AMPK vs mTOR: The Molecular Switch That Controls Muscle, Fat Loss, and Aging
Discover how AMPK vs mTOR controls muscle growth, fat loss, and aging. Learn science-backed strategies to optimize metabolism and longevity.
NUTRITIONEXERCISE
Dr. T.S. Didwal, M.D.(Internal Medicine)
3/28/202615 min read
The balance between AMPK and mTOR acts as a central metabolic switch that regulates whether the body prioritizes energy conservation or growth. AMPK is activated during energy deficit—such as fasting or aerobic exercise—and promotes fat burning, glucose uptake, and cellular repair through autophagy. In contrast, mTOR is activated by nutrient availability, particularly protein and resistance training, driving muscle growth and protein synthesis. Optimal health depends on a cyclical balance between these pathways, where AMPK supports metabolic health and longevity, while mTOR preserves muscle mass and functional capacity.
How to Optimize AMPK and mTOR Balance
Perform resistance training 3–4 times per week to activate mTOR
Include aerobic exercise or fasted walking to stimulate AMPK
Maintain a 12–16-hour overnight fasting window
Consume 20–40g of protein per meal with adequate leucine
Avoid constant snacking to prevent chronic mTOR activation
Prioritize sleep and recovery, which regulate both pathways
Clinical pearls
1. The "Leucine Lock": Sestrin2 and the GATOR Sensor
Scientific Tone: mTORC1 activation is not merely concentration-dependent but sensor-gated. The protein Sestrin2 acts as a molecular brake on the GATOR1/2 complex; only when leucine levels reach a critical threshold (2–3 g) does Sestrin2 release its grip, allowing mTORC1 to translocate to the lysosomal surface for activation.
Think of Leucine as the "ignition key" for muscle growth. Your body has a molecular sensor (Sestrin2) that keeps the engine locked until it detects enough high-quality protein. If you only eat a "trickle" of protein, the key never turns; you need that 2–3 g"bolus" to fully unlock the building process.
2. Circadian Oscillations: Solar-Powered Metabolism
Scientific Tone: The AMPK–mTOR axis is entrained by the suprachiasmatic nucleus (SCN). Generally, mTOR signaling peaks during daylight/feeding hours to favor protein synthesis, while AMPK dominance rises during the dark/fasted phase to facilitate autophagy and rhythmic mitochondrial repair.
Your body follows a natural "Sun Schedule." Daylight and breakfast tell your body it’s time to build (mTOR), while darkness and sleep tell your cells it’s time to "clean house" (AMPK). Disrupting this rhythm—like late-night snacking—confuses your cellular clock and can stall your progress.
3. The "Interference Effect" is a Timing Issue, Not a Hard Stop
Scientific Tone: While acute AMPK activation via high-intensity interval training (HIIT) can transiently inhibit p70S6K (a downstream target of mTOR), this "interference" is short-lived. Separating resistance and aerobic bouts by 6–24 hours allows for the transcriptomic signature of both pathways to be expressed without mutual cancellation.
You can have both cardio health and muscle mass. While doing a long run immediately before heavy lifting might "mute" your growth signals, simply separating them by a few hours or a high-protein meal allows your body to switch gears effectively from "burning" to "building."
4. Muscle as a "Metabolic Sink"
Scientific Tone: Skeletal muscle is the primary site for insulin-stimulated glucose disposal. Maintaining muscle mass via mTOR activation provides a larger "buffer" for glucose, which indirectly prevents the chronic hyperinsulinemia that leads to AMPK suppression and metabolic rigidity.
PMuscle isn't just for show; it’s your body’s largest "sugar sponge." The more muscle you build using mTOR, the easier it is for your body to stay metabolically flexible. Having more muscle actually makes your AMPK "cleaning" phase much more efficient when you fast.
