Validity of the Online Athlete Management System to Assess Training Load.

PURPOSE: To validate the quantification of training load (session rating of perceived exertion [s-RPE]) in an Australian Olympic squad (women's water polo), assessed with the use of a modified RPE scale collected via a newly developed online system (athlete management system). METHODS: Sixteen elite women water polo players (age = 26 [3] y, height = 1.78 [0.05] m, and body mass = 75.5 [7.1] kg) participated in the study. Thirty training sessions were monitored for a total of 303 individual sessions. Heart rate was recorded during training sessions using continuous heart-rate telemetry. Participants were asked to rate the intensity of the training sessions on the athlete management system RPE scale, using an online application within 30 min of completion of the sessions. Individual relationships between s-RPE and both Banister training impulse (TRIMP) and Edwards' method were analyzed. RESULTS: Individual correlations with s-RPE ranged between r = .51 and .79 (Banister TRIMP) and r = .54 and .83 (Edwards' method). The percentages of moderate and large correlation were 81% and 19% between s-RPE method and Banister TRIMP, and 56% and 44% between s-RPE and Edwards' method. CONCLUSIONS: The online athlete management system for assessing s-RPE was shown to be a valid indicator of internal training load and can be used in elite sport.

Stage racing at altitude induces hemodilution despite an increase in hemoglobin mass.

Plasma volume (PV) can be modulated by altitude exposure (decrease) and periods of intense exercise (increase). Cycle racing at altitude combines both stimuli, although presently no data exist to document which is dominant. Hemoglobin mass (Hbmass), hemoglobin concentration ([Hb]), and percent reticulocytes (%Retics) of altitude (ALT; n = 9) and sea-level (SL; n = 9) residents were measured during a 14-day cycling race, held at 1,146-4120 m, as well as during a simulated tour near sea level (SIM; n = 12). Hbmass was assessed before and on days 9 and 14 of racing. Venous blood was collected on days 0, 3, 6, 10, and 14. PV was calculated from Hbmass and [Hb]. A repeated-measures ANOVA was used to assess the impact of racing at altitude over time, within and between groups. [Hb] decreased significantly in all groups over time (P < 0.0001) with decreases evident on the third day of racing. %Retics increased significantly in SL only (P < 0.0001), with SL values elevated at day 6 compared with prerace (P = 0.02), but were suppressed by the end of the race (P = 0.0002). Hbmass significantly increased in SL after 9 (P = 0.0001) and 14 (P = 0.008) days of racing and was lower at the end of the race than midrace (P = 0.018). PV increased in all groups (P < 0.0001). Multiday cycle racing at altitude induces hemodilution of a similar magnitude to that observed during SL racing and occurs in nonacclimatized SL residents, despite an altitude-induced increase in Hbmass. Osmotic regulatory mechanisms associated with intense exercise appear to supersede acute enhancement of oxygen delivery at altitude.

Altitude training and haemoglobin mass from the optimised carbon monoxide rebreathing method determined by a meta-analysis.

OBJECTIVE: To characterise the time course of changes in haemoglobin mass (Hbmass) in response to altitude exposure. METHODS: This meta-analysis uses raw data from 17 studies that used carbon monoxide rebreathing to determine Hbmass prealtitude, during altitude and postaltitude. Seven studies were classic altitude training, eight were live high train low (LHTL) and two mixed classic and LHTL. Separate linear-mixed models were fitted to the data from the 17 studies and the resultant estimates of the effects of altitude used in a random effects meta-analysis to obtain an overall estimate of the effect of altitude, with separate analyses during altitude and postaltitude. In addition, within-subject differences from the prealtitude phase for altitude participant and all the data on control participants were used to estimate the analytical SD. The 'true' between-subject response to altitude was estimated from the within-subject differences on altitude participants, between the prealtitude and during-altitude phases, together with the estimated analytical SD. RESULTS: During-altitude Hbmass was estimated to increase by ∼1.1%/100 h for LHTL and classic altitude. Postaltitude Hbmass was estimated to be 3.3% higher than prealtitude values for up to 20 days. The within-subject SD was constant at ∼2% for up to 7 days between observations, indicative of analytical error. A 95% prediction interval for the 'true' response of an athlete exposed to 300 h of altitude was estimated to be 1.1-6%. CONCLUSIONS: Camps as short as 2 weeks of classic and LHTL altitude will quite likely increase Hbmass and most athletes can expect benefit.

