Effect Of Hypoxic Exposure Research Articles

Hypoxia and Fatigue Impair Rapid Torque Development of Knee Extensors in Elite Alpine Skiers.

This study examined the effects of acute hypoxia on maximal and explosive torque and fatigability in knee extensors of skiers. Twenty-two elite male alpine skiers performed 35 maximal, repeated isokinetic knee extensions at 180°s-1 (total exercise duration 61.25 s) in normoxia (NOR, FiO2 0.21) and normobaric hypoxia (HYP, FiO2 0.13) in a randomized, single-blind design. Peak torque and rate of torque development (RTD) from 0 to 100 ms and associated Vastus Lateralis peak EMG activity and rate of EMG rise (RER) were determined for each contraction. Relative changes in deoxyhemoglobin concentration of the VL muscle were monitored by near-infrared spectroscopy. Peak torque and peak EMG activity did not differ between conditions and decreased similarly with fatigue (p < 0.001), with peak torque decreasing continuously but EMG activity decreasing significantly after 30 contractions only. Compared to NOR, RTD, and RER values were lower in HYP during the first 12 and 9 contractions, respectively (both p < 0.05). Deoxyhemoglobin concentration during the last five contractions was higher in HYP than NOR (p = 0.050) but the delta between maximal and minimal deoxyhemoglobin for each contraction was similar in HYP and NOR suggesting a similar muscle O2 utilization. Post-exercise heart rate (138 ± 24 bpm) and blood lactate concentration (5.8 ± 3.1 mmol.l-1) did not differ between conditions. Arterial oxygen saturation was significantly lower (84 ± 4 vs. 98 ± 1%, p < 0.001) and ratings of perceived exertion higher (6 ± 1 vs. 5 ± 1, p < 0.001) in HYP than NOR. In summary, hypoxia limits RTD via a decrease in neural drive in elite alpine skiers undertaking maximal repeated isokinetic knee extensions, but the effect of hypoxic exposure is negated as fatigue develops. Isokinetic testing protocols for elite alpine skiers should incorporate RTD and RER measurements as they display a higher sensitivity than peak torque and EMG activity.

Hypoxic-Preconditioned Bone Marrow Stem Cell Medium Significantly Improves Outcome After Retinal Ischemia in Rats.

PurposeWe have previously demonstrated the protective effect of bone marrow stem cell (BMSC)-conditioned medium in retinal ischemic injury. We hypothesized here that hypoxic preconditioning of stem cells significantly enhances the neuroprotective effect of the conditioned medium and thereby augments the protective effect in ischemic retina.MethodsRats were subjected to retinal ischemia by increasing intraocular pressure to 130 to 135 mm Hg for 55 minutes. Hypoxic-preconditioned, hypoxic unconditioned, or normoxic medium was injected into the vitreous 24 hours after ischemia ended. Recovery was assessed 7 days after injections by comparing electroretinography measurements, histologic examination, and apoptosis (TUNEL, terminal deoxynucleotidyl transferase–mediated dUTP nick end labeling assay). To compare proteins secreted into the medium in the groups and the effect of hypoxic exposure, we used rat cytokine arrays.ResultsEyes injected with hypoxic BMSC–conditioned medium 24 hours after ischemia demonstrated significantly enhanced return of retinal function, decreased retinal ganglion cell layer loss, and attenuated apoptosis compared to those administered normoxic or hypoxic unconditioned medium. Hypoxic-preconditioned medium had 21 significantly increased protein levels compared to normoxic medium.ConclusionsThe medium from hypoxic-preconditioned BMSCs robustly restored retinal function and prevented cell loss after ischemia when injected 24 hours after ischemia. The protective effect was even more pronounced than in our previous studies of normoxic conditioned medium. Prosurvival signals triggered by the secretome may play a role in this neuroprotective effect.

Effect of Intermittent Normobaric Hypoxic Exposure on Sea-level Performance in Rugby Players