5. Metformin and the Hypertrophy "Blunt"
Scientific Tone: Pharmacological AMPK activation via Metformin may diminish the mechanical loading response of mTORC1 in elderly populations. Clinicians should consider the "Metformin-Exercise Paradox," where the drug may slightly limit the cross-sectional area gains of muscle while still improving overall metabolic health.
If you are taking Metformin for longevity or blood sugar, be aware it’s a "pro-AMPK" drug. It’s excellent for metabolic health, but it might make it a little harder to pack on new muscle. It’s not a reason to stop, but it is a reason to be even more diligent with your weight training and protein intake.
6. Cortisol: The Anabolic Handbrake
Scientific Tone: Chronic glucocorticoid elevation (Cortisol) antagonizes the mTOR pathway by upregulating REDD1, a potent inhibitor of mTORC1 signaling. This creates a state of "anabolic resistance" where the muscle fails to respond to amino acids or mechanical tension.
Stress is the ultimate muscle-killer. When you’re chronically stressed or sleep-deprived, your body floods with Cortisol. This acts like a "handbrake" on your growth machinery, making all those expensive protein shakes and hard gym sessions far less effective.
Unlock Your Metabolic Potential: How to Balance AMPK and mTOR for Optimal Health
Every time you eat, fast, or exercise, your body makes a fundamental decision: Should it build muscle—or repair itself?
This decision is controlled by two master pathways: AMPK and mTOR.”
Modern medicine is beginning to recognize a powerful truth: many of the diseases we treat daily—type 2 diabetes, sarcopenia, cardiovascular disease, and even aspects of aging itself—are not merely the result of isolated organ dysfunction, but of disrupted cellular signaling. At the center of this disruption lies a fundamental biological switch governed by two opposing yet interconnected pathways: AMPK and mTOR. These molecular regulators continuously interpret environmental inputs—nutrient availability, physical activity, and energy status—and translate them into cellular decisions to either build or conserve, grow or repair.
When energy is scarce, AMPK is activated, initiating a survival-oriented program that enhances glucose uptake, promotes fatty acid oxidation, and stimulates autophagy—the essential cellular recycling process that maintains metabolic integrity (Mingzheng & You, 2025; Smiles et al., 2024). In contrast, when nutrients are abundant and mechanical signals from resistance exercise are present, mTOR drives anabolic processes, accelerating protein synthesis, muscle hypertrophy, and tissue repair (Dubek Kazyken et al., 2019). This dynamic interplay is not simply a biochemical curiosity—it is a central determinant of metabolic health and disease progression.
Emerging evidence suggests that chronic imbalance in this axis—persistent mTOR activation in states of overnutrition, or inadequate mTOR signaling in aging muscle—contributes directly to insulin resistance, atherosclerosis, and functional decline (Al-Kuraishy et al., 2025). Conversely, strategic modulation of this pathway through targeted exercise, nutritional timing, and pharmacological interventions offers a powerful, non-invasive means to restore metabolic flexibility and improve long-term health outcomes.
Understanding the AMPK–mTOR axis, therefore, is not just about molecular biology—it is about redefining how we approach prevention, performance, and longevity at their most fundamental level
AMPK: Your Body's Energy Alarm System and Longevity Promoter
AMPK functions as your cellular energy sensor, akin to a smoke detector in every cell. When cellular energy levels drop—such as during fasting, prolonged exercise, or caloric restriction—AMPK is activated. This activation signals the cell to shift into an energy-conservation and repair mode.
What AMPK Does for Your Health:
Boosts Glucose Uptake: Drives glucose into muscle cells, improving insulin sensitivity.
Ramps Up Fat Oxidation: Encourages the body to burn stored fat for fuel.
Stimulates Autophagy: Initiates cellular recycling, clearing damaged proteins and organelles—a critical process for anti-aging and disease prevention.
Enhances Mitochondrial Biogenesis: Builds more cellular power plants" (mitochondria), enhancing overall energy efficiency.
