Research shows that strength training is especially effective at raising EPOC. That’s because, generally speaking, strength-training sessions cause more physiological stress to the body compared to cardiovascular exercise, even higher-intensity cardio intervals. However, it’s worth noting that overall exercise intensity is what makes the biggest impact on EPOC. So squats, deadlifts, and bench presses with heavy weights are going to be much more effective at raising EPOC compared to bicep curls and triceps extensions with light weights.

Our bodies store creatine in our muscles so that we have quick access to it for fast, high-intensity movements, like sprinting or powerlifting, explains Autumn Bates, a certified clinical nutritionist and sports nutritionist in private practice in Manhattan Beach, California. “It's a nonessential amino acid, meaning your body creates it and you don't need to primarily get it from food.”


In standard dosages (5-10g creatine monohydrate) the bioavailability of creatine in humans is approximately 99%,[68][83] although this value is subject to change with different conjugates (forms) of creatine and dosages.[83] Coingestion of cyclocreatine (an analogue) can reduce uptake by about half[131] and coincubation of taurine, choline, glycine, or beta-alanine had minimal attenuation of absorption, which is likely not practically relevant.[131] The inhibition noted with cyclocreatine may be due to receptor saturation.
Due to a combination of its neuroprotective effects and dopaminergic modulatory effects, creatine has been hypothesized in at least one review article to be of benefit to drug rehabilitation.[266] This study used parallels between drug abuse (usually methamphetamines) and traumatic brain injury[267][268] and made note of creatine being able to reduce symptoms of brain trauma, such as headaches, fatigue, and dizziness in clinical settings in two pilot studies.[269][270] No studies currently exist that examine creatine supplementation and drug rehabilitation.
Creatine is classified as a "dietary supplement" under the 1994 Dietary Supplement Health and Education Act and is available without a prescription. Creatine is not subjected to FDA testing, and the purity and hygienic condition of commercial creatine products may be questionable [21]. A 1998 FDA report lists 32 adverse creatine-associated events that had been reported to FDA. These include seizure, vomiting, diarrhea, anxiety, myopathy, cardiac arrhythmia, deep vein thromboses and death. However, there is no certainty that a reported adverse event can be attributed to a particular product [22]. A recent survey of 28 male baseball players and 24 male football players, ages 18 to 23, found that 16 (31%) experienced diarrhea, 13 (25%) experienced muscle cramps, 7 (13%) reported unwanted weight gain, 7 (13%) reported dehydration, and 12 reported various other adverse effects [23].

Wilkinson, S. B., Tarnopolsky, M. A., MacDonald, M. J., MacDonald, J. R., Armstrong, D., & Phillips, S. M. (2007). Consumption of fluid skim milk promotes greater muscle protein accretion after resistance exercise than does consumption of an isonitrogenous and isoenergetic soy-protein beverage. The American Journal of Clinical Nutrition, 85(4), 1031-1040.


Collectively the above investigations indicate that creatine supplementation can be an effective strategy to maintain total creatine pool during a rehabilitation period after injury as well as to attenuate muscle damage induced by a prolonged endurance training session. In addition, it seems that creatine can act as an effective antioxidant agent after more intense resistance training sessions.

In regard to practical interventions, concurrent glycogen loading has been noted to increase creatine stores by 37-46% regardless of whether the tissue was exercised prior to loading phase.[176] It is important to note, however, that creatine levels in response to the creatine loading protocol were compared in one glycogen-depleted leg to the contralateral control leg, which was not exercised.[176] This does not rule out a possible systemic exercise-driven increase in creatine uptake, and the increase in creatine noted above[176] was larger than typically seen with a loading protocol (usually in the 20-25% range). Consistent with an exercise-effect, others have reported that exercise itself increases creatine uptake into muscle, reporting 68% greater creatine uptake in an exercised limb, relative to 14% without exercise.[153]
Creatine citrate is creatine bound to citric acid, or citrate. Creatine citrate does not differ greatly from monohydrate in regard to absorption or kinetics.[83] Note that creatine citrate is more water-soluble than monohydrate,[84] but creatine absorption is generally not limited by solubility. The increased water solubility may play a factor in palatability.
Of course, cardio is an important part of fitness too, but the benefits of strength training are major. Strength training helps build muscle, and lean muscle is better at burning calories when the body is at rest, which is important whether you're trying to lose weight or maintain it. It also helps strengthens joints and bones, avoid injury, improve your muscular endurance, and will help you give it your all during your other workouts, whether that means setting a new PR if you're a runner or pushing (and pulling) a little harder with your legs during your favorite indoor cycling class. 

