Peptides for Energy — The Complete Guide

NAD+/NADH Cycling · Sirtuin Activation · NNMT Inhibition

NAD+ is the central coenzyme of cellular energy metabolism. As an electron carrier in the electron transport chain, NAD+ is reduced to NADH at Complexes I and II, then re-oxidized as NADH donates electrons to drive ATP synthase. NAD+ also activates sirtuins (SIRT1–7), the longevity-associated deacetylase enzymes that regulate mitochondrial biogenesis, DNA repair, and metabolic homeostasis. Published data shows NAD+ levels fall approximately 50% between ages 40 and 60. Direct NAD+ repletion via injectable or nasal spray bypasses oral precursor conversion limitations. 5-Amino-1MQ operates upstream: it inhibits NNMT, the enzyme that diverts nicotinamide away from NAD+ synthesis, raising intracellular NAD+ while simultaneously reducing fat cell hypertrophy.

Alternative Electron Carrier · Cardiolipin Stabilization · ROS Reduction

Even with adequate NAD+ substrate, mitochondrial ATP production fails when the electron transport chain machinery itself is damaged. Methylene Blue functions as an alternative electron carrier, accepting electrons directly from NADH and FADH2 and donating them to cytochrome c, bypassing damaged upstream complexes while reducing electron leak and superoxide formation. Elamiretide (SS31) takes a structural approach, concentrating at cardiolipin in the inner mitochondrial membrane, preserving electron transport chain supercomplex assembly and maintaining membrane potential. Together, they address the functional and structural layers of electron transport chain decline.

AMPK Activation · PGC-1α · ERRα/ERRγ Agonism · Thermogenesis

Peak energy capacity depends on having enough mitochondria per cell. MOTS-C is a mitochondrial-derived peptide that activates AMPK, the master cellular energy sensor, to drive PGC-1α transcription and new mitochondria formation, while improving insulin sensitivity and reducing ROS. SLU-PP-332/BAM15 provides a complementary approach: SLU-PP-332 directly activates ERRα/ERRγ, master transcriptional regulators of mitochondrial biogenesis, while BAM15 is a mitochondrial protonophore that uncouples the membrane, raising metabolic rate and fat oxidation. The combination creates biogenesis signaling plus thermogenic metabolic drive.

Growth Hormone · IGF-1 · Fat Oxidation · Lean Mass · Sleep Quality

Growth hormone governs body composition, metabolic rate, and the anabolic environment in which cellular energy systems operate. GH drives lipolysis, preferential fat oxidation, and lean mass preservation that shift the metabolic set point upward. GH declines approximately 15% per decade after age 30, producing weight gain, reduced muscle mass, increased fatigue, and impaired sleep. CJC-1295/Ipamorelin provides the strongest GH pulse via dual GHRH and ghrelin receptor stimulation. Sermorelin provides more conservative GHRH-analog stimulation. Ibutamoren (MK-677) is the only oral GH secretagogue, offering convenient daily dosing without injection.

Foundation of Every Energy Protocol

• Direct NAD+ delivery to circulation, bypassing oral conversion efficiency limitations
• Restores NAD+/NADH cycling that drives over 90% of cellular ATP production
• Activates sirtuins SIRT1–7, longevity-associated enzymes for mitochondrial biogenesis and DNA repair
• Supports PARP-1 activity for DNA repair in cells undergoing age-related genomic stress
• Higher peak plasma NAD+ elevation than any oral precursor pathway
• Most direct intervention for the NAD+ decline that underlies cellular energy loss

• Non-injectable NAD+ delivery, convenient for patients who prefer to avoid subcutaneous injection
• Nasal mucosal absorption provides rapid systemic bioavailability
• Potential direct CNS access via olfactory route, relevant for cognitive and neurological energy effects
• Multiple doses per day possible, supporting sustained NAD+ elevation between injectable cycles
• 15mL vial provides extended supply at 10mg/0.1mL dosing
• Appropriate as a standalone or as a complement to injectable NAD+ cycles

