scholarly journals Effect of Waters Enriched in O2 by Injection or Electrolysis on Performance and the Cardiopulmonary and Acid–Base Response to High Intensity Exercise

Nutrients ◽  
2021 ◽  
Vol 13 (12) ◽  
pp. 4320
Author(s):  
Frédéric N. Daussin ◽  
François Péronnet ◽  
Antoine Charton ◽  
Evelyne Lonsdorfer ◽  
Stéphane Doutreleau ◽  
...  

Several brands of water enriched with O2 (O2-waters) are commercially available and are advertised as wellness and fitness waters with claims of physiological and psychological benefits, including improvement in exercise performance. However, these claims are based, at best, on anecdotal evidence or on a limited number of unreliable studies. The purpose of this double-blind randomized study was to compare the effect of two O2-waters (~110 mg O2·L−1) and a placebo (10 mg O2·L−1, i.e., close to the value at sea level, 9–12 mg O2·L−1) on the cardiopulmonary responses and on performance during high-intensity exercise. One of the two O2-waters and the placebo were prepared by injection of O2. The other O2-water was enriched by an electrolytic process. Twenty male subjects were randomly allocated to drink one of the three waters in a crossover study (2 L·day−1 × 2 days and 15 mL·kg−1 90 min before exercise). During each exercise trial, the subjects exercised at 95.9 ± 4.7% of maximal workload to volitional fatigue. Exercise time to exhaustion and the cardiopulmonary responses, arterial lactate concentration and pH were measured. Oxidative damage to proteins, lipids and DNA in blood was assessed at rest before exercise. Time to exhaustion (one-way ANOVA) and the responses to exercise (two-way ANOVA [Time; Waters] with repeated measurements) were not significantly different among the three waters. There was only a trend (p = 0.060) for a reduction in the time constant of the rapid component of VO2 kinetics with the water enriched in O2 by electrolysis. No difference in oxidative damage in blood was observed between the three waters. These results suggest that O2-water does not speed up cardiopulmonary response to exercise, does not increase performance and does not trigger oxidative stress measured at rest.

2020 ◽  
Vol 15 (5) ◽  
pp. 741-747 ◽  
Author(s):  
Anna E. Voskamp ◽  
Senna van den Bos ◽  
Carl Foster ◽  
Jos J. de Koning ◽  
Dionne A. Noordhof

Background: Gross efficiency (GE) declines during high-intensity exercise. Increasing extracellular buffer capacity might diminish the decline in GE and thereby improve performance. Purpose: To examine if sodium bicarbonate (NaHCO3) supplementation diminishes the decline in GE during a 2000-m cycling time trial. Methods: Sixteen male cyclists and 16 female cyclists completed 4 testing sessions including a maximal incremental test, a familiarization trial, and two 2000-m GE tests. The 2000-m GE tests were performed after ingestion of either NaHCO3 supplements (0.3 g/kg body mass) or placebo supplements (amylum solani, magnesium stearate, and sunflower oil capsules). The GE tests were conducted using a double-blind, randomized, crossover design. Power output, gas exchange, and time to complete the 2000-m time trials were recorded. Capillary blood samples were analyzed for blood bicarbonate, pH, and lactate concentration. Data were analyzed using magnitude-based inference. Results: The decrement in GE found after the 2000-m time trial was possibly smaller in the male and female groups after NaHCO3 than with placebo ingestion, with the effect in both groups combined being unclear. The effect on performance was likely trivial for males (placebo 164.2 [5.0] s, NaHCO3 164.3 [5.0] s; Δ0.1; ±0.6%), unclear for females (placebo 178.6 [4.8] s, NaHCO3 178.0 [4.3] s; Δ−0.3; ±0.5%), and very likely trivial when effects were combined. Blood bicarbonate, pH, and lactate concentration were substantially elevated from rest to pretest after NaHCO3 ingestion. Conclusions: NaHCO3 supplementation results in an unclear effect on the decrease in GE during high-intensity exercise and in a very likely trivial effect on performance.


