| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
1 School of Human Kinetics and Recreation, Memorial University of Newfoundland, St John's, NL, Canada A1C 5S72 Division de Kinésiologie, Département de Médecine Sociale et Préventive4 Département d'Anatomie et Physiologie, Faculté de Médecine, Université Laval Québec, QC, Canada G1K 7P43 Laboratoire Ergonomie Sportive et Performance, UFR STAPS, Université du Sud Toulon-Var, Avenue de l'Université, BP 132 83957, La Garde Cedex, France
 |
Abstract |
|---|
 Top Abstract IntroductionMethodsResultsDiscussionReferences |
|---|
(Received 27 July 2005;
accepted after revision 16 November 2005; first published online 18 November 2005)
Corresponding author F. A. Basset: School of Human Kinetics and Recreation, Memorial University of Newfoundland, St John's, NL, Canada A1C 5S7. Email: fbasset{at}mun.ca
|
Introduction |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
improvements and/or any changes in other performance-related parameters (Gore et al. 1996; Ashenden et al. 1999a,b, 2000; Gore et al. 2001; Hahn et al. 2001; Townsend et al. 2002). In the present study, SNH was studied because it has been reported to elicit specific hypoxia responses, such as increased circulating erythropoietin (EPO) and red cell mass with several hours of exposure during sleep (Hoppeler & Vogt, 2001). Despite standardization problems related to absolute versus relative exercise intensities, timing, length and degree of hypoxia, a general consensus on the effects of SNH is forming. First, hypoxia stimulation produces physiological adaptations similar to, but not identical to, training adaptations in normoxia (Hoppeler & Vogt, 2001); second, these adaptations to hypoxia are dependent on training conditions and the fitness of the subjects (Bailey et al. 2000); third, short-term exposures can be of sufficient amplitude to initiate adaptive responses while providing periods of recovery that avoid the detrimental effects of altitude (Clanton & Klawitter, 2001). In fact, relatively brief periods of hypoxic exposure via a hypobaric chamber or inhalation of a normobaric hypoxic gas mixture stimulate EPO (Wilber, 2001), which may improve reticulocyte count, haemoglobin and haematocrit in untrained and trained subjects (Vallier, 1995). It seems, then, rational to infer an increase of circulatory oxygen transport. Moreover, even if very low levels of inspired O2 exposure result in a general loss of Krebs cycle enzyme activity (Green et al. 1989) and muscle mass loss (MacDougall et al. 1991), at more modest levels of hypoxia, somewhere above an atmospheric partial pressure of oxygen of 80–100 mmHg, aerobic enzyme activities are particularly stimulated when coupled with exercise (Clanton & Klawitter, 2001). SNH can also increase muscle buffer capacity and carbohydrate oxidation, the latter bringing about better cycling efficiency (Gore et al. 2001).
Several years of scientific research have, however, failed to show conclusive effects of exposure to hypoxia on physical performance, partly because experimental designs used in the literature differ from one study to another (Hoppeler et al. 2003). They differ in terms of sojourn duration (from a few minutes to a lifetime), level of altitude (from 1500 m to the top of Everest) and physical activity (from short sprints to long-lasting aerobic activities). Recently, Hoppeler et al. (2003) proposed a nomenclature based on organism responses that draw boundaries of acute and chronic hypoxia effects. From their thorough review, distinctions are made between native, permanent, long-term, short-term and intermittent hypoxia exposures. As a result, it became clear that the designation of the type of hypoxia intervention varied widely in terms of physiological adaptations from microvasculature to cardiovascular and pulmonary systems.
The present study therefore aimed to assess the effectiveness of an SNH exposure protocol currently used in several Canadian sports centres by highly trained athletes. This protocol has been promoted because it is believed to offer a sufficient stimulus for improving anaerobic and aerobic performance while avoiding symptoms of hypoxia exposure, such as nausea, headaches, loss of appetite, sleeplessness and queasiness. Our objectives were: (1) to verify experimentally the effects of this SNH protocol on physiological parameters (haematological and skeletal muscle histo- and biochemical properties); and (2) to test the efficacy of the protocol in improving physical performance. It was hypothesized that SNH exposure would be sufficient to improve O2 transport-related parameters and skeletal muscle glycolytic and oxidative metabolism potential, and that these physiological improvements would lead to improved physical performance in highly trained athletes.
|
Methods |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
Eight cross-country skiers (5 male; 3 female) from the Centre National d'Entraînement Pierre Harvey and four long track speed skaters (2 male; 2 female) from the Centre National Gaétan Boucher gave their written informed consent (in compliance with the declaration of Helsinki and with Université Laval ethics committee regulations) to participate in this study. During the study, athletes trained on a regular basis, modifying their training sessions for testing periods only. Athletes' characteristics and training profile are shown in Table 1.
|
In a single-blind study, athletes were randomly assigned into two groups, which spent 8 h per night for two consecutive nights per week over a 3 week period under either SNH or normobaric normoxic (NNC) treatments. Following a 3 week washout period, athletes were switched to the other condition (cross-over design; Fig. 1).
|
The study took place during the general preparatory phase in which both groups' training sessions mainly focused on aerobic workouts performed by running and cycling. Two to four 45 min weight training sessions were added per week, with emphasis on muscle hypertrophy. Mean overall volumes -total training hours-were 11 h 24 mm (± 3 h) and 11 h 12 min (± 3) for SNH and (NNC), respectively. In addition, total volumes of intensity (h week–1) were calculated, including all workouts above 75% of maximal aerobic running speed or maximal aerobic cycling workload. Values of total volume of intensity were 1 h 28 min (±0 h 39 min) and 1 h 48 min (±0 h 38 min), representing 13% (± 5) and 17% (± 7) of mean overall volumes for SNH and NNC, respectively, the latter being better indicators of the training density imposed on the athletes.
