Hyperoxia decreases muscle glycogenolysis, lactate production, and lactate efflux during steady-state exercise

Christopher G R Perry 1 | Julie Reid | By Wendy Perry | By Brian A Wilson

Medicine & Science in Sports & Exercise: July 2005 – Volume 37 – Issue 7 – p 1175-1179

The aim of this study was to determine whether the decreased muscle and blood lactate during exercise with hyperoxia (60% inspired O2) vs. room air is due to decreased muscle glycogenolysis, leading to decreased pyruvate and lactate production and efflux. We measured pyruvate oxidation via PDH, muscle pyruvate and lactate accumulation, and lactate and pyruvate efflux to estimate total pyruvate and lactate production during exercise. We hypothesized that 60% O2 would decrease muscle glycogenolysis, resulting in decreased pyruvate and lactate contents, leading to decreased muscle pyruvate and lactate release with no change in PDH activity. Seven active male subjects cycled for 40 min at 70% V̇o2 peak on two occasions when breathing 21 or 60% O2. Arterial and femoral venous blood samples and blood flow measurements were obtained throughout exercise, and muscle biopsies were taken at rest and after 10, 20, and 40 min of exercise. Hyperoxia had no effect on leg O2 delivery, O2 uptake, or RQ during exercise. Muscle glycogenolysis was reduced by 16% with hyperoxia (267 ± 19 vs. 317 ± 21 mmol/kg dry wt), translating into a significant, 15% reduction in total pyruvate production over the 40-min exercise period. Decreased pyruvate production during hyperoxia had no effect on PDH activity (pyruvate oxidation) but significantly decreased lactate accumulation (60%: 22.6 ± 6.4 vs. 21%: 31.3 ± 8.7 mmol/kg dry wt), lactate efflux, and total lactate production over 40 min of cycling. Decreased glycogenolysis in hyperoxia was related to an ∼44% lower epinephrine concentration and an attenuated accumulation of potent phosphorylase activators ADPf and AMPf during exercise. Greater phosphorylation potential during hyperoxia was related to a significantly diminished rate of PCr utilization. The tighter metabolic match between pyruvate production and oxidation resulted in a decrease in total lactate production and efflux over 40 min of exercise during hyperoxia.

ever since the classic work by Hill et. al. (20) and Margaria et. al (34), it has been well known that breathing hyperoxic air (∼60–100% O2) improves exercise performance and decreases steady-state exercise blood lactate concentrations compared with breathing room air (for review, see Ref. 54). Two studies (14, 51) have also reported lower muscle lactate accumulation during exercise lasting longer than 15 min with hyperoxia. These measurements suggest that lactate production and efflux are reduced during exercise under hyperoxic conditions, possibly because of a greater O2 availability and/or greater oxygen partial pressure than during room air breathing.

It has been proposed that the decreased blood lactate with hyperoxia may be due to decreased lactate production resulting from reduced glycogenolysis, glycolysis, and ultimately, a decreased pyruvate production and/or increased lactate clearance (1, 21). Indeed, we (51) recently examined the effect of hyperoxia on skeletal muscle carbohydrate metabolism and reported a ∼33% reduction in glycogen utilization over a 15-min cycling period. We concluded that decreased lactate production via decreased glycogenolysis and pyruvate production with no change in mitochondrial pyruvate oxidation [estimated from pyruvate dehydrogenase (PDH) activity] was the major determinant of the reduced muscle and blood lactate during hyperoxia. However, to clarify these issues it is necessary to measure the production of muscle pyruvate and lactate in normoxic and hyperoxic conditions by measuring muscle pyruvate and lactate accumulations, coupled with measures of pyruvate and lactate release across working muscles during steady-state exercise. Few studies in humans have examined the effects of hyperoxia using arterial and venous (a-v) blood sampling, coupled with blood flow measurements, across the working muscles in humans. These studies found that during whole body cycling (28) or knee extensor exercise (35, 38) there was no effect of hyperoxia on lactate release at either submaximal or peak work rates.