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Several studies have used either beet root juice or pomegranate extract in multi-ingredient performance supplements and have observed improvements in strength, hypertrophy, and performance in resistance-trained men. At this point, however, it's difficult to determine if these benefits are from beet root juice and pomegranate extract working alone or synergistically with other ingredients.[11,12]
How to Take It: If you decide you want to take BCAAs as one of your weight lifting supplements, you can easily get them and take them much like you would protein powders. One scoop provides 2.5g of leucine, 1.25g of isoleucine and 1.25g of valine. Take it before a workout, during or after. As with all supplementation, the aim is to reach your overall daily needs and goals.

Myotonic Dystrophy type I (DM1) is an inhereted muscular disorder caused by an expanded CTG repeat in the DMPK gene on chromosome 19q13.3 (genetic cause of the disorder[561]) resulting in muscular degeneration and myotonia. The related myopathy, Myotonic Dystrophy type II (DM2) which is also known as proximal myotonic myopathy (PROMM) is due to a CCTG repeat on 3q,[562] and is less affected by myotonia and more by muscular pain and weakness. There is no cure for either because they are genetic disorders, so current therapies are aimed at reducing side-effects. Therapies include modafinil for the somnolence[563] and perhaps creatine for the reduction in strength and functionality.[548]


There's good news, though: These temporary muscle pumps are critical to improving muscle hypertrophy, or muscle growth, according to 2014 research in the Strength and Conditioning Journal. So you can think of your weight-room pump as a preview of the muscle results that are to come. Speaking of which, here's an expert-endorsed timeline to reach your muscle-building goals.
In October 1994, the Dietary Supplement Health and Education Act (DSHEA) was signed into law in the USA. Under DSHEA, responsibility for determining the safety of the dietary supplements changed from government to the manufacturer and supplements no longer required approval from the U.S. Food and Drug Administration (FDA) before distributing product. Since that time manufacturers did not have to provide FDA with the evidence to substantiate safety or effectiveness unless a new dietary ingredient was added. It is widely believed that the 1994 DSHEA further consolidated the position of the supplement industry and lead to additional product sales.[6]
A: Eat more frequently, drink less liquids while eating (they compete for stomach volume along with food), eat from larger plates and bowls, add lime or lemon juice to your water with meals (can help to increase production of hydrochloric acid that breaks down food), and consume more liquid calories (especially around the workout if appetite is suffering the rest of the day).
Creatine is known to be present in the retina due to the expression of creatine kinase (CK)[466][39] and the GAMT enzyme of creatine synthesis, which is also present in the mammalian retina.[467] Creatine in the blood can be transported into the retina via the creatine transporter (confirmed in humans[468]), and inhibiting transporter activity (by depleting the medium of chloride and sodium) reduces uptake by 80%.[469] The fact that not all uptake was inhibited suggests that another transporter, such as the monocarboxylate transporter MCT12 (or SLC16A12),[470] plays a role, perhaps moreso in the lens, where its levels were comparable to that of the major creatine transporter SLC6A8.[470] 
Myotonic Dystrophy type I (DM1) is an inhereted muscular disorder caused by an expanded CTG repeat in the DMPK gene on chromosome 19q13.3 (genetic cause of the disorder[561]) resulting in muscular degeneration and myotonia. The related myopathy, Myotonic Dystrophy type II (DM2) which is also known as proximal myotonic myopathy (PROMM) is due to a CCTG repeat on 3q,[562] and is less affected by myotonia and more by muscular pain and weakness. There is no cure for either because they are genetic disorders, so current therapies are aimed at reducing side-effects. Therapies include modafinil for the somnolence[563] and perhaps creatine for the reduction in strength and functionality.[548]
When endothelial cells have a higher creatine concentration, they appear to be mildly less permeable when incubated with 0.5-5mM creatine, while the higher concentration (5mM) is able to fully ablate TNF-α-induced neutrophil adhesion and both E-selectin and ICAM-1 expression.[316] This effect was prevented with ZM241385, an A2A (adenosine) receptor antagonist,[316] and since adenosine released by this receptor is known to be protective of endothelial cells,[317][318] it is thought that creatine works vicariously through this receptor and adenosine release, thought to be due to releasing ATP (occurs in response to stress[319][320]) which protects the cell via the A2A signaling system.[316]
Creatine citrate is creatine bound to citric acid, or citrate. Creatine citrate does not differ greatly from monohydrate in regard to absorption or kinetics.[83] Note that creatine citrate is more water-soluble than monohydrate,[84] but creatine absorption is generally not limited by solubility. The increased water solubility may play a factor in palatability.

