Creatine and fat lose

[R69]

I would like to loose some fat from my body to get leaner.I dont know if its in my head or it is true that when i take creatine i lose fat harder even with 40 min cardio 5 time/week.Just a thought that maybee muscles get contraction energy from creatine and the body dosent have to burn fat for energy as much as without creatine?Creatine does retain whater outside the muscles or not,it bloats you?I think ill get off creatine.

[Warrior]

I would like to loose some fat from my body to get leaner.I dont know if its in my head or it is true that when i take creatine i lose fat harder even with 40 min cardio 5 time/week.Just a thought that maybee muscles get contraction energy from creatine and the body dosent have to burn fat for energy as much as without creatine?Creatine does retain whater outside the muscles or not,it bloats you?I think ill get off creatine.

It doesn't necessarily bloat you - it just needs water to get itself in... thats why it is called Creatine MONOHYDRATE (one molecule of water is required). This increased water in the muscle also carries benefits for other nutrients to help with growth and recovery. Just increase your water intake and stay hydrated to avoid cramping and excess water retention.

Creatine during fat loss cycles might be of benefit when trying to keep your limit strength up while cutting fat... you can get pretty depleted while dieting down. It also depends on the diet you are on... and how much creatine-rich meats you are consuming (dietary sources). If you do carb loads during a cutting diet - that is a really good opportunity refill Creatine stores as well.

[novastepp]

Warrior, not hijacking but just expanding on what u said. what kind of cutting diet would be beneficial to add creatine too? and how much creatine should you use when carbing up?

[Warrior]

Warrior, not hijacking but just expanding on what u said. what kind of cutting diet would be beneficial to add creatine too? and how much creatine should you use when carbing up?

You need to gather around half of your bodies Creatine stores from foods you eat - the rest your body can manufacture on its own. If your cutting diet is limiting creatine-rich foods, like wild game, red meat and fish (herring, salmon and tuna qualify) then you should supplement with it. Keeping strength levels up while dieting is paramount for keeping LBM while losing fat.

When carb loading on a cyclic type diet down - the extra carbs with the Creatine will lead to better overall glycogen supercompensation from the load up, as well as Creatine uptake into the muscle. Be sure you drink a lot of water when carbing up since both the carbs and Creatine will need water for this. I'd say 20-30 grams of creatine would be a good starting point for carb loads... no medical pubs to back that - more might be better... I hit around that for my carb loads...

[Giants11]

Creatine will inhibit fat loss slightly in the short term, because of its effects on on ATP which directly affects AMPk.

However as you diet longer and take creatine, creatine could prove to be beneficial for fat loss. Again because of creatine effects on ATP. Since ATP will provide cell volumazation (which drastically decreases when dieting) it will help prevent the body's starvation response, by signaling a fed state.

[Warrior]

Creatine will inhibit fat loss slightly in the short term, because of its effects on on ATP which directly affects AMPk.

However as you diet longer and take creatine, creatine could prove to be beneficial for fat loss. Again because of creatine effects on ATP. Since ATP will provide cell volumazation (which drastically decreases when dieting) it will help prevent the body's starvation response, by signaling a fed state.

I researched this some more... check these out...

Creatine supplementation affects muscle creatine during energy restriction.

Department of Human Nutrition, Foods, and Exercise, Virginia Tech, Blacksburg 24061-0430, USA.

INTRODUCTION: Anaerobic performance and body protein may decrease with energy restriction practiced by some athletes for weight loss. METHODS: This investigation examined the effects of creatine (Cr) supplementation during energy restriction on muscle Cr, exercise performance (10 sprints of 6 s, with 30-s rest), nitrogen balance, and body composition in male resistance trainers. Creatine supplemented (CrS, 20 g x d(-1) of Cr) and those given a placebo (P1) consumed a formula diet of 75.3 kJ (18 kcal) x kg(-1) x d(-1) (54.7% C, 21.3% P, 24% F) for 4 d. A control group was unsupplemented and continued their normal diet. There were no changes in body composition or performance of the control group. RESULTS: CrS and P1 demonstrated similar decreases in body weight and percent body fat. The percent change in fat-free mass was more for P1 (2.4+/-0.3% reduction) than CrS (1.4+/-0.4%), but urinary nitrogen losses were similar. Significant increases in muscle total Cr and CrP of 15-16% were demonstrated by CrS over the energy restriction period, whereas P1 had no changes in muscle Cr. Total work done during the sprints expressed per body weight tended to be 3.8% higher in CrS and 0.5% less in P1 after the energy restriction (P = 0.058). CONCLUSION: It was concluded that Cr supplementation increased muscle Cr during short-term energy restriction but did not affect body fat or protein loss. The change in muscle creatine was reflected in a tendency for higher total sprint work for the Cr group.

