ArticlePDF Available

Effects of Ribose Supplementation Prior to and during Intense Exercise on Anaerobic Capacity and Metabolic Markers


Abstract and Figures

This study examined whether ribose supplementation before and during intense anaerobic exercise impacts anaerobic capacity and metabolic markers. Twelve moderately trained male cyclists (22.3 +/- 2.2 y; 181 +/- 6 cm, 74.8 +/- 9 kg) participated in the study. Subjects were familiarized and fasted for 8 h after standardizing nutritional intake. In a double blind and crossover manner subjects ingested either a 150 mL placebo or ribose (3 g ribose + 150 microg folate). Subjects rested for 25 min and completed 5 x 30 s anaerobic capacity tests with 3 min passive rest. Six capillary blood samples were taken prior to and after sprints for adenine nucleotide breakdown determination. The experiment was repeated 1 wk later with alternative drink. Data were analyzed by repeated measures ANOVA. No significant interactions were observed for any performance or blood variables. D-ribose supplementation has no impact on anaerobic exercise capacity and metabolic markers after high-intensity cycling exercise.
Content may be subject to copyright.
Kerksick, Rasmussen, Bowden, Leutholtz, Harvey, Greenwood, and Kreider are with the
Exercise and
Sport Nutrition Laboratory, Center for Exercise, Nutrition and Preventive Health Research, Dept of
Health, Human Performance and Recreation. Baylor University, Waco, TX 76798-7313. Earnest is
with the Cooper Institute for Aerobics Research, Division of Epidemiology and Clinical Applications,
Dallas, TX 75230. Almada is with IMAGINutrition, Inc., Laguna Niguel, CA 92677.
International Journal of Sport Nutrition and Exercise Metabolism, 2005, 15, 653-664
© 2005 Human Kinetics, Inc.
Effects of Ribose Supplementation
Prior to and During Intense Exercise
on Anaerobic Capacity and
Metabolic Markers
C. Kerksick, C. Rasmussen, R. Bowden,
B. Leutholtz, T. Harvey, C. Earnest,
M. Greenwood, A. Almada, and R. Kreider
This study examined whether ribose supplementation before and during intense
anaerobic exercise impacts anaerobic capacity and metabolic markers. Twelve
moderately trained male cyclists (22.3 ± 2.2 y; 181 ± 6 cm, 74.8 ± 9 kg) partici-
pated in the study. Subjects were familiarized and fasted for 8 h after standard-
izing nutritional intake. In a double blind and crossover manner subjects ingested
either a 150 mL placebo or ribose (3 g ribose + 150 µg folate). Subjects rested
for 25 min and completed 5 × 30 s anaerobic capacity tests with 3 min passive
rest. Six capillary blood samples were taken prior to and after sprints for adenine
nucleotide breakdown determination. The experiment was repeated 1 wk later
with alternative drink. Data were analyzed by repeated measures ANOVA. No
signicant interactions were observed for any performance or blood variables.
D-ribose supplementation has no impact on anaerobic exercise capacity and
metabolic markers after high-intensity cycling exercise.
Key Words: ATP resynthesis, sport nutrition, ergogenic aids
Single bouts or repeated bouts of high-intensity sprint exercise have been shown to
cause drastic reductions in maximal power output, total work produced, and changes
in creatine phosphate concentration, lactate, ammonia, total adenine nucleotide
(TAN) pool, and inosine-5ʼ-monophosphate (IMP) which are all indications of
extreme fatigue (9, 11, 16, 18). Using muscle biopsies, Zhao (18) and Tullson (16)
concluded that purine inux and efux (TAN, IMP) is greatly increased after a
short-term supramaximal 30 s cycling exercise bout. Consequently, the ability to
effectively handle higher levels of stress is improved. These changes are observed
06Kerksick(653) 10/9/05, 11:07 AM653
654 Kerksick et al.
Ribose Supplementation and Exercise 655
by improving the recovery and quantities of high-energy molecules, greater power
output, work performance, and/or metabolic responses (9).
D-ribose is a naturally occurring 5-carbon carbohydrate that for the last several
years has been marketed with little physiological rationale as an ergogenic aid to
athletes who engage in high-intensity activity. Ribose is a vital molecule for de
novo synthesis and salvage of adenine nucleotides (ATP, ADP, and AMP) which
are intimately involved with energy metabolism. Substantial de novo synthesis of
adenine nucleotides is a lengthy process which could limit the actual ability of any
de novo pathway or ribose supplementation to actually increase ATP resynthesis
during acute, intermittent bouts of high-intensity exercise. Research has suggested,
however, that enhancing the availability of ATP, increasing salvage pathway activ-
ity, and/or maintaining the TAN pool to a greater degree during a single bout or
repeated bouts of high-intensity sprint-type activities increases exercise capacity
(9, 16, 18). Further, research has shown ribose supplementation to increase the
availability of purine nucleotides through either enhanced synthesis or increased
turnover via salvage pathways during exercise (5, 15).
Previous research in clinical populations has provided some promise for ribose
supplementation as an energy-providing supplement (8), enhancing de novo syn-
thesis of purine nucleotides (19), reducing muscle cramping (17), and increasing
exercise tolerance (13). For example, Pliml et al. showed ingestion of ribose in
doses of 60 g/d for 3 d prior to a maximal treadmill test signicantly increased
time until termination in previously diagnosed men with severe coronary artery
disease (13). In addition, Wagner et al. supplemented patients with AMP deaminase
deciency with ribose to determine any possible changes in energy provision and
exercise performance. Every 10 min patients were given 3 g of either placebo or
ribose prior to completing an incremental maximal exercise test. While exercise
performance was not changed, plasma concentrations of lactate and inosine were
increased (P < 0.05). The authors concluded that ribose administration might have
served as an energy source or enhanced the de novo synthesis of purine nucleotides.
In this regard, and despite inconclusive evidence, ribose has been marketed heavily
to athletes for its purported ability to maintain power production during repeated
bouts of intense exercise or to increase the peak power production seen during
these types of activities. Studies in support of ribose supplementation before or
after high-intensity exercise have demonstrated a greater work production during
the exercise bout in addition to an increased recovery of ATP levels in the muscle
several days after exercise (10). To date, no conclusive, performance-enhancing
effect has been reported.
