Effect of acute normobaric hypoxia on peripheral sweat rate

Peripheral sweat rate was measured to determine if acute normobaric hypoxia exerted a local inhibition on sweat gland function. It was hypothesized that peripheral sweat rate would be reduced during hypoxia, following cholinergic stimulation. Nineteen subjects (24 +/- 3 yr; 177 +/- 9 cm; 75.5 +/- 20.1 kg), 8 females and 11 males, were tested once during normobaric hypoxia, simulating an altitude of approximately 3050 m (P(O2) = 13.9%; P(B) approximately 730 mmHg), and once at sea level (200 m; P(O2) = 20.9%; P(B) approximately 730 mmHg). While seated at rest, a approximately 7-cm(2) area of the anterior forearm was stimulated using pilocarpine iontophoresis to produce localized sweating at the site. Following stimulation, sweat was collected from the area for 15 min using a Macroduct Sweat Collection System. One-way repeated measures ANOVA indicated a significantly lower sweat rate during normobaric hypoxia (4.6 +/- 2.6 g x m(-2) x min(-1)) compared to sea level (5.5 +/- 3.0 g x m(-2) x min(-1); p = 0.006). Because sweating was initiated directly at the sweat gland, thus bypassing central nervous system input, changes in sweat rate were likely due to peripheral alterations. Although these peripheral mechanisms warrant further investigation, the results of this study suggest a direct hypoxic influence on sweat gland function as evidenced by a decrease in sweat rate.     

Effect of acute hypoxia on heart rate variability at rest and during exercise

The purpose of this study was to investigate sympathovagal balance as inferred from heart rate variability (HRV) responses to acute hypoxia at rest and during exercise. HRV was evaluated in 12 healthy subjects during a standardized hypoxic tolerance test which consists of four periods alternating rest and moderate exercise (50 % V.O (2)max) in normoxic and hypoxic conditions. Ventilatory responses were determined and HRV indexes were calculated for the last 5 min of each period. In well-tolerant subjects, hypoxia at rest induced a decrease of root-mean-square of successive normal R-R interval differences (RMSSD) (p < 0.05) and of absolute high frequency (HF) power (p < 0.001). All absolute HRV indexes were strongly reduced during exercise (p < 0.001) with no further changes under the additional stimulus of hypoxia. A significant increase (p < 0.05) in the HF/(LF+HF) ratio (where LF is low frequency power) was found during exercise in hypoxia compared to exercise in normoxia, associated with similar mean changes in ventilation and tidal volume. These results indicate a vagal control withdrawal under hypoxia at rest. During exercise at 50 % V.O (2)max, HRV indexes cannot adequately represent cardiac autonomic adaptation to acute hypoxia, or possibly to other additional stimuli, due to the dominant effect of exercise and the eventual influence of confounding factors.     

Simulated rugby performance at 1550-m altitude following adaptation to intermittent normobaric hypoxia

Team-sport athletes who normally reside at sea level occasionally play games at altitudes sufficient to impair endurance performance. To investigate the effect of intermittent normobaric hypoxic exposure on performance in generic and game-specific tests at altitude, 22 senior club level rugby players performed baseline tests before single-blind random assignment to one of three groups: hypoxia-altitude (n = 9), normoxia-altitude (n = 6), and normoxia-sea level (n = 7). The hypoxia-altitude group underwent 9–13 sessions of intermittent hypoxic exposure (concentration of inspired oxygen = 13–10%) over 15 days, then repeated the performance tests within 12 h of travelling to 1550 m. The normoxia-altitude group underwent placebo exposures by breathing room air before repeating the tests at altitude, whereas the normoxia-sea level group underwent placebo exposures before repeating the tests at sea level. Hypoxic exposure consisted of alternately breathing 6 min hypoxic gas and 4 min ambient air for 1 h at rest. Performance measures gathered at each testing session were maximum speed, sub-maximum heart-rate speed and sub-maximum lactate speed during a 20-m incremental running test, mean time in six 70-m sprints, repetitive explosive power and other measures from seven 5.5-min circuits of a rugby simulation. Repetitive explosive power (−16%) and 20-m shuttle performance (−3%) decreased substantially at altitude compared to sea level. Acclimatisation to hypoxia had a beneficial effect on sub-maximum heart rate and lactate speed but little effect on other performance measures. In conclusion, 1550-m altitude substantially impaired some measures of performance and the effects of prior adaptation via 9–13 sessions of intermittent hypoxia were mostly unclear.     

