perhaps, but he said that using creatine is pointless because the water that you retain from it is stored between the muscle and the skin, not actually in the muscle, making it useless
B U L L S H I T....
Enhancement of physical performance by creatine supplementation:
The CK/PCr system is now recognized as an important metabolic regulator during health and disease. Creatine, synthesized in part by the body, but also ingested by food, especially meat and fish (for review see [50]), is taken up into cells by a creatine transporter (CreaT) (for review see [51]). Creatine supplementation in humans leads to an increase in intracellular [Cr] and [PCr], concomitantly improving anaerobic performance of muscle [52,53], shortens muscle relaxation time [83], increases fat free- or lean body mass [94] as well as the cross-sectional area (fiber diameter) of all muscle fiber types [93]. In addition, creatine seems to improve recovery after exhaustive excercise [54] (for review see [55,56]). One could show that creatine supplementation may also have beneficial effects for high-intensity, aerobic long-endurance exercise [57]. In a double-blinded placebo-controlled study, 20 highly trained top athletes were subjected at 1?650 meters above sea level (in Davos, Switzerland) to a series of spiro-ergometric short- and long-term performance tests before and after 10 days of supplementation with 3x3.3 g of Cr per day. In accordance with earlier studies, short performance and maximal work output were both improved by approx. 30 Watt. In a 1 hour spiro-ergometric test at 85% power output of the individually determined anaerobic threshold, the Cr group was able to perform, after Cr supplementation, at the same level of exercise with a significantly lower heart rate (-8.4 beats/min) than before Cr intake. In this group, lactate levels were lower by 0.48 mM/l and Borg scale numbers by 1.35 points. These effects were not observed in the controls. Ventilation, VO2 and respiratory quotient (RQ) were basically unchanged [57]. The effects of Cr on endurance performance seem to be due to increased efficiency of energy utilization by heart and skeletal muscle which may be related to the involvement of CK in the energetics of Ca2+-homeostasis. As a consequence of creatine supplementation, the elevated cellular PCr level is likely to increase the supply of the SR-Ca2+-ATPase with high-energy phosphates via the coupled CK reaction and thus would also increase the efficiency of Ca2+-pumping and delay impaired Ca2+-regulation known to occur under conditions of fatigue [93]. During long-endurance exercise, this process consumes a significant proportion of the available bioenergy. In addition, Cr-stimulated respiration and enhanced resynthesis of PCr after creatine ingestion [54] and/or the recently discovered control of AMP-activated protein kinase by the PCr/Cr ratio [20] and its effects on CK and lipid metabolism in general [20] could be important factors leading to the observed improvement of aerobic exercise described above.
An important new aspect of creatine supplementation was descovered only recently, that is, creatine supplementation in combination with carbohydrate loading after submaximal glycogen-depleting exercise not only markedly improves Cr uptake, but also increases glycogen accumulation in human muslcle [96]. Thus, the highly elevated levels of glycogen reached after combined carbohydrate and creatine loading after glycogen-depleting exercise may, of course, also add to the positive effect of creatine supplementation on long-endurance exercise [57].
The PCr-circuit: a temporal and spatial energy buffering network and regulatory system for energy metabolism in cells with intermittently high energy requirements.
Upper, cytosolic side: the bulk of soluble, cytosolic CK (CKc) equilibrates global ATP/ADP and PCr/Cr ratios by its equilibrium reaction (depicted in the right middle of the figure). In skeletal muscle at rest, these metabolite levels are approximately 3-5 mM/10-20 µM and 20-40 mM/10-15 mM, respectively (see [1,22,47]). One of the main functions of CKc is to keep the concentration of free global ADP very low and thus to maintaing global [ATP] remarkably stable also during cell activation. This part of the PCr-circuit model represents the classical textbook function of CK as a temporal energy buffer, being backed up by adenylate kinase as a second safeguard against declining ATP and rising ADP levels. Some of the cytosolic CKc is functionally coupled to glycolysis and, during periods of anaerobic work-output and recovery, preferentially accepts glycolytic ATP to replenish the very large PCr pool (ATP from glycolysis, depicted in the left middle of the figure). Additionally, however, some fractions of cytosolic CK, are very specifically associated (CKa) with ATP requiring processes at sites of energy consumption. For example, CKa is associated with the contractile apparatus and the sarcoplasmic reticulum, where it forms functionally coupled microcompartments with the acto-myosin ATPase and the SR-Ca2+-ATPase, respectively, or with other ATP requiring processes, like the Na+/K+-ATPase etc. (see top of figure). There, ATP is directly regenerated in situ by CKa via PCr, thus keeping local ATP/ADP ratios very high in the immediate vicinity of these ATPases.
CK is phosphorylated and down-regulated in its activity by AMP-dependent protein kinase (AMPK, top right), which itself is the first enzyme that has been found to be regulated by the PCr/Cr ratio, that is, AMPK is activated by high creatine versus PCr levels [20].
Lower mitochondrial side: mitochondrial Mi-CK is bound to the outer side of the inner mitochondrial membrane (IM) and localized along the cristae membranes, as well as at mitochondrial contact sites, where IM and OM are in close vicinity [48]. At these sites, Mi-CK octamers are forming microcompartments with porin (P) and adenine nucleotide translocase (ANT) for energy transfer from ATP to Cr, followed by vectorial transport of PCr into the cytosol. ATP generated by oxidative phosphorylation is preferentially accepted by Mi-CK octamers, transphosphorylated onto Cr, which is entering through mitochondrial porin (P, or VDAC), to give PCr which then is exported into the cytosol. Thus, under high work-load, PCr would be shuttled from mitochondria to sites of energy consumption (ATPases, top of figure), where it is then used
by CKa to regenerate ATP locally in situ to fuel these ATP-requiring processes and to keep local ATP/ADP ratios very high. Cr would diffuse back to the mitochondria to be recharged again. This part of the model represents the spatial buffering function of the PCr-circuit. In this model, the specifically localized CK isoenzymes at sites of energy consumption and energy production are connected via PCr and Cr as mediators, generating metabolic waves and dampening oscillations of metabolites [22,46].
The dynamic recruitment of either free or membrane-bound Mi-CK octamers (double-arrows 5 or 1, respectively), possibly depending on the metabolic state of the mitochondria, the dynamic octamer/dimer equilibrium of Mi-CK (double arrows 2 and 4), as well as octamerization of Mi-CK dimers bound on the IM (double-arrow 2), all observed in vitro, are schematically visualized as potential modulatory events for long-term metabolic regulation. The interaction of Mi-CK with porin and complex formation of the enzyme with ANT, most likely facilitated by cardiolipin associated with ANT, are also illustrated. Under the conditions expected to prevail in the mitochondrial intermembrane space, however, the equilibria of these reactions, as observed in vitro, would clearly favour the membrane-bound octamer [21,25]. However,since the formation of contact sites and the establishment of the protein complexes are thought to be rather dynamic, a on/off recruitment of Mi-CK octamer into contact sites could easily be envisaged. Finally, these events that are heavily influenced by the exquisite sensitivity of Mi-CK towards peroxynitrite and other ROS [26], may be relevant also for the control of the permeability transition pore [39-41, 45].
http://icbxw.ethz.ch/creatine/creatine_supplementation.html#English
