Καρνιτίνη

[RUHL]

ρε λαιν κανε κοπυ παστε την ερευνα ποιος εχει ορεξη να κατεβαζει απο ραπιντ

τουλαχιστον την περιληψη


παλι καλα κανει κατι η καρνιτινη χαχαχα να δουμε και για γραμμωση αυτες τις ερευνες που δηχνουν οτι χανεις χωρις να κανεις τιποτα απο 1 κιλο την εβδομαδα με την ιδια διατροφη ............................. αχχαχα πλακα κανω δεν θα υπαρξει

[slaine]

Published online June 10, 2005 # Springer-Verlag 2005

Summary. Early research investigating the effects of L-carnitine supplementation has examined its
role in substrate metabolism and in acute exercise performance. These studies have yielded equivocal
findings, partially due to difficulties in increasing muscle carnitine concentrations. However, recent
studies have proposed that L-carnitine may play a different role in exercise physiology, and preliminary
results have been encouraging. Current investigations have theorized that L-carnitine supplementation
facilitates exercise recovery. Proposed mechanism is as follows: 1) increased serum carnitine concentration enhances capillary endothelial function; 2) increased blood flow and reduced hypoxia mitigate
the cascade of ensuing, destructive chemical events following exercise; 3) thus allowing reduced
structural damage of skeletal muscle mediated by more intact receptors in muscle needed for improved
protein signaling. This paradigm explains decreased markers of purine catabolism, free radical formation, and muscle tissue disruption after resistance exercise and the increased repair of muscle proteins
following long-term L-carnitine supplementation.

Keywords. Amino acids; Exercise recovery; Hormones; Metabolism; Skeletal muscle.

Introduction

Carnitine (L-3-hydroxytrimethylaminobutanoate) is a naturally occurring compound that can be synthesized in mammals from the essential amino acids lysine
and methionine [1] or ingested through diet. Primary sources of dietary carnitine
are red meat and dairy products; however, commercially-produced supplements are
also available and have been shown to be safe in humans [2]. Carnitine is stored
primarily in skeletal muscle, but is also found in plasma (although in much smaller
concentrations) [3]. Biologically, carnitine is essential for the transport of longchain (carbon chain length 10) fatty acids across the outer-and inner-mitochondrial membranes (carnitine palmitoyltransferase I and II, respectively). Based on

. Corresponding author. E-mail: William.Kraemer@uconn.edu

W. J. Kraemer et al.
this function, early work investigating the effects of carnitine focused on the paradigm that carnitine supplementation would enhance skeletal muscle carnitine concentrations and increase transport (and thus oxidation) of fatty acids. Studies
investigating this mechanism of action have yielded conflicting results. More
recent studies, however, have focused on a different paradigm: carnitine’s ability
to reduce hypoxic stress and enhance recovery from exercise, which will be the
focus of this review.

Early Research: Carnitine Supplementation and Fat Metabolism

A justification for carnitine supplementation in athletes was provided by Arenas
et al. [4]. Researchers investigated the effects of physical training (6 months) on
carnitine metabolism in sprinters and endurance runners. Participants were supplemented with either L-carnitine (2 g day1 orally) or placebo (P) for the duration of

the study. Athletes receiving P had significantly less muscle carnitine following 6
months of training; alternately, those athletes receiving L-carnitine had a significant
increase in muscle carnitine following training plus supplementation. Although
performance was not measured in this study, the authors hypothesized that 1) reduced muscle carnitine following training could reduce fatty acid metabolism;
and 2) carnitine supplementation during training could negate the decline in
(or even enhance) fatty acid metabolism.

Investigations of carnitine’s effects on acute exercise performance have examined various endpoints, including fat oxidation, aerobic capacity (VO2max), lactate,
and physical performance. These studies have shown equivocal findings in response to various doses and durations of carnitine supplementation (see Table 1).
Some of these studies have shown no increase in muscle carnitine concentrations
[5, 6], which would explain the lack of significant findings on exercise metabolism.

A New Paradigm for Carnitine

A new line of research in the area of L-carnitine and exercise has recently evolved.
Studies have indicated that a novel role for L-carnitine may reside in its ability to
optimize recovery from the hypoxic effects of exercise [7]. Exercise places physiological stress on the body derived from two different stimuli: 1) immediately,

Table 1. Acute effects of L-carnitine supplementation on exercise

Endpoint Finding References
Fat metabolism Increase [30]
No change [6, 31–34]
VO2max Increase [31, 35, 36]
No change [37]
Lactate Decrease [36, 38]
No change [5, 32, 34, 37, 39, 40]
Exercise performance Increase [35]
No change [39, 40]


L-Carnitine and Exercise Recovery

the mechanical forces associated with exercise cause cellular structural damage;
and 2) subsequently, chemical responses related to muscle damage and the tissue
repair process cause tissue alterations that can be observed for up to ten days postexercise.