Reduced AMPK activity is a hallmark of insulin resistance and type 2 diabetes. Medications like metformin work partly by activating AMPK, highlighting its crucial role in metabolic health (Mingzheng and You, 2025)
Key Takeaway: AMPK Benefits
Cellular Energy Sensor: Activated by low energy states (fasting, exercise).
Metabolic Benefits: Improves insulin sensitivity, boosts fat burning.
Longevity Benefits: Promotes autophagy (cellular recycling) and mitochondrial health.
mTOR: Your Body's Master Builder for Muscle Growth
mTOR (mechanistic target of rapamycin) represents the opposite side of the metabolic coin. While AMPK senses scarcity, mTOR senses abundance. When nutrients are plentiful—especially the amino acid leucine—and mechanical stress is applied to muscle (e.g., during resistance training), mTOR activates, driving cellular growth and repair.
mTOR exists in two main complexes: mTORC1 (primary driver of protein synthesis and cell growth) and mTORC2 (involved in cell survival and organisation). Interestingly, AMPK can even activate mTORC2 during acute energetic stress, suggesting a more complex interplay than a simple opposition. (Dubek Kazyken et al. 2019)
How mTOR Gets Activated:
Mechanical Tension: The primary signal from resistance exercise.
Amino Acids: Particularly leucine, which acts as an“ignition key” for muscle growth by releasing a molecular brake (Sestrin2) on mTORC1.
Growth Factors: Hormones like insulin and IGF-1 activate mTORC1, which is why post-exercise carbohydrate intake can amplify mTOR’s anabolic response.
When mTORC1 is active, it accelerates protein synthesis, leading to muscle hypertrophy (muscle growth), satellite cell activation, and tissue repair. This is crucial for preventing sarcopenia (age-related muscle loss) and maintaining functional independence as we age.
Key Takeaway: mTOR Benefits
Growth Regulator: Activated by nutrient abundance (especially leucine) and resistance training.
Anabolic Effects: Drives protein synthesis, muscle hypertrophy, and tissue repair.
Essential for Muscle Mass: Crucial for preventing sarcopenia and maintaining strength.
AMPK vs mTOR: Key Differences
AMPK (Energy Sensor)
Activated by fasting, caloric deficit, and aerobic exercise
Increases fat oxidation and glucose uptake
Stimulates autophagy and cellular repair
Improves insulin sensitivity and metabolic flexibility
mTOR (Growth Regulator)
Activated by protein intake (leucine), insulin, and resistance training
Promotes muscle protein synthesis and hypertrophy
Supports tissue repair and anabolic growth
Essential for preventing sarcopenia
How They Work Together
AMPK inhibits mTOR during energy stress
mTOR suppresses autophagy when nutrients are abundant
Health depends on cyclical activation, not constant dominance
The Molecular Tug-of-War: How AMPK and mTOR Interact
The relationship between AMPK and mTOR is often described as a seesaw or a molecular tug-of-war. They are reciprocally inhibitory, meaning when one is highly active, it tends to suppress the other. This dynamic ensures that the cell prioritizes either energy conservation/repair or growth, but not both simultaneously.
Reciprocal Inhibition:
AMPK inhibits mTORC1: By activating a brake (TSC2) and directly disabling mTORC1 components.
mTOR suppresses AMPK: Active mTOR signaling, often driven by insulin, can reduce AMPK activity
.
This creates a natural cyclical pattern: during periods of energy deficit (fasting, cardio), AMPK dominates. During periods of nutrient surplus and mechanical loading (eating, resistance training), mTOR takes the lead (Smiles et al., 2024).
The "Interference Effect" – Myth vs. Reality
For years, there was concern about the "interference effect"—the idea that combining cardio and weightlifting would cancel out muscle gains due to AMPK suppressing mTOR. Modern science offers a more nuanced view:
Modest Interference: While acute AMPK activation can transiently inhibit mTOR, this effect is short-lived.