• Inhibits NNMT, the enzyme that diverts nicotinamide away from NAD+ synthesis
• Raises intracellular NAD+ by redirecting nicotinamide toward NAD+ recycling
• Reduces fat cell hypertrophy and NNMT-driven adipose metabolic dysfunction
• Oral delivery with convenient daily dosing and no injection required
• Complements direct NAD+ supplementation by optimizing the endogenous synthesis pathway
• Dual energy and body composition benefit from a single mechanism

• Alternative electron carrier that bypasses damaged Complex I/III to maintain ATP output
• Reduces mitochondrial ROS production by intercepting electron leak
• Upregulates PGC-1α and mitochondrial biogenesis genes alongside immediate functional support
• Oral delivery with convenient daily inclusion in energy protocol
• Multiple dose options from 5mg to 25mg; provider determines optimal dose
• Complementary mechanism to NAD+ repletion, addressing electron transport chain function rather than just substrate

• Concentrates at cardiolipin in the inner mitochondrial membrane — unique structural targeting
• Preserves electron transport chain supercomplex assembly for maximum ATP yield
• Protects against cardiolipin oxidation that uncouples the chain and reduces efficiency
• Restores mitochondrial membrane potential in aged and energy-depleted cells
• Particularly effective for patients with established mitochondrial dysfunction or post-illness fatigue
• Addresses the structural deterioration layer that Methylene Blue's functional bypass does not resolve

• Mitochondria-derived peptide, encoded within the mitochondrial genome itself
• Activates AMPK, the master cellular energy sensor that drives PGC-1α and new mitochondria formation
• Improves skeletal muscle insulin sensitivity — more glucose uptake for energy in working muscle
• Reduces reactive oxygen species production at mitochondrial sources
• Anti-inflammatory systemic effects that reduce the chronic inflammation impairing mitochondrial function
• 2mg/mL for moderate biogenesis stimulus; 10mg/mL for more aggressive mitochondrial expansion

• SLU-PP-332 directly activates ERRα and ERRγ — master transcriptional regulators of mitochondrial biogenesis
• BAM15 is a mitochondrial protonophore — uncouples membrane potential to raise metabolic rate
• Combination mimics the energy expenditure and biogenesis signaling of aerobic exercise
• Oral delivery — convenient inclusion for patients who prefer to minimize injections
• Increases fat oxidation and thermogenic metabolic activity via uncoupling mechanism
• ERR activation drives new mitochondria formation independently of AMPK pathway used by MOTS-C

• Dual GHRH analog (CJC-1295) + ghrelin mimetic (Ipamorelin) — most potent GH pulse stimulation
• Increases GH-driven IGF-1 for lean mass preservation, fat oxidation, and metabolic rate elevation
• Preserves pituitary feedback regulation — no GH suppression, maintains natural pulsatility
• Improves sleep quality through GH's role in slow-wave sleep restoration
• Reduces body fat preferentially while maintaining or increasing lean mass — shifts metabolic set point
• The GH secretagogue of choice for patients who want maximum GH stimulation

• Only oral GH secretagogue in the VitalRx catalog — ghrelin receptor agonist
• Stimulates GH release without injection — convenient daily oral dosing
• Raises IGF-1 levels for lean mass, fat metabolism, and recovery support
• Extends slow-wave sleep depth — the primary GH secretion window
• No pituitary suppression — stimulates endogenous GH, does not replace it
• 12.5mg starting dose for tolerability assessment; 25mg for full GH secretagogue effect

The most common age-related energy pattern: pervasive fatigue present even with adequate sleep, poor cellular recovery, and cognitive energy alongside physical energy decline.

Patients with deeper mitochondrial dysfunction — post-viral fatigue, post-chemotherapy energy deficit — where electron transport chain machinery is damaged and substrate repletion alone is insufficient.

Patients with reduced aerobic capacity, exercise intolerance, or metabolic slowdown driven by age-related reduction in mitochondrial number per cell.

Patients where energy presentation includes weight gain despite unchanged diet, reduced lean mass, poor sleep quality, blunted recovery — the classic GH decline phenotype.

