Creatine use among young athletes.

OBJECTIVE: Creatine is a nutritional supplement that is purported to be a safe ergogenic aid in adults. Although as many as 28% of collegiate athletes admit taking creatine, there is little information about creatine use or potential health risk in children and adolescents. Although the use of creatine is not recommended in people less than 18 years of age, numerous anecdotal reports indicate widespread use in young athletes. The purpose of this study was to determine the frequency, risk factors, and demographics of creatine use among middle and high school student athletes. METHODS: Before their annual sports preparticipation physical examinations, middle and high school athletes aged 10 to 18 in Westchester County, a suburb north of New York City, were surveyed in a confidential manner. Information was collected regarding school grade, gender, specific sport participation, and creatine use. RESULTS: Overall, 62 of 1103 participants (5.6%) admitted taking creatine. Creatine use was reported in every grade, from 6 to 12. Forty-four percent of grade 12 athletes surveyed reported using creatine. Creatine use was significantly more common (P <.001) among boys (53/604, 8.8%) than girls (9/492, 1.8%). Although creatine was taken by participants in every sport, use was significantly more common among football players, wrestlers, hockey players, gymnasts, and lacrosse players (P <.001 for all). The most common reasons cited for taking creatine were enhanced performance (74.2% of users) and improved appearance (61.3%), and the most common reason cited for not taking creatine was safety (45.7% of nonusers). CONCLUSIONS: Despite current recommendations against use in adolescents less than 18 years old, creatine is being used by middle and high school athletes at all grade levels. The prevalence in grades 11 and 12 approaches levels reported among collegiate athletes. Until the safety of creatine can be established in adolescents, the use of this product should be discouraged.

Acute elevation and recovery of intracellular [Mg2+] following human focal cerebral ischemia.

We used 31P magnetic resonance spectroscopy (MRS) to investigate changes in brain intracellular [Mg2+] following human focal cerebral ischemia. Mean brain pMg (where pMg = -log[Mg2+]) was significantly lower in the ischemic focus of all stroke patients (pMg = 3.34 +/- 0.28, n = 45, p < 0.01) when compared with normal controls (pMg = 3.50 +/- 0.08, n = 25). Ischemic brain pMg was also significantly reduced when the pH of the stroke region was acidotic (pH < 6.90, pMg = 3.07 +/- 0.44, n = 11, p < 0.01) and when the phosphocreatine index (PCrI = PCr/[PCr+Pi (inorganic phosphate)]) was reduced (PCrI < 0.47, pMg = 3.12 +/- 0.42, n = 13, p < 0.01). Mean brain pMg was significantly reduced at days 0 to 1 (acute) poststroke (pMg = 3.32 +/- 0.28, n = 26, p < 0.01) and at days 2 to 3 (subacute) poststroke (pMg = 3.38 +/- 0.28, n = 21, p = 0.03). There was also a significant (p < 0.01) correlation between decreased pMg and increased relative signal intensity of Pi (normalized by total phosphate signal, Pi/TP) for all stroke groups studied. During the temporal evolution of stroke, pH returned to normal levels by days 2 to 3, and pMg returned to normal by days 4 to 10 (subacute). PCrI and Pi/TP returned toward normal levels after 10 days (chronic), at a time when ischemic brain pH had become significantly alkalotic (pH = 7.10 +/- 0.24, n = 15, p < 0.01). Elevation of ischemic brain [Mg2+] is temporally linked to the acidotic phase of human stroke as well as the breakdown of energy metabolism. These acute changes in [Mg2+] may contribute to, or be a marker for, cellular injury.

Altered brain energy metabolism in demented patients with multiple subcortical ischemic lesions. Working hypotheses.

We report the results of brain metabolic studies (using magnetic resonance spectroscopy) in three groups of individuals: (1) demented patients with multiple subcortical ischemic lesions (n = 18); (2) nondemented, age-matched controls (n = 21); and (3) demented patients with neurodegenerative disease, probably of the Alzheimer type (n = 19). Patients with dementia with subcortical vascular lesions, as demonstrated by appropriate imaging studies, had an increase of phosphate energy charge in areas of the cerebral cortex (especially prominent in the frontal regions) superficial to and excluded from the subcortical lesions. We hypothesize that this increased energy charge might be caused by reduced metabolic activity of disconnected brain tissue or by astrocytic hypertrophy and hyperplasia that accompanies subtle ischemic, cortical alterations.

