) stored in the
muscle
Creatine is chemically known as a non-protein nitrogen
It is synthesized in the liver and pancreas from the amino acids arginine, glycine,
and methionine
Approximately 95% of the body's creatine is stored in skeletal muscle
About two thirds of the creatine found in skeletal muscle is stored as phosphocreatine
(PCr) while the remaining amount of creatine is stored as free creatine
The body breaks down about 1 – 2% of the creatine pool per day (about 1–2 grams/day)
into creatinine in the skeletal muscle
The magnitude of the increase in skeletal muscle creatine content is important because
studies have reported performance changes to be correlated to this increase
"loading" protocol. This protocol is characterized by ingesting approximately
0.3 grams/kg/day of CM for 5 – 7 days (e.g., ≃5 grams taken four times per day) and
3–5 grams/day thereafter [18,22]. Research has shown a 10–40% increase in muscle creatine and PCr stores using this
protocol
Additional research has reported that the loading protocol may only need to be 2–3
days in length to be beneficial, particularly if the ingestion coincides with protein
and/or carbohydrate
A few studies have reported protocols with no loading
period to be sufficient for increasing muscle creatine (3 g/d for 28 days)
Cycling protocols involve the consumption of "loading" doses for 3–5 days every 3
to 4 weeks
Most of these forms of creatine have been reported to be no
better than traditional CM in terms of increasing strength or performance
Recent studies do suggest, however, that adding β-alanine to CM
may produce greater effects than CM alone
These investigations indicate that the
combination may have greater effects on strength, lean mass, and body fat percentage;
in addition to delaying neuromuscular fatigue
creatine
phosphate has been reported to be as effective as CM at improving LBM and strength
Green et al. [24] reported that adding 93 g of carbohydrate to 5 g of CM increased total muscle creatine
by 60%
Steenge et al. [23] reported that adding 47 g of carbohydrate and 50 g of protein to CM was as effective
at promoting muscle retention of creatine as adding 96 g of carbohydrate.
It appears that combining CM with carbohydrate or carbohydrate and protein produces
optimal results
Studies suggest that increasing skeletal muscle creatine uptake may
enhance the benefits of training
Nearly 70% of these studies have
reported a significant improvement in exercise capacity,
Long-term CM supplementation appears to enhance the overall quality of training,
leading to 5 to 15% greater gains in strength and performance
Nearly all studies indicate that "proper" CM supplementation increases body mass
by about 1 to 2 kg in the first week of loading
short-term adaptations reported from
CM supplementation include increased cycling power, total work performed on the bench
press and jump squat, as well as improved sport performance in sprinting, swimming,
and soccer
Long-term adaptations when combining CM supplementation with training include increased
muscle creatine and PCr content, lean body mass, strength, sprint performance, power,
rate of force development, and muscle diameter
subjects taking CM typically gain about twice as much body
mass and/or fat free mass (i.e., an extra 2 to 4 pounds of muscle mass during 4 to
12 weeks of training) than subjects taking a placebo
The gains in muscle mass appear to be a result of an improved ability to perform
high-intensity exercise via increased PCr availability and enhanced ATP synthesis,
thereby enabling an athlete to train harder
there is no evidence to support the notion
that normal creatine intakes (< 25 g/d) in healthy adults cause renal dysfunction
no long-term side effects have been observed in athletes (up to 5 years),
One cohort of patients taking 1.5 – 3 grams/day of CM has been monitored since 1981
with no significant side effects
editorial discussion of the benefit of vitamin D in mitochondrial function. Those in the vitamin D repletion arm of the study had a quicker recovery time to restored phospho-creatinine levels. The quicker the recovery of phospho-creatinine levels, the shorter recovery phase and the likely improvement in athletic performance.
Long-chain polyunsaturated fatty acids, including eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), are highly enriched in neuronal synaptosomal plasma membranes and vesicles
The predominant CNS polyunsaturated fatty acid is DHA
effective supplementation and/or increased ingestion of dietary sources rich in EPA and DHA, such as cold-water fish species and fish oil, may help improve a multitude of neuronal functions, including long-term potentiation and cognition.
multiple preclinical studies have suggested that DHA and/or EPA supplementation may have potential benefit through a multitude of diverse, but complementary mechanisms
pre-injury dietary supplementation with fish oil effectively reduces post-traumatic elevations in protein oxidation
The benefits of pre-traumatic DHA supplementation have not only been independently confirmed,[150] but DHA supplementation has been shown to significantly reduce the number of swollen, disconnected and injured axons when administered following traumatic brain injury.
