The Powerful Energy Ingredient

Better Energy. Better Performance. Bioenergy Ribose®.

For some, high-intensity exercise may mean daily training for a marathon, 10K, or triathlon. For others, it may mean walking to the mailbox, climbing a flight of stairs, or a day at the mall. For most of us, though, it simply means stressing our muscles beyond their normal limit.

Regardless how we individually define high-intensity, the effect on our bodies is the same. Intense exertion taxes our muscles to stay energized. The resulting energy demand/supply mismatch leads to a drain in energy, depleting the cellular energy pool. This loss of cellular energy is a disaster because re-supplying this energy is slow and metabolically costly.

Bioenergy Ribose regulates the body's natural process of energy synthesis. It helps to reduce the loss of energy during stress and accelerates energy and tissue recovery. Through this action, Bioenergy Ribose helps muscles regenerate lost energy and potentially helps minimize any physiological consequences of this energy depletion situation. Whether running a marathon in under three hours or fitting in a daily workout session designed to keep your heart and muscles healthy, Bioenergy Ribose can help keep your muscles energized and feeling strong.

Where to Find Products with Bioenergy Ribose.

Bioenergy Ribose is sold as a bulk ingredient to manufacturers who incorporate it into their food, beverage, sports nutrition or dietary supplement products.  To find some of these consumer products with Bioenergy Ribose, simply do an online search for "Bioenergy Ribose".  The result will show you several companies that make Bioenergy Ribose supplements. You can then do a price comparison and find the product that is right for you. 

How to Use Bioenergy Ribose.

For energy enhancement, 1 to 2 teaspoons (about 2 – 5 grams) is generally adequate. Bioenergy Ribose is mildly sweet and completely soluble. It mixes easily with your favorite juice, coffee, and more.

To maximize athletic performance, or to keep energy pools high during strenuous activity, slightly larger doses may be required. Bioenergy Ribose should be taken just before and just after exercise or activity. For extended exercise, an additional 1 – 2 grams per hour of exercise or activity may be helpful.

Note:  When taking larger doses of Bioenergy Ribose, be sure to take with a carbohydrate (such as juice) to prevent transient hypoglycemia (low blood sugar).

Key Clinical Studies

AMP deamination and purine exchange in human skeletal muscle during and after intense exercise (The Journal of Physiology, 1999)

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Y. Hellsten, E.A. Richter, B. Kiens and J. Bangsbo

The Journal of Physiology. 1999;520;909-920

  1. The present study examined the regulation of human skeletal muscle AMP deamination during intense exercise and quantified muscle accumulation and release of purines during and after intense exercise.
  2. Seven healthy males performed knee extensor exercise at 64·3 W (range: 50-70 W) to exhaustion (234 s; 191-259 s). In addition, on two separate days the subjects performed exercise at the same intensity for 30 s and SO% of exhaustion time (mean, 186 s; range, 153-207 s), respectively. Muscle biopsies were obtained from m.v. lateralis before and after each of the exercise bouts. For the exhaustive bout femoral arterio-venous concentration differences and blood flow were also determined.
  3. During the first 30 s of exercise there was no change in muscle adenosine triphosphate (ATP), inosine monophosphate (IMP) and ammonia (NH3), although estimated free ADP and AMP increased 5- and 45-fold, respectively, during this period. After 186 sand at exhaustion muscle ATP had decreased (P < 0·05) by 15 and 19%, respectively, muscle IMP was elevated (P < 0·05) from 0·20 to 3·65 and 5·67 mmol (kg dry weightf\ respectively, and muscle NH3 had increased (P < 0·05) from 0·47 to 2·55 and 2·33 mmol (kg d.w.f1 , respectively. The concentration of H+ did not change during the first 30 s of exercise, but increased (P < 0·05) to 245·9 nmoll-1 (pH 6·61) after 186 sand to 374·5 nmoll-1 (pH 6·43) at exhaustion.
  4. Muscle inosine and hypoxanthine did not change during exercise. In the first 10 min after exercise the muscle IMP concentration decreased (P < 0·05) by 2·96 mmol (kg d.w.f1 of which inosine and hypoxanthine formation could account for 30%. The total release of inosine and hypoxanthine during exercise and 90 min of recovery amounted to 1·07 mmol corresponding to 46% of the net ATP decrease during exercise or 9% of ATP at rest.
  5. The present data suggest that AMP deamination is inhibited during the initial phase of intense exercise, probably due to accumulation of orthophosphate, and that lowered pH is an important positive modulator of AMP deaminase in contracting human skeletal muscle in vivo. Furthermore, formation and release of purines occurs mainly after intense exercise and leads to a considerable loss of nucleotides.

During intense exercise the rate of ATP utilisation in skeletal muscle is higher than the rate of ATP regeneration, which leads to an accumulation of ADP and AMP. To avoid a large accumulation of AMP within the cell, AMP is deaminated to IMP and ammonia/ammonium (in this paper we will represent both as 'NH3 ') via the enzyme AMP deaminase (Lowenstein, t990). The maximal activity of AMP deaminase is high in skeletal muscle and the accumulation of IMP and NH3 in human muscle after intense exercise may amount to t 0 mmol (kg d.w.f1 (Sahlin et al. 1978; Graham et al. 1990; Bangsbo et al. 1992a; Tullson et al. 1995). The mechanism underlying the regulation of AMP deamination in human skeletal muscle is, however, unclear.