Health risk for athletes at moderate altitude and normobaric hypoxia

Altitudes at which athletes compete or train do usually not exceed 2000-2500 m. At these moderate altitudes acute mountain sickness (AMS) is mild, transient and affects at the most 25% of a tourist population at risk. Unpublished data included in this review paper demonstrate that more intense physical activity associated with high-altitude training or mountaineering does not increase prevalence or severity of AMS at these altitudes. These conclusions can also be extended to the use of normobaric hypoxia, as data in this paper suggest that the severity of AMS is not significantly different between hypobaric and normobaric hypoxia at the same ambient pO(2). Furthermore, high-altitude cerebral or pulmonary oedema do not occur at these altitudes and intermittent exposure to considerably higher altitudes (4000-6000 m) used by athletes for hypoxic training are too short to cause acute high-altitude illnesses. Even moderate altitude between 2000 and 3000 m can, however, exacerbate cardiovascular or pulmonary disease or lead to a first manifestation of undiagnosed illness in older people that may belong to the accompanying staff of athletes. Moderate altitudes may also lead to splenic infarctions in healthy athletes with sickle cell trait.     

Hearing thresholds under acute hypoxia and relationship to slowing in the auditory modality

BACKGROUND: Acute hypoxia slows reaction time to visual stimuli and it has been proposed that this slowing can be accounted for by a decrease in perceived brightness. Auditory slowing could be accounted for in an analogous manner if hypoxia decreases perceived loudness, as reflected by an increase in pure-tone thresholds. However, evidence concerning the effects of hypoxia on auditory thresholds is contradictory and we performed an experiment to clarify this issue. Pilot work suggested that thresholds were raised due to noise from our breathing apparatus used to deliver the low O2 mixtures and we eliminated this artifact by measuring thresholds while the subjects held their breath. METHODS: The six subjects breathed either air as a control through an oro-nasal mask or low O2 mixtures to maintain arterial blood oxygen saturation at 74% while thresholds between 500-4000 Hz were measured with an audiometer during breathholding. RESULTS: Hypoxia produced a statistically significant but practically insignificant decrease in thresholds of 1 dB across all frequencies tested. CONCLUSIONS: Our results are consistent with the view that audition is relatively insensitive to hypoxia and that the slowing observed with auditory stimuli cannot be accounted for by an increase in auditory thresholds. Some alternative hypotheses which could account for this slowing are proposed.     

Predictive validity of ventilatory and lactate thresholds for cycling time trial performance

PURPOSE: To determine which laboratory measurement best predicts 40 km cycling time-trial (TT) performance. METHODS: Fifteen male cyclists performed lactate-threshold (LT), ventilatory-threshold (VT), 5 km and 40 km TT. Key variables of interest were Watts at thresholds. For VT determination we used: breakpoint of ventilatory equivalent of oxygen (VE/VO2); breakpoint of ventilatory equivalent of carbon dioxide (VE/VCO2); V-slope; respiratory exchange ratio (RER)=1 and 0.95. For LT we used Stegmann's individual anaerobic threshold; the stage preceding the second 0.5 mmol L(-1) increase (Baldari); 4 mmol L(-1); 1 mmol L(-1) increase in 3 min; the stage preceding the first 1 mmol L(-1) increase as criterion methods (<1 mmol). Analyses also included peak power during the incremental threshold tests (MaxVT(watts), MaxLT(watts)) and 5 km performance (5K(avgwatts)). RESULTS: Regression analyses between VT variables and 40K(avgwatts) were significant for V-slope (r2=0.63), VE/VO2 (r2=0.64), RER(0.95) (r2=0.53), RER1 (r2=0.57), and MaxVT(watts) (r2=0.65). Regressions between LT variables and 40K(avgwatts) were significant for Baldari (r2=0.52), 4 mmol L(-1) (r2=0.36), <1 mmol (r2=0.35), Keul (r2=0.34), and MaxLT(watts) (r2=0.51). Regressions between 5K variables and 40K(avgwatts) were significant for 5K(avgwatts) (r2=0.58). Paired t-tests between these variables and the 40K(avgwatts) indicated that absolute power outputs at VE/VO2 (P=0.33), RER(0.95) (P=0.93), and 4 mmol L(-1) (P=0.39) were not significantly different from 40K(avgwatts). CONCLUSION: We conclude that VT-based variables are generally superior to LT variables relative to predicting 40K(avgwatts), the simplest of several valid measures appears to be VE/VO2.     

