How PeptiPump™ Enhances Muscle Blood Flow Through Natural ACE Inhibition

PeptiPump™ is primarily marketed as a pump ingredient, but HR Labs would describe it more as a fuel delivery aid. It does support vasodilation, important beyond the subjective sensation of a "pump" but also what determines how much oxygen and nutrient reaches working muscle during a session. But it goes beyond this, boosting glucose uptake into cells for faster delivery of energy substrate to replenish the local muscle stores which can be quickly depleted. This fuel delivery side of performance will always be a limiting factor that more stimulants or other cognitive enhancers will not fix.

This article covers how PeptiPump™ works, the research behind ACE inhibition and exercise blood flow, glucose uptake, and why HR Labs has included it in the newest Defib formulation.

Quick Facts

Main benefit: Supports skeletal muscle blood flow and oxygen delivery during exercise through natural ACE inhibition, promoting vasodilation and improved nutrient delivery to working tissue.

Best for: Athletes in any discipline where sustained muscular output, repeated efforts, and recovery between sets or bouts matter. Particularly relevant for high-volume training where blood flow and nutrient delivery become limiting factors.

Dosage: 500mg PeptiPump™ per serve in Defib.

Timeline: ACE inhibition from food-derived peptides has shown acute effects on vascular function within a single dose period, with continued benefits over consistent use.[5]

What is PeptiPump™ and what does it do?

PeptiPump™ is a lentil protein hydrolysate developed by Nuritas, an Irish biotech company that uses an AI platform called Magnifier to identify networks of bioactive peptides within food proteins. This is exactly how PeptiPump™ was discovered. Rather than isolating a single compound, PeptiPump™ is a profile of peptides that have been identified for their targeted action on ACE inhibition and predicted activity across several complimentary pathways, also including glucose uptake.

The peptides are derived from lentils (Lens culinaris) and have been shown to survive gastrointestinal digestion, meaning they reach circulation in an active form rather than being broken down in the stomach. This digestive resistance is a meaningful distinction from many food-derived peptides, where activity demonstrated in a test tube does not survive the journey through the gut. The ingredient is produced through a controlled process that delivers a consistent peptide profile in every scoop.

Lentil proteins are a particularly effective source of ACE-inhibitory peptides. When lentil protein is broken down, the smallest peptide fragments show the strongest ACE inhibitory activity, and further purification for specific components enhances this further.[3]

The peptides from lentils are characteristically short-chain, shorter than those from other legume sources tested. This matters because shorter peptides are harder for the gut to break down further, meaning they are more likely to survive digestion and reach the bloodstream in an active form. This digestive stability is what makes PeptiPump™ viable as an oral supplement.

Why ACE Inhibition Matters for Exercise

Angiotensin-converting enzyme (ACE) does two things that matter for training. It produces angiotensin II, which narrows blood vessels, and it breaks down bradykinin, which opens them. When ACE activity is high, the balance tips toward constriction: less blood flow to working muscle, reduced oxygen delivery, and impaired glucose uptake. This becomes a real constraint on performance during sustained or repeated high-intensity efforts.[1]

ACE inhibition shifts this balance by reducing the constriction signal and preserving the vasodilation signal by keeping more bradykinin active. More blood reaches working muscle, and more glucose can enter the cells that need it.

Why This Matters for Nitric Oxide

Most blood flow supplement ingredients (arginine, citrulline) work by providing raw material for nitric oxide (NO) production. This is effective, but it has a ceiling. When ACE activity is high, the environment works against NO: angiotensin II promotes oxidative stress that degrades NO before it can act, and the loss of bradykinin removes a direct stimulus for NO production. Providing more precursor does not fully overcome the problem when the enzyme environment is actively suppressing NO signalling.

ACE inhibition addresses this from the other side. Preserving bradykinin keeps signalling for the enzymes that produce nitric oxide. A human trial also showed that ACE inhibition reduces a compound called ADMA, which competes with arginine for access to those same enzymes.[4] When ADMA is high, it blocks arginine from doing its job even when arginine is plentiful. By reducing ADMA, ACE inhibition increases the efficiency of whatever arginine is available, whether from diet, citrulline supplementation, or your body's own production. This means ACE inhibition does not just provide an alternative route to vasodilation, it improves the conditions under which NO precursors like citrulline can do their job.

The ACE Gene and Athletic Performance

The relevance of ACE activity to exercise performance is well demonstrated and the ACE insertion/deletion polymorphism is one of the most studied genetic variants in sports science. Individuals carrying the insertion allele (associated with lower ACE activity) have been consistently overrepresented among endurance athletes. This becomes much more influential as exercise duration extends beyond moderate efforts.

