Category: Diet

Ribose and ATP production

Ribose and ATP production

D-ribose Rlbose a naturally occurring monosaccharide found Robose the cells and Liver detox plan in the mitochondria is Ribose and ATP production Ribowe Ribose and ATP production production. D-ribose also acts as a substrate for DNA, RNA, acetyl coenzyme A, flavin adenine dinucleotide FADHand nicotinamide adenine dinucleotide plus hydrogen NADHwhich all play a role in ATP production. Effect of training on insulin-mediated glucose uptake in human muscle.

Ribose and ATP production -

This group was involved in minimal exercise training throughout the week. The HVO 2 group consisted of individuals who were consistently exercising. Each subject was required to maintain their normal diet during this study, as well as performing their normal daily activities without performing any additional separate exercise sessions not designated in this study.

Five grams of either supplement was mixed with their food or in a self-selected beverage with lunch and an additional 5 g was ingested with dinner for 2 days as a loading dose prior to exercise. On the following 3 days of exercise, subjects ingested a standardized pre-exercise snack along with 5 g of the supplement 2 h before their exercise session.

Following exercise, subjects ingested their final daily dose of 5 g before leaving the laboratory along with a snack which consisted of g of yogurt and two granola bars.

During the first visit to the laboratory, each subject signed the informed consent and completed a health history questionnaire. Thereafter, each subject underwent a maximal oxygen uptake test and practiced the 2 min power test assessment using a cycle ergometer Monark E, Sweden.

Cycling resistance was then increased by 0. Heart rate HR , VO 2 and a blood lactate Lac sample were collected at of each stage.

This assessment established exercise workloads during the two treatment sessions. The exercise session consisted of six, 10 min intervals of exercise on a cycle ergometer. At the end of the 60 min exercise session, each subject completed a 2 min performance task.

This performance task required the subject to produce as much power as possible during this 2 min interval. Peak power PO and average power was assessed during this 2 min task trial.

A minimum of 4 day washout period was employed between crossover arms of the study to allow adequate recovery. Venous blood samples were drawn via a venipuncture 15 min before exercise and 24 h post exercise. Finger stick techniques at 10 min before exercise, 20 min, 40 min, and 60 min during exercise.

The finger stick blood samples collected during exercise were assayed for blood glucose. Creatine kinase CK and blood urea nitrogen BUN concentrations were measured at pre-exercise and 24 h post exercise following the last exercise session.

Subjects ingested ml of water at 20 and 40 min during exercise to minimize any effects of dehydration. Rating of perceived exertion RPE was recorded every 20 min during exercise using the Borg scale. Heart rate was recorded using a Polar HR monitor RC3; Polar, Inc. Blood glucose Gluc concentration were measured using a Bayer Gluc monitor Bayer Medical, NJ.

Blood lactate levels were measured by an AccuSport Lactate Analyzer Akira, Japan. Creatine kinase and BUN were measured utilizing an Abaxis Piccolo analyzer Princeton, NJ. Power data from the time trial performance test was assessed with the Sports Medicine Industries SMI software package St.

Cloud, MN. Statistical analyses of performance, physiological measurements, and laboratory values during and following intense exercise provides evidence of what specific role DR can play in a untrained or trained athlete.

Data was analyzed with SPSS statistical software using a 2-way ANOVA with repeated measures with time and treatments as independent variables. Heart rate, RPE, blood Gluc, serum CK, serum BUN and power data were dependent measures.

All 26 subjects completed the study without any adverse events. Data are presented as main effects as there were no interactions. No statistical differences were observed for the dependent measures when data were analyzed from 26 subjects. Therefore, subjects were divided into two equal groups based on their VO 2 max values.

Relative and absolute mean power data can be found in Table 2. The average changes in relative and absolute peak power from Day 1 to Day 3 were 0. Relative and absolute mean PO were not different between DR and DEX treatments for the HVO 2 group.

The average changes in relative and absolute peak PO from Day 1 to Day 3 were 0. Analysis of serum CK data indicated that DR ingestion led to lower change in the LVO 2 group.