2010 ◽  
Vol 109 (1) ◽  
pp. 135-148 ◽  
Author(s):  
Stephen J. Bailey ◽  
Jonathan Fulford ◽  
Anni Vanhatalo ◽  
Paul G. Winyard ◽  
Jamie R. Blackwell ◽  
...  

The purpose of this study was to elucidate the mechanistic bases for the reported reduction in the O2cost of exercise following short-term dietary nitrate (NO3−) supplementation. In a randomized, double-blind, crossover study, seven men (aged 19–38 yr) consumed 500 ml/day of either nitrate-rich beetroot juice (BR, 5.1 mmol of NO3−/day) or placebo (PL, with negligible nitrate content) for 6 consecutive days, and completed a series of low-intensity and high-intensity “step” exercise tests on the last 3 days for the determination of the muscle metabolic (using31P-MRS) and pulmonary oxygen uptake (V̇o2) responses to exercise. On days 4–6, BR resulted in a significant increase in plasma [nitrite] (mean ± SE, PL 231 ± 76 vs. BR 547 ± 55 nM; P < 0.05). During low-intensity exercise, BR attenuated the reduction in muscle phosphocreatine concentration ([PCr]; PL 8.1 ± 1.2 vs. BR 5.2 ± 0.8 mM; P < 0.05) and the increase in V̇o2(PL 484 ± 41 vs. BR 362 ± 30 ml/min; P < 0.05). During high-intensity exercise, BR reduced the amplitudes of the [PCr] (PL 3.9 ± 1.1 vs. BR 1.6 ± 0.7 mM; P < 0.05) and V̇o2(PL 209 ± 30 vs. BR 100 ± 26 ml/min; P < 0.05) slow components and improved time to exhaustion (PL 586 ± 80 vs. BR 734 ± 109 s; P < 0.01). The total ATP turnover rate was estimated to be less for both low-intensity (PL 296 ± 58 vs. BR 192 ± 38 μM/s; P < 0.05) and high-intensity (PL 607 ± 65 vs. BR 436 ± 43 μM/s; P < 0.05) exercise. Thus the reduced O2cost of exercise following dietary NO3−supplementation appears to be due to a reduced ATP cost of muscle force production. The reduced muscle metabolic perturbation with NO3−supplementation allowed high-intensity exercise to be tolerated for a greater period of time.


2007 ◽  
Vol 293 (1) ◽  
pp. R392-R401 ◽  
Author(s):  
Andrew M. Jones ◽  
Daryl P. Wilkerson ◽  
Nicolas J. Berger ◽  
Jonathan Fulford

We hypothesized that a period of endurance training would result in a speeding of muscle phosphocreatine concentration ([PCr]) kinetics over the fundamental phase of the response and a reduction in the amplitude of the [PCr] slow component during high-intensity exercise. Six male subjects (age 26 ± 5 yr) completed 5 wk of single-legged knee-extension exercise training with the alternate leg serving as a control. Before and after the intervention period, the subjects completed incremental and high-intensity step exercise tests of 6-min duration with both legs separately inside the bore of a whole-body magnetic resonance spectrometer. The time-to-exhaustion during incremental exercise was not changed in the control leg [preintervention group (PRE): 19.4 ± 2.3 min vs. postintervention group (POST): 19.4 ± 1.9 min] but was significantly increased in the trained leg (PRE: 19.6 ± 1.6 min vs. POST: 22.0 ± 2.2 min; P < 0.05). During step exercise, there were no significant changes in the control leg, but end-exercise pH and [PCr] were higher after vs. before training. The time constant for the [PCr] kinetics over the fundamental exponential region of the response was not significantly altered in either the control leg (PRE: 40 ± 13 s vs. POST: 43 ± 10 s) or the trained leg (PRE: 38 ± 8 s vs. POST: 40 ± 12 s). However, the amplitude of the [PCr] slow component was significantly reduced in the trained leg (PRE: 15 ± 7 vs. POST: 7 ± 7% change in [PCr]; P < 0.05) with there being no change in the control leg (PRE: 13 ± 8 vs. POST: 12 ± 10% change in [PCr]). The attenuation of the [PCr] slow component might be mechanistically linked with enhanced exercise tolerance following endurance training.