Environmental conditions (hypoxia and normoxia)
A generator, equipped with a semi-permeable filtration membrane continuously pumping hypoxic air into the tents (204 cm x 153 cm x 165 cm), was used to lower oxygen percentage (to 12–14%) at a flow rate of 96 l min–1 (Hypoxico Inc., New York, NY, USA). After reaching targeted oxygen concentrations, athletes were exposed to the hypoxic environment for 8 h. Oxygen concentrations were monitored before and after SNH (Cambridge Sensotec, St Ives, Cambs, UK). Oxygen saturation of the blood and heart rate were monitored overnight during treatments with a portable oxymeter (3303; BCI Inc., Waukesha, WI, USA). Atmospheric conditions (temperature, barometric pressure and humidity) were collected over the course of the study. For NNC, an identical set-up was used (with active pumps and oxygen concentration monitoring), except that ambient air was pumped into the tents. As well as being asked if they believed they were under SNH or NNC, athletes' comments on discomfort or sleeplessness were recorded during the treatments in order to determine whether athletes were aware of being exposed. Analysis of their responses (not shown) revealed that they could not distinguish between the two conditions.
Hydrostatic weighing
Body density was assessed by hydrostatic weighing as previously described (Wilmore et al. 1999). Prior to hydrostatic weighing, height and body weight were measured (± 0.1 cm, ± 0.1 kg). Lung volume and capacity were determined using the oxygen-dilution principle (Model K520, KL Engineering, Sunnydale, CA, USA). Thereafter, the subjects, immersed in water, were instructed to exhale completely to the point of residual lung volume, at which point a load cell interfaced with a computer was used to obtain the underwater measurement of body weight. Ten measurements were obtained and the three highest values were averaged.
Maximal exercise tests
All athletes were familiar with performance testing procedures because they are regularly used in their training centres. Determination of 
and time-to-exhaustion (Tlim) tests were conducted on a Schwinn cycle ergometer (IC Pro, Schwinn Cycling & Fitness Inc., Louisville, KY, USA) equipped with a 1500 W electronic load generator (Racer Mate Inc., Seattle, WA, USA). This device allowed accurate monitoring of power output (with a random error of ± 2.5%) and cadence. The handlebars and racing seat were adjusted vertically and horizontally according to athletes' preferences. During both tests, athletes wore cycling shoes equipped with toe-clips and maintained a familiar and comfortable pedaling rate greater than 60 r.p.m. through the test. The maximal oxygen uptake determination test was initiated at an initial power output of 200 W for males and of 140 W for females. Increments of 20 W were made every minute until reaching 300 W for males and 200 W for females. Thereafter, the workload was increased by 10 W every minute until exhaustion, allowing a precise assessment of the power output associated with 
for subsequent Tlim tests. In order to calculate Tlim
kinetics, resting metabolic rate was recorded prior to the test by asking athletes to sit quietly on the cycle ergometer for 5–10 min. If O2 values did not reach a 2 min plateau, a longer resting period was allowed to stabilize athlete's resting metabolic rate. After that, the test was initiated with a rapid power output adjustment (within 10 s) and lasted until exhaustion. Briefly, the stopwatch was started when the targeted power output was reached and the test was terminated as soon as subjects were unable to maintain a pedalling rate over 60 r.p.m.; Tlim was then determined (Basset et al. 2003).
Wingate tests were performed on a modified Monark cycle ergometer. A photoelectric cell and a potentiometer allowed the measurement of flywheel revolution and produced tension, respectively. An electrical timing system controlled the input to the microprocessor, and the total work performed for each second was recorded. During the test, athletes were instructed to pedal as fast as possible for 30 s. The resistance was adjusted within 3–4 s. The workload was determined according to body weight (75 g kg–1). Maximal velocity (m s–1), peak power output (W), peak power output per kilogram of body weight (W kg–1) and mean power output (W) were determined by a program previously developed by our team (Bouchard et al. 1991). Fatigue indices were obtained by computing regression equations from raw data.
All tests were conducted following a 15 min warm-up at 100 W for males and at 50 W for females. Athletes were instructed to maintain the same position on the cycle ergometer during the entire test. To ensure a complete recovery, a 48 h rest was allowed between 
, Tlim and Wingate tests. All experimental sessions were conducted at the same time of the day (8.00–12.00 am).
