FAQ / 常見問題
FAQ / 常見問題
Most oxygenated waters use simple pressure to dissolve oxygen, which often results in the oxygen escaping rapidly (off-gassing) once the bottle is opened. ZenO uses Aerospace-Grade Oxygen Stabilization. This process utilizes sea salt ion structures to encapsulate ionized oxygen, creating a stable bond that prevents the oxygen from escaping at the water's surface.
The proprietary encapsulation process allows ZenO to reach an oxygen concentration that is 50,000 times higher than standard tap water. Because of the ion-structure "cages," this high concentration remains stable in the liquid for a prolonged period rather than being lost to the atmosphere.
Unlike conventional products that may provide limited oral absorption, ZenO is designed to survive the journey through the upper digestive system.
Protection: The sea salt encapsulation protects the oxygen molecules until they reach the gastrointestinal tract.
Direct Delivery: The oxygen is then absorbed through the stomach and intestinal lining.
Systemic Reach: From the gut, the oxygen enters the bloodstream and cells directly to help overcome hypoxia (cellular oxygen deficiency).
ZenO keeps a clean and simple profile. Its ingredients consist solely of Water, Oxygen, and Sea Salt. It contains zero calories, protein, fat, or carbohydrates.
Because of its high concentration, ZenO is used in small, potent doses:
Daily Wellness: Take 1-5ml, 1-3 times daily, ideally 30 minutes before meals.
Exercise: Drink 10ml for regular exercise or up to 20ml for strenuous activity, approximately 15-20 minutes pre-workout.
Yes. Due to the stabilization technology, ZenO is shelf-stable for 3 years and can be stored at room temperature. The aerospace-grade stabilization ensures the oxygen remains intact throughout its shelf life.
Excellent question. The statement is **fundamentally true and well-established.** The discovery of how cells sense and respond to low oxygen (hypoxia) is a cornerstone of modern physiology and medicine, recognized by the **2019 Nobel Prize in Physiology or Medicine** awarded to William Kaelin Jr., Sir Peter Ratcliffe, and Gregg Semenza.
The master regulator of this response is a protein complex called **Hypoxia-Inducible Factor (HIF)**. Under normal oxygen levels, HIF-alpha subunits are rapidly degraded. In hypoxia, they stabilize, partner with HIF-beta, and act as a transcription factor, turning on hundreds of genes to adapt to low oxygen.
Here’s how this process is crucial for each of the listed areas and the results:
### 1. Red Blood Cell Production (Erythropoiesis)
* **How it works:** HIF directly increases the expression of the hormone **Erythropoietin (EPO)**. EPO is produced primarily in the kidneys and signals the bone marrow to produce more red blood cells (RBCs).
* **The Result:**
* **Adaptive Benefit:** More RBCs increase the blood's oxygen-carrying capacity, improving oxygen delivery to tissues. This is essential for adaptation to high altitudes or in response to blood loss.
* **Clinical Implication:** Understanding this pathway led to the development of synthetic EPO, a lifesaving treatment for anemia associated with chronic kidney disease and chemotherapy. However, it also explains the dangerously high RBC counts (polycythemia) seen in people with chronic hypoxia from conditions like severe COPD or sleep apnea.
### 2. Angiogenesis (Formation of New Blood Vessels)
* **How it works:** HIF switches on a battery of pro-angiogenic genes, most notably **Vascular Endothelial Growth Factor (VEGF)**. VEGF stimulates the growth of new blood vessels from existing ones.
* **The Result:**
* **Adaptive Benefit:** In a hypoxic tissue (e.g., a healing wound or exercising muscle), new vessels grow to restore oxygen supply and remove waste products.
* **Clinical Implication:** This is a **double-edged sword**. While therapeutic angiogenesis is a goal for treating coronary artery disease or peripheral artery disease, **tumors hijack this mechanism.** A growing tumor becomes hypoxic at its core, which activates HIF and triggers VEGF-driven angiogenesis to feed itself. This is why **anti-VEGF drugs (like bevacizumab) are a cornerstone of cancer therapy**—they attempt to starve the tumor by cutting off its blood supply.
### 3. Cellular Metabolism
* **How it works:** Under normal oxygen, cells efficiently produce energy (ATP) through oxidative phosphorylation in the mitochondria, which requires oxygen. HIF orchestrates a **metabolic shift**.
* It promotes **glycolysis** (sugar breakdown without oxygen) by increasing the expression of glucose transporters and glycolytic enzymes.