Analysis of heart rate and heart rate variation during cardiac CT examinations

RATIONALE AND OBJECTIVES: We sought to examine heart rate and heart rate variability during cardiac computed tomography (CT). MATERIALS AND METHODS: Ninety patients (59.0 +/- 13.5 years) underwent coronary CT angiography (CTA), with 52 patients also undergoing coronary artery calcium scanning (CAC). Forty-two patients with heart rate greater than 70 bpm were pretreated with oral beta-blockers (in five patients, use of beta-blocker was not known). Sixty-four patients were given sublingual nitroglycerin. Mean heart rate and percentage of beats outside a +/-5 bpm region about the mean were compared between baseline (free breathing), prescan hyperventilation, and scan acquisition (breath-hold). RESULTS: Mean scan acquisition time was 13.1 +/- 1.5 seconds for CAC scanning and 14.2 +/- 2.9 seconds for coronary CTA. Mean heart rate during scan acquisition was significantly lower than at baseline (CAC 58.2 +/- 8.5 bpm; CTA 59.2 +/- 8.8 bpm; baseline 62.8 +/- 8.9 bpm; P < .001). The percentage of beats outside a +/-5 bpm about the mean were not different between baseline and CTA scanning (3.5% versus 3.3%, P = .87). The injection of contrast had no significant effect on heart rate (58.2 bpm versus 59.2 bpm, P = .24) or percentage of beats outside a +/-5 bpm about the mean (3.0% versus 3.3%, P = .64). No significant difference was found between gender and age groups (P > .05). CONCLUSIONS: Breath-holding during cardiac CT scan acquisition significantly lowers the mean heart rate by approximately 4 bpm, but heart rate variability is the same or less compared with normal breathing.     

Evidence of decrease in peak heart rate in acute hypoxia: effect of exercise-induced arterial hypoxemia

This study focuses on the influence of the arterial oxygen saturation level at exhaustion on peak heart rate under acute moderate hypoxia, in endurance-trained subjects. Nineteen competing male cyclists performed exhaustive ramp exercise (cycle ergometer) under normoxia and normobaric hypoxia (15 % O (2)). After the normoxic trial, the subjects were divided into those demonstrating exercise-induced arterial hypoxemia during exercise (> 5 % decrease in SaO (2) between rest and the end of exercise, n = 10) and those who did not (n = 9). O (2) uptake, heart rate and arterial O (2) saturation (ear-oximeter) levels were measured. Under hypoxia, peak heart rate decreased for both groups (p < 0.001) and to a greater extent for hypoxemic subjects (p < 0.01). Arterial O (2) saturation under hypoxia was lower for the hypoxemic than for the non-hypoxemic subjects (p < 0.001) and it was correlated to the fall in peak heart rate between normoxia and hypoxia for all subjects (p < 0.01; r = 0.65). Hypoxemic subjects presented greater decrease in maximal O (2) uptake than non-hypoxemic ones (19.6 vs. 15.6 %; p < 0.05). The results confirm the greater decrement in arterial O (2) saturation under hypoxia in hypoxemic subjects and demonstrates a more pronounced reduction in peak heart rate in those subjects compared with non-hypoxemic ones. These data confirm the possible influence of arterial oxygenation on the decrease in peak heart rate in acute hypoxia.     

Temporal dynamics of lactate concentration in the human brain during acute inspiratory hypoxia

Purpose:

To demonstrate the feasibility of measuring the temporal dynamics of cerebral lactate concentration and examine these dynamics in human subjects using magnetic resonance spectroscopy (MRS) during hypoxia.

Materials and Methods:

A respiratory protocol consisting of 10‐minute baseline normoxia, 20‐minute inspiratory hypoxia, and ending with 10‐minute normoxic recovery was used, throughout which lactate‐edited MRS was performed. This was repeated four times in three subjects. A separate session was performed to measure blood lactate. Impulse response functions using end‐tidal oxygen and blood lactate as system inputs and cerebral lactate as the system output were examined to describe the dynamics of the cerebral lactate response to a hypoxic challenge.

Results:

The average lactate increase was 20% ± 15% during the last half of the hypoxic challenge. Significant changes in cerebral lactate concentration were observed after 400 seconds. The average relative increase in blood lactate was 188% ± 95%. The temporal dynamics of cerebral lactate concentration was reproducibly demonstrated with 200‐second time bins of MRS data (coefficient of variation 0.063 ± 0.035 between time bins in normoxia). The across‐subject coefficient of variation was 0.333.