Therefore, the primary aim of this study was to determine whether the decreased muscle lactate accumulation during exercise with hyperoxia is due to decreased muscle glycogenolysis and/or decreased lactate production. We also examined whether a decreased lactate efflux contributed to the lower blood lactate concentration reported during exercise when a hyperoxic gas was breathed. We accomplished this by measuring muscle glycogenolysis, leading to the quantification of the five fates of pyruvate: 1) pyruvate accumulation, 2) pyruvate oxidation [PDH activity (PDHa)], 3) reduction to muscle lactate, 4) lactate efflux, and 5) pyruvate efflux, to estimate total pyruvate and lactate production during 40 min of steady-state cycling at 70% V̇o2 peak when subjects breathed either 21 or 60% O2. We hypothesized that hyperoxia would decrease muscle glycogenolysis, resulting in decreased muscle pyruvate and lactate production and decreased muscle pyruvate and lactate release, with no change in pyruvate oxidation via PDH.


Studies Design

Seven active male subjects volunteered to participate in this study. None were taking medications and all engaged in recreational endurance training no more than five times per week. Their mean (±SE) age, height, weight, and V̇o2 peak were 22.3 ± 1.2 yr, 180 ± 5 cm, 76.1 ± 4.3 kg, and 52.8 ± 3.0 ml·kg−1·min−1, respectively. The experimental protocol and associated risks were explained both orally and in writing to all subjects before written consent was obtained. The ethics committees of the University of Guelph and McMaster University approved the study.


Preexperimental Protocol

Subjects initially performed a continuous, incremental cycling test to exhaustion to determine peak pulmonary oxygen uptake (V̇o2 peak, Quinton Q-plex 1; Quiton Instruments, Seattle, WA) on a cycle ergometer (Lode Instrument, Groningen, The Netherlands). After the V̇o2 peak test, subjects visited the laboratory on three occasions, once for a practice ride and two visits for the experimental protocol. Daily food records were conducted over a 48-h period, and subjects ate the same diet before all experimental trials. In the 24 h before all visits, subjects abstained from intense physical activity and caffeine consumption. Subjects visited the laboratory in the fed state (2–4 h after a standardized meal) for all visits. All subjects underwent a full practice trial, which required them to breathe through a mouthpiece for 20 min at rest and during 40 min of cycling. The practice trial familiarized the subjects with the experimental protocol and breathing through the mouthpiece and confirmed the ∼70% V̇o2 peak power output. The mean (±SE) absolute power output for the trials was 190 ± 18 W, and the relative power output was 72.4 ± 1.9% of V̇o2 peak. Due to the limitations of indirect calorimetry during hyperoxia, V̇o2 and CO2 production (V̇co2) were not assessed during the experimental trials. However, on average the VO2, V̇co2, respiratory exchange ratio (RER), and ventilation during the 40-min normoxic practice ride were 2.90 ± 0.20, 2.71 ± 0.16, 0.93 ± 0.02, and 80.8 ± 5.8 l/min, respectively.


Experimental Protocol

The two experimental trials consisted of 40 min of cycling at 70% V̇o2 peak when subjects breathed either 21 or 60% inspired O2 and were conducted at least 2 wk apart. The trials were randomized and the subjects blinded to the inspired O2 concentration. Before exercise, the radial artery was catheterized percutaneously with a Teflon catheter (20 gauge, 3.2 cm; Baxter, Irvine, CA) after local anesthesia with 0.5 ml of 2% lidocaine, without epinephrine, as previously described (6). The femoral vein was catheterized percutaneously (Thermodilution catheter, model no. 93-135-6F; Baxter) with the use of the Seldinger technique after administration of 3–4 ml of lidocaine (6). Catheters were maintained patent with nonheparinized isotonic saline. A resting (−20 min) arterial blood sample (∼9 ml) was then taken. Leg blood flow was also determined at rest using the thermodilution method, as previously described (3). Specifically, ∼10 ml of nonheparinized saline were injected into the venous catheter, and leg blood flow was determined from the change in temperature as a function of time by use of a portable cardiac output monitor (Spacelab, Redmond, WA). At least three measurements were recorded at each time point and averaged. One leg was then prepared for muscle biopsy sampling; four incisions were made over the vastus lateralis muscle under local anaesthesia (2% lidocaine, no epinephrine).

