Here is some of
the many Research Abstracts from the World's
leading Scientific Journals, that relate to the ingredients
in
Xtreme PUMP and Backup the Science behind this amazing product.
NUCLEOTIDE RESEARCH
Title:
Intense exercise induces the degradation
of adenine nucleotide and purine nucleotide synthesis via
de novo pathway in the rat liver.
Author:
Mikami T , Kitagawa J
Source:
Eur J Appl Physiol, 96(5): 543-50 2006
Abstract:
The purpose of this study was to investigate the influence
of intense exercise on the metabolism of adenine nucleotides
in the liver. In the first experiment, to determine the
degradation of adenine nucleotides, hepatic adenine nucleotides
of rats were labeled by an intraperitoneal administration
of 15N-labeled adenine the day before treadmill running
to exhaustion. In the second experiment, to determine the
de novo synthesis of purine nucleotides after intense exercise,
14C-glycine was intraperitoneally administered to rats performing
intense running on a treadmill. In the first experiment,
hepatic levels of ATP and total adenine nucleotides showed
a reduction immediately after exercise. In contrast, hepatic
levels of AMP, adenosine, hypoxanthine and uric acid showed
an increase immediately after exercise. The hepatic 15N
level continued to decline during the recovery period after
exercise. Urinary excretion of 15N-urate was 40% higher
in the exercised rats than in the control rats. In the second
experiment, the radioactivity of 14C detected in the fraction
of hepatic urate and allantoin was approximately 300% higher
in the exercised rats than in the control rats. 14C-radioactivity
that excreted into urine as urate and allantoin was approximately
200% higher in the exercised rats. Intense exercise led
to the degradation of hepatic adenine nucleotides, which
were not utilized for the re-synthesis of nucleotide and
further degraded to hypoxanthine or uric acid. Intense exercise
induced the synthesis of purine nucleotides in the liver
via a de novo pathway and these synthesized nucleotides
were also degraded to nucleosides and excreted into urine.
Title:
Nitrogenous compounds of interest
in clinical nutrition.
Author:
Fontana Gallego L , Sáez Lara MJ , Santisteban
Bailón R ,
Source:
Nutr Hosp, 21 Suppl 2(): 14-27, 15-29 2006
Abstract:
The term "conditionally essential" (or semi-essential),
initially applied to amino acids, has been generalized to
other nutrients. A conditionally essential nutrient is a
compound usually produced in adequate amounts by endogenous
synthesis but that is exogenously required under certain
circumstances. Thus, arginine, glutamine, cysteine, glycine,
carnitine, choline, and polyamines are conditionally essential
compounds. In addition, dietary nucleotides are considered
semi-essential since some rapidly growing tissues such as
the gut, bone marrow, and lymphocytes, preferentially use
preformed purine and pyrimidine bases for nucleic acid synthesis.
This review discusses the study of conditionally essential
nitrogenous nutrients of interest in clinical nutrition.
Among them we highlight arginine, involved in endothelial,
immune, gastrointestinal, and renal functions, in reproduction,
neonatal development, wound healing, and tumorigenicity;
glutamine, necessary for maintaining bowel integrity, and
with beneficial effects on catabolic states such as sepsis,
infection, trauma, and cancer; and nucleotides, implicated
in cell growth and differentiation, and with various effects
on lipid metabolism, intestinal microbiota, and immune system.
Title:
Sweat lactate, ammonia, and urea in
rugby players.
Author:
Alvear-Ordenes I , GarcÃa-López D ,
De Paz JA , González-Gallego J
Source:
Int J Sports Med, 26(8): 632-7 2005
Abstract:
The purpose of this study was to investigate sweat lactate,
ammonia, and urea excretion in rugby players. Fifteen elite
amateur rugby players volunteered to participate. The study
was conducted during competitive matches in the official
season. Plasma and sweat concentrations of lactate, ammonia,
and urea were measured before and after the matches. Peak
values for creatine kinase activity were observed 24 h after
the match. There was no significant change between time
points for blood lactate concentration but secretion rate
per unit surface and time was significantly reduced after
the match. Sweat ammonia concentration increased significantly
during the match; values were significantly reduced after
24 h and still remained low at 72 h. Secretion rate was
also reduced from 24 h. Urea concentration was significantly
reduced at 48 h, while secretion rates decreased at 24 h
and 48 h. Lactate in blood was significantly elevated during
the match but not thereafter. Blood ammonia was significantly
elevated during the match and did not differ from the resting
values at 24 or 48 h. Urea in blood tended to decrease during
the match, with a significant reduction at 24 h. Significant
positive correlations were observed between blood and sweat
concentrations for urea and ammonia but not for lactate.