2021 ◽  
Vol 12 ◽  
Author(s):  
Jonghyuk Park ◽  
Jimmy Kim ◽  
Toshio Mikami

Regular exercise training induces mitochondrial biogenesis in the brain via activation of peroxisome proliferator-activated receptor gamma-coactivator 1α (PGC-1α). However, it remains unclear whether a single bout of exercise would increase mitochondrial biogenesis in the brain. Therefore, we first investigated whether mitochondrial biogenesis in the hippocampus is affected by a single bout of exercise in mice. A single bout of high-intensity exercise, but not low- or moderate-intensity, increased hippocampal PGC-1α mRNA and mitochondrial DNA (mtDNA) copy number at 12 and 48h. These results depended on exercise intensity, and blood lactate levels observed immediately after exercise. As lactate induces mitochondrial biogenesis in the brain, we examined the effects of acute lactate administration on blood and hippocampal extracellular lactate concentration by in vivo microdialysis. Intraperitoneal (I.P.) lactate injection increased hippocampal extracellular lactate concentration to the same as blood lactate level, promoting PGC-1α mRNA expression in the hippocampus. However, this was suppressed by administering UK5099, a lactate transporter inhibitor, before lactate injection. I.P. UK5099 administration did not affect running performance and blood lactate concentration immediately after exercise but attenuated exercise-induced hippocampal PGC-1α mRNA and mtDNA copy number. In addition, hippocampal monocarboxylate transporters (MCT)1, MCT2, and brain-derived neurotrophic factor (BDNF) mRNA expression, except MCT4, also increased after high-intensity exercise, which was abolished by UK5099 administration. Further, injection of 1,4-dideoxy-1,4-imino-D-arabinitol (glycogen phosphorylase inhibitor) into the hippocampus before high-intensity exercise suppressed glycogen consumption during exercise, but hippocampal lactate, PGC-1α, MCT1, and MCT2 mRNA concentrations were not altered after exercise. These results indicate that the increased blood lactate released from skeletal muscle may induce hippocampal mitochondrial biogenesis and BDNF expression by inducing MCT expression in mice, especially during short-term high-intensity exercise. Thus, a single bout of exercise above the lactate threshold could provide an effective strategy for increasing mitochondrial biogenesis in the hippocampus.


2003 ◽  
Vol 94 (6) ◽  
pp. 2135-2144 ◽  
Author(s):  
Murli Manohar ◽  
Thomas E. Goetz ◽  
Aslam S. Hassan

It is reported that preexercise hyperhydration caused arterial O2 tension of horses performing submaximal exercise to decrease further by 15 Torr (Sosa-Leon L, Hodgson DR, Evans DL, Ray SP, Carlson GP, and Rose RJ. Equine Vet J Suppl 34: 425–429, 2002). Because hydration status is important to optimal athletic performance and thermoregulation during exercise, the present study examined whether preexercise induction of hypervolemia would similarly accentuate the arterial hypoxemia in Thoroughbreds performing short-term high-intensity exercise. Two sets of experiments (namely, control and hypervolemia studies) were carried out on seven healthy, exercise-trained Thoroughbred horses in random order, 7 days apart. In resting horses, an 18.0 ± 1.8% increase in plasma volume was induced with NaCl (0.30–0.45 g/kg dissolved in 1,500 ml H2O) administered via a nasogastric tube, 285–290 min preexercise. Blood-gas and pH measurements as well as concentrations of plasma protein, hemoglobin, and blood lactate were determined at rest and during incremental exercise leading to maximal exertion (14 m/s on a 3.5% uphill grade) that induced pulmonary hemorrhage in all horses in both treatments. In both treatments, significant arterial hypoxemia, desaturation of hemoglobin, hypercapnia, acidosis, and hyperthermia developed during maximal exercise, but statistically significant differences between treatments were not found. Thus preexercise 18% expansion of plasma volume failed to significantly affect the development and/or severity of arterial hypoxemia in Thoroughbreds performing maximal exercise. Although blood lactate concentration and arterial pH were unaffected, hemodilution caused in this manner resulted in a significant ( P < 0.01) attenuation of the exercise-induced expansion of the arterial-to-mixed venous blood O2 content gradient.