Conclusion:

The methods for measuring the dynamics of the cerebral lactate response developed here would be useful to further investigate the brain's response to hypoxia. J. Magn. Reson. Imaging 2013;37:739–745. © 2012 Wiley Periodicals, Inc.     

Differential effects of dietary carbohydrate on RPE at the lactate and ventilatory thresholds.

This study used manipulation of dietary intake and substrate utilization to dissociate the ventilatory (TVE) and lactate (TLAC) thresholds, and investigated the role of the thresholds in perception of effort as measured by the Borg 15-category rating of perceived exertion (RPE) scale. Thirteen males performed graded exercise tests following: a) glycogen depletion (GD) and 3 d on a high-carbohydrate diet (HC, 93% total daily energy intake as carbohydrate), b) GD and 3 d on a low-carbohydrate diet (LC, 21%), and c) a mixed-carbohydrate diet (NC, 51%). During submaximal exercise at intensities between 30 and 90% of peak oxygen uptake (VO2peak), significant differences among conditions (P less than 0.05) were obtained for carbon dioxide elimination, respiratory exchange ratio, and plasma lactate, with HC greater than NC greater than LC. Mean (+/- SD) TLAC occurred at different (P less than 0.05) percentages of VO2peak, with HC (55.6 +/- 2.9%) less than NC (59.6 +/- 2.9%) less than LC (63.8 +/- 2.8%). Means for TVE were not different. RPE at TLAC were significantly different (P less than 0.01) among conditions, with HC (12.6 +/- 0.6) less than NC (13.8 +/- 0.6) less than LC (14.3 +/- 0.7), but RPE at TVE were not different. It was concluded that the perception of exertion as becoming "somewhat hard" to "hard" is more closely linked to TVE than to TLAC.     

急性轻中度缺氧条件下心率及收缩压变异性谱变化

目的：应用心率及收缩压变异性（HRV、SBPV）谱分析方法评价急性轻中度缺氧条件下心血管自主神经调节的变化。方法：10名健康男性青年分别吸入氧13．7％（相当于海拔3500m)和11％（相当于海拔5000m）两种氮－氧混合气各20min,将对照和缺氧条件下的HRV和SBPV谱变化进行对比分析。结果：在两种缺氧条件下,受试者均出现血压下降、心率增快反应,HRV谱总功率（TP）和高频成分（HF）功率均显著减小,低频成分（LF）功率与LF／HF功率比值无显著变化,SBPV谱LF功率显著增大,3名缺氧耐力不良受试者尤为明显。不同水平缺氧之间的数值比较差异均无显著性意义。结论：急性轻中度缺氧条件下,人副交感神经抑制,交感神经兴奋,联合应用HRV与SBPV谱分析方法可对心血管自主神经调节活动进行评定;但HRV的LF成分变化机理较为复杂。     

Correlations between lactate and ventilatory thresholds and the maximal lactate steady state in elite cyclists

We investigated the validity of different lactate and ventilatory threshold methods, to estimate heart rate and power output corresponding with the maximal lactate steady-state (MLSS) in elite cyclists. Elite cyclists (n = 21; 21 +/- 0.4 y; VO2peak, 5.4 +/- 0.2 l x min (-1)) performed either one (n = 10) or two (n = 11) maximal graded exercise tests, as well as two to three 30-min constant-load tests to determine MLSS, on their personal race bicycle which was mounted on an ergometer. Initial workload for the graded tests was 100 Watt and was increased by either 5 % of body mass (in Watt) with every 30 s (T30 s), or 60 % of body mass (in Watt) with every 6 min (T6min). MLSS was defined as the highest constant workload during which lactate increased no more than 1 mmol x l (-1) from min 10 to 30. In T30 s and T6 min the 4 mmol (TH-La4), the Conconi (TH-Con) and dmax (TH-Dm) lactate threshold were determined. The dmax lactate threshold was defined as the point that yields the maximal distance from the lactate curve to the line formed by the lowest and highest lactate values of the curve. In T30 s also ventilatory (TH-Ve) and Vslope (TH-Vs) thresholds were calculated. Time to exhaustion was 36 +/- 1 min for T30 s versus 39 +/- 1 min for T6 min. None of the threshold measures in T30 s, except TH-Vs (r2 = 0.77 for heart rate) correlated with either MLSS heart rate or power output. During T6 min, power output at TH-Dm was closely correlated with MLSS power (r2=0.72). Low correlations were found between MLSS heart rate and heart rate measured at TH-Dm (r2=0.46) and TH-La4 (r2=0.25), respectively, during T6 min. It is concluded that it is not possible to precisely predict heart rate or power output corresponding with MLSS in elite cyclists, from a single graded exercise test causing exhaustion within 35-40 min. The validity of MLSS predicted from an incremental test must be verified by a 30-min constant-load test.     