Timing is Key: Separating resistance and aerobic training by 6-24 hours, or performing resistance training before cardio, largely eliminates meaningful interference. Adequate protein intake around both sessions is also vital.
This means you can achieve both cardiovascular fitness and muscle mass with smart programming.
Key Takeaway: Dynamic Balance
Reciprocal Inhibition: AMPK and mTOR generally oppose each other, ensuring cellular priorities are met.
Cyclical Activation: Optimal health involves alternating periods of AMPK dominance (fasting, cardio) and mTOR dominance (feeding, resistance training).
Interference Effect: Largely mitigated by proper timing and nutrition, allowing for concurrent training.
Autophagy: Where AMPK Becomes a Longevity Tool
One of AMPK’s most clinically significant functions is the induction of autophagy—the cellular "self-cleaning" process. Autophagy is vital for removing damaged mitochondria, misfolded proteins, and cellular debris. This process is critical for preventing neurodegenerative diseases, combating cancer, and promoting healthy aging .
Conversely, when mTOR is highly active, it directly inhibits autophagy. This highlights a fundamental growth-vs-repair trade-off: a cell cannot efficiently build new proteins and dismantle old ones simultaneously. Chronic mTOR overactivation, often seen in conditions like obesity and hyperinsulinemia, impairs autophagy, accelerates cellular aging, and is linked to increased disease risk .
This connection underscores the importance of regular fasting periods, even for otherwise healthy individuals, to allow AMPK to activate and drive these crucial cellular repair mechanisms.
Key Takeaway: Autophagy & Longevity
AMPK Activates Autophagy: Essential for cellular recycling, removing damaged components.
mTOR Inhibits Autophagy: High mTOR activity suppresses this vital repair process.
Fasting Benefits: Regular fasting periods are crucial for activating AMPK and promoting autophagy, contributing to longevity.
Aging, Sarcopenia, and the Paradox of Balance
The interplay between AMPK, mTOR, and aging reveals a fascinating paradox:
Chronic mTOR Overactivation Accelerates Aging: Persistent mTOR signaling (from constant feeding, excess protein without exercise, obesity) suppresses autophagy and is linked to shortened lifespan in animal models. mTOR inhibitors like rapamycin have shown lifespan-extending effects.
mTOR Underactivation Causes Sarcopenia: In older adults, a blunted mTOR response (anabolic resistance) leads to progressive muscle loss (sarcopenia), a major predictor of disability and mortality.
The solution is not to constantly suppress or activate one pathway, but to engage in cyclical activation. This means strategically alternating between periods that favour mTOR (resistance training + protein-rich feeding) and those that favour AMPK (aerobic training + intermittent fasting). This mirrors ancestral human physiology: feast/work/build, then fast/move/clean.
Key Takeaway: The Aging Paradox
Too Much mTOR: Accelerates aging by suppressing repair processes. (Al-Kuraishy et al.2025)
Too Little mTOR: Leads to sarcopenia (muscle loss) in older adults.
The Solution: Cyclical activation—alternating between building (mTOR) and cleaning (AMPK) phases.
Nutritional & Pharmacological Modulators of AMPK and mTOR
Nutritional Control:
Protein Timing & Leucine Loading: Distributing 20-40 grams of high-quality protein across 4 meals daily, each containing a sufficient leucine threshold (2-3g), provides pulsatile mTOR activation without constant overstimulation.
Intermittent Fasting (IF): A 12-16 hour overnight fast activates AMPK, promotes autophagy, and improves insulin sensitivity. This can be done without compromising muscle if daily protein targets are met within the eating window.
Carbohydrate Timing: Consuming carbohydrates around resistance training sessions can amplify mTOR’s anabolic signaling by elevating insulin during peak sensitivity. Avoiding excessive carbs during rest periods helps prevent insulin-driven mTOR suppression of autophagy.