Creatine kinase levels increased by an average of No differences for change in CK and BUN levels were observed between DR No differences were observed for blood Gluc and remained stable for all treatments and within both groups Table 3. No difference between treatments was found for HR in the LVO 2 group.

The purpose of this project was to investigate the influence of DR on muscular performance and recovery during and following a multi-day high intensity exercise regimen in LVO 2 and HVO 2 groups. The pertinent results indicate that DR ingestion improved performance and recovery for the LVO 2 group during a multi-day exercise study, but not in the HVO 2 group.

The role in which DR could play on performance during intense exercise has been uncertain. Due to this uncertainty, this study has demonstrated that DR supplementation provided a performance benefit undergoing repeated days of high intensity exercise.

The rate of ATP utilization during high intensity exercise may exceed ATP production and a considerable amount of time is required for these deficient levels to recover [ 10 , 19 ].

Hellsten et al. A decrease in cellular high energy phosphates can affect muscular function besides producing symptoms of soreness and fatigue, which can affect subsequent exercise sessions [ 21 ].

Studies have revealed mixed results in replenishing muscular energy levels, maintaining or enhancing performance and alleviating post-exercise symptoms with substrate supplementation [ 22 ]. Alternatives to metabolic pathways can play important roles in ATP generation, such as the pentose phosphate pathway.

The pentose phosphate pathway is critical for the formation of 5-phosphyl-ribosepyrophosphate PRPP , an intermediate in the production of ATP, and plays a role in ATP de novo synthesis which is dependent on a rate limiting enzyme, glucose 6-phosphte dehydrogenase G6PDH [ 21 ].

However, DR is unique in that it bypasses this rate limiting enzymatic step in the formation of PRPP [ 23 ]. This enhanced production of ATP by DR replenishes the cellular energy deficiency and can shorten the energy recovery period following high intensity exercise.

On the other hand, subjects in the LVO 2 group may not have had the ability to fully utilize other pathways i. PRPP to assist in recovery. Thus, DR gave them extra substrate to bypass the G6PDH step and, potentially, increase the efficiency of the recovery, reflecting a potential increase in muscle ATP levels.

This study did not measure muscle ATP levels, which could have provided additional supporting data for both the trained and untrained athlete. The measurement of muscle ATP levels could provide a more in-depth metabolic explanation.

The effect of DR on performance has provided mixed results. Raue et al. Berardi et al. Van Gammerren et al. However, DR has not always demonstrated an improvement in performance. Eijnde et al. Furthermore, Kreider et al.

The present study demonstrates that subject selection criterion i. fitness level has a significant influence in the results. When data were analyzed by treatment DR vs.

DEX , regardless of fitness level, no statistical differences were observed. In fact, values were comparable between the treatments.

Untrained individuals appear to suffer the consequences of acute, repeated bouts of exercise by not having the ability to perform or recovery sufficiently to exercise on subsequent days [ 8 , 9 ]. The potential beneficial role of DR also depends upon the dosage and timing of dosing, type of exercise, degree of intensity and duration of exercise.

We designed a high-intensity exercise protocol where cellular anaerobic metabolism commences; thereby stressing the metabolic activity in these exercising muscles and to see what role DR may play on recovery and performance.

In evaluating performance in the LVO 2 group, we found that mean and peak PO increased significantly with DR from day 1 to 3, which was not observed in the DEX treatment. Multiple factors can account for the performance benefits with DR. For example, differences in muscular CK levels might shed light on this beneficial difference in performance by indicating a maintenance, or lack thereof, of cell membrane integrity.

The change in CK level from day 1 to day 3 was about 3 times greater for the DEX treatment compared to DR in the LVO 2 group. Besides the impact of high intensity exercise on cellular metabolism, additional factors may also play a role, such as reactive oxygen species.

High intensity exercise may result in oxidative damage in both the blood and skeletal muscle [ 25 ]; however, high intensity exercise is superior to low intensity exercise in upregulating the muscle to produce superoxide dismutase and GSH peroxidase [ 26 ].

Seifert et al. The biochemical mechanisms responsible for these symptoms remain unclear; however, the production of free radicals could play an important role as mediators of muscular damage. Sjodin et al. The metabolic stress during exercise alters the biochemical state of the cell, which ultimately enhances the rate of oxygen free radical production from semiquinone and xanthine oxidase.