Why glucose uptake matters for exercise

During exercise, your muscles rely heavily on glucose as fuel. Glucose comes from two sources: glycogen stored inside the muscle itself, and blood glucose delivered via circulation. Local glycogen is finite and can be substantially depleted during sustained or high-intensity efforts. Once local stores run low, the muscle becomes increasingly dependent on glucose from the bloodstream. How fast that glucose can cross into the muscle cell becomes a genuine bottleneck.

This is governed primarily by a glucose transporter protein called GLUT4. Think of GLUT4 as a gate in the muscle cell wall. Normally, most of these gates sit inside the cell doing nothing. When you exercise or when insulin rises, GLUT4 gates move to the cell surface and open up, allowing glucose to flow in. The more GLUT4 at the surface, the faster glucose enters the cell.[6]

This matters most in two scenarios. First, during prolonged or repeated high-intensity exercise where glycogen is being burned faster than it can be replenished from circulation. Second, during recovery between bouts or sessions, where the speed of glycogen refuelling determines how quickly the muscle is ready to perform again. Research has shown that GLUT4 increases after exercise and that this increase directly correlates with how fast glycogen stores are rebuilt in the hours following a session.[10] Anything that gets more GLUT4 to the cell surface during and after exercise has the potential to improve both sustained performance and recovery.

This is where the ACE inhibition mechanism becomes relevant beyond blood flow. Bradykinin, preserved by ACE inhibition, has been shown to directly enhance glucose transport in skeletal muscle through a pathway that works alongside but is separate from insulin. The result is the same: more GLUT4 gates move to the cell surface, allowing more glucose in.[7] This has been demonstrated in both animal models and human studies, where ACE inhibition increased muscle glucose uptake beyond what improved blood flow alone could explain.[9]

ACE inhibition helps glucose uptake from two directions at once. On one side, preserving bradykinin stimulates a signalling chain through nitric oxide that drives more GLUT4 to the cell surface. On the other side, reducing angiotensin II removes a signal that actively suppresses GLUT4 movement. More of the "open the gates" signal, less of the "keep them closed" signal.

What is understood about PeptiPump™ and glucose transport

PeptiPump™ was identified through Nuritas' AI-driven screening specifically for networks of peptides with ACE-inhibitory activity. The glucose uptake effect is a predicted downstream consequence of that ACE inhibition, operating through the bradykinin to nitric oxide to GLUT4 pathway described above. This is consistent with the broader literature on food-derived ACE-inhibitory peptides and glucose metabolism. Research on another food-derived bioactive peptide with ACE-related activity demonstrated improved glucose tolerance and increased GLUT4 activity in skeletal muscle.[11]

While PeptiPump™-specific glucose uptake data is not yet published, the mechanistic pathway from ACE inhibition to enhanced muscle glucose transport is well established across multiple peer-reviewed studies using both pharmaceutical ACE inhibitors and food-derived peptides. The relevance for training is that this pathway offers a route to improved fuel delivery that is distinct from simply increasing blood flow or providing more carbohydrate. By helping glucose cross into muscle cells faster, ACE inhibition from PeptiPump™ has the potential to support both sustained energy availability during a session and the speed of glycogen recovery between sessions.

PeptiPump™ in the Defib Preworkout

Defib, available in New Zealand through Strom Sports, includes PeptiPump™ at 500mg per serve. Also included alongside for blood flow support is citrulline malate, which provides substrate for the nitric oxide synthesis pathway via the arginine-citrulline cycle.

These two ingredients address blood flow from complementary angles. Citrulline malate provides more raw material (arginine) for nitric oxide production. PeptiPump™ works on the environment in which that production happens: preserving bradykinin (which stimulates the enzymes that make nitric oxide) and reducing ADMA (which blocks arginine from reaching those enzymes). The practical result is that PeptiPump™ improves the conditions under which citrulline can be effective, rather than duplicating the same mechanism. One provides the fuel, the other clears the road. On top of this, PeptiPump™ adds the glucose transport benefit through GLUT4, an effect that citrulline does not address.

This blood flow stack ensures vasodilation is managed from multiple angles to produce an outcome not achievable by any single ingredient alone, giving a more complete approach to fuel delivery during training.

For the full breakdown of how all Defib ingredients work together across stimulation, cognition, blood flow, and hydration, see the Defib article.

Frequently Asked Questions

Is there a published clinical trial on PeptiPump™?

Not at the time of writing, though one is registered and data is expected. The ACE inhibition mechanism behind PeptiPump™ is well established in human research, including randomised controlled trials on food-derived ACE-inhibitory peptides showing improved vascular function.[5] This article will be updated as PeptiPump™-specific data becomes available.

How does this relate to the "pump" I feel during training?