Physiological measurements
For maximal oxygen uptake determination and time-to-exhaustion tests, 
, minute ventilation 
and respiratory exchange ratio (RER) were continuously recorded with an automated breath-by-breath system (K4B2, Cosmed, Rome, Italy) using a Nafion filter tube and a turbine flowmeter (opto-electric). Prior to testing, gas analysers and volume were calibrated with medically certified calibration gases (15% O2 and 5% CO2) and with a 3 l calibration syringe, respectively. Heart rate values were collected with a Polar Vantage XL heart rate monitor (PolarElectro, Kempele, Finland). The criterion used for determination of 
was a plateau in oxygen uptake, corresponding to less than 50 ml min–1 raise (Astorino et al. 2000) despite increasing power output. In order to determine maximal O2 values, time-averaged 15 s intervals were used.
kinetics for time to exhaustion
To reduce the breath-by-breath noise, 
data were smoothed with a five-breath moving average filter (MatLab, MathWorks Inc,, Natick, MA, USA). The time course of the 
response after the onset of exercise was described in terms of a mono-exponential function, by using iterative non-linear regression:
|
|
is the oxygen consumption at baseline, 
(ml min–1) and A1 are asymptotic values, TD is a not-fixed time delay for each exponential term and 
is a time constant (min) to reach 63% of amplitude A1. This function was used to examine the fast component modifications only, and because most of the athletes had too short time-to-exhaustion values to observe a slow component phenomenon. Blood sampling
Blood samples were drawn from the antecubital vein under standardized conditions in a supine position after an overnight fast. Samples were collected within the hour after the second night during treatments, except for the first sample, which was collected following an overnight (12 h) fast and served as a control. All blood samples were withdrawn between 7.00 and 8.00 am. Red blood cell (RBC) count, reticulocyte cell count, white blood cell (WBC) count and platelet count were determined using an automated cytological cell counter (Model General-S, Berkman Coulter, Fullerton, CA, USA). Ferritin and transferrin were assessed by a fluorogenic enzyme-linked immunoassay (ELISA, Dade Behring, Mississauga, ON, Canada) and by chemoluminescence immunoassay (Dade Behring), respectively. Serum iron measurement was assessed by immunoenzymatic assay (Vitros Chemistry, Raritan, NJ, USA) and EPO concentration was determined by an enzyme-linked immunosorbent assay (ELISA, Labotech Biomech Chem, Franklin Lakes, NJ, USA).
Muscle biopsies
Athletes underwent muscle biopsies before and after treatments. Muscle biopsies were obtained in the morning following an overnight (12 h) fast from the middle portion of the right vastus lateralis muscle (i.e. about 15 cm above the patella and about 2 cm away from the epimysium) by the percutaneous needle biopsy technique as previously described by (Evans et al. 1982) and regularly used in our laboratory (Simoneau & Bouchard, 1995). Muscle samples were divided into two parts: one part was immediately frozen in liquid nitrogen for subsequent determination of muscle enzyme activities; the other part was trimmed, mounted on corkboard, and frozen in isopentane cooled on liquid nitrogen for subsequent histochemical analyses. All samples were then stored at –80°C until used.
Skeletal muscle histochemistry
Cross-sections (10 µm) of isopentane-frozen muscle were cut with a microtome at –20°C and stained for myosine ATPase (mATPase) and capillaries (Simoneau et al. 1986). The single-step staining procedure allowed the identification of three fibre types (I, Ia and IIb) in the same section. To measure the cross-sectional area of the different fibre types, sections were examined under a light microscope (Leitz Dialux 20), which was connected to a CCD camera (Sony C-350), with an analog-to-digital conversion system. Image analysis was performed with a Power Macintosh computer using the public domain NIH Image program (developed at the US National Institutes of Health and available on the Internet at http://rsb.info.nih.gov/nih-image/). The mean cross-sectional area was determined by averaging the measurement of 30 randomly selected fibres of each type that had been obtained from the mATPase-stained sections.
Skeletal muscle enzyme activities
Small pieces of muscle (
10 mg) were homogenized in a glass–glass homogenizer with 39 volumes of ice-cold extracting medium (0.1 M Na-K-phosphate, 2 mM EDTA, pH 7.2), and enzyme activities were measured as previously described (Simoneau et al. 1986). The enzymes measured were creatine kinase (CK; EC 2.7.3.2
[EC]
), citrate synthase (CS; EC 4.1.3.7
[EC]
), cytochrome c oxidase (COX; EC 1.9.3.1
[EC]
), phosphofructokinase (PFK; EC 2.7.1.11
[EC]
), glyceraldehyde phosphate dehydrogenase (GAPDH; EC 1.2.1.12
[EC]
), ß-hydroxyacyl CoA dehydrogenase (HADH; EC 1.1.1.35
[EC]
), hexokinase (HK; EC 2.7.1.1
[EC]
) and glycogen phosphorylase (GPHOS; EC 2.4.1.1
[EC]
). The enzyme activities are expressed in units of micromoles of substrate converted per minute per gram of wet tissue (U g–1). The intraindividual reproducibility of this measurement has previously been reported (Simoneau et al. 1986).