Blood lactate and heart rate during national and international women's basketball

AIM: In order to measure game intensity in female basketball players, 2 teams (Olympic National Team - I -and a team at 1(st) National Division - N) were studied for a total of 12 games (10 official competitions and 2 practice games -P). METHODS: Both blood lactate concentration ([La](b)) and mean heart rate (HR) were measured during the games and then compared with a progressive field test where maximal blood lactate (max[La](b)), individual lactate threshold and maximal heart rate (HR max) values were obtained. All different categories (International, National and Practice) and positions (Guard, Forward and Center) were taken into account in this study. RESULTS: Differences (p<0.05) in HR were found between all positions (Guard=185+/-5.9; Forward=175+/-11 and Center=167+/-12 beats x min(-1)) and between the International team and the rest of the categories (International=186+/-6; National=175+/-13 and Practice=170+/-11 beats x min(-1)). The [La](b) differed between the Guard and the other 2 positions (Guard=5.7+/-2.1; Forward=4.2+/-2.1 and Center=3.9+/-2.0 mmol x L(-1)) and between Practice and the rest of the categories (International=5.0+/-2.3; National=5.2+/-2.0 and Practice=2.7+/-1.2 mmol x L(-1)). The game intensity of International players reached 94.6% of their maximum HR value, whereas National players reached 90.8%, this percentage descending to 89.8% during Practice. International games reached the individual lactate threshold at 89.2% of the maximum HR; National games at 88.6%. CONCLUSION: We can conclude that the game intensity of female basketball increases according to the level of competition. It may also differ according to playing position, being greatest in guards. The game intensity at international level surpasses the individual lactate threshold, whereas it reaches a lower level in training games.     

Comparison of heart rate to lactate threshold and to Conconi's threshold in children

The heart rate (HR) at the lactate threshold was determined on a treadmill in 59 children with an average age of 11.8 years. 45 minutes later, they had to go through a vita maxima test on a bicycle ergometer. The load was increased stepwise by 10 Watt/min. During the tests HR was registered continually and stored every 5 seconds. In 52 children the characteristic break point was evident; in 7 children no break point could be found - in 2 children, because they had stopped the exercise before reaching the lactate threshold, and in 5 children because their HR increased linearly from the beginning until the end of the load application. HR at the break point correlated very strongly with HR at the lactate threshold (r = 0.99). Therefore the authors are of the opinion that the introduced modification of the Conconi test can substitute the invasive lactate threshold determination in children.     

RPE association with lactate and heart rate during high-intensity interval cycling

PURPOSE: Physiological and perceptual measures during interval exercise are not well understood. The current study therefore examined the correspondence between RPE, HR, and blood lactate concentration ([La]) during interval cycling. METHODS: VO2peak and the 4.0 mmol x L(-1) lactate threshold were determined. In session 2, subjects (N = 12) warmed up (10 min, 0 W) and completed five 2-min intervals (INT) at >4 mmol x L(-1) workload, each separated by 3 min of recovery (REC) (60 rpm, 0 W). HR, RPE, and [La] were recorded at 10 min, at the conclusion of each INT, and each REC and 5- and 10-min recovery. RESULTS: Repeated-measures ANOVA showed [La], HR, and RPE increased significantly across time (INT and REC). At each time point, repeated-measures ANOVA was used to compare standardized data (alpha = 0.05). RPE (at INT) intensified concurrently with HR and [La] at INT. Correlations were significant for INT (P < or = 0.05) (HR-RPE: r = 0.63, [La]-RPE: r = 0.43). Similarly, RPE and HR for REC systematically increased with [La]. Correlations for REC were also significant (HR-RPE: r = 0.44, [La]-RPE: r = 0.34). Correlations were also significant for INT and REC combined (HR-RPE: r = 0.70, [La]-RPE: r = 0.22). CONCLUSIONS: INT and REC independently showed moderate correspondence for RPE-[La] and RPE-HR. However, tighter overall coupling of HR with RPE (vs [La] with RPE) and a dissociation between RPE-[La] suggest RPE during intervals of intense cycling were more sensitive to acute metabolic demand (evidenced by HR) versus [La].     