Consequently, several studies have sought to determine an ergogenic property
to ribose supplementation during high-intensity exercise. Results from these stud-
ies have concluded that supplementation with ribose for 3 to 6 d in doses ranging
from 8 to 50 g/d while participating in repeated bouts of high-intensity exercise
(e.g., Wingate sprints or maximal knee extensions) did not increase performance
over those subjects who were taking a placebo (4, 11, 12). While some ndings did
indicate improved maintenance of total work (11) or peak power (4) with ribose,
the authorsʼ in these studies concluded that ribose did not signicantly improve
More research is needed to investigate the potential ergogenic value of ribose
supplementation particularly at the dosages recommended by various supplement
06Kerksick(653) 10/9/05, 11:07 AM654
654 Kerksick et al.
Ribose Supplementation and Exercise 655
manufacturers. Currently, studies need to be conducted to investigate any possible
role of ribose administration prior to maximal exercise and/or during recovery from
a maximal exercise bout. Subsequently, the purpose of this study was to determine
if acute supplementation of ribose in dosages that are commonly marketed as an
ergogenic aid (2 doses of 3 g ribose + 150 µg folate) prior to a maximal exercise bout
or during the recovery period prior to a subsequent exercise bout has any benecial
impact on the performance of repeated sprint exercise with limited recovery.
Twelve apparently healthy moderately trained male cyclists between the ages of
18 and 40 were recruited for this investigation. All subjects signed informed con-
sent documents and the study was approved by the Baylor University Institutional
Review Board prior to any data collection. To qualify for participation, all subjects
were: 1) experienced cyclists who had been previously involved in a cycling pro-
gram for at least 3 h/wk for 3 months and were part of a competitive club cycling
program at large National Collegiate Athletic Association Division I institution; 2)
not taking any nutritional supplements purported to have ergogenic effects (e.g.,
creatine monohydrate, ribose, caffeine, sodium phosphates, bicarbonates, etc.);
and 3) not taking or have never taken any anabolic steroids.
During initial familiarization sessions, subjects were informed of testing pro-
cedures, completed all necessary paperwork, and were familiarized to all exercise
testing on two different occasions prior to beginning the experimental protocol.
Descriptive characteristics of the subjects were as follows: age, 22.3 ± 2.2 y; body
weight, 74.9 ± 9.6 kg; height, 180.9 ± 6.1 cm; and body fat, 18.2 ± 5.4%. Prior to
data collection, all subjects had been training for competitive events which were
typically shorter distance (20 to 30 miles), higher-paced events which led them to
maintain an average of 1.8 ± 0.5 h/d, 3.1 ± 1.3 d/wk for 76.8 ± 51.6 miles/wk.
Experimental Design
Throughout two familiarization sessions, subjects completed informed consent
documents, medical and training history questionnaires, and personal informa-
tion sheets, and were then familiarized with the testing protocol. Subjects were
instructed to record their training for 5 d and food and uid intake for 24 h prior
to their initial testing session (T1). All training and dietary intake was then subse-
quently replicated prior to the second testing session (T2). Subjects were required
to refrain from exercise for 48 h and fast for 8 h prior to their testing sessions. All
subjects consumed a standardized carbohydrate/protein (240 kcals, 40 g protein,
16 g carbohydrate, 3 g fat) meal replacement drink (RTD40 Met-Rx, Boca Raton,
FL) 4 h prior to their testing session to standardize nutritional intake for 12 h prior
to testing.
Figure 1 illustrates the testing design. Subjects provided their rst blood
sample from a clean, pre-warmed nger prior to consuming the rst dose of the
supplement. Pre-exercise blood samples were taken within 15 min of reporting to
the lab and followed by 25 min of quiet rest. Subjects warmed up for 5 min on a
06Kerksick(653) 10/9/05, 11:07 AM655
656 Kerksick et al.
Ribose Supplementation and Exercise 657
Figure 1—Schematic diagram of testing conditions.
06Kerksick(653) 10/9/05, 11:07 AM656
656 Kerksick et al.
Ribose Supplementation and Exercise 657
bicycle ergometer at a standardized work rate (2 kg @ 60 rpm; 120 W) and rested
for 5 min. Subjects then performed 3 × 30 s Wingate anaerobic capacity tests each
separated by 3 min of standardized passive recovery. Immediately after the third
sprint, a second blood sample was taken and a second identical dose of the supple-
ment was ingested. The second dose of the supplement was consumed within 5 min
of completion of the third sprint and all subjects consumed the drink within 30 s in
view of the investigators. Five minutes after ingestion of the supplement, a third
blood sample was taken and subjects then sat at quiet rest for a total of 25 min. A
fourth blood sample was then obtained. Subjects began to free spin at 80 rpm with
no resistance for 30 s prior to the each Wingate test. Subjects then completed the
fourth and fth Wingate tests with 3 min passive rest between both trials; a fth
blood sample was taken immediately upon completion of the fth sprint. A sixth
and nal blood sample was taken 5 min after completion of the last sprint.
In a double blind, randomized, and crossover manner, subjects were admin-
istered either 3 g of D-ribose with 150 µg of the vitamin folate (folic acid) or 3
g of a maltodextrin placebo. Folate was included for its role in normal ribose
metabolism but it does not possess any known ergogenic properties. All supple-
ments were prepared in powdered form and packaged in ready-to-mix containers
for double blind administration by Royal Numico Research B.V. (Wageningen,
The Netherlands) to ensure similar taste, color, consistency, and texture. Supple-
ments were mixed immediately prior to ingestion with 150 mL of cold water and
consumed in front of researchers to ensure proper administration. Subsequent
testing sessions were completed 1 wk later at the same time of day in an identical
fashion as described above.