Buffer capacity and muscle pH
The buffer capacity (ßm) measurement used in the present study was based upon that of Gore et al. (2001). The muscle sample was dissected free of any remaining connective tissue, fat and blood prior to homogenization on ice with a manual glass homogenizer. The muscle samples were homogenized (1:40 dilution) in 145 mmol l–1 KCl, 10 mmol l–1 NaCl, and 5 mmol l–1 sodium iodoacetate (NaIAA), pH 7.0. The pH of the homogenate was measured at 37°C using a microelectrode (Accumet Engineering Corporation, Hudson, MA, USA), and was adjusted to pH 7.2 by addition of NaOH (10 mmol l–1). Homogenates, briefly vortexed, were titrated from pH 7.2 to 6.1 with successive additions of 2 µl aliquots of 10 mmol l–1 HCl. Results are expressed as µmol H+ (g muscle)–1 (pH unit)–1.
Salivary cortisol
Salivary cortisol was measured as a marker of physiological response to acute stress (Schulz et al. 1998). Samples were obtained immediately after waking and 30 min later following treatments, under the same conditions used for blood sampling. Samples were collected by stimulating saliva flow by chewing on a salivette (IBL, Hamburg, Germany) for 1 min. Soaked salivettes were carefully placed in an aseptic and airtight tube and stored at –80°C prior to further analysis. After thawing, salivettes were centrifuged at 2000 g at 4°C for 5 min, and 100 µl of the recovered supernatant was used for duplicate analysis employing a time-resolved immunoassay with fluorescence detection (Medicor Inc., Montréal, QC, Canada) as previously described (Dressendorfer et al. 1992).
Statistical analysis
All variables are presented as means (±S.D.) and 90% confidence intervals. Levene tests for equality of variances were performed and, if significant, logarithmic adjustments were made. One-way analysis of variance (Pre to Post) was performed on anthropometrics characteristics, training status, haematological parameters, muscle histo- and biochemical parameters, and anaerobic and aerobic performance parameters independently for each treatment (SNH and NNC). In addition, a mixed linear model was used to account for error of measurement in the estimate of differences in the change on haematological parameters, muscle histo- and biochemical parameters, and anaerobic and aerobic performance parameters caused by treatments. Within-athlete coefficients of variation (c.v.) were also obtained for each parameter and averaged to yield between-athlete coefficients of variation for both treatments. Three-way analysis of variance [2 experimental conditions (SNH and NNC) x 2 periods (Pre and Post) x 2 times (waking and waking +30 min)] for repeated measures was computed for salivary cortisol. In order to look at intra- and interindividual variations, the mean change in each parameter has been derived from pre- and post-treatment values by computing the following:
|
|
|
Results |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
No weight loss was recorded either by weighing scale or by hydrostatic weighing throughout the study. Even though no training profile difference was observed between speed skaters and cross-country skiers, the latter showed a higher training volume over the course of the study (Table 1). Moreover, no difference was observed between SNH and NNC on training parameters (mean overall volume and volume of intensity training).
Environmental conditions, and overnight blood oxygen saturation and heart rate
Averages of ambient (outside the tent) environmental conditions were 19.7 (0.8) and 19.3 (0.9)°C, 100.6 (0.6) and 100.3 (1.2) kPa, and 54.9 (19.2) and 57.5 (13.7)% humidity for SNH and NNC, respectively. The average O2 concentration within tents during SNH was 13.4 ± 0.5% and ranged from 12.5 to 14.5%, simulating an average altitude of 3636 m. Blood oxygen saturation was significantly lower [84.4 (1.1) and 97.8 (0.4)%] and heart rate significantly higher [60.2 (2.5) and 51.5 (1.3) beats min–1] during SNH compared to NNC. In addition, a significant simple negative linear relationship between heart rate and blood oxygen saturation was observed (r2=–0.42).
Measures of performance
No significant change was observed in aerobic or anaerobic performance following SNH or NNC exposure (Table 2). Also, no differences were noted in performance between SNH and NNC. To investigate further the effect of SNH and NNC, we report coefficients of variation, percentage change and mean difference along with confidence intervals. For the sake of brevity, we present only variables of interest. Coefficients of variation for 
were 3.7 and 3.8% for SNH and NNC, respectively. 
percentage changes between pre- and post-treatments were 3.5 (90%CI = 0.1–6.8) and 4.3% (90%CI = 0.8–7.8) for SNH and NNC, respectively, and the mean difference of 
between post-SNH and post-NNC was 20.4 ml min–1 (90%CI =–540–580 ml min–1). Coefficients of variation for oxygen uptake reached during Tlim
had a similar range of variation, 3.6 and 4.8% for SNH and NNC, respectively. Even though oxygen uptake reached during 
percentage changes between pre- and post-treatments were lower, with values of 0.4 (90%CI =–3.5–4.3) and 2.5 (90%CI =–2.4–7.4) compared to those obtained in 
, confidence intervals were greater. On the basis of the confidence intervals (90%CI =–646–612 ml min–1), and although Tlim
mean difference between post-SNH and post-NNC was smaller (16.7 ml min–1), it is clearly more variable compared to 
values. Although c.v.s for the Tlim tests seem large (16.0% for SNH and 17.0% for NNC), they are similar in magnitude in both treatments, which did not correspond to Tlim percentage changes, since means were 5.2 (90%CI =–15.3–25.6) and 13.5% (90%CI =–4.4–31.4) for SNH and NNC, respectively. Wingate peak power output also showed important c.v.s (8.6 and 13.3%), and the mean difference between post-SNH and post-NNC was 66.4 W (90%CI =–108.5–241.3 W). The Wingate peak power output percentage changes were 3.6 (90%CI =–5.1–12.3) and 6.2% (90%CI =–5.7–18.3) for SNH and NNC, respectively. Finally, no significant correlation was found between mean change in performance and mean change in haematological and muscle phenotype parameters.