Ten days of simulated live high:train low altitude training increases Hbmass in elite water polo players.

OBJECTIVES: Water polo requires high aerobic power to meet the demands of match play. Live high:train low (LHTL) may enhance aerobic capacity at sea level. Before the Olympics, the Australian women's water polo team utilised LHTL in an attempt to enhance aerobic fitness. METHODS: Over 6 months, 11 players completed three normobaric LHTL exposures (block 1:11 days at 3000 m; block 2+3:9 days at 2500 m, 11 days normoxia, 10 days at 2800 m). Haemoglobin mass (Hbmass) was measured through carbon monoxide-rebreathing. Before each block, the relationship between Hbmass and water polo-specific aerobic fitness was investigated using the Multistage Shuttle Swim Test (MSST). Effect size statistics were adopted with likely, highly likely and almost certainly results being >75%, >95%, >99%, respectively. A Pearson product moment correlation was used to characterise the association between pooled data of Hbmass and MSST. RESULTS: Hbmass (mean ± SD, pre 721 ± 66 g) likely increased after block 1 and almost certainly after block 2+3 (% change; 90% confidence limits: block 1: 3.7%; 1.3-6.2%, block 2+3: 4.5%; 3.8-5.1%) and the net effect was almost certainly higher after block 2+3 than before block 1 (pre) by 8.5%; 7.3-9.7%. There was a very large correlation between Hbmass (g/kg) and MSST score (r=0.73). CONCLUSIONS: LHTL exposures of <2 weeks induced approximately 4% increase in Hbmass of water polo players. Extra Hbmass may increase aerobic power, but since match performance is nuanced by many factors it is impossible to ascertain whether the increased Hbmass contributed to Australia's Bronze medal.

Within-subject variation in hemoglobin mass in elite athletes.

UNLABELLED: Illicit autologous blood transfusion to improve performance in elite sport is currently undetectable, but the stability of longitudinal profiles of an athlete's hemoglobin mass (Hbmass) might be used to detect such practices. PURPOSE: Our aim was to quantify within-subject variation of Hbmass in elite athletes, and the effects of potentially confounding factors such as reduced training or altitude exposure. METHODS: A total of 130 athletes (43 females and 87 males) were measured for Hbmass an average of six times during a period of approximately 1 yr using carbon monoxide rebreathing. Linear mixed models were used to quantify within-subject variation of Hbmass and its associated analytical and biological components for males and females, as well as the effects of reduced training and moderate altitude exposure in certain athletes. RESULTS: The maximum within-subject coefficient of variation (CV) for Hbmass was 3.4% for males and 4.0% for females. The analytical CV was ~2.0% for both males and females, and the long-term biological CV, after allowing for analytical variation, was 2.8% for males and 3.5% for females. On average, self-reported reduced training resulted in a 2.8% decrease in Hbmass and altitude exposure increased Hbmass by 1.5% to 2.9%, depending on the duration and type of exposure. CONCLUSIONS: The within-subject CV for Hbmass of ~4% indicates that athletes may experience changes up to ~20% with a 1-in-1000 probability. Changes of this magnitude for measures taken a few months apart suggest that Hbmass has a limited capacity to detect autologous blood doping. However, changes in Hbmass may be a useful indicator when combined with other measures of blood manipulation.

Standardising analysis of carbon monoxide rebreathing for application in anti-doping.