Total body mass was measured on a calibrated digital scale with a precision of ±
0.02 kg (Sterling Scale Co., Southeld, MI). Skinfold body composition measures
were taken prior to each testing session for descriptive purposes using standard
skinfold techniques (Lange calipers) following American College of Sports Medi-
cine guidelines (2). Standard nger-stick phlebotomy techniques from a clean,
pre-warmed nger were used to collect each 200 to 400 µL whole blood sample
into lithium heparin-treated Microtainer tubes (Becton Dickinson, Franklin
Lakes, NJ). The tubes were centrifuged for 15 min using a bench-top centrifuge
(VanGuard V6500, Hamilton Bell Co., Montvale, NJ). Plasma was assayed
for ammonia, lactate, and glucose using an Analox MicroStat GM7 analyzer
(Analox Instruments, Ltd., London, UK). Inter-assay variances for ammonia,
lactate, and glucose were ±10 µmol/L, ±0.05-0.07 mmol/L, and 1.4% at 10
mmol/L, respectively.
Wingate anaerobic capacity tests were performed on a computerized Lode
Excalibur Sport (Lode BV, Groningen, The Netherlands) cycle ergometer equipped
with toe clips at a standardized torque factor 0.7. The torque factor setting was
set to the manufacturerʼs guidelines relative to the population being tested. Seat
position, seat height, handlebar height, and handlebar position were determined
during familiarization sessions and repeated for both testing sessions. Subjects
were instructed to begin sprinting 5 s prior to beginning of data collection to ensure
optimal force and power production at the beginning of the test and to remain
06Kerksick(653) 10/9/05, 11:07 AM657
658 Kerksick et al.
Ribose Supplementation and Exercise 659
sprinting for the entire duration of the test. All visual feedback was removed during
testing and subjects were instructed to remain in the saddle for the entire duration
of the test while researchers provided verbal encouragement. The ergometer was
connected via an RS-232 parallel interface to a Dell Optiplex GX 260 computer
(Dell Computer Corp., Austin, TX) using Wingate for Windows software version
1 (Lode BV, Groningen, The Netherlands). Crank frequency was measured using
magnetic encoders (4/revolution). The Excalibur Sport has a range of 0 to -2000 W
with typical variation of measurement less than 2% with the sampling frequency
of data at 5 times/s. Test to test variability in performing repeated Wingate tests in
our lab has yielded correlation coefcients of r = 0.981± 15% for mean power.
Statistical Analysis
Descriptive variables and all other data were analyzed using a 2 × 5 (group ×
sprints) repeated measures ANOVA for all performance variables and a 2 × 6
(group × blood sample) repeated measures ANOVA using SPSS for Windows
version 11.5 (SPSS Inc., Chicago, IL) with an added correction factor to control
test effect bias. Alpha level was set at 0.05. Effect sizes were calculated for any
signicant trends using the mean differences. Data was considered signicantly
different when the probability of a Type I error was 0.05 or less. Data are presented
as means ± standard deviation.
Side Effects
No subjects reported adverse events or responses to the supplementation and
training protocol. No reports of medical problems or symptoms were indicated in
post-study questionnaires administered in a blinded manner.
Sprint Performance
Peak power (P = 0.006) and total work (P = 0.005) both signicantly decreased
across sprint trials with no signicant differences between groups. No signicant
interactions were found (P > 0.05) for average power, peak power, time to peak
power, rate of fatigue, and total work between the two groups. No signicant group ×
time interactions were found for any of the ve sprint tests throughout the study.
Metabolic Markers
The Wingate sprint tests signicantly increased lactate (P < 0.001) across time for
both groups. No signicant group × time interactions (P > 0.05) were observed
among groups in these metabolic parameters. Due to an inability to retrieve an
adequate amount of sample and/or to analyze some samples within a few hours after
exercise, ammonia analysis was only performed on 9 subjects (ribose = 4, placebo
= 5). Complete analysis was conducted on all other variables. Figure 2 indicates the
changes in peak power, mean power, rate of fatigue, glucose, lactate, and ammonia
levels throughout all ve sprint tests for both the ribose and placebo groups.
06Kerksick(653) 10/9/05, 11:07 AM658
658 Kerksick et al.
Ribose Supplementation and Exercise 659
Figure 2Peak power, average power, rate to fatigue, glucose, lactate and ammonia
values observed for the ribose (solid square) and placebo (grey diamond) groups prior to
and following supplementation. Peak power, average power and total work are shown top
to bottom in the left panel; plasma glucose, lactate and ammonia are shown top to bottom
in the right panel. Data are means ± standard deviation.
06Kerksick(653) 10/9/05, 11:07 AM659
660 Kerksick et al.
Ribose Supplementation and Exercise 661
Figure 2—(continued)
06Kerksick(653) 10/9/05, 11:07 AM660
660 Kerksick et al.
Ribose Supplementation and Exercise 661
This study was developed to determine if the pattern and timing of ribose supple-
mentation at acute dosage levels (2 doses of 3 g ribose + 150 µg folate) of what is
commonly marketed as an ergogenic aid affected the outcome of repeated sprint
performance with limited recovery. The timing of administration and dosages were
chosen to mimic both the dosage amounts marketed to athletes as well as provide
a similar layout to what is commonly experienced by many competitive athletes
(e.g., heats in swimming, sprinting, etc.). The pharmokinetics of ribose suggest that
88 to 100% of an oral dose (up to 200 mg × kg
× h
) is absorbed from the small
intestine and distributed to various tissues including skeletal muscle (1). The dosage
used in the present study (3 g) was only 20% of this expected upper limit of ribose
bioavailability, suggesting the doses of ribose were indeed able to be absorbed to
some degree prior to the exercise bouts. It was expected that the Wingate anaerobic
capacity tests would be a good, reliable measure of anaerobic capacity (6, 9). It
is possible that slight reductions in peak power performance might have occurred
due to a possible loss of optimal neuromuscular coordination and resulting force
production as a result of extremely high cadence rates (typically 180 to 200 rpm
during the 5 s “superspin” period prior to the beginning of the test). The authors,
however, believe that this effect is negligible due to the sprint cycling experience of
the participants and the standardization of the testing procedures. Furthermore, the
tests and protocol were anticipated to stimulate a degradation of the TAN pool in
addition to changes in metabolic activity based on previous research (6, 9, 11).