|
Statistical analysis revealed a significant increase in RBC count, haemoglobin, haematocrit, platelets and EPO following SNH (Table 3). No changes to haematological parameters were observed following NNC. Coefficient of variation, percentage change and mean difference have been reported to illustrate how the O2 transport-related parameters varied with treatments. Coefficients of variation for RBC count were 4.3 and 1.7% for SNH and NNC, respectively. RBC count percentage changes between pre- and post-treatments were 6.1 (90%CI = 4.4–7.8) and 0.6% (90%CI =–1.7–2.8), and the mean difference between post-SNH and post-NNC was 0.19% (90%CI =–0.11–0.49). Haemoglobin showed the same pattern of variation, since the SNH c.v. was higher (4.0%) compared to NNC c.v. (2.2%), whereas percentage changes were 5.8 (90%CI = 4.2–7.4) and –0.8% (90%CI =–3.4–1.8). The mean difference between post-SNH and post-NNC reached 5.5% (90%CI =–3.6–14.7). For haematocrit, the c.v.s were 3.9 and 1.9%; percentage changes between pre- and post-treatments were 5.5 (90%CI = 3.8–7.1) and 0.6% (90%CI =–1.7–2.9). The mean difference between post-SNH and post-NNC was 0.16% (90%CI =–0.10–0.42). EPO demonstrated the most important variation among haematological parameters. SNH c.v. was higher (52.7%) compared to the NNC value (27.3%). This was accompanied by a high percentage change and a wide confidence interval in SNH, 143.4% (53.4–233.3). However, in NNC the corresponding values were smaller, only reaching 18.8% (–12.0–49.9). This was reflected by a mean difference of 9.6% (90%CI = 1.7–17.5) between post-treatments.
|
Except for a modest (–9.7%) but significant decrease in PFK activity, SNH exposure had no effect of the activities of a number of enzymes of energy metabolism, muscle buffer capacity, capillary contacts, fibre type distribution or fibre size (Table 4). The mixed linear model output showed that c.v.s for PFK were 9.4 and 11.7% for SNH and NNC, respectively. PFK percentage changes between pre- and post-treatments were –9.0 (90%CI =–16.1–1.8) and 6.5% (90%CI =–9.7–22.7), for SNH and NNC, respectively, and the mean difference between post-SNH and post-NNC was –6.4% (90%CI =–11.9–0.9).
|
Significant time (waking versus waking +30 min) and period (Pre versus Post) effects were observed on salivary cortisol concentrations. Mean values for waking and waking +30 min were 0.68 Ng · dL–1 (90%CI = 0.59–0.77) and 0.87 (90%CI = 0.73–1.00), and 0.76 (90%CI = 0.63–0.89) and 1.05 (90%CI = 0.91–1.2) for pre- and post-NNC, respectively; whereas SNH mean values for waking and waking +30 min were 0.77 (90%CI = 0.64–0.89) and 0.99 (90%CI = 0.84–1.1), 0.66 (90%CI = 0.57–0.75) and 0.92 (90%CI = 0.81–1.04), for pre- and post-SNH, respectively. However, no significant effect of treatment (SNH versus NNC) was observed.
|
Discussion |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
The effect of short-term normobaric hypoxia on haematological parameters and on salivary cortisol
Results of the present study clearly showed that SNH increased blood O2 transport-related parameters (Table 3). This increase is in accordance with previous reports (Monge & Leon-Velarde, 1991; Mairbaurl, 1994) and has been considered as the main organism adaptation to hypoxia. In this study, increases in RBC count, haematocrit and haemoglobin certainly reflect general erythropoiesis activation in response to presumed renal tissue hypoxia (Calbet et al. 2002). In this regard, Klausen et al. (1991) have studied the time course response in haematological parameters, demonstrating that EPO was the first adaptive mechanism during hypoxia, accompanied by asynchronous haematological variations. Previously, Eckardt et al. (1989) observed a rapid increase in plasma EPO values in the early phase of hypoxia exposure (between 4 and 6 h), with higher values at 4000 than at 3000 m. Recently, Heinicke et al. (2003) confirmed that EPO is released in the first 48 h of hypoxia exposure, elevated levels lasting for 4–7 days. Contrary to our results, Ashenden et al. (1999a,b, 2000) failed to observe any change in haematological parameters, which may be due to the fact that O2 concentration level and athlete characteristics were quite different. In the studies of Ashenden et al. (1999a,b, 2000), subjects have sojourned from 12 to 23 nights at a simulated altitude of 2650–3000 m. By comparison, O2 concentrations in the present 6 day SNH protocol were lower (3636 m), possibly inducing a greater EPO response. In that way, the 13.4% average O2 concentration measured in the tents during short-term normobaric hypoxia was, as expected, associated with significantly decreased values of arterial O2 saturation and increased heart rate. This latter finding is undoubtedly a mechanism to compensate for decreased blood oxygen saturation, as indicated by a significant negative relationship between these measures (r2=–0.42).