The subjects then breathed 21 or 60% O2, balance N2, through a mouthpiece for 20 min at rest in the seated position. Inspired gases were automatically mixed, analyzed for proper O2 concentration, and stored in a 150-L tissot spirometer. Immediately before exercise, a resting (0 min) arterial blood sample was drawn, and a resting biopsy was taken, with subjects on the bed, and instantly frozen in liquid N2 for later analysis. Subjects then moved to the cycle ergometer and commenced cycling for 40 min at a power output to elicit ∼70% V̇o2 peak. Another arterial blood sample was drawn 5 min into exercise, and then both arterial and femoral venous blood samples, combined with leg blood flow measurements, were taken at 10, 20, 30, and 40 min during exercise. Additional muscle samples were taken after 10, 20, and 40 min of cycling and immediately frozen in liquid N2. Less than 40 s elapsed between cessation of exercise, the obtaining of the muscle biopsy, and recommencement of cycling.


Muscle Analyses

A small piece of frozen wet muscle (∼10–15 mg) was removed under liquid N2 for the determination of PDH activity, as described previously (41). The remainder of the muscle sample was freeze-dried, dissected free of visible blood and connective tissue, and powdered for metabolite and glycogen analyses. An aliquot of freeze-dried muscle (∼10–12 mg) was extracted with 0.5 M perchloric acid (HClO4) containing 1 mM EDTA and neutralized with 2.2 M KHCO3. The supernatant was used for the determination of creatine (Cr), phosphocreatine (PCr), ATP, and lactate by enzymatic spectrophotometric assays (5) and acetyl-CoA and acetylcarnitine with radiometric measurements (7). Pyruvate and citrate were analyzed fluorometrically (36). Muscle glycogen content was determined from a second aliquot of freeze-dried muscle (∼4–6 mg) from the resting (0 min) and 40-min biopsy samples. All muscle measurements were normalized to the highest total Cr content measured among the 8 biopsies from each subject.


Blood Sampling and Analysis

Two separate arterial and venous blood samples were drawn at each time point into heparinized plastic syringes and placed on ice. One portion of the first sample was deproteinized in a 1-to-5 ratio with 0.6% PCA (wt/vol). This supernatant was stored at −80°C and analyzed for glucose and lactate (5). A second portion of blood was immediately centrifuged, and 400 μl of plasma were added to 100 μl of NaCl and incubated at 56°C for 30 min to inactivate lipoprotein lipase activity. The plasma was stored at −80°C and analyzed for free fatty acids (FFA) with a colorometric assay (Wako NEFA C test kit; Wako Chemicals, Richmond, VA). A third portion of blood (1.5 ml) was added to 30 μl of EGTA-GSH, mixed thoroughly, and centrifuged. The supernatant was stored at −80°C and subsequently analyzed for plasma epinephrine by radioimmunoassay (Epinephrine RIA; Labor Diagnostika Nord, Nordhorn, Germany). The second arterial and venous sample drawn at each time point was analyzed for Po2, Pco2, pH, and hematocrit via the GEM Premier 3000 blood gas analyzer (Instrumentation Laboratory, Richmond Hill, ON, Canada) and O2 saturation and hemoglobin (Hb) concentration (OSM3 Hemoximeter; Radiometer, Copenhagen, Denmark).

FIGURE 1—Gas delivery system through which subjects inspired either hyperoxia or normoxia during the work intervals.