The sensation of a muscular pump during resistance training is driven by increased blood flow to working muscle and the accumulation of metabolites that draw fluid into muscle cells. ACE inhibition supports the vasodilation side of this equation, promoting greater blood delivery to active tissue. The effect is functional, not just cosmetic: more blood means more oxygen and substrate delivery, better metabolic waste clearance, and improved capacity for sustained output.

Will PeptiPump™ lower my blood pressure?

Food-derived ACE-inhibitory peptides have shown vascular benefits in human trials without significant changes in systemic blood pressure in normotensive individuals.[5] The mechanism supports local vasodilation in active tissue rather than a systemic blood pressure reduction. That said, if you have existing blood pressure concerns or are on antihypertensive medication, consult your healthcare provider.

Is it safe for drug-tested athletes?

PeptiPump™ is a food-derived lentil protein hydrolysate with no prohibited substances. Always verify against your specific organisation's banned substance list.

Does PeptiPump™ overlap with nitrate supplements?

Both support vasodilation, but through different pathways. Nitrates (like those in OxyStorm®) provide raw material that your body converts directly into nitric oxide. PeptiPump™ works through ACE inhibition, which preserves bradykinin (a vasodilator) and reduces angiotensin II (a vasoconstrictor), while also improving the conditions for your body's own nitric oxide production. The two mechanisms are complementary.

For the full science on nitrate pathways and how they complement citrulline under anaerobic conditions, see the nitrates article.

Shop DEFIB™ Pre-Workout here

MADE FOR PROGRESS

References

1. Dietze GJ, Henriksen EJ. Angiotensin-converting enzyme in skeletal muscle: sentinel of blood pressure control and glucose homeostasis. J Renin Angiotensin Aldosterone Syst. 2008;9(2):75-88.
2. Puthucheary Z, Skipworth JRA, Rawal J, Loosemore M, Van Someren K, Montgomery HE. The ACE gene and human performance: 12 years on. Sports Med. 2011;41(6):433-448.
3. Chang SKC, Zhang Y, Pechan T. Structures, antioxidant, and angiotensin I-converting enzyme (ACE)-inhibitory activities of peptides derived from protein hydrolysates of three phenolics-rich legume genera. J Food Sci. 2025;90(2):e70069.
4. Chen JW, Hsu NW, Wu TC, Lin SJ, Chang MS. Long-term angiotensin-converting enzyme inhibition reduces plasma asymmetric dimethylarginine and improves endothelial nitric oxide bioavailability and coronary microvascular function in patients with syndrome X. Am J Cardiol. 2002;90(9):974-982.
5. Hirota T, Ohki K, Kawagishi R, et al. Casein hydrolysate containing the antihypertensive tripeptides Val-Pro-Pro and Ile-Pro-Pro improves vascular endothelial function independent of blood pressure-lowering effects: contribution of the inhibitory action of angiotensin-converting enzyme. Hypertens Res. 2007;30(6):489-496.
6. Henriksen EJ, Jacob S. Modulation of metabolic control by angiotensin converting enzyme (ACE) inhibition. J Cell Physiol. 2003;196(1):171-179.
7. Henriksen EJ, Jacob S, Kinnick TR, Youngblood EB, Schmit MB, Dietze GJ. ACE inhibition and glucose transport in insulinresistant muscle: roles of bradykinin and nitric oxide. Am J Physiol. 1999;277(1):R332-336.
8. Shiuchi T, Cui TX, Wu L, et al. ACE inhibitor improves insulin resistance in diabetic mouse via bradykinin and NO. Hypertension. 2002;40(3):329-334.
9. Dietze GJ, Wicklmayr M, Rett K, Jacob S, Henriksen EJ. Potential role of bradykinin in forearm muscle metabolism in humans. Diabetes. 1996;45(Suppl 1):S110-114.
10. Kuo CH, Browning KS, Ivy JL. Regulation of GLUT4 protein expression and glycogen storage after prolonged exercise. Acta Physiol Scand. 1999;165(2):193-201.
11. de Campos Zani SC, Son M, Bhullar KS, Chan CB, Wu J. IRW (Isoleucine-Arginine-Tryptophan) improves glucose tolerance in high fat diet fed C57BL/6 mice via activation of insulin signaling and AMPK pathways in skeletal muscle. Biomedicines. 2022;10(6):1235.

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This content is for educational purposes only and does not intend to cure or diagnose disease, nor make any health claims. There is no intent to slander in any way, but rather produce an informed and accurate third party perspective on the product. Always consult your accredited medical professional before introducing a new supplement. This content is not to be copied or repurposed in any form without express permission from the author.

First published for HRLABS.co.uk 23rd January 2026