Statistical analysis revealed a significant effect of time (waking and waking +30 min) on salivary cortisol, in addition to a significant effect of period (Pre and Post). These outcomes are in accordance with those of Schulz et al. (1998). Thus, salivary cortisol values decreased over the course of the study. The confidence intervals clearly confirmed this effect. No effect of SNH was recorded, however, suggesting that SNH exposure did not induce an important additional physiological stress.
The effect of short-term normobaric hypoxia on skeletal muscle
Our SNH protocol had very little impact on a number of muscle phenotypes. No significant effects were noted for most activities of enzymes related to energy metabolism (except a modest but significant decrease in PFK activity), and there were no significant changes in capillary contacts with fibres or capillary density, muscle fibre type distribution or size, or buffer capacity. Several factors could explain these results. First, athletes involved in this project had an average of 10 years of highly intensive training that has probably optimized their cardiovascular and muscular systems. These long-term training effects undoubtedly induced glycolytic and oxidative enzymatic pathway adaptations resulting from high-intensity exercises, as in the exercise-induced hypoxia concept (Costill et al. 1976; Foster et al. 1978). Second, according to our results and supported by several years of scientific research (Wilber, 2001), it seems that SNH benefits are not clearly dissociated from training adaptations. In fact, Vallier et al. (1996) reported that aerobic metabolism, which is already optimized in highly trained athletes, did not respond to additional effects of hypoxia, whereas significant effects of hypobaric hypoxia on physical performance were observed in sedentary subjects. One can postulate that the sojourn duration of the present study was not of sufficient duration to elicit adaptation, but recent studies conducted by Gore et al. (2001) and Clark et al. (2004) showed that 20–23 days of exposure to hypoxia did not induce skeletal muscle enzyme activity modifications but increased muscle ßm in parallel with a decrease in lactate production. Earlier, Mizuno et al. (1990) showed significant decreases in PFK, CS and HADH activities after 2 weeks of altitude training (2700 m) without effects on 
. Nevertheless, their athletes improved time to exhaustion, accompanied by a 6% increase in muscle ßm. In the above-mentioned studies (Mizuno et al. 1990; Gore et al. 2001; Clark et al. 2004), hypoxia intervention brought about increased ßm, suggesting a compensation mechanism for oxidative enzymatic pathway depression. The threshold O2 concentrations and sojourn duration required to induce muscle adaptation in highly trained athletes have yet to be determined.
The effect of short-term normobaric hypoxia on physical performance
In this study, no significant SNH effect was observed on physical performance, in agreement with some (Gore et al. 1996, 2001; Emonson et al. 1997; Hahn et al. 2001; Townsend et al. 2002; Roberts et al. 2003; Clark et al. 2004; Julian et al. 2004) but contrary to other previous studies (Levine et al. 1992; Levine & Stray-Gundersen, 1992, 1997; Chapman et al. 1998; Truijens et al. 2003). In a study of a 4 week intermittent hypobaric hypoxia period (live high–train low), Levine & Stray-Gundersen (1997) observed a significant increase of 
and aerobic performance in athletes having a recent 5000 m personal best in running (< 16 min 30 s for males; < 18 min 30 s for females). However, these authors reported a mere 5% increase in 
, leading to questions about the ability to discriminate between biological variation and measurement error. To control for biological variations, Chapman et al. (1998) identified responder and non-responder athletes to altitude training. They reported that, in addition to increased EPO values and total red cell volume, responders improved their 
and maximal steady-state exercise, confirming data from Levine & Stray-Gundersen (1997). From these studies, physiological improvements appear to contribute to the enhancement of the sea-level performances. However, following 23 nights of simulated altitude (3000 m), Gore et al. (2001) showed a significant decrease of 
(–7%) with a significant increase in muscle ßm, inducing anaerobic performance improvement in highly trained athletes. Thus, the reduced availability of oxygen did not lead to enhanced transportation and utilization of O2 in exercising muscle. In addition, Roberts et al. (2003) confirmed that anaerobic capacity increased with short-term hypoxia exposure by showing a significant increase in maximal accumulated oxygen deficit, while Hahn et al. 2001) noticed that after a period of sleeping in moderate hypoxia, many athletes seem able to generate more work per litre of oxygen consumed and therefore it seems that any performance benefit is likely to stem from either increased anaerobic capacity or greater efficiency of aerobic metabolism (perhaps from a switch to carbohydrate oxidation). Nummela & Rusko (2000) also reported that changes in the acid–base balance and lactate metabolism might be responsible for the improvement in sprint performance, concluding that hypoxia-induced changes might be related to changes in anaerobic capacity and muscle ßm. Several authors (Boning, 1997; Baker & Hopkins, 1998; Wilber, 2001) agree that long-term hypoxia exposure modifies skeletal muscle enzymatic activities in parallel with an increase in lactate metabolism and an increase in anaerobic performance. In the present study, since no significant increases were observed in 
or anaerobic power, we conclude that the present protocol was unable to induce positive physiological changes leading to improved performance in highly trained athletes. Finally, controversy remains because some authors observed an increase in glycolytic enzymatic activities in parallel with a decrease in oxidative enzymatic activities without improvement in aerobic and anaerobic performances (Vallier, 1995; Wilber, 2001). Therefore, in addition to the poor efficacy of the protocol, intra- and interindividual variability seems to be a key factor. Hence, individual responses to SNH vary widely, as shown by the coefficients of variation and the 90% confidence intervals. It can be argued from these results that this substantial interindividual variability in the adaptive response to hypoxia could represent non-physiological factors influencing exercise performance as well as insensitivity of physiological markers to hypoxia-induced adaptation.