Determination of total haemoglobin mass (Hbmass) via carbon monoxide (CO) depends critically on repeatable measurement of percent carboxyhaemoglobin (%HbCO) in blood with a hemoximeter. The main aim of this study was to determine, for an OSM3 hemoximeter, the number of replicate measures as well as the theoretical change in percent carboxyhaemoglobin required to yield a random error of analysis (Analyser Error) of ≤1%. Before and after inhalation of CO, nine participants provided a total of 576 blood samples that were each analysed five times for percent carboxyhaemoglobin on one of three OSM3 hemoximeters; with approximately one-third of blood samples analysed on each OSM3. The Analyser Error was calculated for the first two (duplicate), first three (triplicate) and first four (quadruplicate) measures on each OSM3, as well as for all five measures (quintuplicates). Two methods of CO-rebreathing, a 2-min and 10-min procedure, were evaluated for Analyser Error. For duplicate analyses of blood, the Analyser Error for the 2-min method was 3.7, 4.0 and 5.0% for the three OSM3s when the percent carboxyhaemoglobin increased by two above resting values. With quintuplicate analyses of blood, the corresponding errors reduced to .8, .9 and 1.0% for the 2-min method when the percent carboxyhaemoglobin increased by 5.5 above resting values. In summary, to minimise the Analyser Error to ∼≤1% on an OSM3 hemoximeter, researchers should make ≥5 replicates of percent carboxyhaemoglobin and the volume of CO administered should be sufficient increase percent carboxyhaemoglobin by ≥5.5 above baseline levels.

Carbon monoxide uptake kinetics of arterial, venous and capillary blood during CO rebreathing.

The uptake and distribution of CO throughout the circulatory system during two different methods of CO rebreathing (2 min 'Schmidt' and 40 min 'Burge' methods) were determined in nine healthy volunteers. Specifically, the impact of (i) differences in circulatory mixing time (t(mix)), (ii) CO diffusion to myoglobin (Mb) and (iii) CO wash-out was assessed on calculated haemoglobin mass (Hb(mass)). Arterial (a), muscle venous (vm) and capillary samples (c) were obtained simultaneously at 0, 1, 2, 3.5, 5, 7.5, 10, 12.5, 15, 20, 30 and 40 min for determination of carboxyhaemoglobin (HbCO). Carbon monoxide wash-out was measured from expired air following rebreathing. The rate of CO diffusion to Mb was calculated using the change in HbCO after t(mix), and the rate of CO wash-out. In both methods, HbCOa and HbCOc followed a near-identical time course, peaking within the first 2 min and decreasing thereafter. The HbCOvm increased slowly and was significantly lower at 1, 2 and 3.5 min in both methods (P < 0.01). The HbCOa peaked significantly higher in the Schmidt method (P = 0.03). Circulatory mixing had occurred by 10 min in most but not all subjects. The rate of CO wash-out was 0.25 ± 0.13 ml min⁻¹ in the Schmidt and 0.25 ± 0.16 ml min⁻¹ in the Burge method. The rate of CO diffusion to Mb was 0.22 ± 0.11 and 0.16 ± 0.13 ml min⁻¹ (P = 0.63) in Schmidt and Burge methods, respectively. Inhalation of a CO bolus during the Schmidt method results in faster HbCOa uptake but does not greatly shorten t(mix) or influence rates of CO wash-out and flux to Mb. The calculated Hb(mass) depends substantially on the plateau level of HbCO; therefore, it is paramount to ensure HbCO is mixed completely prior to blood sampling, as well as accounting for potential within-subject alterations of CO exhalation and CO flux to Mb.

Daily training with high carbohydrate availability increases exogenous carbohydrate oxidation during endurance cycling.