1996 ◽  
Vol 81 (6) ◽  
pp. 2611-2617 ◽  
Author(s):  
Hunter Gillies ◽  
Wayne E. Derman ◽  
Timothy D. Noakes ◽  
Peter Smith ◽  
Alicia Evans ◽  
...  

Gillies, Hunter, Wayne E. Derman, Timothy D. Noakes, Peter Smith, Alicia Evans, and Gary Gabriels.Pseudoephedrine is without ergogenic effects during prolonged exercise. J. Appl. Physiol. 81(6): 2611–2617, 1996.—This study was designed to measure whether a single dose of 120 mg pseudoephedrine ingested 120 min before exercise influences performance during 1 h of high-intensity exercise. The effects of exercise on urinary excretion of the drug were also studied. Ten healthy male cyclists were tested on two occasions, separated by at least 7 days, by using a randomly assigned, double-blind, placebo-controlled, crossover design. Exercise performance was tested during a 40-km trial on a laboratory cycle ergometer, and skeletal muscle function was measured during isometric contractions. On a third occasion, subjects ingested 120 mg pseudoephedrine but did not exercise [control (C)]. Pseudoephedrine did not influence either time trial performance [drug (D) vs. placebo: 58.1 ± 1.4 (SE) vs. 58.7 ± 1.5 min] or isometric muscle function. Urinary pseudoephedrine concentrations were significantly increased 1 h after exercise (D vs. C: 114.3 ± 27.2 vs. 35.4 ± 13.1 μg/ml; P < 0.05). Peak plasma pseudoephedrine concentrations ( P < 0.05) but not time taken to reach peak plasma concentrations or the area under the plasma pseudoephedrine concentration vs. time curve was significantly increased in the total group with exercise (D vs. C). In three subjects, plasma pseudoephedrine concentrations were not influenced by exercise. Only these subjects showed increased urinary pseudoephedrine excretion during exercise. We conclude that a single therapeutic dose of pseudoephedrine did not have a measurable ergogenic effect during high-intensity exercise of 1-h duration, but plasma drug concentrations and urinary excretion were altered by exercise. These findings have practical relevance to doping control regulations in international sporting competitions.


Author(s):  
Lukas Beis ◽  
Yaser Mohammad ◽  
Chris Easton ◽  
Yannis P. Pitsiladis

Oral supplementation with glycine-arginine-α-ketoisocaproic acid (GAKIC) has previously been shown to improve exhaustive high-intensity exercise performance. There are no controlled studies involving GAKIC supplementation in well-trained subjects. The aim of the current study was to examine the effects of GAKIC supplementation on fatigue during high-intensity, repeated cycle sprints in trained cyclists. After at least 2 familiarization trials, 10 well-trained male cyclists completed 2 supramaximal sprint tests each involving 10 sprints of 10 s separated by 50-s rest intervals on an electrically braked cycle ergometer. Subjects ingested 11.2 g of GAKIC or placebo (Pl) during a period of 45 min before the 2 experimental trials, administered in a randomized and double-blind fashion. Peak power declined from the 1st sprint (M ± SD; Pl 1,332 ± 307 W, GAKIC 1,367 ± 342 W) to the 10th sprint (Pl 1,091 ± 229 W, GAKIC 1,061 ± 272 W) and did not differ between conditions (p = .88). Mean power declined from the 1st sprint (Pl 892 ± 151 W, GAKIC 892 ± 153 W) to the 10th sprint (Pl 766 ± 120 W, GAKIC 752 ± 138 W) and did not differ between conditions (p = .96). The fatigue index remained at ~38% throughout the series of sprints and did not differ between conditions (p = .99). Heart rate and ratings of perceived exertion increased from the 1st sprint to the 10th sprint and did not differ between conditions (p = .11 and p = .83, respectively). In contrast to previous studies in untrained individuals, these results suggest that GAKIC has no ergogenic effect on repeated bouts of high-intensity exercise in trained individuals.