Dissociation of the ventilatory and lactate thresholds following caffeine ingestion

Caffeine ingestion prior to the start of exercise has been shown to have an effect on ventilatory parameters and substrate utilization. Changes in either substrate utilization or ventilatory parameters may influence the determination of the lactate threshold (LT) and/or the ventilatory threshold (VT). Therefore, it was the purpose of this investigation to determine whether the VT and LT occur at similar metabolic rates and what effect caffeine ingestion will have on these two measures. Ten male subjects completed two maximal exercise bouts on the treadmill using a single blind procedure. One trial was performed 45 min after the ingestion of caffeine citrate (CC) in an amount equal to 7.0 mg of anhydrous caffeine.kg-1 body weight. The second trial was performed 45 min after the ingestion of a gelatin powdered placebo (P). Ventilatory parameters were monitored on a breath-by-breath basis, and blood for lactate determination was obtained from an antecubital vein every minute. Maximal oxygen consumption did not differ significantly between the CC (60.3 +/- 5.2 ml.kg-1.min-1) and P (59.7 +/- 5.6 ml.kg-1.min-1) trials. Oxygen consumption (VO2) values during the P trial at the VT (40.2 +/- 6.1 ml.kg-1.min-1) and the LT (38.6 +/- 3.3 ml.kg-1.min-1) were not significantly different (P less than 0.05). During the CC trial, VO2 values at the VT (44.4 +/- 6.6 ml.kg-1.min-1) and the LT (39.7 +/- 5.8 ml.kg-1.min-1) were significantly different. When comparing the VO2 at the LTs between the CC and P trials, there was no significant difference. There was, however, a significant difference in VO2 at the VTs when comparing the two trials. These data demonstrate a dissociation between the VT and LT following caffeine ingestion and suggest that the use of the VT as an indicator of the LT may be inappropriate following ingestion of moderate dosages of caffeine.     

Effect of short-term and intermittent normobaric hypoxia on endogenous erythropoietin isoforms

The aim of the present study was to evaluate whether the Epo isoforms in blood, induced by short-term and intermittent hypoxia, are different from those at normoxia at sea level and if this could be an impediment to the use of a direct Epo doping test based upon the electric charge of the Epo isoforms. Ten healthy subjects, 9 men and 1 woman, participated in the study. Median age was 22 years (range 20-32). Normobaric hypoxia was administered differently in 3 sub-groups; two groups with 12 h hypoxia and 12 h normoxia up to 10 days: IM 2000 and IM 2700 living in 16.2% and 14.9% O2, corresponding to 2000 and 2700 m above sea level, respectively, and training in normoxia. The third group, C 2700, lived in hypoxia, 14.9% O2 corresponding to 2700 m, continuously for 48 h. The mean serum Epo level increased from 10.9 IUL(-1) (range 8.8-12.5) to 23.5 IUL(-1) (15.6-29.1) after 2 days followed by 19.7 IUL(-1) (16.1-24.1) after 10 days exposure for intermittent hypoxia. The highest values 39.5 IUL(-1) (31.5-50) were obtained for the group exposed for continuous hypoxia for 48 h. The median electrophoretic mobility of the serum Epo isoforms was above the cut-off limit of 670 AMU, previously estimated for discrimination between recombinant and endogenous Epo, in all samples taken before and after exposure to hypoxia. The highest values, mean 730 mAMU (range 703-750) were obtained after 10 days of intermittent hypoxia. CONCLUSION: If the method had been used as a doping test, no false positive results would have been registered for the 15 serum samples from the 10 individuals exposed for hypoxia. Thus, the results indicate that the basic principle for direct detection of recombinant Epo doping, based upon the change in electric charge on Epo, can be used also on individuals having lived in a hypoxic milieu.     

Differences in cardio-ventilatory responses to hypobaric and normobaric hypoxia: a review

The presence of differences in physiological response to a lowered inspired Po2 mediated by hypobaric hypoxia (HH) or normobaric hypoxia (NH) is controversial. This review examines the brief, acute, and subacute respiratory, cardiovascular, and subjective symptom response to intermediate and severe hypoxic exposure in NH and HH. Brief exposures lead to similar physiological responses; this is not the case in acute/subacute exposures. Extrapolating data from NH studies to HH in longer exposures is inappropriate as physiological responses to hypoxia seem to be influenced by the prevailing ambient pressure, especially in chronic exposures where acute mountain sickness severity is greater in HH than NH. Explanations for the discrepancy between the two modalities include differences in ventilatory patterns, alveolar gas disequilibrium, and dissimilar acute hypoxic ventilatory responses. Awareness and consideration of these key differences between NH and HH is essential to their proper application to kinesiology, altitude, and aviation medicine.