Following the theoretical rationale and marketing campaigns of nutritional
supplement companies for ribose supplementation, we hypothesized that if acute
ribose ingestion improves the availability of ATP (increase de novo synthesis or
increased salvage of these nucleotides) during the sprints and/or during recovery,
then: 1) an increase in peak power would have been determined after the rst or
fourth sprints; 2) a greater maintenance of power (average power) or total work
output would be observed after either group of sprints; or 3) an improved main-
tenance of the metabolic markers (i.e., glucose, lactate, and ammonia) measured
would have been observed between groups throughout the protocol. While many
different considerations could have been made that might have elucidated vary-
ing conclusions, the rest periods and end points (i.e., peak ammonia, glucose, and
lactate levels) chosen in this study were hypothesized to provide the most realistic
picture of what would be experienced by athletes using ribose supplementation
throughout their workouts (4, 6).
Results from the present study indicate that the exercise protocol employed
was successful at producing a signicant metabolic challenge. A 23% decrease in
total work output, a 16.5% decrease in peak power, a six-fold increase in blood
lactate, and a 180% increase in ammonia levels from the rst to the third sprint
was found, which was similar to the ndings of Hargreaves et al. when they had
subjects complete 3 × 30 s sprints on a cycle ergometer with 4 min rest between
each sprint. In this study, a 34% decrease in total work was found in addition to
a thirteen-fold increase in serum lactate (9). While the supplementation protocols
were different, the changes in the present study for total work, lactate, and ammonia
were similar to changes reported by Kreider et al. (11) in which they used only
2 × 30 s anaerobic capacity tests. Furthermore, the magnitude of change in the
06Kerksick(653) 10/9/05, 11:07 AM661
662 Kerksick et al.
Ribose Supplementation and Exercise 663
present study is 1 to 4 times greater than previously reported by other investigators.
Opʼt Eijnde and colleagues (12) performed two bouts of isokinetic knee extensions
(15 sets × 12 contractions each with 15 s rest) which promoted a signicant 20 to
25% decrease in TAN. In comparison to these two previous studies, the present
study used subjects who had been participating in a cycling program that included
either sprint work or intense interval work compared to recreational subjects. The
specic adaptations made in response to their training status are thought to explain
the somewhat decreased magnitude of change in peak power and lactate response.
The present studyʼs ndings are limited due to the absence of any direct assess-
ment of muscle TAN levels via muscle biopsy. The present study, however, when
compared with other published reports (11, 12), provides evidence (e.g., changes in
indirect markers such as lactate, ammonia, and power output) that the study design
used likely produced a decrease in TAN in addition to challenging the metabolic
systems. For example, Zhao and colleagues had seven male subjects complete
only one 30 s maximal sprint and reported a ~ 33% decrease in TAN using muscle
biopsies (18) in addition to the ndings by Hargreaves in which he noted an ~ 11%
decrease in TAN after three maximal 30 s sprints (9)
In contrast to the present ndings in which no signicant increases or improve-
ment in performance were noted, recent studies have suggested that ribose could be
effective at maintaining or attenuating the amount of work completed in addition to
promoting a greater maintenance of high-energy compounds (e.g., ATP, ADP, etc.)
used during high-intensity exercise (3, 7, 10, 11, 14). Antonio and colleagues (3)
concluded that ribose supplementation (10 g/d in 5 g doses prior to and following
workouts) resulted in a greater number of repetitions performed during 10 sets to
failure in the bench press. Kreider and colleagues (11) reported that subjects who
were supplemented with ribose (50 g/d × 5 d) were better able to sustain total
work output after 2 × 30 s Wingate cycle ergometer sprints compared to a matched
double-blind placebo, which resulted in a more drastic decrease in total work output.
Lastly, Hellsten and colleagues (10) trained subjects for 7 d and then supplemented
subjects for 3 d in a double-blind manner (600 mg × kg
× d
) prior to completing
an identical exercise bout used in the training period. Muscle biopsy samples were
taken 5, 24, and 72 h after this exercise bout and found a signicantly increased
level of muscle ATP at 72 h post-exercise. Furthermore, ribose supplementation was
found in two related studies (20 g/d for 3 d prior to training, during a 5 d training
period, and for 3 d following training) to have no impact on performance but did
help to attenuate the decrease in the TAN pool following acute, intense exercise
as well as after a 65 h recovery period (7, 14). While limited evidence is provided
for ribose to increase performance, these ndings do support a possible benet
for ribose supplementation to sustain work production or promotion of long-term
recovery by enhancing ATP availability. In summary, these previously published
studies help to provide the collective evidence indicating why manufacturers of
ribose have marketed these supplements to athletes (3, 7, 10, 11, 14).
While some studies have suggested ergogenic properties for ribose administra-
tion, the results from the present study do not support any ergogenic role for acute
ribose supplementation compared with a placebo on markers of performance and
metabolic activity before or during repeated high-intensity intermittent exercise.
This provides additional support to previous research that has suggested no ergo-
genic benet of ribose supplementation (8 to 50 g/d for 3 to 6 d) while completing
06Kerksick(653) 10/9/05, 11:07 AM662
662 Kerksick et al.
Ribose Supplementation and Exercise 663
various forms of high-intensity exercise (e.g., 6 to 15 × 10 to 30 s sprints with 60
to 180 s recovery as well as nding no difference in plasma metabolites (lactate,
ammonia, uric acid, glucose, or creatine kinase) and muscle adenine nucleotides
(ATP, ADP, AMP, IMP, or TAN) (4, 7, 11, 12). Lastly, and in accordance with the
ndings showing no performance increase after ribose supplementation, de novo
synthesis of ATP is a slow process with limited evidence of its ability to increase
resting muscle ATP levels during an acute bout of high-intensity, intermittent
exercise (7, 10). Under these circumstances, it is possible that any acute admin-
istration of ribose in a single day or exercise bout would not have enough time to
have a physiological impact; the popularity of ribose supplementation, however,
warranted the investigation.
