A recently published paper reviews the role of mitochondrial metabolism on heart failure with preserved ejection fraction (HFpEF), and the potential mechanism by which ubiquinol and d-ribose may support mitochondrial function.
A recent paper published in The Annals of Medicine and Surgery1 reviews the role of mitochondrial metabolism on heart failure with preserved ejection fraction (HFpEF), and the potential mechanism by which ubiquinol and d-ribose may support mitochondrial function. The research was funded by the National Institutes of Health, National Institute on Aging and the Department of Health and Human Services, and the research was conducted by faculty at the University of Kansas Medical Center.
Ejection fraction is the percentage of how much blood is pumped out of the left ventricle of the heart with each contraction. Normal ejection fraction is between 50-70%, meaning that 50-70% of the blood in the left ventricle is pushed out with each heartbeat. HFpEF occurs when the left ventricle does not properly fill with blood during the diastolic (filling) phase, but the normal percentage of blood is pumped out. While ejection fraction may be normal, the lack of blood from the diastolic phase means that not enough blood was pumped to meet the body’s needs. It is also called diastolic heart failure.
Unfortunately, patients with HFpEF are often misdiagnosed because they describe symptoms such as dyspnea on exertion, which are non-specific. As a result, physicians have a hard time distinguishing HFpEF from heart failure with reduced ejection fraction on a clinical basis alone. And, because of our incomplete understanding of the pathophysiology of HFpEF, it is difficult to determine an optimal treatment related to underlying biological mechanisms. The study proposes reduced myocardial bioenergetics, namely reduced ATP production in the myocardium, as a potential mechanism. Therefore, because mitochondria produce ATP, researchers are investigating agents that target mitochondrial function as a treatment strategy.
“The ability of CoQ10 to be oxidized and reduced allows it to function as an antioxidant to stabilize ROS [reactive oxygen species]. The myocardium contains an abundance of mitochondria in order to produce the energy needed to function. Damage to the myocardiocytes may led [sic] to low CoQ10 levels and high ROS levels that contribute to a decrease in ATP production,” the researchers state. “Supplementation of ubiquinol could improve the disease progression of heart failure by increasing depleted levels of CoQ10, thus decreasing ROS levels and increasing ATP. Further research trials are needed to study ubiquinol as a potential treatment for heart failure.
A signature feature of HFpEF is the presence of metabolic syndrome, which is manifested by impaired mitochondrial respiration and oxidative stress with associated inflammation, decreased mitochondrial calcium, and depressed oxygen supply which directly reduces ATP synthesis. For patients with HFpEF, factors that contribute to mitochondrial dysfunction include: “1) increased sympathetic tone with associated hypertension; 2) oxidative stress with associated inflammation; 3) pro-inflammatory cytokines with microvascular dysfunction; and 5) a buildup of lipids in the myocardium due to diabetes.”
When it comes to d-ribose, it is a monosaccharide naturally produced within the body within the pentose pathway, the study explains. It is a critically important pentose sugar molecule that is part of the DNA and essential for cellular ATP production. Building on the body of research supporting the use of d-ribose to support heart health, the researchers announced a study of their own that is underway that hypothesizes d-ribose supplementation bypasses enzymatic steps to increase myocardial ATP production.
“Though we are unable to measure myocardial ATP levels directly, we are obtaining blood ATP measurements in HFpEF patients receiving 15 g of d-ribose or placebo over 12 weeks. Since this current blinded study is still in progress, we are unable to report these data, but we will have a more in-depth metabolic explanation after study completion,” state the researchers.
“Since Stephen Sinatra, MD proposed the nutritional triad of d-ribose, CoQ10 and L-carnitine for cardiac health in the 1990s, extensive research has been conducted on these ingredients with good results. However, little has been done to study these ingredients in combination,” said Alex Xue, PhD, executive vice president and chief scientific officer of Bioenergy Life Science (BLS), in a press release. BLS pioneered the d-ribose category with its proprietary Bioenergy D-Ribose. “This University of Kansas study is a formal clinical trial examining the combination of d-ribose and ubiquinol (a form of CoQ10) in heart failure patients. This ingredient combination should synergistically generate and maintain ATP levels in cardiac muscles, which may significantly help to preserve their ejection fraction,” he continued.
“We predict a good outcome for this study,” added BLS director of scientific affairs and technology Michael Crabtree, ND., in a press release. “This news is already significant to the heart health category at a time when interest in conservative approaches to managing heart health is building. In addition to its ubiquinol synergies with respect to ATP production, d-ribose supports the pliability of the aortic tunnel, helping it to relax after the heart pulses which provides for greater ejection fraction.”