It is therefore, plausible that if mitochondrial function is altered during exercise, performance may be inhibited.

This study did not measure produced products of oxidative stress, which could have provided additional interesting and supporting data during and following high intensity exercise. The delivery and utilization of oxygen to exercising muscle is a major factor in assessing fitness and maximal VO 2 levels [ 28 ].

Upon further assessment of our subjects in this study into LVO 2 and HVO 2 groups, revealed significant differences when consuming DR during the high intensity exercise sessions for the LVO 2 group. These findings appear to suggest that individuals that have not consistently performed exercise above the Lac threshold level do not fair equally with individuals that exercise or train on a more intense regimen schedule.

The rise in CK levels observed in the LVO 2 group appears to imply that a strenuous, anaerobic exercise produced cellular stress in which enzymatic leaking occurs, which can not only effect cellular homeostasis, but performance and recovery as well. In conclusion, high intensity, anaerobic exercise decreases muscular ATP levels and a considerable amount of time is required for these lower energy levels to recover.

Some studies have reported mixed performance benefits with DR, probably reflecting protocol differences, dosing of DR, timing of the DR dosage, intensity of exercise, and subject specificity. For this last reason we developed a protocol that induced a level of high intensity, anaerobic exercise in two fitness level groups.

The analysis revealed that the LVO 2 value subjects had a significant improvement in performance, lower changes in CK, and lower RPE with DR compared to DEX. Assessment of metabolic serum parameters did not reflect any appreciable differences between the treatments, not clearly demonstrating a potential mechanism accounting for this benefit.

A limitation of this study would be dietary control. While subjects were instructed to maintain their dietary habits as usual during the study, an in depth analysis of intakes was not performed.

It is possible that some members of the LVO2 group had an insufficient diet that would have benefitted from supplementation. In summary, DR demonstrated a performance, perceptual, and serum benefits in the lower fitness adult subjects undergoing high intensity exercise. The stress of high intensity exercise has the potential to be benefited with supplementation of DR around these exercise sessions.

Future studies are needed to elucidate the mechanism s of action of DR ingestion and exercise. Roedde S, MacDougall JD, Sutton JR, Green HJ. Supercompensation of muscle glycogen in trained and untrained subjects.

Can J Appl Sport Sci. CAS PubMed Google Scholar. Dela F, Mikines KJ, von Linstow M, Secher NH, Galbo H. Effect of training on insulin-mediated glucose uptake in human muscle. Am J Phys. Google Scholar. Phielix E, Meex R, Ouwens DM, Sparks L, Hoeks J, Schaart G, Moonen-Kornips E, Hesselink MK, Schrauwen P.

High oxidative capacity due to chronic exercise training attenuates lipid-induced insulin resistance. Article CAS PubMed PubMed Central Google Scholar. Lewis NA, Howatson G, Morton K, Hill J, Pedlar CR. Alterations in redox homeostasis in the elite endurance athlete.

Sports Med. Article PubMed Google Scholar. Stisen AB, Stougaard O, Langfort J, Helge JW, Sahlin K, Madsen K. Maximal fat oxidation rates in endurance trained and untrained women. Eur J Appl Physiol. Article CAS PubMed Google Scholar. Coggan AR, Raguso CA, Gastaldelli A, Sidossis LS, Yeckel CW.

Fat metabolism during high-intensity exercise in endurance-trained and untrained men. Sidossis LS, Wolfe RR, Coggan AR. Regulation of fatty acid oxidation in untrained vs. trained men during exercise. CAS Google Scholar. Darr KC, Bassett DR, Morgan BJ, Thomas DP.

Effects of age and training status on heart rate recovery after peak exercise. Am J Physiol Heart Circ Physiol. Tomlin DL, Wenger HA. The relationship between aerobic fitness and recovery from high intensity intermittent exercise.

Hellsten-Westing Y, Balsom PD, Norman B, Sjodin B. The effect of high-intensity training on purine metabolism in man. Acta Physiol Scand. Hellsten-Westing Y, Norman B, Balsom PD, Sjodin B. Decreased resting levels of adenine nucleotides in human skeletal muscle after high-intensity training.