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Decreased resting levels of adenine nucleotides in human skeletal muscle after high-intensity training (J. Appl. Physiol. 74(5): 2523-2528, 1993)

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Ylva Hellsten-Westing, Barbarba Norman, Paul D. Balsom, and Bertil Sjodin

Department of Physiology 111, Karolinska Institute, S-11486 Stockholm; and Department of Clinical Physiology, Huddinge Hospital, S14186 Huddinge, Sweden

J. Appl. Physiol. 74(5): 2523-2528, 1993

The effect of high-intensity intermittent training on the adenine nucleotide content of skeletal muscle was studied. Eleven male subjects (group A) performed high-intensity intermittent training on a cycle ergometer three times per week for 6 wk, followed by 1 wk of the same kind of training with two sessions per day. Nine males (group B) exclusively performed 1 wk of training with two sessions per day. In group A, skeletal muscle total adenine nucleotide (TAN) levels decreased from 25.1 ± 0.7 (SE) to 22.0 ± 0.6 mmollkg dry wt over the 6-wk period (P < 0.01). The subsequent intensive week did not further alter TAN levels. In group B, the intensive week of training reduced TAN levels from 25.1 ± 0.5 to 19.4 ± 0.6 mmol/kg dry wt (P < 0.001). The decrease was sustained 72 h after training (P < 0.001). During the intensive week, there was no change in plasma creatine kinase activity in either group A or group B. The plasma activity was, however, higher in group B than in group A on days 4 and 7 of the intensive week (P < 0.05). The results from this study indicate that high-intensity intermittent exercise causes a decrease in resting levels of skeletal muscle adenine nucleotides without a concomitant indication of muscle damage. A training-induced adaptation appears to occur with training by which a further loss of adenine nucleotides is prevented despite an increased training dose.

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Effects of Oral Ribose on Muscle Metabolism during Bicycle Ergometer in AMPD-Deficient Patients (Ann Nutr Metab, 1991)

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D.R. Wagner, U.Gresser, N. Zollner

Medizinishe Poliklinik der Universitat Munchen, FRG

Ann Nutr Metab 1991:35:297-302

Abstract. Three patients with AMP deaminase deficiency (AMPD deficiency) performed exercise on a bicycle ergometer with increasing work load \~hout and with administration of ribose (3 g p.o. every l 0 min. beginning l h before exercise until the end). The patients performed exercise until heart rate was 200 minus age. Maximum capacity was not increased by administration of ribose. but postexertional muscle stiffness and cramps disappeared almost completely in 2 of 3 AMPD-deficient patients. Plasma concentrations of lactate and inosine were increased in AMPD-deficient patients after oral administration of ribose. Our data suggest that ribose may both serve as an energy source and enhance the de novo synthesis of purine nucleotides.

AMP deaminase deficiency (AMPD deficiency) is a relatively frequent enzyme defect of skeletal muscle ( 1.5% of muscle biopsies) [ 1]. Clinically, it is characterized by postexertional muscle stiffness and cramps. AMP deaminase (myoadenylate deaminase) is one component of the purine nucleotide cycle. The disruption of the purine nucleotide cycle induced by AMPD deficiency is probably the cause of the muscular disorder. So far, the only successful therapeutic approach has been the oral administration of ribose. The beneficial effect of ribose in AMPD deficiency has only been achieved by high oral doses (3-4 g) administered continuously (every I 0 min) during exercise, as first described by Zollner et al. [2]. Lower and not exercise-related doses of 500 mg ribose 4 times a day were not successful. Besides occasionally occurring diarrhea no side effects have been noted during ribose therapy. The beneficial effect of ribose has mainly been attributed to an additional energy source [2] and possibly also to enhanced de novo synthesis of purine nucleotides [3].

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Ribose Administration during Exercise: Effects on Substrates and Products of Energy Metabolism in Healthy Subjects and a Patient with Myoadenylate Deaminase Deficiency (1991)

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M. Gross. B. Kormann, and N. Zollner

Yledizinische Po!iklinik der Universitat Miinchen, FRG

Klin Wochenschrift (1991) 69: 151-155

Summary. Nine healthy men and a patient with myoadenylate deaminase deficiency were exercised on a bicycle ergometer (30 minutes, 125 Watts) with and without oral ribose administration at a dose of 2 g every 5 minutes of exercise. Plasma or serum levels of glucose, free fatty acids, lactate, ammonia and hypoxanthine and the urinary hypoxanthine excretion were determined. After 30 minutes of exercise without ribose intake the healthy subjects showed significant increases in plasma lactate (p < 0.05), ammonia (p < 0.01) and hypoxanthine (p <0.05) concentrations and a decrease in serum glucose concentration (p<0.05). When ribose was administered, the plasma lactate concentration increased significantly higher (p < 0.05) and the increase in plasma hypoxanthine concentration was no longer significant. The patient showed the same pattern of changes in serum or plasma concentrations with exercise with the exception of hypoxanthine in plasma which increased higher when ribose was administered.

The deficiency of the muscle isoform of adenylate deaminase (myoadenylate deaminase deficiency) was first described in 1978 as a new disease of skeletal muscle [3]. It is now considered to be the most common known enzyme defect in muscle, found in about 2% of all muscle biopsies (18]. The spectrum of symptoms ranges from asymptomatic carriers of the disease to patients that suffer from exercise-induced muscle pain and cramps and includes cases of rhabdomyolysis [16].

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It was previously suggested that in the myocytes of these patients AMP is degraded during exercise to adenosine which can then easily diffuse out of the cell. It has also been shown that ribose accelerates de novo adenine nucleotide synthesis in cardiac muscle [19]. For that reasons ribose was administered in these patients to increase the adenine nucleotide synthesis [9]. It has been shown that continuous administration of D-ribose during exercise (10-20 g per hour) can, in some patients, prevent or decrease the symptoms [20].

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