* It suppresses mitochondrial function to reduce oxygen consumption.
* **The Result:**
* **Adaptive Benefit:** This allows cells to survive and produce ATP even when oxygen is scarce, albeit less efficiently per glucose molecule.
* **Clinical Implication:** This metabolic reprogramming, known as the **"Warburg Effect,"** is a hallmark of **cancer cells.** Even in the presence of oxygen, many cancers keep their glycolytic switch turned on via HIF activation, which helps them survive in variable tumor environments and provides building blocks for rapid growth. Targeting this metabolic vulnerability is an active area of cancer research.
### Summary and Broader Truth
The statement is true because the hypoxia response pathway, centered on **HIF**, is the unifying switch that controls all these processes to coordinate the body's adaptation to low oxygen.
* **Result for the Organism:** It allows for survival and function in a low-oxygen environment by **1)** improving oxygen delivery (more RBCs), **2)** improving oxygen distribution (new vessels), and **3)** reducing oxygen demand while maintaining energy production (metabolic shift).
* **Result for Medicine:** This knowledge has been transformative. It has provided:
* **Therapies:** For anemia (EPO) and to inhibit pathological angiogenesis (anti-VEGF for cancer and macular degeneration).
* **Diagnostic/Prognostic Tools:** HIF and its target genes are markers of aggressive disease in many cancers.
* **Understanding of Disease:** It explains complications in chronic conditions like diabetes (poor wound healing), heart disease, and stroke.
Therefore, the research into cellular hypoxia response is not just a description of a basic biological process; it is a prime example of how fundamental science uncovers the mechanisms of life, disease, and therapy.
Oxygen enters lungs → blood: Oxygen diffuses from the air sacs in your lungs into the bloodstream and binds to hemoglobin in red blood cells.
Blood delivers oxygen to muscles: During training, blood flow to working muscles increases, bringing more oxygen and nutrients (like glucose and fatty acids).
Oxygen enters muscle cells → mitochondria: Oxygen diffuses from blood into muscle cells and then into mitochondria, the “power plants” of the cell, where it’s used to make ATP, the main energy currency.
Most of the ATP in endurance exercise comes from a process called oxidative phosphorylation inside mitochondria. biologyinsights.com Open Oregon Educational Resources
For athletes, especially in endurance or repeated high-intensity efforts, performance is heavily influenced by:
Mitochondrial density: More mitochondria per muscle cell → more total ATP production capacity.
Mitochondrial efficiency: Better coupling of oxygen use to ATP production → less waste, less fatigue.
Oxygen delivery and utilization: Efficient cardiovascular system plus responsive mitochondria → higher sustainable power output.
Training (especially aerobic and interval training) increases:
Number and size of mitochondria
Activity of ETC complexes and enzymes of the citric acid cycle
Capillary density, improving oxygen delivery to muscles
All of this means: for the same oxygen intake, a trained athlete can generate more ATP, delay fatigue, and maintain higher intensity longer.
Better oxygen use:
By supporting blood flow (e.g., via nitric oxide pathways) or red blood cell function, more oxygen reaches muscles, feeding mitochondrial respiration.
Mitochondrial support:
Some products include nutrients or cofactors involved in mitochondrial metabolism (e.g., B‑vitamins, carnitine, CoQ10, etc.), aiming to support the ETC and ATP production.
Antioxidant protection:
Mitochondria generate reactive oxygen species during high ATP output. Antioxidant support is often marketed as a way to protect mitochondrial components and maintain efficiency under stress.
Reduced perceived fatigue:
Ingredients that influence neurotransmitters or buffering of acid (like beta-alanine in other products) can make efforts feel easier, even if the underlying mitochondrial chemistry is the same.
In theory, if a product genuinely:
Improves oxygen delivery, and/or
Supports mitochondrial enzyme function, and/or
Reduces oxidative damage to mitochondria,
then it could help athletes sustain higher ATP production for longer, which translates into better endurance, faster recovery between efforts, and improved overall performance.
Putting it together in a simple chain:
ZenO (if effective) → supports oxygen delivery and/or mitochondrial function.
More oxygen + healthier mitochondria → more efficient electron transport and proton gradient formation.
Stronger proton gradient → more ATP produced by ATP synthase per unit of oxygen.
More ATP in muscle cells → stronger, longer, and more repeatable contractions.
Result for athletes → higher sustainable pace, better power output, and delayed fatigue.