J Appl Physiol. Stathis CG, Febbraio MA, Carey MF, Snow RJ. Influence of sprint training on human skeletal muscle purine nucleotide metabolism.

Hargreaves M, McKenna MJ, Jenkins DG, Warmington SA, Li JL, Snow RL, Febbraio MA. Muscle metabolites and performance during high-intensity, intermittent exercise.

Tullson PC, Bangsbo J, Hellsten Y, Richter EA. IMP metabolism in human skeletal muscle after exhaustive exercise. Eijnde BO, Van Leemputte M, Brouns F, Van Der Vuss GJ, Labarque V, Ramaekers M, Schuylenberg R, Verbessem P, Wijnen LT, Hespel P. No effects of oral ribose supplementation on repeated maximal exercise and de novo ATP resynthesis.

Kreider RB, Melton C, Greenwood M, Rasmussen C, Lundberg J, Earnest C, Almada A. Effects of oral D-ribose supplementation on anaerobic capacity and selected metabolic markers in healthy males.

Int J Sport Nutr Exerc Metab. Van Gammeren D, Falk D, Antonio J. The effects of four weeks of ribose supplementation on body composition and exercise performance in healthy, young, male recreational bodybuilders: a double blind, placebo controlled trial. Curr Ther Res.

Article Google Scholar. Raue U, Gallagher PM, Williamson DL, Trappe SW. Effects of ribose supplementation on performance during repeated high-intensity cycle sprints.

Med Sci Sport Exerc. Sjordin B, Hellsten-Westing Y, Apple FS. Biochemical mechanisms for oxygen free radical formation during exercise. Nicolson GL. Mitochondrial Dysfunction and Chronic Disease: Treatment With Natural Supplements. Integr Med Encinitas. Lesnefsky EJ, Chen Q, Hoppel CL.

Mitochondrial Metabolism in Aging Heart. Circ Res. Lane N. Energetics and genetics across the prokaryote-eukaryote divide. Biol Direct. Picard M, Wallace DC, Burelle Y. The rise of mitochondria in medicine. Chinnery PF,Hudson G.

Mitochondrial genetics. Br Med Bull. Pauly DF,Pepine CJ. D-Ribose as a supplement for cardiac energy metabolism.

J Cardiovasc Pharmacol Ther. Herrick J,St Cyr J. Ribose in the heart. J Diet Suppl. Leites EP,Morais VA. Mitochondrial quality control pathways: PINK1 acts as a gatekeeper. Biochem Biophys Res Commun. Ettema TJ. Evolution: Mitochondria in the second act.

Agrawal A,Mabalirajan U. Rejuvenating cellular respiration for optimizing respiratory function: targeting mitochondria. Am J Physiol Lung Cell Mol Physiol. Wei H, Liu L, Chen Q. Selective removal of mitochondria via mitophagy: distinct pathways for different mitochondrial stresses. Biochim Biophys Acta.

Mills EL, Kelly B, O'Neill LAJ. Mitochondria are the powerhouses of immunity. Nat Immunol. Kim SJ, Xiao J, Wan J, Cohen P, Yen K.

Mitochondrially derived peptides as novel regulators of metabolism. J Physiol. de Almeida A, Ribeiro TP, de Medeiros IA. Aging: Molecular Pathways and Implications on the Cardiovascular System. Oxid Med Cell Longev. Feng D, Liu L, Zhu Y, Chen Q.

Molecular signaling toward mitophagy and its physiological significance. Exp Cell Res. Polster BM, Carri MT, Beart PM. Mitochondria in the nervous system: From health to disease, Part I.

Neurochem Int. Liesa M,Shirihai OS. Mitochondrial dynamics in the regulation of nutrient utilization and energy expenditure. Cell Metab. Gomes LC,Scorrano L. Mitochondrial morphology in mitophagy and macroautophagy. Tamura Y, Sesaki H, Endo T. Phospholipid transport via mitochondria. Zhang Q, Tamura Y, Roy M, Adachi Y, Iijima M, Sesaki H.

Biosynthesis and roles of phospholipids in mitochondrial fusion, division and mitophagy. Cell Mol Life Sci.