In summary, the results of this study indicate that acute ribose supplementation
(2 doses of 3 g each) during ve repeated, high-intensity, short-term (30 s) exercise
bouts provides no ergogenic benet. Previous ndings have alluded that possible
benets from ribose supplementation might not be elucidated until several days
after supplementation (10) suggesting additional studies should evaluate the impact
on the TAN pool and performance of ingesting varying doses of ribose before,
during, and after exercise. Investigations should also focus on the pharmokinetic
pattern of ribose to the muscle during acute dosing studies and more research is
needed to evaluate the effects of ribose supplementation on recovery from intense
exercise and training adaptations. Nevertheless, results from this study indicate
that acute ribose supplementation does not improve performance or recovery in
trained cyclists.
We would like to thank the subjects who participated in this study and the laboratory assis-
tants in the Exercise and Sport Nutrition Laboratory at Baylor University who assisted
in data acquisition and analysis. This study was funded in part by Royal Numico;
none of the investigators who participated in the study have a nancial interest in the
outcome of this research. The conclusions and ndings of this study are not meant in
any way to suggest an endorsement of the products used or the companies that funded
the research.
1. PDR for Nutritional Supplements. Montvale, NJ: Medical Economics, Thomson
Healthcare, 2001.
2. ACSM. ACSMʼs Guidelines for Exercise Testing and Prescription. Philadelphia: Lip-
pincott Williams & Wilkins, 2000.
3. Antonio, J., D. Falk and D. Gammeren. Ribose administration in recreation bodybuild-
ers. Med. Sci. Sports Exerc. 33:S166 (Abstract), 2001.
4. Berardi, J.M. and T.N. Ziegenfuss. Effects of ribose supplementation on repeated sprint
performance in men. J. Strength Cond. Res. 17:47-52, 2003.
5. Dodd, S.L., C.A. Johnson, K. Fernholz, and J.A. St. Cyr. The role of ribose in human
skeletal muscle metabolism. Med. Hypotheses. 62:819-824, 2004.
6. Febbraio, M.A. and J. Dancey. Skeletal muscle energy metabolism during prolonged,
fatiguing exercise. J. Appl. Physiol. 87:2341-2347, 1999.
06Kerksick(653) 10/9/05, 11:07 AM663
664 Kerksick et al.
7. Gallagher, P.M., D.L. Williamson, M.P. Godard, J.R. Witter, and S.W. Trappe. Effects of
ribose supplementation on adenine nucleotide concentration in skeletal muscle follow-
ing high-intensity cycle exercise. Med. Sci. Sports Exerc. 33:S167 (Abstract), 2001.
8. Gross, M., B. Kormann, and N. Zollner. Ribose administration during exercise: effects
on substrates and products of energy metabolism in healthy subjects and a patient with
myoadenylate deaminase deciency. Klin Wochenschr. 69:151-155, 1991.
9. Hargreaves, M., M.J. McKenna, D.G. Jenkins, S.A. Warmington, J.L. Li, R.J. Snow,
M.A. Febbraio. Muscle metabolites and performance during high-intensity intermittent
exercise. J. Appl. Physiol. 84:1687-1691, 1998.
10. Hellsten, Y., L. Skadhauge, and J. Bangsbo. Effect of ribose supplementation on
resynthesis of adenine nucleotides after intense intermittent training in humans. Am.
J. Physiol. Regul. Integr. Comp. Physiol. 286:R182-R188, 2004.
11. Kreider, R.B., C. Melton, M. Greenwood, C. Rasmussen, J. Lundberg, C. Earnest,
and A. Almada. Effects of oral D-ribose supplementation on anaerobic capacity and
selected metabolic markers in healthy males. Int. J. Sport Nutr. Exerc. Metab. 13:76-86,
12. Op ʻt Eijnde, B., M. Van Leemputte, F. Brouns, G.J. Van Der Vusse, V. Labarque, M.
Ramaekers, R. Van Schuylenberg, P. Verbessem, H. Wijnen, and P. Hespel. No effects
of oral ribose supplementation on repeated maximal exercise and de novo ATP resyn-
thesis. J. Appl. Physiol. 91:2275-2281, 2001.
13. Pliml, W., T. von Arnim, A. Stablein, H. Hofmann, H.G. Zimmer, and E. Erdmann.
Effects of ribose on exercise-induced ischemia in stable coronary artery disease. Lancet.
340:507-510, 1992.
14. Raue, U., P.M. Gallagher, D.L. Williamson, M.P. Godard, and S.W. Trappe. Effects of
ribose supplementation on performance during repeated high-intensity cycle sprints.
Med. Sci. Sports Exerc. 33:S44 (Abstract), 2001.
15. Stout, J. Maintaining muscle cell energy: the possible role of D-ribose. In: Sports
Supplements, Antonio, J. and J. Stout. Philadelphia: Lippincott Williams & Wilkins,
pp. 248-249, 2001.
16. Tullson, P.C., J. Bangsbo, Y. Hellsten, and E.A. Richter. IMP metabolism in human
skeletal muscle after exhaustive exercise. J. Appl. Physiol. 78:146-152, 1995.
17. Wagner, D.R., U. Gresser, and N. Zollner. Effects of oral ribose on muscle metabolism
during bicycle ergometer in AMPD-decient patients. Ann. Nutr. Metab. 35:297-302,
18. Zhao, S., R.J. Snow, C.G. Stathis, M.A. Febbraio, and M.F. Carey. Muscle adenine
nucleotide metabolism during and in recovery from maximal exercise in humans. J.
Appl. Physiol. 88:1513-1519, 2000.
19. Zimmer, H.G. Restitution of myocardial adenine nucleotides: acceleration by admin-
istration of ribose. J. Physiol. (Paris). 76:769-775, 1980.
06Kerksick(653) 10/9/05, 11:07 AM664
... Research regarding the effects of ribose supplementation on muscular ATP reserves, athletic performance and ATP replenishment are conflicting [1,5,7,10,12,13,15,16]. Interestingly, there is no study that has looked specifically at athletic performance and fatiguing substance markers during recovery from exercise. ...
... There are a few studies investigating the effects of ribose on anaerobic performance and ATP replenishment [1,5,7,10,12,13,15,16]. Ribose supplementation immediately before exercise has not been found effective for anaerobic capacity and peak power [12,15]. ...