Creatine supplementation influences substrate utilization at rest.

Department of Nutrition, Arizona State University, Mesa, Arizona 85212, USA.

The influence of creatine supplementation on substrate utilization during rest was investigated using a double-blind crossover design. Ten active men participated in 12 wk of weight training and were given creatine and placebo (20 g/day for 4 days, then 2 g/day for 17 days) in two trials separated by a 4-wk washout. Body composition, substrate utilization, and strength were assessed after weeks 2, 5, 9, and 12. Maximal isometric contraction [1 repetition maximum (RM)] leg press increased significantly (P < 0.05) after both treatments, but 1-RM bench press was increased (33 +/- 8 kg, P < 0.05) only after creatine. Total body mass increased (1.6 +/- 0.5 kg, P < 0.05) after creatine but not after placebo. Significant (P < 0.05) increases in fat-free mass were found after creatine and placebo supplementation (1.9 +/- 0.8 and 2.2 +/- 0.7 kg, respectively). Fat mass did not change significantly with creatine but decreased after the placebo trial (-2.4 +/- 0.8 kg, P < 0.05). Carbohydrate oxidation was increased by creatine (8.9 +/- 4.0%, P < 0.05), whereas there was a trend for increased respiratory exchange ratio after creatine supplementation (0.03 +/- 0.01, P = 0.07). Changes in substrate oxidation may influence the inhibition of fat mass loss associated with creatine after weight training.

Creatine monohydrate supplementation on body weight and percent body fat.

Department of Physical Education and Athletic Training, Palm Beach Atlantic University, West Palm Beach, Florida 33416, USA. [email protected]

Seventeen active males (age 22.9 +/- 4.9 year) participated in a study to examine the effects of creatine monohydrate supplementation on total body weight (TBW), percent body fat, body water content, and caloric intake. The TBW was measured in kilograms, percent body fat by hydrostatic weighing, body water content via bioelectrical impedance, and caloric intake by daily food log. Subjects were paired and assigned to a creatine or placebo group with a double-blind research design. Supplementation was given for 4 weeks (30 g a day for the initial 2 weeks and 15 g a day for the final 2 weeks). Subjects reported 2 days a week for supervised strength training of the lower extremity. Significant increases before and after the study were found in TBW (90.42 +/- 14.74 to 92.12 +/- 15.19 kg) and body water content (53.77 +/- 1.75 to 57.15 +/- 2.01 L) for the creatine group (p = 0.05). No significant changes were found in percent body fat or daily caloric intake in the creatine group. No significant changes were noted for the placebo group. These findings support previous research that creatine supplementation increases TBW. Mean percent body fat and caloric intake was not affected by creatine supplementation. Therefore weight gain in lieu of creatine supplementation may in part be due to water retention.

[Giants11]

These do not really encompass what I was saying.

My response is based more on leptin and the cellular reponse of the body when dieting:

Leptin signaling, adiposity, and energy balance.

Jequier E.