Mechanical stress to muscle tissue is primarily mediated by the intensity of the
eccentric muscle actions (muscle lengthening under force). Loading that is greater
than concentric (muscle shortening) maximal strength (e.g., lowering weights with
105–120% of the weight that can be raised) can lead to significant damage to
contractile units. The mechanical stress of such overload can create muscle tissue
damage and produce dramatic deformation in the geometrical organization of
muscle fibers sarcomeres [8]. Such damage can be significant, if not injurious,
due to the loss of the structural integrity and contractile function [9]. Under such
conditions, the structure of the circulatory vessels is altered by changes in capillary
luminal shapes and areas [10].

Whereas most exercise results in some disruption of muscle fibers due to
mechanical stress, chemical factors associated with exercise stress can result in
more long term dysfunction due to free radical scavenging, which can continue to
degrade tissue structures over the recovery period of 5 to 10 days [11, 12]. This
problem is exacerbated by the increased release of cortisol, which has negative
effects on immune cell activation. These chemical responses to the mechanical
stress of exercises cause physical performance decrements and delayed-onset muscle soreness (DOMS) [13].

A new role of L-carnitine may rest in its ability to reduce chemical damage to
tissues and help the process of muscle tissue repair and remodeling. Potentially, Lcarnitine may improve blood flow during and following exercise, and optimize the
signals supporting tissue repair processes. Over the past several years, we have
investigated this theoretical potential and developed a new paradigm for the use of
L-carnitine in exercise.

Reduction of Tissue Hypoxia and Free Radical Damage

Figure 1 shows the underlying components of our paradigm. Independent of
mechanical damage, exercise results in breakdown of adenosine triphosphate
(ATP), accumulation of adenosine diphosphate (ADP) within the smooth muscle
of the pre-capillary sphincter (Fig. 1, #1a), and activation of the enzyme adenylate
kinase (Fig. 1, #1b). Adenylate kinase then catalyzes the formation of ATP and
adenosine monophosphate (AMP) from two molecules of ADP (Fig. 1, #1c). Accumulation of AMP leads to the formation of hypoxanthine that diffuses out of the
capillary endothelial cell. Hypoxia induced by exercise (Fig. 1, #2a) also causes a
mismatch between ATP supply and demand resulting in the malfunction of ATPdependent calcium pumps (Fig. 1, #2b) and intracellular accumulation of calcium.

The increase in intracellular calcium activates calcium-dependent proteases
(Fig. 1, #2c) that lead to the proteolytic cleavage of a portion of xanthine dehydrogenase converting it to xanthine oxidase (Fig. 1, #2d) [14]. Recent work by
Hellsten et al. [15] provides evidence for an increase in xanthine oxidase in human
vascular cells of skeletal muscle following exercise. Xanthine oxidase then catalyzes the formation of xanthine from hypoxanthine (Fig. 1, #3a) and converts it to


W. J. Kraemer et al.
Fig. 1. Theoretical paradigm for the role of L-carnitine in exercise recovery; numbers indicate areas
of recent or current research; see text for details

uric acid (Fig. 1, #3b). These reactions utilize molecular oxygen as an electron
acceptor and form a superoxide radical (Fig. 1, #3c). The superoxide radical can
combine with iron and form reactive hydroxy radicals that attack polyunsaturated
fatty acids in cell membranes (Fig. 1, #4). This attack initiates a chain of lipid
peroxidation reactions.

Lipid peroxidation results in the formation of numerous aldehydes of different
chain lengths, such as the 3-carbon product malondialdehyde (MDA) (Fig. 1, #5).
MDA is thus used as a plasma marker of free radical damage. The disruption to the
cell membrane results in leakage of cytosolic proteins such as creatine kinase (CK)
(Fig. 1, #6). Finally, superoxide radicals also form intermediates (Fig. 1, #7a) that
attract neutrophils (Fig. 1, #7b), furthering membrane disruption.

L-Carnitine may have a role in reducing the hypoxic stress of tissues. Studies
have attempted to show that L-carnitine has vasodilation properties. Ischemia in
endothelial cells can result in carnitine release, increased oxidative stress, and compromised blood flow [16]. These responses can be ameliorated by carnitine administration [17].