Human focal cerebral ischemia: evaluation of brain pH and energy metabolism with P-31 NMR spectroscopy.

The authors investigated early human focal ischemia with phosphorus-31 nuclear magnetic resonance spectroscopy at 1.89 T to characterize the temporal evolution and relationship of brain pH and phosphate energy metabolism. Data from 65 symptomatic patients were prospectively studied; none of the patients had had ischemic stroke in the internal carotid artery territory before. Twenty-eight neurologically normal individuals served as control subjects. Serial ischemic brain pH levels indicated a progression from early acidosis to subacute alkalosis. When acidosis was present there was a significant elevation in the relative signal intensity of inorganic phosphate (Pi) and significant reductions in signal intensities of alpha-adenosine triphosphate (ATP) and gamma-ATP compared with those of control subjects. Ischemic brain pH values directly correlated with the relative signal intensity of phosphocreatine (PCr) and the PCr index and inversely correlated with the signal intensity of Pi. There was a general lack of correlation between either ischemic brain pH or phosphate energy metabolism and the initial clinical stroke severity. The data suggest a link between high-energy phosphate metabolism and brain pH, especially during the period of ischemic brain acidosis, and the authors propose that effective acute stroke therapy should be instituted during this period.

In vivo 31P NMR profiles of Alzheimer's disease and multiple subcortical infarct dementia.

We used in vivo phosphorus 31 nuclear magnetic resonance (31P NMR) spectroscopy to study regional high-energy phosphate and phospholipid metabolism in brains of patients with dementia associated with probable Alzheimer's disease (AD) and multiple subcortical cerebral infarctions (MSID). The MSID patients demonstrated elevations of the phosphocreatine (PCr)/inorganic orthophosphate (Pi) ratio in both the temporoparietal and frontal regions. Phosphomonoesters (PME) and the ratio of PME to phosphodiesters were elevated in the temporoparietal region of AD. Pi was also elevated in the frontal and temporoparietal regions of AD. Findings from 31P NMR were accurate in distinguishing MSID from AD. Values of PCr/Pi accurately classified 100% of the MSID patients and 92% of AD. Pi and PME, considered jointly, also accurately classified all MSID and all but 1 AD. Findings from in vivo 31P NMR spectroscopy appear to yield metabolic profiles useful in distinguishing AD from MSID.

Preliminary observations on brain energy metabolism in migraine studied by in vivo phosphorus 31 NMR spectroscopy.

We measured brain energy phosphate metabolism and intracellular pH (pHi) in a cross-sectional study of migraine patients by in vivo phosphorus 31 NMR spectroscopy. During a migraine attack the ratio ATP/total phosphate signal (mole % ATP) was preserved, but there was a decrease in mole % phosphocreatine (PCr) and an increase in mole % inorganic phosphate (Pi) resulting in a decrease of the PCr/Pi ratio, an index of brain phosphorylation potential. This was found in classic but not common migraine. Mole % Pi was also increased in combined brain regions between attacks. There was no alteration in brain pHi during or between attacks. Energy phosphate metabolism but not pHi appears disordered during a migraine attack.

Effect of nimodipine on blood pressure in acute ischemic stroke in humans.

Nimodipine is currently under investigation for the treatment of acute stroke. Although relatively specific for the cerebrovasculature, acute reductions in blood pressure after a dose may adversely affect neurologic outcome. We studied 29 consecutive acute ischemic stroke patients treated with placebo (n = 9) or either 120 (n = 10) or 240 (n = 10) mg/day of nimodipine. Blood pressure was recorded before and 30 and 60 minutes after a dose for the first 8 days. Ten neurologic physicians were asked to predict the treatment group (placebo or drug) of randomly selected patients based on blood pressure results. Only those patients on 240 mg/day of nimodipine had significant decreases in blood pressure after a dose (p less than 0.001); however, these were minimal (average 10 mm Hg systolic). Only 26 of 48 treatment predictions (54%) were correct. At the studied doses, nimodipine has a minimal effect on blood pressure in the acute stroke period.