... There are a few studies investigating the effects of ribose on anaerobic performance and ATP replenishment [1,5,7,10,12,13,15,16]. Ribose supplementation immediately before exercise has not been found effective for anaerobic capacity and peak power [12,15]. Berardi et al. [1] found that oral supplementation with ribose before exercise did not affect mean or peak power gains although it has led to a significant increase in mean power and peak power in only one of six modified Wingate trials [1]. ...
... We have now demonstrated that there is a deficiency of AMPD1 as well as hypoxanthine and other AMP breakdown products in myositis mice, but treatment of these mice with daily oral doses of D-ribose showed no beneficial effects. These results in our mouse disease model are consistent with other reports indicating that D-ribose has no effect on muscle performance in healthy patients or in patients with other metabolic diseases [15,16,17]. We also propose that low expression levels of the enzyme ribokinase may contribute to inefficient utilization of Dribose in skeletal muscle. ...
... The infiltration of lymphocytes is not typically seen until the animals reach 13 weeks of age or older. AMPD1 enzyme activity and muscle function continue to decrease up to 16 ...
... A comparison of RBKS expression profiles in humans and mice using publicly available data (NCBI UniGene Hs.11916 ) suggests that both humans and mice have low basal expression of RBKS in skeletal muscle. While we cannot directly extrapolate from this mouse model, the suggestion that Dribose cannot be utilized by skeletal muscle tissue is in agreement with prior publications in humans showing that D-ribose has no effect on muscle function in healthy patients [15,16,17]. ...
Full-text available
Current treatments for idiopathic inflammatory myopathies (collectively called myositis) focus on the suppression of an autoimmune inflammatory response within the skeletal muscle. However, it has been observed that there is a poor correlation between the successful suppression of muscle inflammation and an improvement in muscle function. Some evidence in the literature suggests that metabolic abnormalities in the skeletal muscle underlie the weakness that continues despite successful immunosuppression. We have previously shown that decreased expression of a purine nucleotide cycle enzyme, adenosine monophosphate deaminase (AMPD1), leads to muscle weakness in a mouse model of myositis and may provide a mechanistic basis for muscle weakness. One of the downstream metabolites of this pathway, D-ribose, has been reported to alleviate symptoms of myalgia in patients with a congenital loss of AMPD1. Therefore, we hypothesized that supplementing exogenous D-ribose would improve muscle function in the mouse model of myositis. We treated normal and myositis mice with daily doses of D-ribose (4 mg/kg) over a 6-week time period and assessed its effects using a battery of behavioral, functional, histological and molecular measures. Treatment with D-ribose was found to have no statistically significant effects on body weight, grip strength, open field behavioral activity, maximal and specific forces of EDL, soleus muscles, or histological features. Histological and gene expression analysis indicated that muscle tissues remained inflamed despite treatment. Gene expression analysis also suggested that low levels of the ribokinase enzyme in the skeletal muscle might prevent skeletal muscle tissue from effectively utilizing D-ribose. Treatment with daily oral doses of D-ribose showed no significant effect on either disease progression or muscle function in the mouse model of myositis.
... No prior controlled studies have been conducted on the effects of D-ribose supplementation on exercise-induced DOMS. Nevertheless, the potential benefits of D-ribose supplementation for improving exercise performance and/or recovery [22][23][24], and for reducing markers of ROS production [25] has been explored, though some studies didn't support this hypothesis [24,[26][27][28]. Seifert et al. [24] suggested that a failure to support the potential benefit of D-ribose may be due to the difference of fitness level of subjects. ...
Full-text available
Abstract Objective Previous investigations suggest that appropriate nutritional interventions may reduce delayed onset muscle soreness (DOMS). This study examined the effect of D-ribose supplementation on DOMS induced by plyometric exercise. Methods For the purpose of inducing DOMS, 21 untrained male college students performed a lower-limb plyometric exercise session that involved 7 sets of 20 consecutive frog hops with 90-s of rest between each set. Muscle soreness was measured with a visual analogue scale 1-h before, 24-h after, and 48-h after exercise. Subjects were then randomly placed into the D-ribose group (DRIB, n = 11) and the placebo group (PLAC, n = 10) to assure equivalent BMI and muscle soreness. After a 14-d washout/recovery period, subjects performed the same exercise session, with DRIB ingesting a 200 ml solution containing 15 g D-ribose 1-h before, 1-h, 12-h, 24-h, and 36-h after exercise, and PLAC ingesting a calorically equivalent placebo of the same volume and taste containing sorbitol and β-cyclodextrin. Muscle soreness and isokinetic muscle strength were measured, and venous blood was assessed for markers of muscle damage and oxidative stress 1-h before, 24-h and 48-h after exercise. Results In DRIB, muscle soreness after 24-h and 48-h in the second exercise session were significantly lower (p
... A 2006 study [685] investigated the effects of supplementing with either ribose or dextrose over 8 weeks on rowing performance and concluded that ribose was outperformed by the dextrose control [685]. Kreider and associates [684] and Kerksick and colleagues [686] investigated ribose supplementation on measures of anaerobic capacity in trained cyclists and concluded ribose had no positive impact on performance. In 2017, Seifert and investigators [687] had 26 healthy subjects supplement with either 10 g of ribose or 10 g of dextrose for 5 days while completing a single bout of interval exercise and a two-minute power output test. ...
Full-text available
Background: Sports nutrition is a constantly evolving field with hundreds of research papers published annually. In the year 2017 alone, 2082 articles were published under the key words 'sport nutrition'. Consequently, staying current with the relevant literature is often difficult. Methods: This paper is an ongoing update of the sports nutrition review article originally published as the lead paper to launch the Journal of the International Society of Sports Nutrition in 2004 and updated in 2010. It presents a well-referenced overview of the current state of the science related to optimization of training and performance enhancement through exercise training and nutrition. Notably, due to the accelerated pace and size at which the literature base in this research area grows, the topics discussed will focus on muscle hypertrophy and performance enhancement. As such, this paper provides an overview of: 1.) How ergogenic aids and dietary supplements are defined in terms of governmental regulation and oversight; 2.) How dietary supplements are legally regulated in the United States; 3.) How to evaluate the scientific merit of nutritional supplements; 4.) General nutritional strategies to optimize performance and enhance recovery; and, 5.) An overview of our current understanding of nutritional approaches to augment skeletal muscle hypertrophy and the potential ergogenic value of various dietary and supplemental approaches. Conclusions: This updated review is to provide ISSN members and individuals interested in sports nutrition with information that can be implemented in educational, research or practical settings and serve as a foundational basis for determining the efficacy and safety of many common sport nutrition products and their ingredients.