The “live-high/train-low” approach to altitude training produces worthwhile gains in endurance performance at sea level, but the effects of this approach using normobaric hypoxia to simulate altitude are more contentious. The effects of hypoxic exposure on brief high-intensity performance similar to that of team games also need further investigation. PURPOSE: To determine the effects of normobaric intermittent hypoxic exposure on sea-level performance in professional rugby players. METHODS: Ten players were randomly assigned to two groups. Players in each group received 9–14 sessions of either hypoxic (10–15% O2) or normoxic (21% O2) exposure over 14 days in a single-blind fashion. Each session consisted of six 6-min intervals of exposure delivered via a hand-held mask interspersed with 4-min recovery periods breathing room air. Performance measures obtained consecutively in a single testing session pre- and post-exposure were: maximum speed in a 20-m incremental running test, mean time in six 70-m repeated sprints, various mean measures in seven 5.5-min circuits of a rugby simulation, and mean time in a second set of sprints. Blood sampling was performed 7 and 14 days before and 2 days following exposure. Performance tests were performed 1–3 days prior to and 1–4 days after exposure. RESULTS: Effects of hypoxic exposure on maximum speed and sprint times were trivial (< 1.0%) but unclear (90% likely range ±5% to ±9%). In the rugby simulation, hypoxic exposure produced clear impairments of peak power in two scrums (15%, ±8%; 9%, ±7%) and clear impairments of time in offensive sprints (7%, ±8%) and tackle sprints (11 %, ±9%). Impairments were also observed in the 20-m sprint (1.6%, ±7.0%), 30-m sprint (2.0%, ±4.5%), and defensive sprint (3.5%, ±4.7%), although these were unclear. The effect on ball-passing accuracy was also unclear (2%, ±19%), as were effects on hemoglobin concentration (−2.0, ±4.7%), reticulocytes (0.7, ±36%) andferritin(11,±22%). CONCLUSIONS: Pending further research, rugby players would be unwise to use normobaric intermittent hypoxic exposure to prepare for games at sea level. Supported by the New Zealand Rugby Union.

Effects of live high, train low hypoxic exposure on lactate metabolism in trained humans.

We determined the effect of 20 nights of live high, train low (LHTL) hypoxic exposure on lactate kinetics, monocarboxylate lactate transporter proteins (MCT1 and MCT4), and muscle in vitro buffering capacity (betam) in 29 well-trained cyclists and triathletes. Subjects were divided into one of three groups: 20 consecutive nights of hypoxic exposure (LHTLc), 20 nights of intermittent hypoxic exposure [four 5-night blocks of hypoxia, each interspersed with 2 nights of normoxia (LHTLi)], or control (Con). Rates of lactate appearance (Ra), disappearance (Rd), and oxidation (Rox) were determined from a primed, continuous infusion of l-[U-14C]lactic acid tracer during 90 min of steady-state exercise [60 min at 65% peak O2 uptake (VO(2 peak)) followed by 30 min at 85% VO(2 peak)]. A resting muscle biopsy was taken before and after 20 nights of LHTL for the determination of betam and MCT1 and MCT4 protein abundance. Ra during the first 60 min of exercise was not different between groups. During the last 25 min of exercise at 85% VO(2 peak), Ra was higher compared with exercise at 65% of VO(2 peak) and was decreased in LHTLc (P < 0.05) compared with the other groups. Rd followed a similar pattern to Ra. Although Rox was significantly increased during exercise at 85% compared with 65% of VO(2 peak), there were no differences between the three groups or across trials. There was no effect of hypoxic exposure on betam or MCT1 and MCT4 protein abundance. We conclude that 20 consecutive nights of hypoxia exposure decreased whole body Ra during intense exercise in well-trained athletes. However, muscle markers of lactate metabolism and pH regulation were unchanged by the LHTL intervention.

LIVE-HIGH, TRAIN-LOW HYPOXIC EXPOSURE DOES NOT ALTER LACTATE KINETICS OR MUSCLE BUFFERING IN TRAINED HUMANS

Changes in the anaerobic pathways have recently been suggested as a mechanism by which exercise performance at sea level is improved after live-high, train-low (LHTL) hypoxic exposure. PURPOSE To determine the effect of 20 nights of LHTL (2,650 m) on resting lactate kinetics and muscle buffering (βm) in well-trained athletes. METHODS 29 cyclists/triathletes were divided into three groups:20 consecutive nights of hypoxic exposure (LHTLc), 20 nights of intermittent hypoxic exposure (four 5-night blocks of hypoxia, each interspersed with 2 nights of normoxia (LHTLi), or control (CON). Rates of lactate appearance (Ra), and disappearance (Rd) were determined from a primed, continuous infusion of L-[U-14C] tracer during 90 min of exercise (60 min at 65% VO2peak followed by 30 min at 85% VO2peak). Resting muscle biopsies were taken pre and post 20 nights of LHTL for the determination of in-vitro βm. RESULTS Ra ranged between 65–90 μmol.kg−1.min−1 during the first 60 min of exercise and was not different between either the two hypoxic conditions or CON. Ra averaged during the last 25 min of exercise at 85% VO2peak was ∼230 μmol.kg −1. min−1 for all three groups, and was higher (P < 0.05) compared with exercise at 65% of VO2peak. However there was no difference in Ra between groups either pre or post hypoxic exposure. Rd followed a similar pattern to Ra. μm capacity averaged 147 μ mol H+.g muscle dw−1. pH−1 (range 141–151 μmol H +.g muscle dw−1. pH−1) and there was no effect of hypoxic exposure. CONCLUSION 20 nights of LHTL had no effect on lactate kinetics during exercise nor muscle buffering capacity. Supported by ARC grant C00002552

Effect of hypoxic exposure on Na+/H+ antiport activity, isoform expression, and localization in endothelial cells.

