Natural Products Insider

MAR-APR 2019

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Page 32 of 92

from Longwood University, Virginia. 3 "Due to limitations within FA transport across the cell and mitochondrial membranes, FAox is limited at higher exercise intensities." They noted fatty acid oxidation is at its max during moderate-intensity exercise, about 45 to 60 percent VO 2 max, and reaches it limit at greater intensities— exercise above 65 percent V O 2 max prefers carb-driven energy. To be oxidized into coenzyme A, fatty acids must get into the mitochondria. This job falls to carnitine, found mostly in skeletal muscle; carnitine can be ingested from meat, but supplemental carnitine is a popular way to boost muscle stores and promote increased energy from fatty acid oxidation. Medium-chain fatty acids are more easily digested and transported throughout the body than are long chain fatty acids. Medium-chain triglycerides (MCTs) more quickly reach the muscles, where they are oxidized for energy, and the liver, where they are converted into ketone bodies. There are a few dietary sources of MCTs, but supplemental MCTs, mostly synthesized from coconut oil, are a popular way to get an energy boost for exercise, especially among keto dieters. When carbohydrate consumption plummets and blood glucose levels are very low, low insulin levels trigger liver mitochondria to convert coenzyme A to ketone bodies, including acetoacetate and beta-hydroxybutyrate (BHB). The liver lacks the enzymes needed to use these ketones to produce energy, but other tissues in the body can do so—the brain struggles with fatty acid metabolism and so favors glucose for energy production, but ketones can be a fuel source for the brain under very low glucose conditions, such as fasting or a very low-carb/keto diet. The use of ketones to make energy spares the glucose system and inhibits gluconeogenesis, the process of making glucose, which spares the use of protein to make glucose. Some researchers have reported the use of ketones generates more ATP than does the same amount of glucose. 4 For all its stages, the krebs cycle doesn't produce many ATPs, but it produces byproducts that carry many electrons that go through a process called oxidative phosphorylation to make ATP. Central to this process is the electron transport chain (ETC). Electrons from the krebs byproducts reach the ETC and are then repeatedly transferred down the chain, which is comprised of proteins and other organic molecules. These reactions create energy that forms a proton gradient and releases hydrogen ions. The fl ow of these ions across the gradient is harnessed by enzymes to turn ADP and phosphate into ATP. Of all the ways to make energy molecules, oxidative phosphorylation produces the most amount of ATP per glucose molecule. Coenzyme Q10 (CoQ10) helps carry electrons down this chain, making it an essential nutrient for ATP production. CoQ10 is popular for increasing energy in heart patients, particularly those with chronic heart failure (CHF), but it also has been highlighted for its energy benefi ts in sports nutrition. Editor's note: Turn to page 64 for more information on CoQ10's benefi ts. The mineral magnesium is a cofactor of many enzymes crucial to ATP production, 5 including creatine kinase in the phosphagen system, pyruvate kinase and others in the glycolytic system and dehydrogenases in the kreb cycle. This mineral, which may also help protect ATP, has been added to many sports nutrition formulas, including pre-workouts containing creatine. Magnesium is critical for everyday and athletic performance, assured Samantha Cassetty, R.D., chief nutrition offi cer for OMG! Nutrition, which uses magnesium glycinate (magnesium bisglycinate chelate). Sports Nutrition: Energy 1. Kalman DS, Rood-Ojalvo S, Komorowski J., Comparison of cellular nitric oxide production from various sports nutrition ingredients. JISSN. 2016; 13(Suppl 1):P33. 2. Evans M, Zakaria N, Marzuk M, Perez Ojalvo S, Sylla S, Komorowski J. An evaluation of the effects of inositol-stabilized arginine silicate (ASI; Nitrosigine ® ) in preventing the decline in cognitive function caused by strenuous exercise. JISSN. 2018; (Suppl 1) TBD. U.S. Patent Nos.: 6,803,456; and 7,576,132. DRA1672102918 Visit for more information Nitrosigine ® Superiority 1 In Vitro Study PLACEBO *p ≤ 0.05 vs palcebo NITROSIGINE ® Clinical Cognition Test 2 30 25 20 15 10 5 0 -5 -10 56% SECONDS Nitrosigine ® produces 5x the N.O. than other ingredients. Nitrosigine ® prevents cognitive function decline following strenuous exercise.* *p < 0.01 vs. other compounds 1.4 1.2 1 0.8 0.6 0.4 0.2 0 μM NITRITE Agmatine Sulfate NITROSIGINE ® L-Citrulline Malate L-Arginine L-Arginine AKG L-Citrulline *These statements have not been evaluated by the Food and Drug Administration. This product is not intended to diagnose, treat, cure, or prevent any disease. The carotenoid astaxanthin, found in red plant foods and seafood, is another antioxidant protector of the mitochondria that can help manage the energy-fatigue balance.

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