Pharmacological Consideration
Metformin: A common diabetes drug, metformin activates AMPK and improves metabolic health. However, it may modestly blunt the hypertrophic response to resistance training .
Berberine: A plant-derived compound, berberine also activates AMPK and is gaining interest for metabolic syndrome management.
Rapamycin: Directly inhibits mTORC1 and is studied for its longevity potential, though chronic use has immunosuppressive risks
Best Foods to Activate AMPK
Polyphenol-rich foods (green tea, berries, dark chocolate) stimulate AMPK via antioxidant signaling pathways
Low-glycemic, high-fibre foods improve insulin sensitivity and indirectly enhance AMPK activity
Healthy fats (olive oil, nuts) support metabolic flexibility and fat oxidation
Caloric restriction/fasting states remain the most potent nutritional triggers of AMPK
Functional compounds: Berberine and resveratrol mimic AMPK activation similar to exercise
Best Exercises for mTOR Activation
Resistance training (primary driver): Compound lifts (squats, deadlifts, presses) create mechanical tension → mTORC1 activation
Moderate-to-high intensity loading: 6–12 reps, progressive overload maximizes hypertrophic signaling
Post-exercise protein intake (20–40g, leucine-rich): Amplifies mTOR activation
Explosive training (power movements): Enhances neuromuscular signaling and anabolic response
Consistency > volume: Repeated stimulation produces cumulative mTOR signaling
AMPK vs mTOR for Fat Loss
AMPK drives fat loss: Increases lipolysis, fatty acid oxidation, and mitochondrial activity
mTOR preserves lean mass: Prevents muscle loss during caloric deficit
Best strategy = dual activation:
AMPK → fasting + aerobic training
mTOR → resistance training + protein
Excess AMPK without mTOR → muscle loss
Excess mTOR without AMPK → fat gain & metabolic rigidity
Clinical Insight: Sustainable fat loss requires high AMPK activity with periodic mTOR stimulation to maintain metabolic rate and muscle mass.
Practical Applications: Your Weekly Blueprint for Metabolic Flexibility
To achieve "Metabolic Flexibility"—the ability to efficiently switch between burning fat and building muscle—your weekly routine should integrate periods that favor each pathway.
The Metabolic Cycle Protocol: Programming for Longevity
The Build Phase (mTOR Activation)
Goal: Muscle protein synthesis, structural repair, hypertrophy.
Mechanism: Activating mTOR via mechanical tension and amino acid signaling.
Execution: Resistance training (3-4 sessions/week, compound movements). Consume a high-leucine protein meal (30-40g) within 2 hours post-session to maximize the "mTOR surge."
The Clean Phase (AMPK Activation)
Goal: Autophagy, fat oxidation, improved insulin sensitivity.
Mechanism: Triggering AMPK by creating a temporary energy deficit.
Execution: Fasted movement (Zone 2 aerobic exercise or brisk 30-minute walk in a fasted state, ideally morning). Maintain a consistent 12-16-hour overnight fast.
The Transition Phase (Concurrent Training)
Goal: Balancing cardiovascular endurance with muscle preservation.
Mechanism: Navigating "cross-talk" where both pathways are stimulated within the same 24-hour window.
Execution: The "Lift-First" Rule: Perform resistance training before aerobic work if done in the same session. Separate sessions by at least 6 hours if possible. Prioritize post-session protein.
Weekly Prescription Example:
Resistance Training: 3-4 sessions/week (compound movements, 3-4 sets, 6-12 reps). Follow each with 30-40g leucine-rich protein.
Aerobic Training: 2-3 sessions/week (30-45 min Zone 2 cardio), ideally fasted in the morning or 6+ hours after resistance training.
Protein Distribution: 1.6-2.2g protein/kg body weight daily, divided across 4 meals for pulsatile mTOR activation.
Fasting Window: Consistent 12-hour overnight fast; extend to 14-16 hours 2-3 times/week for amplified AMPK/autophagy benefits.