Institute of Physiology, University of Lausanne, Switzerland. [email protected]

A chronic minor imbalance between energy intake and energy expenditure may lead to obesity. Both lean and obese subjects eventually reach energy balance and their body weight regulation implies that the adipose tissue mass is "sensed", leading to appropriate responses of energy intake and energy expenditure. The cloning of the ob gene and the identification of its encoded protein, leptin, have provided a system signaling the amount of adipose energy stores to the brain. Leptin, a hormone secreted by fat cells, acts in rodents via hypothalamic receptors to inhibit feeding and increase thermogenesis. A feedback regulatory loop with three distinct steps has been identified: (1) a sensor (leptin production by adipose cells) monitors the size of the adipose tissue mass; (2) hypothalamic centers receive and integrate the intensity of the leptin signal through leptin receptors (LRb); (3) effector systems, including the sympathetic nervous system, control the two main determinants of energy balance-energy intake and energy expenditure. While this feedback regulatory loop is well established in rodents, there are many unsolved questions about its applicability to body weight regulation in humans. The rate of leptin production is related to adiposity, but a large portion of the interindividual variability in plasma leptin concentration is independent of body fatness. Gender is an important factor determining plasma leptin, with women having markedly higher leptin concentrations than men for any given degree of fat mass. The ob mRNA expression is also upregulated by glucocorticoids, whereas stimulation of the sympathetic nervous system results in its inhibition. Furthermore, leptin is not a satiety factor in humans because changes in food intake do not induce short-term increases in plasma leptin levels. After its binding to LRb in the hypothalamus, leptin stimulates a specific signaling cascade that results in the inhibition of several orexigenic neuropeptides, while stimulating several anorexigenic peptides. The orexigenic neuropeptides that are downregulated by leptin are NPY (neuropeptide Y), MCH (melanin-concentrating hormone), orexins, and AGRP (agouti-related peptide). The anorexigenic neuropeptides that are upregulated by leptin are alpha-MSH (alpha-melanocyte-stimulating hormone), which acts on MC4R (melanocortin-4 receptor); CART (cocaine and amphetamine-regulated transcript); and CRH (corticotropin-releasing-hormone). Obese humans have high plasma leptin concentrations related to the size of adipose tissue, but this elevated leptin signal does not induce the expected responses (i.e., a reduction in food intake and an increase in energy expenditure). This suggests that obese humans are resistant to the effects of endogenous leptin. This resistance is also shown by the lack of effect of exogenous leptin administration to induce weight loss in obese patients. The mechanisms that may account for leptin resistance in human obesity include a limitation of the blood-brain-barrier transport system for leptin and an inhibition of the leptin signaling pathways in leptin-responsive hypothalamic neurons. During periods of energy deficit, the fall in leptin plasma levels exceeds the rate at which fat stores are decreased. Reduction of the leptin signal induces several neuroendocrine responses that tend to limit weight loss, such as hunger, food-seeking behavior, and suppression of plasma thyroid hormone levels. Conversely, it is unlikely that leptin has evolved to prevent obesity when plenty of palatable foods are available because the elevated plasma leptin levels resulting from the increased adipose tissue mass do not prevent the development of obesity. In conclusion, in humans, the leptin signaling system appears to be mainly involved in maintenance of adequate energy stores for survival during periods of energy deficit. Its role in the etiology of human obesity is only demonstrated in the very rare situations of absence of the leptin signal (mutations of the leptin gene or of the leptin receptor gene), which produces an internal perception of starvation and results in a chronic stimulation of excessive food intake.

[Giants11]

The above is relevent because creatine can cause cellular swelling:

Muscle glycogen supercompensation is enhanced by prior creatine supplementation.

Nelson AG, Arnall DA, Kokkonen J, Day R, Evans J.

Department of Kinesiology, Louisiana State University, Baton Rouge, LA 70803, USA. [email protected]