We determined the effects of varying daily carbohydrate intake by providing or withholding carbohydrate during daily training on endurance performance, whole body rates of substrate oxidation, and selected mitochondrial enzymes. Sixteen endurance-trained cyclists or triathletes were pair matched and randomly allocated to either a high-carbohydrate group (High group; n = 8) or an energy-matched low-carbohydrate group (Low group; n = 8) for 28 days. Immediately before study commencement and during the final 5 days, subjects undertook a 5-day test block in which they completed an exercise trial consisting of a 100 min of steady-state cycling (100SS) followed by a 7-kJ/kg time trial on two occasions separated by 72 h. In a counterbalanced design, subjects consumed either water (water trial) or a 10% glucose solution (glucose trial) throughout the exercise trial. A muscle biopsy was taken from the vastus lateralis muscle on day 1 of the first test block, and rates of substrate oxidation were determined throughout 100SS. Training induced a marked increase in maximal citrate synthase activity after the intervention in the High group (27 vs. 34 micromol x g(-1) x min(-1), P < 0.001). Tracer-derived estimates of exogenous glucose oxidation during 100SS in the glucose trial increased from 54.6 to 63.6 g (P < 0.01) in the High group with no change in the Low group. Cycling performance improved by approximately 6% after training. We conclude that altering total daily carbohydrate intake by providing or withholding carbohydrate during daily training in trained athletes results in differences in selected metabolic adaptations to exercise, including the oxidation of exogenous carbohydrate. However, these metabolic changes do not alter the training-induced magnitude of increase in exercise performance.

An attempt to quantify the placebo effect from a three-week simulated altitude training camp in elite race walkers.

PURPOSE: To quantify physiological and performance effects of hypoxic exposure, a training camp, the placebo effect, and a combination of these factors. METHODS: Elite Australian and International race walkers (n = 17) were recruited, including men and women. Three groups were assigned: 1) Live High:Train Low (LHTL, n = 6) of 14 h/d at 3000 m simulated altitude; 2) Placebo (n = 6) of 14 h/d of normoxic exposure (600 m); and 3) Nocebo (n = 5) living in normoxia. All groups undertook similar training during the intervention. Physiological and performance measures included 10-min maximal treadmill distance, peak oxygen uptake (VO2peak), walking economy, and hemoglobin mass (Hbmass). RESULTS: Blinding failed, so the Placebo group was a second control group aware of the treatment. All three groups improved treadmill performance by approx. 4%. Compared with Placebo, LHTL increased Hbmass by 8.6% (90% CI: 3.5 to 14.0%; P = .01, very likely), VO2peak by 2.7% (-2.2 to 7.9%; P = .34, possibly), but had no additional improvement in treadmill distance (-0.8%, -4.6 to 3.8%; P = .75, unlikely) or economy (-8.2%, -24.1 to 5.7%; P = .31, unlikely). Compared with Nocebo, LHTL increased Hbmass by 5.5% (2.5 to 8.7%; P = .01, very likely), VO2peak by 5.8% (2.3 to 9.4%; P = .02, very likely), but had no additional improvement in treadmill distance (0.3%, -1.9 to 2.5%; P = .75, possibly) and had a decrease in walking economy (-16.5%, -30.5 to 3.9%; P = .04, very likely). CONCLUSION: Overall, 3-wk LHTL simulated altitude training for 14 h/d increased Hbmass and VO2peak, but the improvement in treadmill performance was not greater than the training camp effect.

Time course of haemoglobin mass during 21 days live high:train low simulated altitude.

The aim of this study was to determine the time course of changes in haemoglobin mass (Hb(mass)) in well-trained cyclists in response to live high:train low (LHTL). Twelve well-trained male cyclists participated in a 3-week LHTL protocol comprising 3,000 m simulated altitude for ~14 h/day. Prior to LHTL duplicate baseline measurements were made of Hb(mass), maximal oxygen consumption (VO(2max)) and serum erythropoietin (sEPO). Hb(mass) was measured weekly during LHTL and twice in the week thereafter. There was a 3.3% increase in Hb(mass) and no change in VO(2max) after LHTL. The mean Hb(mass) increased at a rate of ~1% per week and this was maintained in the week after cessation of LHTL. The sEPO concentration peaked after two nights of LHTL but there was only a trivial correlation (r = 0.04, P = 0.89) between the increase in sEPO and the increase in Hb(mass). Athletes seeking to gain erythropoietic benefits from moderate altitude need to spend >12 h/day in hypoxia.