Special Consideration for Older Adults: Higher protein (2.0-2.2g/kg), slightly longer leucine boluses (3-4g), and prioritized resistance training to offset anabolic resistance. Individualize aggressive fasting protocols to avoid muscle loss.
Frequently Asked Questions
1. Can I activate both AMPK and mTOR at the same time?
Not optimally in the same cell at the same moment — they reciprocally inhibit each other. However, over the course of a day or week, you can structure exercise and nutrition to activate each pathway at appropriate times. Morning fasted cardio activates AMPK; afternoon resistance training + protein activates mTOR. The key is temporal separation.
2. Is intermittent fasting safe if I'm trying to build muscle?
Yes, when designed correctly. A 12–16 hour overnight fast does not meaningfully impair muscle protein synthesis if daily protein targets (1.6–2.2g/kg) are met during the feeding window. The AMPK activation from fasting actually improves insulin sensitivity and mitochondrial health, supporting long-term training capacity.
3. Does metformin prevent muscle growth?
Evidence suggests metformin may blunt some hypertrophic signaling from resistance training by activating AMPK during the post-exercise mTOR window. The effect appears modest in most patients but is worth monitoring in individuals specifically training for hypertrophy. The cardiovascular and metabolic benefits of metformin almost always outweigh this concern.
4. What foods best activate mTOR?
Leucine-rich protein sources are the most potent dietary mTOR activators: whey protein, eggs, chicken breast, beef, salmon, and Greek yogurt. A meal containing at least 2–3g of leucine is generally considered sufficient to cross the mTOR activation threshold.
5. What is "anabolic resistance" and how do I overcome it?
Anabolic resistance is the blunted mTOR response to protein and exercise seen in older adults (generally over 60). The muscle's sensitivity to leucine and mechanical loading diminishes with age. Practical solutions include increasing per-meal protein to 35–40g, ensuring leucine content of 3–4g, performing resistance training consistently, and considering supplemental creatine, which has independent evidence for sensitizing mTOR signaling in aging muscle.
6. How does sleep affect the AMPK–mTOR balance?
Sleep deprivation suppresses mTOR signaling and impairs muscle protein synthesis while simultaneously dysregulating AMPK — the worst of both worlds. Poor sleep also elevates cortisol, which directly inhibits anabolic signaling. Optimizing sleep (7–9 hours) is arguably as important as nutrition and training for managing this axis.
7. Can supplements like berberine or NMN meaningfully shift this balance?
Berberine has solid evidence for AMPK activation comparable to low-dose metformin in metabolic syndrome patients. NMN (nicotinamide mononucleotide) is a precursor to NAD+, which supports AMPK activation indirectly through SIRT1. Neither is a substitute for exercise and nutrition, but in appropriately selected patients, they may augment the AMPK arm of the balance.
8 .What is the best time to activate AMPK?
The optimal time to activate AMPK is during energy-deficit states, such as morning fasted periods or aerobic exercise sessions. Overnight fasting (12–16 hours) naturally increases AMPK activity, promoting fat oxidation and cellular repair.
9 .Does fasting increase autophagy?
Yes. Fasting is one of the most potent activators of autophagy, primarily through AMPK activation and suppression of mTOR. Autophagy typically increases after 12–16 hours of fasting, enhancing cellular cleanup and metabolic health.
10 .How to activate mTOR naturally?
mTOR is best activated through a combination of resistance training and adequate protein intake, especially leucine-rich sources (20–40g protein per meal). Post-exercise nutrition and mechanical muscle loading are the strongest natural stimulators of mTOR signaling.
Call to Action — How to Take This Further
Understanding AMPK and mTOR is not just academic. It is a blueprint for how to structure your training, your meals, and your clinical decisions in ways that genuinely change metabolic outcomes.
Your Next Steps
Audit your current week. How many resistance sessions are you doing? How many aerobic sessions? Is there a 12-hour fasting window most nights? Where are the gaps?
