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 LVO2 and HVO2 groups. The pertinent results indicate that DR ingestion improved performance and recovery for the LVO2 group during a multi-day exercise study, but not in the HVO2 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.  reported in subjects supplementing with oral DR around high-intensity, intermittent exercise showed that ATP synthesis increased and ATP levels return to normal after 72 h; however, this benefit was not found in the control group. A decrease in cellular high energy phosphates can affect muscular function besides producing symptoms of soreness and fatigue, which can affect subsequent exercise sessions . Studies have revealed mixed results in replenishing muscular energy levels, maintaining or enhancing performance and alleviating post-exercise symptoms with substrate supplementation .
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-ribose-1-pyrophosphate (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) . However, DR is unique in that it bypasses this rate limiting enzymatic step in the formation of PRPP . This enhanced production of ATP by DR replenishes the cellular energy deficiency and can shorten the energy recovery period following high intensity exercise. It is plausible that subjects in the present study’s HVO2 group, had well developed energy-producing systems that when stressed, were able to overcome the exercise stress through other various recovery processes. On the other hand, subjects in the LVO2 group may not have had the ability to fully utilize other pathways (i.e. 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.  reported that 220 g of DR supplementation (20 g/d) produced a significant increase in average power output during high intensity exercise. Berardi et al.  found that DR supplementation prior to exercise produced an increase in peak PO from 2.2 to 7% and increased their average PO from 2 to 10%. Van Gammerren et al.  reported that 280 g of DR supplementation (10 g/d) increased muscular power assessment in weight lifting increased muscular strength and total work performed in amateur bodybuilders. However, DR has not always demonstrated an improvement in performance. Eijnde et al.  found that the use of 16 g/d of DR during knee contraction exercise did not produce a benefit in PO nor in ATP synthesis in physically active subjects. Furthermore, Kreider et al.  reported that supplementing 10 g/day for 5 days of DR around exercise did not demonstrate a significant difference from control subjects when undergoing anaerobic exercise capacity test in trained subjects, as well as not reflecting an improvement in metabolic parameters.
The present study demonstrates that subject selection criterion (i.e. 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 LVO2 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 LVO2 group. This could indicate that there was a mechanism by which the cells were able to recover energy for the next day’s exercise and be able to continue to demonstrate at least an adequate level of performance in that 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 ; however, high intensity exercise is superior to low intensity exercise in upregulating the muscle to produce superoxide dismutase and GSH peroxidase . Seifert et al.  reported that DR ingestion led to significantly lower production of free radical markers compared to the control treatment during exercise under hypoxic conditions. 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.  reported that during exercise, two potentially harmful free radical sources are mitochondrial semiquinone and xanthine oxidase in the endothelial cells. 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 VO2 levels . Upon further assessment of our subjects in this study into LVO2 and HVO2 groups, revealed significant differences when consuming DR during the high intensity exercise sessions for the LVO2 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 LVO2 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.