For normoxic trainers, room air was inspired by setting the two-way valve open directly to room air, whereas for hyperoxic trainers the valve was open to the reservoir bags containing the humidified hyperoxic gas mixture. There were several ways in which subjects were blind to the gas they were inspiring. First, subjects were unable to see at which opening the two-way valve was set. In addition, the humidification of the hyperoxic air made it feel similar to inspiring room air. Also, each bag could supply one subject, allowing for two athletes to ride at the same time. This made it difficult for subjects to tell whether they were inspiring from the bags or from room air.


Results are expressed as mean ± standard error of the mean (SEM). All trial comparisons were tested with a two-way, repeated measures ANOVA. If a significant F-ratio was obtained, a Student–Newman–Keuls post hoc test was used to analyze the difference between treatments. The level of significance was established at P < 0.05 for all statistics.


Hyperoxia allowed subjects to train throughout the 6-wk program at a power output that was 8.1 ± 0.5% greater than the work rate in normoxia (Fig. 2). This equates to a mean difference of 18 ± 1.3 W. Both groups trained at 92% of their HRmax. Both groups also increased their training power output throughout the 6-wk sessions.

FIGURE 2—Progression of training intensity over 6 wk. Hyperoxic training power outputs were on average 8.1% greater than those achieved in normoxic conditions across the entire 6 wk of training

Both H and N training improved performance time to exhaustion at 90% O2max, with the H condition demonstrating a significantly superior improvement over N (Fig. 3). Hyperoxic trainers improved from 5.1 ± 0.4 min to 11.1 ± 1.4 min (mean increase of 117%), whereas training in normoxia improved the time from 5.6 ± 0.6 min to 8.5 ± 1.1 min (mean increase of 50%). No statistically significant difference existed between the two pretraining trials, suggesting that subjects had successfully detrained between the two 6-wk sessions.

FIGURE 3—Performance time to exhaustion for hyperoxic and normoxic training at 90%* indicates significant difference between pre- and posttraining performance time. # indicates significant difference between the performance improvements for hyperoxia vs normoxia. There was no significant difference between the two pretraining trials.

FIGURE 4—Pre- and posttraining JOURNAL/mespex/04.02/00005768-200507000-00014/root/v/2017-07-20T223005Z/r/text-xmlO2max data for hyperoxic and normoxic conditions. *indicates significant increases in posttraining values for both hyperoxia and normoxia. Hyperoxia increased by 8.3% (± 3.4), whereas normoxia increased by 6.0% (± 3.7). There was no significant difference between improvement in both training conditions.

Steady-state HR during the 8-min ride at 80% O2max was lower posttraining for both H and N conditions (Fig. 6). In normoxia, steady-state HR improved from 172 ± 4 bpm to 163 ± 4 bpm (mean decrease of 9 ± 2 bpm), whereas in hyperoxia the change was from 169 ± 5 bpm to 162 ± 5 bpm (mean decrease of 7 ± 2 bpm). There was no significant difference between the H and N improvements. Steady-state E showed a similar response, in that both groups showed a comparable posttraining drop in E (Fig. 7). Steady-state E changed from 104.9 ± 6.2 L·min−1 to 91.2 ± 5.8 L·min−1 (mean decrease of 13.7 ± 2.7 L·min−1) for N training, and from the change was from 96.7 ± 4.4 L·min−1 to 86 ± 3.6 L·min−1 (mean decrease of 10.7 ± 4.0 L·min−1) for H training.

FIGURE 5—JOURNAL/mespex/04.02/00005768-200507000-00014/root/v/2017-07-20T223005Z/r/text-xmlEmax during JOURNAL/mespex/04.02/00005768-200507000-00014/root/v/2017-07-20T223005Z/r/text-xmlO2max test pre- and posttraining for hyperoxic and normoxic conditions. There was no significant improvement for either training condition.