|
Footnotes |
|---|
In memory of Dr Guy Falgairette who passed away suddenly on 17 February 2005 
|
References |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
Ashenden MJ, Gore CJ, Dobson GP & Hahn AG (1999a). ‘Live high, train low’ does not change the total haemoglobin mass of male endurance athletes sleeping at a simulated altitude of 3000 m for 23 nights. Eur J Appl Physiol 80, 479–484.
Ashenden MJ, Gore CJ, Martin DT, Dobson GP & Hahn AG (1999b). Effects of a 12-day ‘live high, train low’ camp on reticulocyte production and haemoglobin mass in elite female road cyclists. Eur J Appl Physiol 80, 472–478.
Astorino TA, Roberts RA, Ghiasvand F, Marks D & Burns S (2000). Incidence of the oxygen plateau at 
during exercise testing to volitional fatigue. J Exerc Physiol 3, 1–12.
Bailey DM, Davies B & Baker J (2000). Training in hypoxia: modulation of metabolic and cardiovascular risk factors in men. Med Sci Sports Exerc 32, 1058–1066.[Medline]
Baker A & Hopkins WG (1998). Altitude training for sea-level competition. In Sportscience, DOI: http://sportsci.org/traintech/altitude/wgh.html.
Basset FA, Chouinard R & Boulay MR (2003). Training profile counts for time-to-exhaustion performance. Can J Appl Physiol 28, 654–666.[Medline]
Boning D (1997). Altitude and hypoxia training – a short review. Int J Sports Med 18, 565–570.[Medline]
Bouchard C, Taylor AW, Simoneau JA & Dulac S (1991). Testing anaerobic power and capacity. In Physiological Testing of the High-Performance Athlete, vol. 2, ed. MacDougall JD, Wenger HA & Green HJ, pp. 175–221. Canadian Association of Sport Sciences, Champaign.
Calbet JA, Radegran G, Boushel R, Sondergaard H, Saltin B & Wagner PD (2002). Effect of blood haemoglobin concentration on 
and cardiovascular function in lowlanders acclimatised to 5260 m. J Physiol 545, 715–728.
Chapman RF, Stray-Gundersen J & Levine BD (1998). Individual variation in response to altitude training. J Appl Physiol 85, 1448–1456.
Clanton TL & Klawitter PF (2001). Invited review: Adaptive responses of skeletal muscle to intermittent hypoxia: the known and the unknown. J Appl Physiol 90, 2476–2487.
Clark SA, Aughey RJ, Gore CJ, Hahn AG, Townsend NE, Kinsman TA, Chow CM, McKenna MJ & Hawley JA (2004). Effects of live high, train low hypoxic exposure on lactate metabolism in trained humans. J Appl Physiol 96, 517–525.
Costill DL, Daniels J, Evans W, Fink W, Krahenbuhl G & Saltin B (1976). Skeletal muscle enzymes and fiber composition in male and female track athletes. J Appl Physiol 40, 149–154.
Dressendorfer RA, Kirschbaum C, Rohde W, Stahl F & Strasburger CJ (1992). Synthesis of a cortisol-biotin conjugate and evaluation as a tracer in an immunoassay for salivary cortisol measurement. J Steroid Biochem Mol Biol 43, 683–692.[CrossRef][Medline]
Eckardt KU, Boutellier U, Kurtz A, Schopen M, Koller EA & Bauer C (1989). Rate of erythropoietin formation in humans in response to acute hypobaric hypoxia. J Appl Physiol 66, 1785–1788.
Emonson DL, Aminuddin AH, Wight RL, Scroop GC & Gore CJ (1997). Training-induced increases in sea level 
and endurance are not enhanced by acute hypobaric exposure. Eur J Appl Physiol 76, 8–12.[CrossRef]
Evans WJ, Phinney SD & Young VR (1982). Suction applied to a muscle biopsy maximizes sample size. Med Sci Sports Exerc 14, 101–102.[Medline]
Foster C, Costill DL, Daniels JT & Fink WJ (1978). Skeletal muscle enzyme activity, fiber composition and 
in relation to distance running performance. Med Sports Sci 11, 338–344.
Gore CJ, Hahn AG, Aughey RJ, Martin DT, Ashenden MJ, Clark SA, Garnham AP, Roberts AD, Slater GJ & McKenna MJ (2001). Live high: train low increases muscle buffer capacity and submaximal cycling efficiency. Acta Physiol Scand 173, 275–286.[CrossRef][Medline]
Gore CJ, Hahn AG, Scroop GC, Watson DB, Norton KI, Wood RJ, Campbell DP & Emonson DL (1996). Increased arterial desaturation in trained cyclists during maximal exercise at 580 m altitude. J Appl Physiol 80, 2204–2210.