PURPOSE: Recently, it was shown that glycogen supercompensation tended (P = 0.06) to be greater if creatine and glycogen were loaded simultaneously. Because the authors suggested that creatine loading increased cell volumes and, therefore, enhanced glycogen supercompensation, we decided to determine whether an enhanced glycogen supercompensation could be realized if the glycogen loading protocol was preceded by a 5-d creatine load. METHODS: Twelve men (19-28 yr) performed two standard glycogen loading protocols interspersed with a standard creatine load of 20 g.d(-1) for 5 d. The vastus lateralis muscle was biopsied before and after each loading protocol. RESULTS: The initial glycogen loading protocol showed a significant 4% increase (P < 0.05) in muscle glycogen (Delta upward arrow 164 +/- 87 mmol.kg(-1) d.m.), and no change (P > 0.05) in total muscle creatine. Biopsies pre- and post-creatine loading showed significant increases in total muscle creatine levels in both the left leg (Delta upward arrow 41.1 +/- 31.1 mmol.kg(-1) d.m.) and the right leg (Delta upward arrow 36.6 +/- 19.8 mmol.kg(-1) d.m.), with no change in either leg's muscle glycogen content. After the final glycogen loading, a significant 53% increase in muscle glycogen (Delta upward arrow 241 +/- 150 mmol.kg-1 d.m.) was detected. Finally, the postcreatine load total glycogen content (694 +/- 156 mmol.kg(-1) d.m.) was significantly (P < 0.05) greater than the precreatine load total glycogen content (597 +/- 142 mmol.kg(-1) d.m.). CONCLUSION: It is suggested that a muscle's glycogen loading capacity is influenced by its initial levels of creatine and the accompanying alterations in cell volume.

[Giants11]

And that is relevent becuase, as dieting continues. Cells begin to shrink due to the lack of food. As cells shrink leptin decreases, which as you can see above, increases appitite, suppresses thyroid function as well as, upregualtes corticotropin-releasing-hormone (not good).

By using creatine you are able to load the muscle with ATP (a fuel source) and swell the size of cells. Which all in the long run will help make the body think its in the fed state. Which will help with the decline in Leptin which makes long term dieting like trying to swin upstream.

[Warrior]

Kewl... never saw the tie-in with Creatine and Leptin before. This would suggest that Creatine supplementation while cutting calories can help stop plummeting leptin levels via it's cell volumizing effect... but I don't think on it's own, supplemental Creatine use would be strong enough to cause a real difference... but rather potentiate other concurent methods... Lyle McDonald wrote on this before (regarding the short term AMPk activation), "if you look at the single study on the topic, the change in resting RER was pretty miniscule. I think if you're absolutely trying ot maximize everything, worry about it."

I was going by this idea for a CKD approach: the depletion phase prior to a carb load is filled with high protein, Creatine-rich foods... eating like this lowers blood sugar and subsequently insulin while exerting a diuretic effect. The carb load is filled with carbohydrates and less meats/fats... the higher blood sugar, insulin and hydration levels can help additional supplemental Creatine uptake better and fully saturate the muscles.

Perhaps Creatine should only used during a carb up period of a CKD-type dieting method, since at that time fat loss is not the number one priority... but rather glycogen supercompensation and resetting things like leptin...

In the end - it seems like Creatine use while losing fat can be a toss up... long term benefits with some short term possible set backs... but I'd have to say the long term effects out-weigh the short term possibilities...

[R69]

Thanks for the posts...it was a very good read....

[Giants11]

Kewl... never saw the tie-in with Creatine and Leptin before. This would suggest that Creatine supplementation while cutting calories can help stop plummeting leptin levels via it's cell volumizing effect... but I don't think on it's own, supplemental Creatine use would be strong enough to cause a real difference... but rather potentiate other concurent methods... Lyle McDonald wrote on this before (regarding the short term AMPk activation), "if you look at the single study on the topic, the change in resting RER was pretty miniscule. I think if you're absolutely trying ot maximize everything, worry about it."

I was going by this idea for a CKD approach: the depletion phase prior to a carb load is filled with high protein, Creatine-rich foods... eating like this lowers blood sugar and subsequently insulin while exerting a diuretic effect. The carb load is filled with carbohydrates and less meats/fats... the higher blood sugar, insulin and hydration levels can help additional supplemental Creatine uptake better and fully saturate the muscles.

Perhaps Creatine should only used during a carb up period of a CKD-type dieting method, since at that time fat loss is not the number one priority... but rather glycogen supercompensation and resetting things like leptin...

In the end - it seems like Creatine use while losing fat can be a toss up... long term benefits with some short term possible set backs... but I'd have to say the long term effects out-weigh the short term possibilities...

Exactly, I wouldn't be so concerned with the short term lowering of AMPk.

Anyhoo.....Creatine would be a nice addition to a cell volumizing stack which includes more goodies....

Taurine, Guanidinopropionic Acid, Glycerol Mono Sterate etc...