STROMUSC Aicar 10mg*100 For Bodybuilding CAS:3031-94-5

   What is AICAR? The Metabolic Decoy

    AICAR is not a synthetic hormone or typical anabolic agent. It's a naturally occurring purine nucleotide analogue. Think of it as a molecular decoy mimicking AMP (Adenosine Monophosphate), the cell's fundamental signal for low energy status. When cellular energy (primarily ATP) is depleted, AMP levels rise. AICAR exploits this natural signaling pathway.

    ●Core Mechanism: AICAR is readily taken up by cells and phosphorylated to become ZMP (5-Aminoimidazole-4-carboxamide-1-β-D-ribofuranosyl monophosphate). ZMP is the active metabolite that convincingly mimics AMP.

    ●AMPK Activation: ZMP's primary target is the master metabolic regulator AMP-activated Protein Kinase (AMPK). By binding to the regulatory γ-subunit of AMPK, ZMP tricks the enzyme into thinking cellular energy (ATP) is critically low, even when it isn't. This forces AMPK into its active state.

    Activated AMPK orchestrates a profound cellular shift towards energy conservation and production:

    ●Catabolic Switch: AMPK rapidly shuts down energy-consuming processes (anabolism) like protein synthesis (mTOR inhibition), fatty acid synthesis, and glycogen synthesis.

    ●Energy Production Boost: Simultaneously, it flips the switch on energy-producing (catabolic) pathways:

    ○Enhanced Glucose Uptake: Increases translocation of GLUT4 glucose transporters to the cell membrane, pulling more glucose into muscle and fat cells for fuel.

    ○Increased Glycolysis: Speeds up the breakdown of glucose for energy.

    ○Fatty Acid Oxidation: Drives the breakdown of stored fats (triglycerides) into free fatty acids and promotes their transport into mitochondria to be burned for energy (beta-oxidation).

    ○Mitochondrial Biogenesis: Chronically, AMPK activation signals the cell to produce more mitochondria (the cellular power plants), potentially enhancing long-term aerobic capacity.

    ●Impact on Muscle Fiber Type: Research (primarily rodent) suggests chronic AMPK activation can promote a shift from fast-twitch (glycolytic, powerful but fatigue-prone, Type IIb/x) muscle fibers towards more slow-twitch (oxidative, endurance-oriented, fatigue-resistant, Type I/IIa) fibers. This is mediated through effects on transcription factors like PGC-1α.

    Bodybuilders are theoretically attracted to AICAR for two primary, interconnected reasons:

    ●Enhanced Endurance & Work Capacity: By promoting mitochondrial biogenesis and shifting muscle fiber composition towards the fatigue-resistant Type I/IIa fibers, AICAR could theoretically allow for:

    ○Longer, more intense cardio sessions.

    ○Increased training volume in the gym (more sets/reps with less fatigue).

    ○Faster recovery between sets. This is its most touted potential benefit.

    ●Fat Loss Acceleration: By forcibly activating AMPK, AICAR ramps up fatty acid oxidation and glucose uptake/utilization, potentially creating a significant calorie deficit at the cellular level, independent of intense exercise (though exercise synergizes). This targets stubborn adipose tissue.

    Crucially, these applications are largely extrapolated from in vitro and rodent studies. Robust human data, especially in healthy athletes, is extremely limited.

    ●Increased Aerobic Capacity: Potential boost to VO2 max and endurance performance.

    ●Improved Workout Efficiency: Ability to sustain higher training volumes with perceived less fatigue during workouts.

    ●Enhanced Fat Oxidation: Potential to increase the proportion of fat used as fuel during low-moderate intensity exercise and potentially at rest.

    ●Muscle Sparing During Caloric Deficit? Highly speculative. AMPK's inhibition of mTOR (the key driver of muscle protein synthesis) directly conflicts with muscle growth. While increased endurance might allow for more muscle-stimulating volume, the direct biochemical signal from AICAR is anti-anabolic. Any muscle sparing would likely be indirect and contingent on other factors (diet, training, other compounds). It is NOT a muscle-builder.

    ●Insulin Sensitivity: AMPK activation improves glucose uptake, potentially enhancing insulin sensitivity, beneficial in fat loss phases.

    ●Dosage: Human data is scarce. Extrapolation from rodent studies (using metabolic equivalent scaling) and anecdotal reports suggest a range of 100mg to 500mg per day. Common starting points are often around 200-250mg daily. Due to its short half-life (see below), splitting the dose (e.g., AM/PM) is common, especially if pre-workout endurance is a goal.

    ●Administration: Typically administered via subcutaneous (SubQ) injection. Oral bioavailability is very poor (<10%) due to degradation in the gut/liver.