Green HJ, Sutton JR, Cymerman A, Young PM & Houston CS (1989). Operation Everest II: adaptations in human skeletal muscle. J Appl Physiol 66, 2454–2461.
Hahn AG, Gore CJ, Martin DT, Ashenden MJ, Roberts AD & Logan PA (2001). An evaluation of the concept of living at moderate altitude and training at sea level. Comp Biochem Physiol 128, 777–789.
Heinicke K, Prommer N, Cajigal J, Viola T, Behn C & Schmidt W (2003). Long-term exposure to intermittent hypoxia results in increased hemoglobin mass, reduced plasma volume, and elevated erythropoietin plasma levels in man. Eur J Appl Physiol 88, 535–543.[Medline]
Hoppeler H & Vogt M (2001). Muscle tissue adaptations to hypoxia. J Exp Biol 204, 3133–3139.
Hoppeler H, Vogt M, Weibel ER & Fluck M (2003). Response of skeletal muscle mitochondria to hypoxia. Exp Physiol 88, 109–119.[Abstract]
Julian CG, Gore CJ, Wilber RL, Daniels JT, Fredericson M, Stray-Gundersen J, Hahn AG, Parisotto R & Levine BD (2004). Intermittent normobaric hypoxia does not alter performance or erythropoietic markers in highly trained distance runners. J Appl Physiol 96, 1800–1807.
Klausen T, Mohr T, Ghisler U & Nielsen OJ (1991). Maximal oxygen uptake and erythropoietic responses after training at moderate altitude. Eur J Appl Physiol 62, 376–379.
Levine BD, Friedman DB, Engfred K, Hanel B, Kjaer M, Clifford PS & Secher NH (1992). The effect of normoxic or hypobaric hypoxic endurance training on the hypoxic ventilatory response. Med Sci Sports Exerc 24, 769–775.[Medline]
Levine BD & Stray-Gundersen J (1992). A practical approach to altitude training: where to live and train for optimal performance enhancement. Int J Sports Med 13, 209–212.
Levine BD & Stray-Gundersen J (1997). ‘Living high-training low’: effect of moderate-altitude acclimatization with low-altitude training on performance. J Appl Physiol 83, 102–112.
MacDougall JD, Green HJ, Sutton JR, Coates G, Cymerman A, Young P & Houston CS (1991). Operation Everest II: structural adaptations in skeletal muscle in response to extreme simulated altitude. 142, 421–427.
Mairbaurl H (1994). Red blood cell function in hypoxia at altitude and exercise. Int J Sports Med 15, 51–63.[Medline]
Mizuno M, Juel C, Bro-Rasmussen T, Mygind E, Schibye B, Rasmussen B & Saltin B (1990). Limb skeletal muscle adaptation in athletes after training at altitude. J Appl Physiol 68, 496–502.
Monge C & Leon-Velarde F (1991). Physiological adaptation to high altitude: oxygen transport in mammals and birds. Physiol Rev 71, 1135–1172.
Nummela A & Rusko H (2000). Acclimatization to altitude and normoxic training improve 400-m running performance at sea level. J Sports Sci 18, 411–419.[CrossRef][Medline]
Roberts AD, Clark SA, Townsend NE, Anderson ME, Gore CJ & Hahn AG (2003). Changes in performance, maximal oxygen uptake and maximal accumulated oxygen deficit after 5, 10 and 15 days of live high: train low altitude exposure. Eur J Appl Physiol 88, 390–395.[Medline]
Schulz P, Kirschbaum C, Prubner J & Hellhammer DH (1998). Increased free cortisol secretion after awakening in chronically stressed individuals due to work overload. Stress Med 14, 91–97.
Simoneau JA & Bouchard C (1995). Skeletal muscle metabolism and body fat content in men and women. Obes Res 3, 23–29.[Medline]
Simoneau JA, Lortie G, Boulay MR, Thibault MC & Bouchard C (1986). Repeatability of fibre type and enzyme activity measurements in human skeletal muscle. Clin Physiol 6, 347–356.[Medline]
Townsend NE, Gore CJ, Hahn AG, McKenna MJ, Aughey RJ, Clark SA, Kinsman T, Hawley JA & Chow CM (2002). Living high-training low increases hypoxic ventilatory response of well-trained endurance athletes. J Appl Physiol 93, 1498–1505.
Truijens MJ, Toussaint HM, Dow J & Levine BD (2003). Effect of high-intensity hypoxic training on sea-level swimming performances. J Appl Physiol 94, 733–743.
Vallier JM (1995). Effets d'un entraînement en chambre hypobare sur les performances physiques. PhD Dissertation, Université de Paris, Paris.
Vallier JM, Chateau P & Guezennec CY (1996). Effects of physical training in a hypobaric chamber on the physical performance of competitive triathletes. Eur J Appl Physiol 73, 471–478.[CrossRef]
Wilber RL (2001). Current trends in altitude training. Sports Med 31, 249–265.[CrossRef][Medline]
Wilmore JH, Despres JP, Stanforth PR, Mandel S, Rice T, Gagnon J, Leon AS, Rao D, Skinner JS & Bouchard C (1999). Alterations in body weight and composition consequent to 20 wk of endurance training: the HERITAGE Family Study. Am J Clin Nutr 70, 346–352.
|
Acknowledgements |
|---|
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