Sweat rate correlated positively with sweat lactate secretion.
The fact that part of the ammonia formed during exercise
is lost with sweat indicates the importance of the purine
nucleotide cycle during rugby matches. Our data also confirm
that sweat lactate concentration is not influenced by circulatory
blood lactate in rugby players.
BRAIN RESEARCH
Title:
Cytidine and Uridine Increase Striatal
CDP-Choline Levels Without Decreasing Acetylcholine Synthesis
or Release.
Author:
Ismail Ulus, Carol Watkins, Mehmet Cansev, Richard Wurtman
Source:
Cell Mol Neurobiol. 2006 Apr 25
Abstract:
Treatments that increase acetylcholine release from brain
slices decrease the synthesis of phosphatidylcholine by,
and its levels in, the slices. We examined whether adding
cytidine or uridine to the slice medium, which increases
the utilization of choline to form phospholipids, also decreases
acetylcholine levels and release. Methods: We incubated
rat brain slices with or without cytidine or uridine (both
25-400 muM), and with or without choline (20-40 muM), and
measured the spontaneous and potassium-evoked release of
acetylcholine. Results: Striatal slices stimulated for 2
h released 2650+/-365 pmol of acetylcholine per mg protein
when incubated without choline, or 4600+/-450 pmol/mg protein
acetylcholine when incubated with choline (20 muM). Adding
cytidine or uridine (both 25-400 muM) to the media failed
to affect acetylcholine release whether or not choline was
also added, even though the pyrimidines (400 muM) did enhance
choline;s utilization to form CDP-choline by 89 or 61%,
respectively. The pyrimidines also had no effect on acetylcholine
release from hippocampal and cortical slices. Cytidine or
uridine also failed to affect acetylcholine levels in striatal
slices, nor choline transport into striatal synaptosomes.
Conclusion: These data show that cytidine and uridine can
stimulate brain phosphatide synthesis without diminishing
acetylcholine synthesis or release.
Title:
Oral uridine-5'-monophosphate (UMP)
increases brain CDP-choline levels in gerbils.
Author:
Mehmet Cansev, Carol J Watkins, Eline M van der Beek, Richard
J Wurtman
Source:
Brain Res. 2006 Apr 19
Abstract: We examined the biochemical pathways
whereby oral uridine-5'-monophosphate (UMP) increases membrane
phosphatide synthesis in brains of gerbils. We previously
showed that supplementing PC12 cells with uridine caused
concentration-related increases in CDP-choline levels, and
that this effect was mediated by elevations in intracellular
uridine triphosphate (UTP) and cytidine triphosphate (CTP).
In the present study, adult gerbils received UMP (1 mmol/kg),
a constituent of human breast milk and infant formulas,
by gavage, and plasma samples and brains were collected
for assay between 5 min and 8 h thereafter. Thirty minutes
after gavage, plasma uridine levels were increased from
6.6 +/- 0.58 to 32.7 +/- 1.85 muM (P < 0.001), and brain
uridine from 22.6 +/- 2.9 to 89.1 +/- 8.82 pmol/mg tissue
(P < 0.001). UMP also significantly increased plasma
and brain cytidine levels; however, both basally and following
UMP, these levels were much lower than those of uridine.
Brain UTP, CTP, and CDP-choline were all elevated 15 min
after UMP (from 254 +/- 31.9 to 417 +/- 50.2, [P < 0.05];
56.8 +/- 1.8 to 71.7 +/- 1.8, [P < 0.001]; and 11.3 +/-
0.5 to 16.4 +/- 1, [P < 0.001] pmol/mg tissue, respectively),
returning to basal levels after 20 and 30 min. The smallest
UMP dose that significantly increased brain CDP-choline
was 0.05 mmol/kg. These results show that oral UMP, a uridine
source, enhances the synthesis of CDP-choline, the immediate
precursor of PC, in gerbil brain.
Title:
Evidence for a supraspinal contribution
to human muscle fatigue.
Author:
Taylor JL , Todd G , Gandevia SC
Source:
Clin Exp Pharmacol Physiol, 33(4): 400-5 2006
Abstract:
1. Muscle fatigue can be defined as any exercise-induced
loss of ability to produce force with a muscle or muscle
group. It involves processes at all levels of the motor
pathway between the brain and the muscle. Central fatigue
represents the failure of the nervous system to drive the
muscle maximally. It is defined as a progressive exercise-induced
reduction in voluntary activation or neural drive to the
muscle. Supraspinal fatigue is a component of central fatigue.