2012 ◽  
Vol 37 (5) ◽  
pp. 976-981 ◽  
Author(s):  
John Jakeman ◽  
Simon Adamson ◽  
John Babraj

High-intensity training (HIT) involving 30-s sprints is an effective training regimen to improve aerobic performance. We tested whether 6-s HITs can improve aerobic performance in triathletes. Six subelite triathletes (age, 40 ± 9 years; weight, 86 ± 11 kg; body mass index, 26 ± 3 kg·m–2) took part in cycle HIT and 6 endurance-trained subelite athletes (age, 36 ± 9 years; weight, 82 ± 11 kg; BMI, 26 ± 3 kg·m–2) maintained their normal training routine. Before and after 2 weeks of HIT, involving 10 × 6-s sprints or normal activity, participants performed a self-paced 10-km time trial and a time to exhaustion test on a cycle ergometer. Finger prick blood samples were taken throughout the time to exhaustion test to determine blood lactate concentration. Two weeks of HIT resulted in a 10% decrease in self-paced 10-km time trial (p = 0.03) but no significant change in time to exhaustion. The time taken to reach onset of blood lactate accumulation (OBLA, defined as the point where blood lactate reaches 4 mmol·L–1) was significantly increased following 2 weeks of HIT (p = 0.003). The change in time trial performance was correlated to the change in time taken to reach OBLA (R2 = 0.63; p = 0.001). We concluded that a very short duration HIT is a very effective training regimen to improve aerobic performance in subelite triathletes and this is associated with a delay in blood lactate build-up.


2020 ◽  
Vol 41 (14) ◽  
pp. 1061-1066 ◽  
Author(s):  
Camila S. Padilha ◽  
Francois Billaut ◽  
Caique Figueiredo ◽  
Valéria Leme Gonçalves Panissa ◽  
Fabrício Eduardo Rossi ◽  
...  

AbstractTo investigate the effect of acute capsaicin (CAP) supplementation on time to exhaustion, physiological responses and energy systems contribution during continuous high-intensity exercise session in runners. Fifteen recreationally-trained runners completed two randomized, double-blind continuous high-intensity exercises at the speed eliciting 90% V̇O2peak (90% s V̇O2peak), 45 minutes after consuming capsaicin or an isocaloric placebo. Time to exhaustion, blood lactate concentration, oxygen consumption during and 20-min post-exercise, energy systems contribution, time to reach V̇O2peak, heart rate and the rate of perceived exertion (RPE) were evaluated. There was no significant difference between conditions for time to reach V̇O2peak (CAP:391.71±221.8 vs. PLA:298.20±174.5 sec, ES:0.58, p=0.872), peak lactate (CAP:7.98±2.11 vs. PLA:8.58±2.15 µmol, ES:−0.28, p=0.257), time to exhaustion (CAP:654.28±195.44 vs. PLA:709.20±208.44 sec, ES:−0.28, p=0.462, end-of-exercise heart rate (CAP:177.6±14.9 vs. PLA:177.5±17.9 bpm, ES:−0.10, p=0.979) and end-of-exercise RPE (CAP: 19±0.8 vs. PLA: 18±2.4, ES: 0.89, p=0.623). In conclusion, acute CAP supplementation did not increase time to exhaustion during high-intensity continuous exercise nor alter physiological responses in runners.


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