Steady-state HR during the 8-min ride at 80% O2max was lower posttraining for both H and N conditions (Fig. 6). In normoxia, steady-state HR improved from 172 ± 4 bpm to 163 ± 4 bpm (mean decrease of 9 ± 2 bpm), whereas in hyperoxia the change was from 169 ± 5 bpm to 162 ± 5 bpm (mean decrease of 7 ± 2 bpm). There was no significant difference between the H and N improvements. Steady-state E showed a similar response, in that both groups showed a comparable posttraining drop in E (Fig. 7). Steady-state E changed from 104.9 ± 6.2 L·min−1 to 91.2 ± 5.8 L·min−1 (mean decrease of 13.7 ± 2.7 L·min−1) for N training, and from the change was from 96.7 ± 4.4 L·min−1 to 86 ± 3.6 L·min−1 (mean decrease of 10.7 ± 4.0 L·min−1) for H training.

FIGURE 6—Heart rate during steady-state work at 80% JOURNAL/mespex/04.02/00005768-200507000-00014/root/v/2017-07-20T223005Z/r/text-xmlO2max pre- and posttraining for hyperoxic and normoxic conditions. * indicates a significant decrease in heart rate for both training conditions. There were no significant differences posttraining between both conditions.

FIGURE 7—Ventilation during steady-state tests at 80% JOURNAL/mespex/04.02/00005768-200507000-00014/root/v/2017-07-20T223005Z/r/text-xmlO2max pre- and posttraining for hyperoxic and normoxic conditions. * indicates significant decreases in JOURNAL/mespex/04.02/00005768-200507000-00014/root/v/2017-07-20T223005Z/r/text-xmlE posttraining for both conditions. There was no significant difference between the decrease in JOURNAL/mespex/04.02/00005768-200507000-00014/root/v/2017-07-20T223005Z/r/text-xmlE observed in both conditions.


It has been observed repeatedly that hyperoxia enhances exercise performance (1,2,9,14,15,18). The present study has demonstrated that this effect can be carried through a training regimen for at least 6 wk in duration. Subjects were, in fact, able to select and train at a power output that was 8.1% higher when exercising in hyperoxia as compared with normoxia for the same training HR. This would suggest that subjects could reach a training intensity in hyperoxia that was unattainable under normoxic conditions. The exact mechanism that allows for this increased power output during hyperoxia is not completely understood. However, the increased O2max, lower lactate, and RPE reported under hyperoxic conditions may play a significant role (1,4,14,15).

The intensity and duration of the 6-wk training protocol was sufficient to bring about improvements in O2max and performance for both hyperoxic and normoxic trainers. Hyperoxic training improved performance to a greater extent than normoxic training. There was also a trend for a greater increase in O2max after hyperoxic training, but this difference was not significant. Because the power outputs used in the posttraining time trials were the same absolute intensity used in the pretraining time trials (i.e., 90% of pretraining O2max), the increase in O2max observed after training in both conditions means that this power output was now less than 90% of the posttraining O2max. Although the mean improvements in O2max were not statistically different between training conditions, the power output used for the time trial was still a smaller proportion of the posttraining O2max after training in hyperoxia (83.1% O2max) as compared with after training in normoxia (84.9% O2max). Ploutz-Snyder et al. (10) also observed that hyperoxic training did not improve O2max significantly more than normoxic training. However, the power outputs maintained throughout training in their study differed from the present study. The present study had subjects train at 92% of their HRmax for 1 h·d−1, 3× wk−1 for 6 wk using interval training (4 min on, 2 min off). The study by Ploutz-Snyder et al. (10) trained subjects for 40 min·d−1 (no intervals) at 70% of their normoxic or hyperoxic O2max, 5 d·wk−1 for 5 wk. However, neither hyperoxic training regimens elicited a significantly greater improvement in O2max.

