Ribose and its Effect on Energy Recovery in Heart and Skeletal Muscle

by Terri L. Butler, Ph.D.
Bioenergy, Inc.

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Ribose Effects in the Heart

Knowledge concerning the effect of ribose in the heart has been gathered from many laboratory and clinical studies of human and animal myocardial tissue and function. These studies have documented several positive effects of ribose including improved ventricular function and enhanced recovery of myocardial ATP and adenine nucleotide levels following ischemia, increased exercise tolerance in patients with stable coronary artery disease, and improved thallium-201 redistribution in cardiac imaging applications.

Myocardial tissue becomes oxygen depleted when blood flow to the heart is restricted. A persistent consequence of this ischemia is a substantial lowering of tissue energy, as evidenced by decreased myocardial ATP levels. These lowered energy levels are in turn correlated with depressed cardiac function.2,3

The correlation between decreased ATP levels and depressed myocardial performance has spurred researchers to develop methods of metabolic intervention into adenine nucleotide degradation and/or biosynthesis in order to restore myocardial ATP levels.

In a series of oxygen depletion studies in the myocardium using asphyxia recovery and ATP depletion models evidence was gathered that PRPP availability limits adenine nucleotide synthesis by both the de novo and salvage pathways.12,13,24,25

By providing ribose to the myocardium a pronounced stimulatory effect on PRPP synthesis occurs. The presence of ribose allows the rate-limiting step in the pentose phosphate pathway, the G-6-PDH enzymatic reaction, to be bypassed, leading to the production of PRPP. This increase in PRPP levels is noted to be accompanied by accelerated cardiac adenine nucleotide synthesis and improved global heart function. Thus, ribose restores cardiac energy reserves and positively affects myocardial function.

The effect of orally-administered ribose on exercise tolerance in stable coronary artery disease patients has also been studied.26 Two positive baseline treadmill studies were performed for eligibility into this study. The criterion for inclusion was development of moderate angina and/or ST-segment depression (an indicator of ischemia) on the electrocardiogram.

Patients were randomized into two groups. Ten patients received placebo (glucose) for three days and another 10 patients received ribose dissolved in water for the same time period. A final treadmill evaluation was performed in all patients after taking the supplement. In the ribose-treated group, the mean walking time to ST-segment depression was significantly greater than in the placebo group (p < 0.002).

The time to both ST-segment depression and onset of moderate angina was also prolonged significantly in the ribose group compared to its pre-ribose baseline (p<0.005). These results show that patients who had been given ribose were able to exercise longer without chest pain or evidence of ischemia than patients who did not receive ribose.

Ribose also enhances the detection of hibernating myocardium during diagnostic procedures such as thallium imaging or dobutamine stress echocardiography. In two swine models, ribose infusion after transient ischemia modified thallium-201 (201TI) clearance in both ischemic and non-ischemic myocardial regions, resulting in faster 201TI redistribution.27,28 Furthermore, placebo-controlled clinical trials have also found that intravenous ribose infusion enhances thallium-201 redistribution in humans.29,30

One such trial addressed whether or not an intravenous infusion of ribose could facilitate 201TI redistribution after transient myocardial ischemia in patients with coronary artery disease and thus improve the ability to detect jeopardized but viable myocardium.29

Seventeen patients with documented coronary artery disease and chronic, stable angina were enrolled. Each patient underwent two separate exercise tests, one with saline infusion and one with ribose, performed 1 - 2 weeks apart. In each test an injection of 201TI was given and two subsequent imaging procedures were performed. Post-exercise and initial imaging, patients received the infusion of either ribose or saline. Imaging was performed again at 1 hour, followed by a rest period of 4 hours. Following the rest period imaging was performed one final time.

The results revealed that at both 1 and 4 hours post-exercise there were significantly more reversible defects identified when patients were given ribose versus saline. In another 201TI study with a similar protocol, but with imaging at 4 and 24 hours, results showed that there were more defects detected at 4 hours post-exercise when ribose infusion was given than at 4 and 24 hours with saline infusion.30

The conclusions from both of these studies imply that ribose substantially improves the identification of viable ischemic myocardium using 201TI imaging after exercise, suggesting improved post-ischemic myocardial function with ribose administration.

Another research study reported that ribose infusion in conjunction with dobutamine stress echocardiography increases the contractile response in hibernating regions of the heart.31 In a placebo-controlled double-blind study twenty-five patients with ischemic cardiomyopathy were infused with either D-ribose or dextrose placebo for the 4 hours prior to dobutamine stress echocardiography.

On day two the patients were crossed over to the alternate treatment. During dobutamine stress echocardiography more dysfunctional wall segments responded with improved wall motion when D-ribose was infused prior to the procedure as compared to placebo (p = 0.02).

In patients who then underwent coronary artery bypass surgery the predictive sensitivity for functional recovery of the segments identified during the D-ribose infusion was greater than those identified during placebo infusion.

A recent review provides the background and rationale for the use of ribose in metabolic support of the heart.32 Evidence such as that discussed above is presented in support of the main hypothesis that ribose is the rate-limiting component in the pathways necessary for the heart to restore depleted adenine nucleotide levels.

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