It can be defined as an exercise-induced decline in force
caused by suboptimal output from the motor cortex. 2. When
stimulus intensity is set appropriately, transcranial magnetic
stimulation (TMS) over the motor cortex during an isometric
maximal voluntary contraction (MVC) of the elbow flexors
commonly evokes a small twitch-like increment in flexion
force. This increment indicates that, despite the subject's
maximal effort, motor cortical output at the moment of stimulation
was not maximal and was not sufficient to drive the motoneurons
to produce maximal force from the muscle. An exercise-induced
increase in this increment demonstrates supraspinal fatigue.
3. Supraspinal fatigue has been demonstrated during fatiguing
sustained and intermittent maximal and submaximal contractions
of the elbow flexors where it accounts for about one-quarter
of the loss of force of fatigue. It is linked to activity
and the development of fatigue in the tested muscles and
is little influenced by exercise performed by other muscles.
4. The mechanisms of supraspinal fatigue are unclear. Although
changes in the behaviour of cortical neurons and spinal
motoneurons occur during fatigue, they can be dissociated
from supraspinal fatigue. One factor that may contribute
to supraspinal fatigue is the firing of fatigue-sensitive
muscle afferents that may act to impair voluntary descending
drive.
Title:
Exercise starts and ends in the brain.
Author:
Kayser B
Source:
Eur J Appl Physiol, 90(3-4): 411-9 2003
Abstract:
Classically the limit to endurance of exercise is explained
in terms of metabolic capacity. Cardio-respiratory capacity
and muscle fatigue are thought to set the limit and the
majority of studies on factors limiting endurance exercise
discuss issues such as maximal oxygen uptake (VO2max), aerobic
enzyme capacity, cardiac output, glycogen stores, etc. However,
this paradigm does not explain the limitation to endurance
exercise with large muscle groups at altitude, when at exhaustion
exercise is ended without limb locomotor muscle fatigue
and with sub-maximal cardiac output. A simple fact provides
a basis for an explanation. Voluntary exercise starts and
ends in the brain. It starts with spatial and temporal recruitment
of motor units and ends with their de-recruitment. A conscious
decision precedes a voluntary effort. The end of effort
is again volitional and a forced conscious decision to stop
precedes it, but it is unknown what forces the off-switch
of recruitment at exhaustion although sensation of exertion
certainly plays a role. An alternative model explaining
the limitation of exercise endurance thus proposes that
the central nervous system integrates input from various
sources all related to the exercise and limits the intensity
and duration of recruitment of limb skeletal muscle to prevent
jeopardizing the integrity of the organism. This model acknowledges
the cardio-respiratory and muscle metabolic capacities as
prime actors on the performance scene, while crediting the
central nervous system for its pivotal role as the ultimate
site where exercise starts and ends.
Title:
Synaptic proteins and phospholipids
are increased in gerbil brain by administering uridine plus
docosahexaenoic acid orally.
Author:
Richard J Wurtman, Ismail H Ulus, Mehmet Cansev, Carol J
Watkins, Lei Wang, George Marzloff
Abstract:
The synthesis of brain phosphatidylcholine may utilize three
circulating precursors: choline; a pyrimidine (e.g., uridine,
converted via UTP to brain CTP); and a PUFA (e.g., docosahexaenoic
acid); phosphatidylethanolamine may utilize two of these,
a pyrimidine and a PUFA. We observe that consuming these
precursors can substantially increase membrane phosphatide
and synaptic protein levels in gerbil brains. (Pyrimidine
metabolism in gerbils, but not rats, resembles that in humans.)
Animals received, daily for 4 weeks, a diet containing choline
chloride and UMP (a uridine source) and/or DHA by gavage.
Brain phosphatidylcholine rose by 13-22% with uridine and
choline alone, or DHA alone, or by 45% with the combination,
phosphatidylethanolamine and the other phosphatides increasing
by 39-74%. Smaller elevations occurred after 1-3 weeks.
The combination also increased the vesicular protein Synapsin-1
by 41%, the postsynaptic protein PSD-95 by 38% and the neurite
neurofibrillar proteins NF-70 and NF-M by up to 102% and
48%, respectively. However, it had no effect on the cytoskeletal
protein beta-tubulin. Hence, the quantity of synaptic membrane
probably increased. The precursors act by enhancing the
substrate saturation of enzymes that initiate their incorporation
into phosphatidylcholine and phosphatidylethanolamine and
by UTP-mediated activation of P2Y receptors. Alzheimer's
disease brains contain fewer and smaller synapses and reduced
levels of synaptic proteins, membrane phosphatides, choline
and DHA. The three phosphatide precursors might thus be
useful in treating this disease.
BULGARIA
U.K.
GERMANY
ROMANIA