DHA has provided neuroprotection in experimental models of both focal and diffuse traumatic brain injury
potential mechanisms of neuroprotection, in addition to DHA and EPA's well-established anti-oxidant and anti-inflammatory properties
Despite abundant laboratory evidence supporting its neuroprotective effects in experimental models, the role of dietary DHA and/or EPA supplementation in human neurological diseases remains uncertain
Several population-based, observational studies have suggested that increased dietary fish and/or omega-3 polyunsaturated fatty acid consumption may reduce risk for ischemic stroke in several populations
Randomized control trials have also demonstrated significant reductions in ischemic stroke recurrence,[217] relative risk for ischemic stroke,[2] and reduced incidence of both symptomatic vasospasm and mortality following subarachnoid hemorrhage
Clinical trials in Alzheimer's disease have also been largely ineffective
The clinical evidence thus far appears equivocal
curcumin has gained much attention from Western researchers for its potential therapeutic benefits in large part due to its potent anti-oxidant[128,194,236] and anti-inflammatory properties
Curcumin is highly lipophilic and crosses the blood-brain barrier enabling it to exert a multitude of different established neuroprotective effects
in the context of TBI, a series of preclinical studies have suggested that pre-traumatic and post-traumatic curcumin supplementation may bolster the brain's resilience to injury and serve as a valuable therapeutic option
Curcumin may confer significant neuroprotection because of its ability to act on multiple deleterious post-traumatic, molecular cascades
studies demonstrated that both pre- and post-traumatic curcumin administration resulted in a significant reduction of neuroinflammation via inhibition of the pro-inflammatory molecules interleukin 1β and nuclear factor kappa B (NFκB)
no human studies have been conducted with respect to the effects of curcumin administration on the treatment of TBI, subarachnoid or intracranial hemorrhage, epilepsy or stroke
studies have demonstrated that resveratrol treatment reduces brain edema and lesion volume, as well as improves neurobehavioral functional performance following TBI
green tea consumption or supplementation with its derivatives may bolster cognitive function acutely and may slow cognitive decline
At least one population based study, though, did demonstrate that increased green tea consumption was associated with a reduced risk for Parkinson's disease independent of total caffeine intake
a randomized, placebo-controlled trial demonstrated that administration of green tea extract and L-theanine, over 16 weeks of treatment, improved indices of memory and brain theta wave activity on electroencephalography, suggesting greater cognitive alertness
Other animal studies have also demonstrated that theanine, another important component of green tea extract, exerts a multitude of neuroprotective benefits in experimental models of ischemic stroke,[63,97] Alzheimer's disease,[109] and Parkinson's disease
Theanine, like EGCG, contains multiple mechanisms of neuroprotective action including protection from excitotoxic injury[97] and inhibition of inflammation
potent anti-oxidant EGCG which is capable of crossing the blood-nerve and blood-brain barrier,
Epigallocatechin-3-gallate also displays neuroprotective properties
More recent research has suggested that vitamin D supplementation and the prevention of vitamin D deficiency may serve valuable roles in the treatment of TBI and may represents an important and necessary neuroprotective adjuvant for post-TBI progesterone therapy
Progesterone is one of the few agents to demonstrate significant reductions in mortality following TBI in human patients in preliminary trials
in vitro and in vivo studies have suggested that vitamin D supplementation with progesterone administration may significantly enhance neuroprotection
Vitamin D deficiency may increase inflammatory damage and behavioral impairment following experimental injury and attenuate the protective effects of post-traumatic progesterone treatment.[37]
emerging evidence has suggested that daily intravenous administration of vitamin E following TBI significantly decreases mortality and improves patient outcomes
high dose vitamin C administration following injury stabilized or reduced peri-lesional edema and infarction in the majority of patients receiving post-injury treatment
it has been speculated that combined vitamin C and E therapy may potentiate CNS anti-oxidation and act synergistically with regards to neuroprotection
one prospective human study has found that combined intake of vitamin C and E displays significant treatment interaction and reduces the risk of stroke
Pycnogenol has demonstrated the ability to slow or reduce the pathological processes associated with Alzheimer's disease
Pcynogenol administration, in a clinical study of elderly patients, led to improved cognition and reductions in markers of lipid peroxidase
One other point of consideration is that in neurodegenerative disease states like Alzheimer's disease and Parkinson's disease, where there are high levels of reactive oxygen species generation, vitamin E can tend to become oxidized itself. For maximal effectiveness and to maintain its anti-oxidant capacity, vitamin E must be given in conjunction with other anti-oxidants like vitamin C or flavonoids
These various factors might account for the null effects of alpha-tocopherol supplementation in patients with MCI and Alzheimer's disease
preliminary results obtained in a pediatric population have suggested that post-traumatic oral creatine administration (0.4 g/kg) given within four hours of traumatic brain injury and then daily thereafter, may improve both acute and long-term outcomes
Acutely, post-traumatic creatine administration seemed to reduce duration of post-traumatic amnesia, length of time spent in the intensive care unit, and duration of intubation
At three and six months post-injury, subjects in the creatine treatment group demonstrated improvement on indices of self care, communication abilities, locomotion, sociability, personality or behavior and cognitive function when compared to untreated controls
patients in the creatine-treatment group were less likely to experience headaches, dizziness and fatigue over six months of follow-up
CNS creatine is derived from both its local biosynthesis from the essential amino acids methionine, glycine and arginine
Studies of patients with CNS creatine deficiency and/or murine models with genetic ablation of creatine kinase have consistently demonstrated significant neurological impairment in the absence of proper creatine, phosphocreatine, or creatine kinase function; thus highlighting its functional importance
chronic dosing may partially reverse neurological impairments in human CNS creatine deficiency syndromes
Several studies have suggested that creatine supplementation may also reduce oxidative DNA damage and brain glutamate levels in Huntington disease patients
Another study highlighted that creatine supplementation marginally improved indices of mood and reduced the need for increased dopaminergic therapy in patients with Parkinson's disease