Try the cycle model for 4 weeks. Apply the build/clean framework above, track energy, body composition, and how you feel. The AMPK–mTOR balance responds to lifestyle inputs within days, not months.
Share this with your clinician. If you are managing diabetes, obesity, or sarcopenia, bring this framework to your next appointment. The translation from molecular biology to prescriptive lifestyle medicine is precisely what personalized care looks like.
Author’s Note — A Clinician’s Perspective
As a physician working at the intersection of metabolic disease, aging, and exercise physiology, I have come to view the balance between AMPK and mTOR not as an abstract biochemical concept but as a daily clinical reality. Every patient encounter—whether involving type 2 diabetes, obesity, frailty, or cardiovascular risk—reflects some degree of dysregulation within this axis.
In traditional practice, we often treat downstream manifestations: elevated glucose, reduced muscle mass, or lipid abnormalities. However, what becomes increasingly clear is that these are surface expressions of deeper signaling imbalances. A sedentary, overnourished patient with insulin resistance is, at a cellular level, chronically mTOR-dominant and AMPK-suppressed. Conversely, an older patient experiencing sarcopenia often demonstrates inadequate mTOR responsiveness despite sufficient nutritional intake—a phenomenon we recognize as anabolic resistance.
This duality presents a clinical challenge: the goal is not to suppress one pathway in favor of the other, but to restore physiological rhythm between them. In practice, this means prescribing not just medications, but structured behavioral interventions—resistance training to stimulate anabolic signaling, aerobic activity and fasting windows to activate cellular repair mechanisms, and precise nutritional strategies to synchronize both.
Pharmacological tools such as metformin and, in select cases, mTOR inhibitors provide additional leverage, but they cannot replace the foundational role of lifestyle-driven signaling modulation. The most meaningful improvements I observe in patients occur when these pathways are engaged through consistent, cyclical patterns of stress and recovery.
Ultimately, understanding the AMPK–mTOR axis shifts the clinician’s role—from reactive disease management to proactive metabolic programming. It allows us to move beyond symptom control and toward designing interventions that align with human physiology at its most fundamental level.
This article is intended for educational purposes only and does not constitute medical advice. Always consult a qualified healthcare provider before beginning a new exercise or nutrition program, especially if you have an existing medical condition.
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References
Al-Kuraishy, H. M., Sulaiman, G. M., Mohsin, M. H., Mohammed, H. A., Dawood, R. A., Albuhadily, A. K., Al-Gareeb, A. I., Albukhaty, S., & Abomughaid, M. M. (2025). Targeting of AMPK/MTOR signaling in the management of atherosclerosis: Outmost leveraging. International Journal of Biological Macromolecules, 309(Pt 2), 142933. https://doi.org/10.1016/j.ijbiomac.2025.142933
Audet-Walsh, É., Vernier, M., & Viollet, B. (2021). Editorial: AMPK and mTOR beyond signaling: Emerging roles in transcriptional regulation. Frontiers in Cell and Developmental Biology, 8, 641552. https://doi.org/10.3389/fcell.2020.641552
Dubek Kazyken, D., et al. (2019). AMPK directly activates mTORC2 to promote cell survival during acute energetic stress. Science Signaling, 12, eaav3249. https://doi.org/10.1126/scisignal.aav3249
Mingzheng, X., & You, W. (2025). AMPK/mTOR balance during exercise: Implications for insulin resistance in aging muscle. Molecular and Cellular Biochemistry, 480, 5941–5953. https://doi.org/10.1007/s11010-025-05362-4
Smiles, W. J., Ovens, A. J., Kemp, B. E., Galic, S., Petersen, J., & Oakhill, J. S. (2024). New developments in AMPK and mTORC1 cross-talk. Essays in Biochemistry, 68(3), 321–336. https://doi.org/10.1042/EBC20240007