The effect of acute simulated moderate altitude on power, performance and pacing strategies in well-trained cyclists.

Athletes regularly compete at 2,000-3,000 m altitude where peak oxygen consumption (VO2peak) declines approximately 10-20%. Factors other than VO2peak including gross efficiency (GE), power output, and pacing are all important for cycling performance. It is therefore imperative to understand how all these factors and not just VO2peak are affected by acute hypobaric hypoxia to select athletes who can compete successfully at these altitudes. Ten well-trained, non-altitude-acclimatised male cyclists and triathletes completed cycling tests at four simulated altitudes (200, 1,200, 2,200, 3,200 m) in a randomised, counter-balanced order. The exercise protocol comprised 5 x 5-min submaximal efforts (50, 100, 150, 200 and 250 W) to determine submaximal VO2 and GE and, after 10-min rest, a 5-min maximal time-trial (5-minTT) to determine VO2peak and mean power output (5-minTT(power)). VO2peak declined 8.2 +/- 2.0, 13.9 +/- 2.9 and 22.5 +/- 3.8% at 1,200, 2,200 and 3,200 m compared with 200 m, respectively, P < 0.05. The corresponding decreases in 5-minTT(power) were 5.8 +/- 2.9, 10.3 +/- 4.3 and 19.8 +/- 3.5% (P < 0.05). GE during the 5-minTT was not different across the four altitudes. There was no change in submaximal VO2 at any of the simulated altitudes, however, submaximal efficiency decreased at 3,200 m compared with both 200 and 1,200 m. Despite substantially reduced power at simulated altitude, there was no difference in pacing at the four altitudes for athletes whose first trial was at 200 or 1,200 m; whereas athletes whose first trial was at 2,200 or 3,200 m tended to mis-pace that effort. In conclusion, during the 5-minTT there was a dose-response effect of hypoxia on both VO2peak and 5-minTT(power) but no effect on GE.

Nonhematological mechanisms of improved sea-level performance after hypoxic exposure.

Altitude training has been used regularly for the past five decades by elite endurance athletes, with the goal of improving performance at sea level. The dominant paradigm is that the improved performance at sea level is due primarily to an accelerated erythropoietic response due to the reduced oxygen available at altitude, leading to an increase in red cell mass, maximal oxygen uptake, and competitive performance. Blood doping and exogenous use of erythropoietin demonstrate the unequivocal performance benefits of more red blood cells to an athlete, but it is perhaps revealing that long-term residence at high altitude does not increase hemoglobin concentration in Tibetans and Ethiopians compared with the polycythemia commonly observed in Andeans. This review also explores evidence of factors other than accelerated erythropoiesis that can contribute to improved athletic performance at sea level after living and/or training in natural or artificial hypoxia. We describe a range of studies that have demonstrated performance improvements after various forms of altitude exposures despite no increase in red cell mass. In addition, the multifactor cascade of responses induced by hypoxia includes angiogenesis, glucose transport, glycolysis, and pH regulation, each of which may partially explain improved endurance performance independent of a larger number of red blood cells. Specific beneficial nonhematological factors include improved muscle efficiency probably at a mitochondrial level, greater muscle buffering, and the ability to tolerate lactic acid production. Future research should examine both hematological and nonhematological mechanisms of adaptation to hypoxia that might enhance the performance of elite athletes at sea level.

Loss of discrete memory B cell subsets is associated with impaired immunization responses in HIV-1 infection and may be a risk factor for invasive pneumococcal disease.

Invasive pneumococcal infection is an important cause of morbidity and mortality in HIV-1-infected individuals. B cells play an important role in maintaining serologic memory after infection. IgM memory B cells are significantly reduced in HIV-1-infected patients and their frequency is similar to that observed in other patient groups (splenectomized individuals and patients with primary Ab deficiency) who are also known to have an increased risk of invasive pneumococcal infection. Antiretroviral therapy does not restore marginal zone B cell percentages. Immunization with the 23-valent polysaccharide pneumococcal vaccine shows that HIV-1-infected patients have impaired total IgM and IgG pneumococcal vaccines compared with healthy controls. Loss of switched memory B cells was associated with impaired tetanus toxoid IgG vaccine responses. Results of this study demonstrate that defects in B cell memory subsets are associated with impaired humoral immune responses in HIV-1 patients who are receiving antiretroviral therapy and may be a contributory factor to the increased risk of invasive pneumococcal infection observed in HIV-1 infection.

