Though weight training can stimulate the cardiovascular system, many exercise physiologists, based on their observation of maximal oxygen uptake, argue that aerobics training is a better cardiovascular stimulus. Central catheter monitoring during resistance training reveals increased cardiac output, suggesting that strength training shows potential for cardiovascular exercise. However, a 2007 meta-analysis found that, though aerobic training is an effective therapy for heart failure patients, combined aerobic and strength training is ineffective; "the favorable antiremodeling role of aerobic exercise was not confirmed when this mode of exercise was combined with strength training".
Escolar, D. M., Buyse, G., Henricson, E., Leshner, R., Florence, J., Mayhew, J., Tesi-Rocha, C., Gorni, K., Pasquali, L., Patel, K. M., McCarter, R., Huang, J., Mayhew, T., Bertorini, T., Carlo, J., Connolly, A. M., Clemens, P. R., Goemans, N., Iannaccone, S. T., Igarashi, M., Nevo, Y., Pestronk, A., Subramony, S. H., Vedanarayanan, V. V., and Wessel, H. CINRG randomized controlled trial of creatine and glutamine in Duchenne muscular dystrophy. Ann Neurol 2005;58:151-155. View abstract.
One study on 27 otherwise healthy men supplementing creatine (0.3g/kg loading for a week, 0.05g/kg thereafter for 8 weeks) with a thrice weekly exercise regiment noted that alongside greater increase in lean mass and power relative to placebo at 4 and 8 weeks, myostatin in serum decreased to a greater extent with creatine (around 17% at 8 weeks, derived from graph) than it did with placebo (approximately 7%). Increases in GASP-1, a serum protein that inhibits the actions of myostatin by directly binding to it, were not different between groups.
If you want to take creatine as a supplement for bigger and stronger muscles, then the standard protocol is to have a “loading period” where you significantly increase your creatine intake for a few days or weeks. “This can prime your muscles to increase the amount of creatine that they ‘hold,’” explains Bates. “During the loading period, you generally take 5 g of creatine four times per day. After the loading period, you decrease the amount of creatine you take to a ‘maintenance’ level of 3 to 5 g per day.” (That’s also the recommendation from the International Society of Sports Nutrition.) (5)
2. What's your training like? Are you crushing 25 sets for chest like the average juiced out bodybuilder? If so, there's a pretty good chance you might be working above your MRV (maximal recoverable volume) and as such any physiological adaptation which could have taken place is going to be minimal given the cellular environment which occurs in a state of functional overreaching.
AAKG β-hydroxy β-methylbutyrate Carnitine Chondroitin sulfate Cod liver oil Copper gluconate Creatine/Creatine supplements Dietary fiber Echinacea Elemental calcium Ephedra Fish oil Folic acid Ginseng Glucosamine Glutamine Grape seed extract Guarana Iron supplements Japanese Honeysuckle Krill oil Lingzhi Linseed oil Lipoic acid Milk thistle Melatonin Red yeast rice Royal jelly Saw palmetto Spirulina St John's wort Taurine Wheatgrass Wolfberry Yohimbine Zinc gluconate
Most causes of brain injury (calcium influx, excitotoxicity, lipid peroxidation, reactive oxygen intermediates or ROIs) all tend to ultimately work secondary to damaging the mitochondrial membrane and reducing its potential, which ultimately causes cellular apoptosis. Traumatic brain injuries are thought to work vicariously through ROIs by depleting ATP concentrations. Creatine appears to preserve mitochondrial membrane permeability in response to traumatic brain injury (1% of the rat’s diet for four weeks), which is a mechanism commonly attributed to its ATP-buffering ability.
In recent years, the related areas of fitness and figure competition have increased in popularity, surpassing that of female bodybuilding, and have provided an alternative for women who choose not to develop the level of muscularity necessary for bodybuilding. McLish would closely resemble what is thought of today as a fitness and figure competitor, instead of what is now considered a female bodybuilder. Fitness competitions also have a gymnastic element to them. A study by the Clinical Journal of Sport Medicine found that female bodybuilders who are taking anabolic steroids are more likely to have qualified for substance dependence disorder, to have been diagnosed with a psychiatric illness, or to have a history of sexual abuse.
Children: Creatine is POSSIBLY SAFE in children when taken by mouth appropriately. Creatine 3-5 grams daily for 2-6 months has been taken safely in children 5-18 years of age. Creatine 2 grams daily for 6 months has been taken safely in children 2-5 years of age. Additionally, creatine 0.1-0.4 grams/kg daily for up to 6 months has been taken safely in both infants and children.
Gordon, P. H., Cheung, Y. K., Levin, B., Andrews, H., Doorish, C., Macarthur, R. B., Montes, J., Bednarz, K., Florence, J., Rowin, J., Boylan, K., Mozaffar, T., Tandan, R., Mitsumoto, H., Kelvin, E. A., Chapin, J., Bedlack, R., Rivner, M., McCluskey, L. F., Pestronk, A., Graves, M., Sorenson, E. J., Barohn, R. J., Belsh, J. M., Lou, J. S., Levine, T., Saperstein, D., Miller, R. G., and Scelsa, S. N. A novel, efficient, randomized selection trial comparing combinations of drug therapy for ALS. Amyotroph.Lateral.Scler. 2008;9(4):212-222. View abstract.
Negative regulators of the creatine transporter (CrT) are those that, when activated, reduce the activity of the CrT and overall creatine uptake into cells. As noted above, CrT activity is positively regulated by mTOR. Consistent with the well-known role of AMPK as a suppressor mTOR signaling, CrT activity has also been shown to be inhibited in response to AMPK activation in kidney epithelial cells. Since AMPK suppresses mTOR via upstream TSC2 activation, the negative regulation of AMPK on CrT activity in these cells appears to occur through an indirect mechanism. Although indirect, activation of AMPK has been noted to reduce the Vmax of the CrT without altering creatine binding, and is involved in internalizing the receptors. This pathway seems to max out at around 30% suppression, with no combination of mTOR antagonists and AMPK inducers further suppressing creatine uptake.
It is known that intracellular energy depletion (assessed by a depletion of ATP) stimulates AMPK activity in order to normalize the AMP:ATP ratio, and when activated AMPK (active in states of low cellular energy and colocalizes with creatine kinase in muscle tissue) appears to inhibit creatine kinase via phosphorylation (preserving phosphocreatine stores but attenuating the rate that creatine buffers ATP). While phosphocreatine technically inhibits AMPK, this does not occur in the presence of creatine at a 2:1 ratio. It seems that if the ratio of phosphocreatine:creatine increases (indicative of excess cellular energy status) that AMPK activity is then attenuated, since when a cell is in a high energy status, there is less AMP to directly activate AMPK.