Incorporating this theory into an exercise model, Giamberadino et al. [18],
demonstrated that 3 grams of L-carnitine day1 for 3 weeks attenuated eccentric

exercise-induced. This was evidenced by reduced creatine kinase concentrations
(a marker of sarcolemmal damage) and subjective indicators of muscle pain and
tenderness. The authors suggested that L-carnitine enhanced oxygen availability,


L-Carnitine and Exercise Recovery

which subsequently attenuated the accumulation of free radicals that is common
after exercise stress. From these suggestions, we have developed our model for the
role of L-carnitine in recovery following exercise.

Our research group recently tested this paradigm by examining the influence of
L-CARNIPURE+ , L-carnitine L-tartrate (LCLT), on markers of purine catabolism,
free radical formation, and muscle tissue disruption after resistance exercise [7].
Using a balanced, crossover design (1 wk washout), ten resistance-trained men
consumed a placebo or LCLT supplement (2 g L-carnitine day1) for three weeks.

Blood samples were obtained on six consecutive days (D1 to D6). On D2, subjects
reported to the laboratory for pre-exercise blood draws, a hypoxic back squat
protocol (5 sets of 15–20 repetitions at 50% one-repetition maximum), and serial
post-exercise blood draws. Muscle tissue damage at the mid-thigh was assessed
using magnetic resonance imaging (MRI) prior to exercise (D1) and following
exercise (D3 and D6). Exercise-induced increases in plasma markers of purine
catabolism (hypoxanthine, xanthine oxidase, and serum uric acid) and circulating
cytosolic proteins (myoglobin, fatty acid binding protein, and CK) were significantly ( p<0.05) attenuated by LCLT. Similarly, exercise-induced increases in
plasma malondialdehyde returned to resting values sooner during LCLT supplementation compared to placebo. The amount of muscle disruption assessed via
MRI was 41–45% lower following LCLT than placebo supplementation.

These data indicated that LCLT supplementation was effective in enhancing
exercise recovery and mediating muscle damage, and therefore supported our
experimental paradigm for the role of L-carnitine in exercise recovery. The supplementation regimen used in this study (2 g L-carnitine day1 for three weeks)

resulted in increased serum carnitine concentrations [7]. We propose that enhanced
serum carnitine leads to accumulation within endothelial cells and enhanced
(directly or indirectly) vasodilation of the capillary vessel. The subsequent increase
in blood flow and delivery of oxygen to muscle tissue may reduce the magnitude of
exercise-induced hypoxia and thus attenuate the cascade of events that lead to free
radical formation and membrane disruption.

Hormones in the Recovery Process Paradigm

A host of hormones are involved with the signaling of protein synthesis and
immune cell function following tissue damage. The mechanisms by which such
signals are involved remain a topic of current research. Primary anabolic hormones
are growth hormone(s), growth factors, and androgens, which have all been viewed
as potential players in the normal exercise recovery process. In addition, cortisol
has been cast as an important hormone in the repair process due to 1) its role in
contractile protein breakdown in attempt to spare muscle glycogen and 2) its
negative effects on immune cell activation during the inflammatory process.

Previous research has investigated L-carnitine’s influence on hormonal responses to physical stress. Uptake of carnitine occurs in the central nervous system

[19] and the testes [20]. Studies have indicated that carnitine is involved in the
central (hypothalamic=pituitary) regulation and peripheral (testes) production of
testosterone. At the level of the hypothalamus, carnitine has been shown to restore
lutenizing hormone pulsatility and gonadal function in those with hypothalamic

W. J. Kraemer et al.
disorder [21]. Furthermore, supplementation stimulated in vitro K.-induced gonadotropin releasing hormone (GnRH) from the hypothalamus [22, 23]. In the testes,
carnitine may be involved in the transport of fatty acids into mitochondria and=or
serve as an energy substrate [24]. Thus, L-carnitine could be influencing recovery,
from brain-level signaling processes to substrate availability and transport in the
testes [25].

Direct influence of L-carnitine on stress=recovery responses has been investigated. In rats exposed to chronic intermittent cold-water swimming, supplementation with acetyl-L-carnitine mediated the decline in testosterone observed
following P supplementation [26]. L-Carnitine could help mediate enhanced tissue
repair following exercise due to improvement of blood flow.