Sleep disturbance at simulated altitude indicated by stratified respiratory disturbance index but not hypoxic ventilatory response.

At high altitudes, the clinically defined respiratory disturbance index (RDI) and high hypoxic ventilatory response (HVR) have been associated with diminished sleep quality. Increased RDI has also been observed in some athletes sleeping at simulated moderate altitude. In this study, we investigated relationships between the HVR of 14 trained male endurance cyclists with variable RDI and sleep quality responses to simulated moderate altitude. Blood oxygen saturation (SpO2%), heart rate, RDI, arousal rate, awakenings, sleep efficiency, rapid eye movement (REM) sleep, non-REM sleep stages 1, 2 and slow wave sleep as percentages of total sleep time (%TST) were measured for two nights at normoxia of 600 m and one night at a simulated altitude of 2,650 m. HVR and RDI were not significantly correlated with sleep stage, arousal rate or awakening response to nocturnal simulated altitude. SpO2 was inversely correlated with total RDI (r = -0.69, P = 0.004) at simulated altitude and with the change in arousal rate from normoxia (r = -0.65, P = 0.02). REM sleep response to simulated altitude correlated with the change, relative to normoxia, in arousal (r = -0.63, P = 0.04) and heart rate (r = -0.61, P = 0.04). When stratified, those athletes at altitude with RDI >20 h(-1) (n = 4) and those with <10 h(-1) (n = 10) exhibited no difference in HVR but the former had larger falls in SpO2 (P = 0.05) and more arousals (P = 0.03). Neither RDI (without stratification) nor HVR were sufficiently sensitive to explain any deterioration in REM sleep or arousal increase. However, the stratified RDI provides a basis for determining potential sleep disturbance in athletes at simulated moderate altitude.

Hypoxic ventilatory response is correlated with increased submaximal exercise ventilation after live high, train low.

This study tested the hypothesis that live high, train low (LHTL) would increase submaximal exercise ventilation (V(E)) in normoxia, and the increase would be related to enhanced hypoxic ventilatory response (HVR). Thirty-three cyclists/triathletes were divided into three groups: 20 consecutive nights of hypoxia (LHTLc, n = 12), 20 nights of intermittent hypoxia (4x5-night 'blocks' of hypoxia interspersed by two nights of normoxia, LHTLi, n = 10), or control (CON, n = 11). LHTLc and LHTLi slept 8-10 h per night in normobaric hypoxia (2,650 m), and CON slept under ambient conditions (600 m). Resting, isocapnic HVR (DeltaV(E)/Deltablood oxygen saturation) was measured in normoxia before (PRE) and after 15 nights (N15) hypoxia. Submaximal cycle ergometry was conducted PRE and after 4, 10, and 19 nights of hypoxia (N4, N10, and N19 respectively). Mean submaximal exercise V(E) was increased (P < 0.05) from PRE to N4 in LHTLc [74.4 (5.1) vs 80.0 (8.4) l min(-1); mean (SD)] and in LHTLi [69.0 (7.5) vs 76.9 (7.3) l min(-1)] and remained elevated in both groups thereafter, with no changes observed in CON at any time. Prior to LHTL, submaximal V(E) was not correlated with HVR, but this relationship was significant at N4 (r = 0.49, P = 0.03) and N19 (r = 0.77, P < 0.0001). Additionally, the increases in submaximal V(E) and HVR from PRE to N15-N19 were correlated (r = 0.51, P = 0.02) for the pooled data of LHTLc and LHTLi. These results suggest that enhanced hypoxic chemosensitivity contributes to increased exercise V(E) in normoxia following LHTL.