    ●Cycle Length: Cycles are typically short, ranging from 2 to 8 weeks, due to cost, limited knowledge of long-term effects, and the potential for mitochondrial adaptations to plateau. 4-6 weeks is a common experimental timeframe.

    ●Timing: Often taken daily. If targeting workout endurance, a dose 60-90 minutes pre-workout might be used (sometimes alongside the daily dose).

    ●Important Caveats:

    ○No Established Protocols: There are no clinically established or universally agreed-upon dosing protocols for athletes. This is pure experimentation.

    ○Cost Prohibitive: Pure, research-grade AICAR is extremely expensive, making long-term or high-dose use impractical for most.

    ○Purity Concerns: Sourcing poses significant risks of contamination or mislabeling.

    ●Half-Life: AICAR has a relatively short half-life in humans, estimated at around 1.5 to 2 hours.

    ●Implication: The active effects of a single dose are transient, lasting perhaps 4-6 hours. This short duration necessitates multiple daily injections (e.g., twice daily) to maintain elevated AMPK activation throughout the day, especially if sustained effects on fat oxidation or endurance are desired beyond a specific workout window. The ZMP metabolite may persist longer, but the primary pharmacological effect is tied to the presence of AICAR/ZMP.

    ●No Hormonal Impact: Unlike anabolic steroids or SARMs, AICAR does not interact with the Hypothalamic-Pituitary-Gonadal (HPG) axis (testosterone production) or the Hypothalamic-Pituitary-Adrenal (HPA) axis (cortisol regulation). It works purely through the AMPK metabolic pathway.

    ●No Suppression: It does not suppress natural testosterone or estrogen production.

    ●Therefore: Traditional PCT (SERMs like Tamoxifen/Clomid, or hCG) is NOT required or beneficial after an AICAR cycle. The primary "recovery" needed is simply allowing cellular signaling (AMPK, mTOR) to return to baseline homeostasis, which occurs naturally as the compound clears the system.

    ●Anti-Anabolic (mTOR Inhibition): This is the BIGGEST CONTRADICTION for bodybuilding. AMPK activation directly inhibits mTORC1, the master regulator of muscle protein synthesis. While endurance might improve, the direct biochemical signal from AICAR actively opposes muscle hypertrophy. Using it during a muscle-building phase is counterproductive.

    ●Human Efficacy Uncertain: Promising rodent data does not reliably translate to humans, especially in the context of athletic performance enhancement. Human studies are limited and often show less dramatic effects.

    ●Cost: Prohibitively expensive for meaningful, sustained use.

    ●Injection Burden: Requires frequent SubQ injections.

    ●Mitochondrial Stress: Chronic, forced AMPK activation might theoretically lead to excessive mitochondrial biogenesis or dysfunction, though long-term human risks are unknown.

    ●Potential Side Effects: Reported anecdotally (lack of clinical data) include lethargy, headaches, hypoglycemia (especially if not eating enough carbs), and injection site reactions. Its long-term safety profile is unknown.

    ●Synergy Misconceptions: While sometimes stacked with compounds like GW501516 (Cardarine) for a "stamina/fat loss stack," this amplifies cost, injection burden, and unknown risks without proven synergistic benefits in humans. Cardarine works via PPARδ (increasing fatty acid oxidation and endurance genes), so the mechanisms differ but potentially overlap on fat burning/endurance.

    ●Not a Magic Bullet: Effects on fat loss and endurance, if present, are likely subtle and far less impactful than proper diet, training consistency, sleep, and proven supplements (caffeine, creatine, beta-alanine).

Brand	STROMUSC
Trade names	Aminoimidazole carboxamide ribonucleotide, AICA ribonucleotide, ZMP
CAS	3031-94-5
Molar mass	338.213
MF	C9H15N4O8P
Purity	Above 98%
Apprarance	10mg*100

 

 

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    AICAR is a fascinating research compound that mechanistically targets AMPK to potentially enhance endurance and fat oxidation. However, its application in bodybuilding is highly experimental, exceptionally costly, and fundamentally limited by its potent anti-anabolic (mTOR inhibiting) effect. The theoretical benefits for workout endurance and fat loss are overshadowed by the direct biochemical conflict with the primary goal of muscle growth.

    For bodybuilders seeking endurance, traditional methods (progressive overload, conditioning work, beta-alanine, citrulline malate, proper fueling) are far more reliable and cost-effective. For fat loss, caloric deficit, macronutrient manipulation, and proven thermogenics (caffeine, yohimbine HCL in specific contexts) are superior choices. AICAR remains a tool of scientific inquiry, not a practical or advisable strategy for achieving bodybuilding goals. The risks, costs, and biochemical trade-offs simply do not justify its use outside of controlled research settings. Its niche appeal is vastly outweighed by its significant practical and physiological limitations for the aspiring physique athlete.

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