The synthesis of creatine (from guanidinoacetate via GAMT) also requires SAMe as a cofactor and is implicated in homocysteine production. While supplementation of guanidinoacetate at 0.36% (prior to SAMe) can increase homocysteine by up to 50% in rats, supplementation of creatine (0.4%) is able to suppress homocysteine by up to 25%, secondary to reducing creatine synthesis,[309] and has been replicated elsewhere with 2% of the rat diet, while a loading phase did not alter the benefits.[124]
Syrotuik and Bell [57] investigated the physical characteristics of responder and non-responder subjects to creatine supplementation in recreationally resistance trained men with no history of CM usage. The supplement group was asked to ingest a loading dosage of 0.3 g/kg/d for 5 days. The physiological characteristics of responders were classified using Greenhaff et al [58] criterion of >20 mmol/kg dry weight increase in total intramuscular creatine and phosphocreatine and non responders as <10 mmol/kg dry weight increase, a third group labeled quasi responders were also used to classify participants who fell in between the previously mentioned groups (10-20 mmol/kg dry weight). Overall, the supplemented group showed a mean increase in total resting muscle creatine and phosphocreatine of 14.5% (from 111.12 ± 8.87 mmol/kg dry weight to 127.30 ± 9.69 mmol/kg dry weight) whilst the placebo group remained relatively unaffected (from 115.70 ± 14.99 mmol/kg dry weight to 111.74 ± 12.95 mmol/kg dry weight). However when looking at individual cases from the creatine group the results showed a variance in response. From the 11 males in the supplemented group, 3 participants were responders (mean increase of 29.5 mmol/kg dry weight or 27%), 5 quasi responders (mean increase of 14.9 mmol/kg dry weight or 13.6%) and 3 non-responders (mean increase of 5.1 mmol/kg dry weight or 4.8%). Using muscle biopsies of the vastus lateralis, a descending trend for groups and mean percentage fiber type was observed. Responders showed the greatest percentage of type II fibers followed by quasi responders and non-responders. The responder and quasi responder groups had an initial larger cross sectional area for type I, type IIa and type IIx fibers. The responder group also had the greatest mean increase in the cross sectional area of all the muscle fiber types measured (type I, type IIa and type IIx increased 320, 971 and 840 μm2 respectively) and non-responders the least (type I, type IIa and type IIx increased 60, 46 and 78 μm2 respectively). There was evidence of a descending trend for responders to have the highest percentage of type II fibers; furthermore, responders and quasi responders possessed the largest initial cross sectional area of type I, IIa and IIx fibers. Responders were seen to have the lowest initial levels of creatine and phosphocreatine. This has also been observed in a previous study [17] which found that subjects whose creatine levels were around 150 mmol/Kg dry mass did not have any increments in their creatine saturation due to creatine supplementation, neither did they experience any increases of creatine uptake, phosphocreatine resynthesis and performance. This would indicate a limit maximum size of the creatine pool.
In regard to the blood brain barrier (BBB), which is a tightly woven mesh of non-fenestrated microcapillary endothelial cells (MCECs) that prevents passive diffusion of many water-soluble or large compounds into the brain, creatine can be taken into the brain via the SLC6A8 transporter.[192] In contrast, the creatine precursor (guanidinoacetate, or GAA) only appears to enter this transporter during creatine deficiency.[192] More creatine is taken up than effluxed, and more GAA is effluxed rather than taken up, suggesting that creatine utilization in the brain from blood-borne sources[192] is the major source of neural creatine.[193][192] However, “capable of passage” differs from “unregulated passage” and creatine appears to have tightly regulated entry into the brain in vivo[193]. After injecting rats with a large dose of creatine, creatine levels increased and plateaued at 70uM above baseline levels. These baseline levels are about 10mM, so this equates to an 0.7% increase when superloaded.[193] These kinetics may be a reason for the relative lack of neural effects of creatine supplementation in creatine sufficient populations.
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