The mechanism for the larger increase in performance with hyperoxic training is unclear. The present study found no significant difference in the improvements in O2max between both training conditions. Furthermore, we did not show significant differences in the responses of submax HR and VE at 80% O2max for both hyperoxic and normoxic training. These data do not provide any evidence for a greater training effect of hyperoxia versus normoxia for submax HR or VE, suggesting other central or peripheral factors may play a role in the maximum performance improvement seen for hyperoxic trainers. This suggests that peripheral changes due to the training overload at the muscle may be responsible for the training advantage seen for hyperoxia. Direct measurements of muscle adaptations to the N and H training will be necessary to test this hypothesis. The ability to sustain higher training workloads under hyperoxia may be due to an increase in intracellular PO2 (12,13) and muscle O2 (6,16).

With regard to the validity of the performance test, some studies have suggested that using time to exhaustion as a performance criterion is less valid then performing a given amount of work in the shortest period of time possible. Jeukendrup et al. (5) found that time to exhaustion had a coefficient of variation of 26.6%, whereas a time trial protocol had 3.35%. However, this should not play a significant role in the present study as the mean improvement in performance time to exhaustion was approximately 117%, which far exceeded the increase of 50% for normoxic trainers.

The training protocol in the present study could be considered an extension of the LHTL model being a “live low train even lower” design. Of course, the trainers in this model would not receive any of the beneficial effects of live high trainers such as increased erythrocyte volume but should show similar responses to the train low subjects. The present study demonstrates that the LHTL model may be extended to a “live high train very low” model (LHTVL) with hyperoxic breathing. Our data show that training under hyperoxic conditions can augment both O2max and high-intensity performance. Although the exact physiological mechanisms for this response are unclear, it does appear to be related to the increased training intensity found during hyperoxic conditions. This may prove to be an important technique for increasing training load in elite athletes where plateaus in training intensity are often found.


1. Adams, R. P., and H. G. Welch. Oxygen uptake, acid-base status, and performance with varied inspired O2 fractions. J.Appl. Physiol. 49:863–868, 1980. | Cited Here

2. Adams, R. P., P. A. Cashman, and J. C. Young. Effect of hyperoxia on substrate utilization during intense submaximal exercise. J. Appl. Physiol. 61:523–529, 1986. | Cited Here

3. Ekblom, B., R. Huot, E. M. Stein, and A. T. Thorstensson. Effect of changes in arterial oxygen content on circulation and physical performance. J. Appl. Physiol. 39:71–75, 1975.| Cited Here

4. Graham, T. E., P. K. Pedersen, and B. Saltin. Muscle and blood ammonia and lactate responses to prolonged exercise with hyperoxia. J. Appl. Physiol. 63:1457–1462, 1987. | Cited Here

5. Jeukendrup, A., W. H. M. Saris, F. Brouns, and A. D. M. Kester. A new validated endurance performance test. Med. Sci. Sports Exerc. 28:266–270, 1996. | Cited Here | View Full Text | PubMed | CrossRef

6. Knight, D. R., W. Schaffartzik, D. C. Poole, M. C. Hogan, D. E. Bebout, and P. D. Wagner. Effects of hyperoxia on maximal leg O2 supply and utilization in men. J. Appl. Physiol. 75:2586–2594, 1993. | Cited Here | PubMed

7. Levine, B. D. Intermittent hypoxic training: fact or fancy. High Alt. Med. Biol. 3:177–193, 2002. | Cited Here | PubMed | CrossRef

8. Morris, D. M., J. T. Kearney, and E. R. Burke. The effects of breathing supplemental oxygen during altitude training on cycling performance. J. Sci. Med. Sport 3:165–175, 2000. | Cited Here | PubMed | CrossRef

9. Plet, J., P. K. Pedersen, F. B. Jensen, and J. K. Hansen. Increased working capacity with hyperoxia in humans. Eur. J. Appl. Physiol. 65:171–177, 1992. | Cited Here |PubMed | CrossRef