Gonzalez, AM, Pinzone, AG, Bram, J, Salisbury, JL, Lee, S, and Mangine, GT. Effect of multi-ingredient preworkout supplementation on repeated sprint performance in recreationally active men and women. J Strength Cond Res XX(X): 000-000, 2019-The purpose of this investigation was to examine the effects of acute supplementation of a multi-ingredient preworkout supplement (MIPS), containing a proprietary blend of ancient peat and apple extracts, creatine monohydrate, taurine, ribose, and magnesium, on sprint cycling performance. Seventeen recreationally active men and women (23.2 ± 5.9 years; 172.9 ± 14.3 cm; 82.4 ± 14.5 kg) underwent 2 testing sessions administered in a randomized, counterbalanced, double-blind fashion. Subjects were provided either MIPS or placebo (PL) one hour before performing a sprint cycling protocol, which consisted of ten 5-second "all-out" sprints interspersed by 55 seconds of unloaded pedaling. Average power (PAVG), peak power (PPK), average velocity (VAVG), and distance covered were recorded for each sprint. Separate linear mixed models revealed decrements (p < 0.05) compared to the first sprint in PAVG (75-229 W) and PPK (79-209 W) throughout all consecutive sprints after the initial sprint during PL. Likewise, diminished (p ≤ 0.029) VAVG (3.37-6.36 m·s) and distance covered (7.77-9.00 m) were noted after the third and fifth sprints, respectively, during PL. By contrast, during MIPS, only VAVG decreased (2.34-5.87 m·s, p ≤ 0.002) on consecutive sprints after the first sprint, whereas PAVG and PPK were maintained. In addition, a significant decrease (p = 0.045) in distance covered was only observed on the ninth sprint during MIPS. These data suggest that recreational athletes who consumed the MIPS formulation, one hour before a repeated sprinting session on a cycle ergometer, better maintained performance compared with PL.
Full-text available
Abstract Sport nutrition is a constantly evolving field with literally thousands of research papers published annually. For this reason, keeping up to date with the literature is often difficult. This paper presents a well-referenced overview of the current state of the science related to how to optimize training through nutrition. More specifically, this article discusses: 1.) how to evaluate the scientific merit of nutritional supplements; 2.) general nutritional strategies to optimize performance and enhance recovery; and, 3.) our current understanding of the available science behind weight gain, weight loss, and performance enhancement supplements. Our hope is that ISSN members find this review useful in their daily practice and consultation with their clients.
It is critical to keep in mind, especially in this chapter that multiple lifestyle options exists that can improve or actually not improve and even exacerbate side effects from cancer treatments. And there are many integrative medicines, especially dietary supplements that can improve, have no impact or actually cause a side effect from cancer treatment to become worse! The purpose of this chapter just like the rest of this book is to cover all of those integrative medicines that work, have no effect or are worthless for multiple cancer treatment side effects. When applicable prescription drug treatments are mentioned and reviewed. Still, this chapter and the book is not intended to provide a summary or exhaustive list of the conventional prescription treatment options for these side effects from A to Z because it would not only create an unreadable voluminous text, but this also would not serve the purpose of this text—to simply provide a non-biased and objective review of the medical research in the area of breast cancer and integrative medicines, especially in regard to lifestyle changes and dietary supplements. This is the area of oncology that appears to have arguably the greatest current needs for more objective and educational attention to this issue.
Full-text available
Six men were studied during four 30-s "all-out" exercise bouts on an air-braked cycle ergometer. The first three exercise bouts were separated by 4 min of passive recovery; after the third bout, subjects rested for 4 min, exercised for 30 min at 30-35% peak O2 consumption, and rested for a further 60 min before completing the fourth exercise bout. Peak power and total work were reduced (P < 0. 05) during bout 3 [765 +/- 60 (SE) W; 15.8 +/- 1.0 kJ] compared with bout 1 (1,168 +/- 55 W, 23.8 +/- 1.2 kJ), but no difference in exercise performance was observed between bouts 1 and 4 (1,094 +/- 64 W, 23.2 +/- 1.4 kJ). Before bout 3, muscle ATP, creatine phosphate (CP), glycogen, pH, and sarcoplasmic reticulum (SR) Ca2+ uptake were reduced, while muscle lactate and inosine 5'-monophosphate were increased. Muscle ATP and glycogen before bout 4 remained lower than values before bout 1 (P < 0.05), but there were no differences in muscle inosine 5'-monophosphate, lactate, pH, and SR Ca2+ uptake. Muscle CP levels before bout 4 had increased above resting levels. Consistent with the decline in muscle ATP were increases in hypoxanthine and inosine before bouts 3 and 4. The decline in exercise performance does not appear to be related to a reduction in muscle glycogen. Instead, it may be caused by reduced CP availability, increased H+ concentration, impairment in SR function, or some other fatigue-inducing agent.
Full-text available
There is no established treatment specifically aimed at protecting or restoring cardiac energy metabolism, which is greatly impaired by ischaemia. Even after reperfusion, myocardial content of ATP remains low for more than 72 h. Long-term post-ischaemic dysfunction and irreversibility of ischaemic damage have been associated with low ATP content. Evidence that the pentose sugar ribose stimulates ATP synthesis and improves cardiac function led us to test the possibility that ribose increases tolerance to myocardial ischaemia in patients with coronary artery disease (CAD). 20 men with documented severe CAD underwent two symptom-limited treadmill exercise tests on 2 consecutive days; we postulated that the ischaemia induced might bring about changes in ATP metabolism lasting for several days. Patients whose baseline tests showed reproducibility were randomly allocated 3 days of treatment with placebo or ribose 60 g daily in four doses by mouth. Exercise testing was repeated after treatment on day 5. At that time mean (95% confidence interval) treadmill walking time until 1 mm ST-segment depression was significantly greater in the ribose than in the placebo group (276 [220-331] vs 223 [188-259] s; p = 0.002). The groups did not differ significantly in time to moderate angina. In the ribose-treated group the changes from baseline to day 5 in both time to ST depression and time to moderate angina were significant (p less than 0.005), but these changes were not significant in the placebo group. In patients with CAD, administration of ribose by mouth for 3 days improved the heart's tolerance to ischaemia. The presumed effects on cardiac energy metabolism offer new possibilities for adjunctive medical treatment of myocardial ischaemia.