Days 1–14

Acute NAD+ and Mitochondrial Support Effects

NAD+ injectable patients typically notice the fastest effects — improved mental clarity, reduced fatigue with exertion, and improved post-activity recovery within the first 1–2 weeks. Methylene Blue effects on cognitive energy and mental clarity are often reported within the first 1–2 weeks. Elamiretide mitochondrial membrane restoration effects begin within days at the cellular level, with functional improvement accumulating over weeks.

Weeks 2–6

Mitochondrial Biogenesis and GH Pulse Restoration

MOTS-C and SLU-PP-332/BAM15 biogenesis effects develop as new mitochondria form and mature — patients describe improved exercise tolerance, better aerobic capacity, and faster recovery by weeks 4–6. GH secretagogue users notice improved sleep quality within 2 weeks, with body composition, energy, and exercise recovery improvements through weeks 4–8. 5-Amino-1MQ body composition effects develop over 4–8 weeks.

Months 2–4 and Beyond

Sustained Metabolic Restoration

The most significant energy improvements — body composition shift from GH secretagogues, full mitochondrial biogenesis from MOTS-C, and sustained NAD+ elevation — develop and consolidate over months. Most patients report qualitatively different energy from stimulant effects: more sustained throughout the day, better overnight recovery, improved stress tolerance, and a general sense of metabolic capacity restoration.

NAD+ Injectable — 10mL (100mg/mL)

Direct NAD+ repletion via subcutaneous injection. Highest peak plasma NAD+ elevation.

NAD+ Nasal Spray — 15mL (10mg/0.1mL)

Non-injectable NAD+ delivery. Rapid nasal mucosal absorption with potential CNS access.

5-Amino-1MQ — from $124.65 (25mg, 30ct)

NNMT inhibitor. Raises intracellular NAD+ via endogenous synthesis pathway. Oral daily dosing.

Methylene Blue Oral Capsules — from $98 (5mg, 20ct)

Mitochondrial electron carrier. Electron transport bypass, ROS reduction, PGC-1α upregulation.

Elamiretide (SS31) — 5mL Injectable

Cardiolipin-targeted mitochondrial antioxidant for electron transport chain structural integrity.

MOTS-C Injectable — 2mg/mL, 5mL

Mitochondrial-derived peptide. AMPK activation for mitochondrial biogenesis and insulin sensitivity.

SLU-PP-332 / BAM15 Capsules — 30ct

ERRα/ERRγ agonism + mitochondrial uncoupling. Exercise-mimetic biogenesis and thermogenic metabolism.

CJC-1295 / Ipamorelin — 5mL Injectable

Dual GH secretagogue. Strongest pituitary GH pulse stimulation for metabolic restoration.

Ibutamoren (MK-677) — from $118.30 (12.5mg, 30ct)

Oral GH secretagogue. Ghrelin receptor agonist — the only oral GH support option in the catalog.

Identify Your Primary Energy Pattern

Is your fatigue pervasive and constant — suggesting NAD+ depletion or mitochondrial dysfunction? Is it tied to exercise intolerance and reduced aerobic capacity — suggesting mitochondrial biogenesis decline? Or does it come with weight gain, poor sleep, and reduced lean mass — the GH decline phenotype? Your primary pattern guides which mechanism to start with.

Complete Your Async Provider Consultation

Answer a brief health intake questionnaire at your own pace — no video call, no waiting room. Describe your energy pattern, history, sleep quality, activity level, and any relevant labs. A licensed provider reviews your submission, recommends compounds and dosing, and issues your prescription when clinically appropriate.

Receive Your Order

Your prescription is filled by Optimal Balance Pharmacy — a licensed compounding pharmacy — and shipped via FedEx Standard Overnight to your door. Syringes and alcohol swabs included with all injectable orders.

Build and Layer Over Time

Energy protocols often start with one or two foundational compounds and expand as the primary deficit is addressed and secondary layers become the focus. Most patients begin with NAD+ or GH secretagogues depending on their dominant pattern, then layer in biogenesis compounds. Follow-up consultations adjust the protocol based on your response.