We [27] examined the influence of LCLT supplementation on the normal
tissue repair recovery response signals (i.e., testosterone [T], immunofunctional
and immunoreactive growth hormone, insulin-like growth factor-1 [IGF-1], and
insulin-like growth factor-binding protein-3 [IGFBP-3]) to acute resistance exercise using a balanced, cross-over, placebo-controlled research design. Ten healthy,
recreationally weight-trained men volunteered and were matched for body size and
strength. After 3 weeks of supplementation (2 g d1 LCLT or P), fasting morning

blood samples were obtained on six consecutive days (D1–D6). On D2, participants performed the same squat protocol as used previously in our laboratory
(5 sets of 15–20 repetitions). Blood samples were obtained before exercise and 0,
15, 30, 120, and 180 minutes post-exercise. After a 1-week washout period, participants then consumed the other supplement for a 3-week period, and the same
experimental protocol was repeated. Similar to our previous research [7], LCLT
reduced the amount of exercise-induced muscle tissue damage assessed via MRI of
the thigh. Exercise induced increases in GH, IGFBP-3, and T. LCLT supplementation significantly ( p<0.05) increased IGFBP-3 concentrations prior to and at 30,
120, and 180 minutes after acute exercise. No other direct effects of LCLT supplementation were observed in absolute concentrations of the hormones examined.
Blood flow enhancement to tissues may help mediate quicker recovery following
exercise stress.

In a recent meeting [28] we presented the first evidence that LCLT supplementation by improving blood flow under hypoxic conditions may enhance recovery at
the level of the tissue receptor (e.g., androgen receptor (AR). The combination of
food ingestion as well as LCLT enhanced recovery of muscle per our improved
blood flow mechanisms allowing greater interactions with protein repair mechanisms [29]. These results did provide some initial indications that repair of muscle
tissue via improved blood flow, reduced free radicals, and more intact tissue aids
recovery and was enhanced by LCLT supplementation.

The timing of increased protein synthesis via intake of nutrients may well be
linked to the interface of optimal use of LCLT supplementation. With the use of
such supplementation each day concomitant with meals and physical training,
LCLT appeared to augment recovery response of muscle at rest and may be important during physical training or periods of high activity in an active lifestyle.
Nevertheless, such data has started to shed light on the interaction of LCLT with
the recovery process of which nutrient intake and protein synthesis are intimately
involved.


L-Carnitine and Exercise Recovery

Summary

The role of L-carnitine in the recovery process from exercise is a new paradigm for
the study of this chemical compound. L-Carnitine’s impact on hypoxia related
tissue damage has opened an innovative area of study. Future research may have
an impact not only on our understanding of exercise-induced damage and repair
processes, but also other physiological challenges, from surgery to spaceflight, in
which recovery plays an important role. The physiological roles of L-carnitine
related to exercise recovery remains an exciting new vista for further investigation.

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[RUHL]

εδω ειμαστε ωραιος παντα τετοια

[Muscleboss]

θα πρότεινα όταν ανεβάζετε έρευνες, ή να βάζετε μόνο την περίληψη, ή όταν βάζετε όλο το άρθρο να υπογραμμίζετε τα σημεία που είναι σημαντικά για να διαβάσουμε, καθώς πολλοί από εμάς δε θα κάτσουμε να το διαβάσουμε όλο παρά μόνο τα σημεία που είναι σημαντικά.

anyway, καλός slaine.

δεν κάθησα να διαβάσω το άρθρο, αλλά από τη στιγμή που είναι αμινοξύ είναι λογικό να βοηθάει στην ανάπτυξη και ανάρρωση...

ΜΒ

[tezaman]

καρνιτιν ιτ ιζ δεν 8)

[Muscleboss]

καρνιτιν ιτ ιζ δεν 8)

αυτό μόνο ο τεζας μπορει να το γράψει...

ΜΒ

[slaine]

^^γιου γκατ δατ ράιτ

[tezaman]

καρνιτιν ιτ ιζ δεν 8)

αυτό μόνο ο τεζας μπορει να το γράψει...

ΜΒ

Μπός δεν μου έχεις δόση άξες στα ΑΑΣ

θα είμαι καλό παιδί δεν θα σπαμάρω

[pikolo]

οχι μη του δωσεις θα καταστρεψει ολα τα τοπικ....!

[tezaman]

για εμένα μιλάμε 8)

[Fotis_Patra]

Εσυ για ποιον πιστευεις να λεει?

[tezaman]

για κάνεναν σπάμερ .. KATERINHS144 πχ

[pikolo]

πωπω καντε ενα ban τον teza καταστρεφει τα τοπικ!!!

[tezaman]

είσαι κακός άνθρωπος 8)

[ikamak]

Ωραία έρευνα !!!

Πρέπει να έχει κι άλλες το site που τη βρήκες. Μπορείς να δώσεις το link pls;