Little is known about the effects of prolonged hypoxic exposure on membrane ion transport activity. The Na+/H+ antiport is an ion transport site that regulates intracellular pH in mammalian cells. We determined the effect of prolonged hypoxic exposure on human pulmonary arterial endothelial cell antiport activity, gene expression, and localization. Monolayers were incubated under hypoxic or normoxic conditions for 72 h. Antiport activity was determined as the rate of recovery from intracellular acidosis. Antiport isoform identification and gene expression were determined with RT-PCR and Northern and Western blots. Antiport localization and F-actin cytoskeleton organization were defined with immunofluorescent staining. Prolonged hypoxic exposure decreased antiport activity, with no change in cell viability compared with normoxic control cells. One antiport isoform [Na+/H+ exchanger isoform (NHE) 1] that was localized to the basolateral cell surface was present in human pulmonary arterial endothelial cells. Hypoxic exposure had no effect on NHE1 mRNA transcript expression, but NHE1 protein expression was upregulated. Immunofluorescent staining demonstrated a significant alteration of the F-actin cytoskeleton after hypoxic exposure but no change in NHE1 localization. These results demonstrate that the decrease in NHE1 activity after prolonged hypoxic exposure is not related to altered gene expression. The change in NHE1 activity may have important consequences for vascular function.

Modulation of duodenal iron uptake by hypoxia and fasting in the rat

The effect of hypoxic exposure on invitroduodenal Fe uptake kinetics was studied in tissue fragments from rats that were fed or fasted overnight before study. Hypoxic exposure was for 3 d at 0·5 atm and fasting was for the last 18-24 h before Fe uptake determinations. The non-permeable Fe2+chelator 3-(2-pyridyl)-5,6-bis-(4-phenyl-sulphonic acid)-l,2,4-triazine (ferrozine), and medium deoxygenation inhibited uptake in all experimental groups. Ferrozine sensitivity and mucosal Fe3+reductase activity were greatest in hypoxic animals. Fe uptake was inhibited by membrane depolarization only after fasting or hypoxic exposure of the rats. The data demonstrated that Fe uptake by rat duodenal fragments involves at least two mechanisms: a membrane-potentialindependent mechanism which is not responsive to hypoxia and a second mechanism, induced by fasting or hypoxia, which is inhibited by membrane depolarization. Uptake is partially dependent on reduction of Fe3+to Fe2+and this is primarily associated with the second mechanism for uptake. These properties have been reported also in mouse and human Fe uptake, suggesting that the rat is a useful model for the study of basic mechanisms of Fe absorption

Effect of hypoxic exposure on iron absorption in heterozygous hypotransferrinaemic mice.

Heterozygous hypotransferrinaemic mice show serum iron, haemoglobin and reticulocyte levels similar to those of normal (+/+) controls but the plasma apotransferrin level is significantly reduced. Male heterozygous hypotransferrinaemic Balb/cJ mice and control (+/+) littermates were exposed to 1-3 days' hypoxia at 0.5 atmospheres. Controls increased their haemoglobin and iron absorption significantly during the first day of exposure; serum transferrin levels were increased and iron absorption had returned to normal levels by the third day or serum transferrin above normal levels and the elevated iron absorption persisted for longer than in controls. Serum iron levels were lower following hypoxic exposure than in controls. Liver iron loading was significantly enhanced by hypoxia in heterozygotes, but not in controls. These observations demonstrate the importance of the reservoir of plasma apotransferrin in the initial phase of enhanced erythropoiesis, and that the ability to enhance plasma levels of iron-bound transferrin is required in order to increase haemoglobin levels under the hypoxic stress.

Hypoxic coordinate regulation of mitochondrial enzymes in mammalian cells.

The effect of hypoxic exposure on various mitochondrial enzymes and on cell mitochondrial genomic content was studied in two types of mammalian cells. Hypoxia depressed the activity of six enzymes to the same degree. The kinetics of depression and of recovery during reexposure to normoxia were statistically similar for three marker enzymes. Despite the global and symmetrical decrease in enzyme activities, mitochondrial DNA remained constant. This suggests either symmetrical loss of mitochondrial enzymes from all mitochondria or complete loss of enzymes from a subpopulation of mitochondria with retention of an intact mitochondrial genome.

Effect of Hypoxic Exposure on Lutein Cell Ultrastructure in the Pregnant Mouse

Effect of Hypoxic Exposure on Lutein Cell Ultrastructure in the Pregnant Mouse