10. Ploutz-Snyder, L. L., J. A. Simoneu, R. M. Gilders, R. S. Staron, and F. C. Hagerman. Cardiorespiratory and metabolic adaptations to hyperoxic training. Eur. J. Appl. Physiol. 73:38–48, 1996. | Cited Here | PubMed | CrossRef

11. Randall, L. W., P. L. Holm, D. M. Morris, G. M. Dallam, and S. D. Callan. Effect of FIO2 on physiological responses and cycling performance at moderate altitude. Med. Sci. Sports Exerc. 35:1153–1159, 2003. | Cited Here | View Full Text | PubMed | CrossRef

12. Richardson, R. S., B. Grassi, T. P. Gavin, et al. Evidence of O2 supply-dependent O2max in the exercise-trained human quadriceps. J. Appl. Physiol. 86: 1048–1053, 1999. | Cited Here | PubMed

13. Richardson, R. S., J. S. Leigh, P. D. Wagner, and E. A. Noyszewski. Cellular PO2 as a determinant of maximal mitochondrial O(2) consumption in trained human skeletal muscle. J. Appl. Physiol. 87:325–331, 1999. | Cited Here | PubMed

14. Welch, H. G. Hyperoxia and human performance: a brief review. Med. Sci. Sports Exerc. 14:253–262, 1982. | Cited Here | View Full Text | PubMed | CrossRef

15. Welch, H. G., and P. K. Petersen. Measurement of metabolic rate in hyperoxia. J. Appl. Physiol. 51:725–731, 1981. | Cited Here | PubMed

16. Wilson, B. A., and W. N. Stainsby. Effects of O2 breathing on RQ, blood flow, and developed tension in situ dog muscle. Med. Sci. Sports. 10:167–170, 1978. | Cited Here | PubMed

17. Wilson, B. A., H. G. Welch, and J. N. Liles. Effects of hyperoxic gas mixtures on energy metabolism during prolonged work. J. Appl. Physiol. 39:267–271, 1975. | Cited Here | PubMed

18. Wilson, G. D., and H. G. Welch. Effects of hyperoxic gas mixtures on exercise tolerance in man. Med. Sci. Sports 7: 48–52, 1975. | Cited Here | View Full Text | PubMed


Up your game, gain that extra edge and crush your workouts like never before. Hypermax Oxygen is the ultimate game changer for athletes ready to take control of their body’s oxygen levels and achieve a higher level of performance.


If your training program needs that extra push to boost revenue and help your clients achieve their fitness goals, HyperMax Oxygen sessions could provide that big break you’ve been waiting for.


Ready for a renewed buzz and record memberships at your gym? Get started today by adding a few HyperMax Oxygen Sport Systems to your facility. Special pricing available on orders of multiple systems.


As all good coaches know—champions are made in the off-season. Jumpstart your workouts by adding HyperMax Oxygen to your practices and give your players that extra advantage on game day.

Harness the power of Oxygen.

Oxygen heals & energizes, improves mental performance, strengthens the physical body and stimulates your sex drive. In scientific studies, test subjects improved their memory an average of 20%, and reaction times in certain activities an average of 15%. And the HyperMax Oxygen Health and Fitness System is certified for 93% oxygen purity, so you know what you’re getting with every breath.

Holistic Science

Human cells need oxygen above all else to survive and thrive. Better oxygen means a better mind and a better body. That’s what HyperMax Oxygen is all about. 300% more oxygen purity than you’re breathing right now.

Early Adopters

The use of oxygen for health and fitness isn’t new, but HyperMax certainly is. Our revolutionary approach to exercising with oxygen is at a breakthrough technological level, awaiting health-minded pioneers who love to be first.


The top building block in the body is oxygen. No matter how you map your personal eco-system, all roads connect with oxygen. HyperMax is the superhighway to better wellness. It delivers three times more oxygen purity than you’re breathing right this minute.