Regulation of fuel metabolism by preexercise muscle glycogen content and exercise intensity.

To date, the results of studies that have examined the effects of altering preexercise muscle glycogen content and exercise intensity on endogenous carbohydrate oxidation are equivocal. Differences in the training status of subjects between investigations may, in part, explain these inconsistent findings. Accordingly, we determined the relative effects of exercise intensity and carbohydrate availability on patterns of fuel utilization in the same subjects who performed a random order of four 60-min rides, two at 45% and two at 70% of peak O(2) uptake (Vo(2 peak)), after exercise-diet intervention to manipulate muscle glycogen content. Preexercise muscle glycogen content was 596 +/- 43 and 202 +/- 21 mmol/kg dry mass (P < 0.001) for high-glycogen (HG) and low-glycogen (LG) conditions, respectively. Respiratory exchange ratio was higher for HG than LG during exercise at both 45% (0.85 +/- 0.01 vs. 0.74 +/- 0.01; P < 0.001) and 70% (0.90 +/- 0.01 vs. 0.79 +/- 0.01; P < 0.001) of Vo(2 peak). The contribution of whole body muscle glycogen oxidation to energy expenditure differed between LG and HG for exercise at both 45% (5 +/- 2 vs. 45 +/- 5%; P < 0.001) and 70% (25 +/- 3 vs. 60 +/- 3%; P < 0.001) of Vo(2 peak). Yet, despite marked differences in preexercise muscle glycogen content and its subsequent utilization, rates of plasma glucose disappearance were similar under all conditions. We conclude that, in moderately trained individuals, muscle glycogen availability (low vs. high) does not influence rates of plasma glucose disposal during either low- or moderate-intensity exercise.

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.

Living high-training low increases hypoxic ventilatory response of well-trained endurance athletes.

This study determined whether "living high-training low" (LHTL)-simulated altitude exposure increased the hypoxic ventilatory response (HVR) in well-trained endurance athletes. Thirty-three cyclists/triathletes were divided into three groups: 20 consecutive nights of hypoxic exposure (LHTLc, n = 12), 20 nights of intermittent hypoxic exposure (four 5-night blocks of hypoxia, each interspersed with 2 nights of normoxia, LHTLi, n = 10), or control (Con, n = 11). LHTLc and LHTLi slept 8-10 h/day overnight in normobaric hypoxia (approximately 2,650 m); Con slept under ambient conditions (600 m). Resting, isocapnic HVR (DeltaVE/DeltaSp(O(2)), where VE is minute ventilation and Sp(O(2)) is blood O(2) saturation) was measured in normoxia before hypoxia (Pre), after 1, 3, 10, and 15 nights of exposure (N1, N3, N10, and N15, respectively), and 2 nights after the exposure night 20 (Post). Before each HVR test, end-tidal PCO(2) (PET(CO(2))) and VE were measured during room air breathing at rest. HVR (l. min(-1). %(-1)) was higher (P < 0.05) in LHTLc than in Con at N1 (0.56 +/- 0.32 vs. 0.28 +/- 0.16), N3 (0.69 +/- 0.30 vs. 0.36 +/- 0.24), N10 (0.79 +/- 0.36 vs. 0.34 +/- 0.14), N15 (1.00 +/- 0.38 vs. 0.36 +/- 0.23), and Post (0.79 +/- 0.37 vs. 0.36 +/- 0.26). HVR at N15 was higher (P < 0.05) in LHTLi (0.67 +/- 0.33) than in Con and in LHTLc than in LHTLi. PET(CO(2)) was depressed in LHTLc and LHTLi compared with Con at all points after hypoxia (P < 0.05). No significant differences were observed for VE at any point. We conclude that LHTL increases HVR in endurance athletes in a time-dependent manner and decreases PET(CO(2)) in normoxia, without change in VE. Thus endurance athletes sleeping in mild hypoxia may experience changes to the respiratory control system.