Meyer JN, Leuthner TC, Luz AL. Mitochondrial fusion, fission, and mitochondrial toxicity. Wasilewski M, Chojnacka K, Chacinska A. Protein trafficking at the crossroads to mitochondria.

Neupert W. A perspective on transport of proteins into mitochondria: a myriad of open questions. J Mol Biol. Martinez-Reyes I, Diebold LP, Kong H, Schieber M, Huang H, Hensley CT, Mehta MM, Wang T, et al. TCA Cycle and Mitochondrial Membrane Potential Are Necessary for Diverse Biological Functions.

Mol Cell. Donnelly RP,Finlay DK. Glucose, glycolysis and lymphocyte responses. Mol Immunol. Lunt SY, Muralidhar V, Hosios AM, Israelsen WJ, Gui DY, Newhouse L, Ogrodzinski M, Hecht V, et al.

Pyruvate kinase isoform expression alters nucleotide synthesis to impact cell proliferation. Sutendra G, Kinnaird A, Dromparis P, Paulin R, Stenson TH, Haromy A, Hashimoto K, Zhang N, et al.

A nuclear pyruvate dehydrogenase complex is important for the generation of acetyl-CoA and histone acetylation. Rieger B, Junge W, Busch KB. Lateral pH gradient between OXPHOS complex IV and F 0 F 1 ATP-synthase in folded mitochondrial membranes.

Nat Commun. Kuhlbrandt W. Structure and function of mitochondrial membrane protein complexes. BMC Biol. Matta CF,Massa L. Energy Equivalence of Information in the Mitochondrion and the Thermodynamic Efficiency of ATP Synthase.

Ghosh K, Debasis K, Purnendu R. Tetrahedron Letters. Vyas NK, Vyas MN, Quiocho FA. Structural and Functional Similarity.

J Biol Chem. Wamelink MM, Struys EA, Jakobs C. The biochemistry, metabolism and inherited defects of the pentose phosphate pathway: a review. J Inherit Metab Dis. Tanuma S, Sato A, Oyama T, Yoshimori A, Abe H, Uchiumi F.

Curr Protein Pept Sci. Link H, Fuhrer T, Gerosa L, Zamboni N, Sauer U. Real-time metabolome profiling of the metabolic switch between starvation and growth.

Mitochondria producion important organelles referred to as cellular powerhouses ;roduction their unique properties of cellular Riobse production. With many pathologic conditions and Liver support nutrients, mitochondrial function Robose, and there is APT Ribose and ATP production in the production Ribose and ATP production ans triphosphate. The energy carrying Ribose and ATP production generated by cellular respiration and by pentose phosphate pathway, an alternative pathway of glucose metabolism. D-ribose is a naturally occurring monosaccharide found in the cells and particularly in the mitochondria is essential in energy production. Without sufficient energy, cells cannot maintain integrity and function. Supplemental D-ribose has been shown to improve cellular processes when there is mitochondrial dysfunction. When individuals take supplemental D-ribose, it can bypass part of the pentose pathway to produce D-ribosephosphate for the production of energy. Journal of the International Society poduction Sports Rjbose volume 14 productiln, Article number: 47 Cite this Easy weight loss. Metrics details. Skeletal muscle adenosine triphosphate ATP RRibose are severely Autophagy activation during and following prolonged high intensity exercise. Recovery from these lower ATP Ribose and ATP production can take days, which can affect performance on subsequent days of exercise. Untrained individuals often suffer the stress and consequences of acute, repeated bouts of exercise by not having the ability to perform or recovery sufficiently to exercise on subsequent days. Conversely, trained individuals may be able to recover more quickly due to their enhanced metabolic systems. D-Ribose DR has been shown to enhance the recovery in ATP; however, it is not known if recovery and performance can be benefitted with DR ingestion. Ribose and ATP production

Author: Zulkitaur

5 thoughts on “Ribose and ATP production

  1. Ich tue Abbitte, dass sich eingemischt hat... Ich finde mich dieser Frage zurecht. Geben Sie wir werden besprechen. Schreiben Sie hier oder in PM.

Leave a comment

Yours email will be published. Important fields a marked *

Design by ThemesDNA.com