Three patients with AMP deaminase deficiency (AMPD deficiency) performed exercise on a bicycle ergometer with increasing work load without and with administration of ribose (3 g p.o. every 10 min, beginning 1 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.
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 less than 0.05), ammonia (p less than 0.01) and hypoxanthine (p less than 0.05) concentrations and a decrease in serum glucose concentration (p less than 0.05). When ribose was administered, the plasma lactate concentration increased significantly higher (p less than 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.
In the present study, the influence of ribose on the biosynthesis of myocardial adenine nucleotides was examined in rats in vivo utilizing two experimental models which are characterized by a reduction in the adenine nucleotide content; recovery from oxygen deficiency and application of isoproterenol. 1. The biosynthesis (= de novo synthesis) of cardiac adenine nucleotides was enhanced by 90% during the first 60 min of recovery from five intermittent periods of asphyxia of 4.5 min duration (Table I). 2. Isoproterenol induced a stimulation of myocardial adenine nucleotide synthesis in a dose-dependent manner amounting to 640% three hours after s.c. administration of 25 mg/kg (Fig. 1). 3. Ribose which bypasses the hexose monophosphate shunt in the myocardium and which leads to an elevation of the available pool of 5-phosphoribosyl-1-pyrophosphate (PRPP), stimulated the biosynthesis of adenine nucleotides in the heart, but not in liver and kidney, of rats one hour after i.v. application of a single dose of 100 mg/kg from 6 nmoles/g/h to 27 nmoles/g/h (Fig. 2). 4. When ribose was constantly infused during the first 60 min of recovery from asphyxia, the enhancement of cardiac adenine nucleotide biosynthesis was further stimulated from 12.6 nmoles/g/h to 20.5 nmoles/g/h (with 500 mg ribose/kg/h) and to 43.4 nmoles/g/h (with 1 000 mg ribose/kg/h) (Fig. 3). 5. Continuous I.V. infusion of ribose (200 mg/kg/h) for 24 hours in isoproterenol-treated rats during a 13-fold increase in myocardial adenine nucleotide biosynthesis compared with the control (Fig. 4). In this condition, the isoproterenol-induced decline in the adenine nucleotide level did not occur (Table II).
This study addressed whether AMP deaminase (AMPD)myosin binding occurs with deamination during intense exercise in humans and the extent of purine loss from muscle during the initial minutes of recovery. Male subjects performed cycle exercise (265 +/- 2 W for 4.39 +/- 0.04 min) to stimulate muscle inosine 5'-monophosphate (IMP) formation. After exercise, blood flow to one leg was occluded. Muscle biopsies (vastus lateralis) were taken before and 3.6 +/- 0.2 min after exercise from the occluded leg and 0.7 +/- 0.0, 1.1 +/- 0.0, and 2.9 +/- 0.1 min postexercise in the nonoccluded leg. Exercise activated AMPD; at exhaustion IMP was 3.5 +/- 0.4 mmol/kg dry muscle. Before exercise, 16.0 +/- 1.6% of AMPD cosedimented with the myosin fraction; the extent of AMPD:myosin binding was unchanged by exercise. Inosine content increased about threefold during exercise and twofold more during recovery; by 2.9 min postexercise it was 0.43 +/- 0.02 mmol/kg dry muscle. IMP decreased 2.1 +/- 0.3 mmol/kg dry muscle with no change in total adenylates. Total purines declined significantly (P < 0.05) during the recovery period in the nonoccluded leg, consistent with a loss of purines to the circulation, whereas total purines were unchanged in the occluded leg. Regulation of muscle purine content is a dynamic process that must accommodate rapid changes due to degradation and efflux.
A depletion of phosphocreatine (PCr), fall in the total adenine nucleotide pool (TAN = ATP + ADP + AMP), and increase in TAN degradation products inosine 5'-monophosphate (IMP) and hypoxanthine are observed at fatigue during prolonged exercise at 70% maximal O(2) uptake in untrained subjects [J. Baldwin, R. J. Snow, M. F. Carey, and M. A. Febbraio. Am. J. Physiol. 277 (Regulatory Integrative Comp. Physiol. 46): R295-R300, 1999]. The present study aimed to examine whether these metabolic changes are also prevalent when exercise is performed below the blood lactate threshold (LT). Six healthy, untrained humans exercised on a cycle ergometer to voluntary exhaustion at an intensity equivalent to 93 +/- 3% of LT ( approximately 65% peak O(2) uptake). Muscle biopsy samples were obtained at rest, at 10 min of exercise, approximately 40 min before fatigue (F-40 =143 +/- 13 min), and at fatigue (F = 186 +/- 31 min). Glycogen concentration progressively declined (P < 0.01) to very low levels at fatigue (28 +/- 6 mmol glucosyl U/kg dry wt). Despite this, PCr content was not different when F-40 was compared with F and was only reduced by 40% when F was compared with rest (52. 8 +/- 3.7 vs. 87.8 +/- 2.0 mmol/kg dry wt; P < 0.01). In addition, TAN concentration was not reduced, IMP did not increase significantly throughout exercise, and hypoxanthine was not detected in any muscle samples. A significant correlation (r = 0.95; P < 0. 05) was observed between exercise time and glycogen use, indicating that glycogen availability is a limiting factor during prolonged exercise below LT. However, because TAN was not reduced, PCr was not depleted, and no correlation was observed between glycogen content and IMP when glycogen stores were compromised, fatigue may be related to processes other than those involved in muscle high-energy phosphagen metabolism.