Live High-train Low Research Articles

Point: Counterpoint: Hypobaric hypoxia induces/does not induce different responses from normobaric hypoxia

Point: Counterpoint: Hypobaric hypoxia induces/does not induce different responses from normobaric hypoxia

Live-High Train-Low Altitude Training on Maximal Oxygen Consumption in Athletes: A Systematic Review and Meta-Analysis: A Response to Commentary

Live-High Train-Low Altitude Training on Maximal Oxygen Consumption in Athletes: A Systematic Review and Meta-Analysis: A Response to Commentary

Live-High Train-Low Altitude Training on Maximal Oxygen Consumption in Athletes: A Systematic Review and Meta-Analysis

We quantified the effects of four different protocols of Live-high Train-low altitude training on maximal aerobic capacity. A systematic search of PubMed for published studies, up to July 2010 was performed using appropriate search terms. Eleven studies met inclusion criteria. Combined analysis showed athletes exposed to hypoxia had higher maximal oxygen consumption compared to those undertaking normoxic training, Weighted Mean Difference (WMD) 1.51 ml. kg−1.min−1 [0.44, 2.58, p=0.006]; hemoglobin (WMD) 0.57 mg/dl−1 [0.38, 0.75, p<0.00001], lower maximum heart rate (WMD) −1.77 beats.minute−1 [−3.03, −0.50, p=0.006], and peak exercise blood lactate (WMD) −3.03 mmol. L−1 [−4.57, −1.49, p=0.0001]. Studies utilizing minimum hypoxic exposure of 9.5 hours daily showed a significantly greater weighted mean difference in maximal oxygen consumption WMD 3.45 ml.kg−1.min−1 [0.30, 6.60] p=0.03, in the hypoxic subjects. Protocols using altitudes between 2,500 to 3,500m for a minimum of 9.5 hours daily for at least 2 weeks elicited greatest performance effects.

Live-High Train-Low Altitude Training on Maximal Oxygen Consumption in Athletes: A Systematic Review and Meta-Analysis

INTRODUCTION Lancaster and Smart have provided us with an altitude training / hypoxic exposure metaanalysis, which includes a group of 11 studies utilizing a wide variety of hypoxia delivery mechanisms, exposure times, and subject cohorts. Meta-analysis is a quantitative analysis of the results of individual empirical studies [1] and is often used as a means to review previous studies, test theoretical propositions, and/or make generalizations about an entire population. Meta-analysis can be quite useful and is utilized in a number of fields, most prominently in medicine [2]. However, meta-analysis is not without limitations. With any meta-analysis, there is an underlying assumption that the combined studies share commonalities, particularly with regard to components such as treatments, subject characteristics, and measurements. If these components are quite similar, then a meta-analysis can be a helpful tool. However, if the studies under consideration have fundamental differences in experimental design or underlying physiological rationale, then a meta-analysis may in fact just be combining noise, ultimately comparing apples and oranges. In giving weight to the Lancaster and Smart analysis, the reader should be fully aware of some of the many issues involved with training studies in general and altitude training / hypoxic exposure studies in particular [3], many of which go well beyond the limitations noted by the authors in their paper. Each of these issues, if not controlled for, can add substantial variability to the outcome measures being examined. Additionally, there are substantial differences in both the research methodologies and hypoxic doses used in the studies utilized in this particular meta-analysis. We question if it is useful and proper to compare the outcomes of these studies to each other under a global umbrella of “Live High – Train Low.” Each of these theoretical issues is addressed below.

Ineffective normobaric LHTL: room confinement or inappropriate training intensity?

to the editor: To explain an ineffective live high-train low (LHTL) in normobaric hypoxia (e.g., where the athletes slept in hypoxic chamber), Siebenman et al. ([4][1]) suggested that the recommended 16 h/day of room confinement may lead to a reduction in plasma volume: 13.8% and 20.1% in the

Influence of altitude training modality on performance and total haemoglobin mass in elite swimmers

We compared changes in performance and total haemoglobin mass (tHb) of elite swimmers in the weeks following either Classic or Live High:Train Low (LHTL) altitude training. Twenty-six elite swimmers (15 male, 11 female, 21.4 ± 2.7 years; mean ± SD) were divided into two groups for 3 weeks of either Classic or LHTL altitude training. Swimming performances over 100 or 200 m were assessed before altitude, then 1, 7, 14 and 28 days after returning to sea-level. Total haemoglobin mass was measured twice before altitude, then 1 and 14 days after return to sea-level. Changes in swimming performance in the first week after Classic and LHTL were compared against those of Race Control (n = 11), a group of elite swimmers who did not complete altitude training. In addition, a season-long comparison of swimming performance between altitude and non-altitude groups was undertaken to compare the progression of performances over the course of a competitive season. Regardless of altitude training modality, swimming performances were substantially slower 1 day (Classic 1.4 ± 1.3% and LHTL 1.6 ± 1.6%; mean ± 90% confidence limits) and 7 days (0.9 ± 1.0% and 1.9 ± 1.1%) after altitude compared to Race Control. In both groups, performances 14 and 28 days after altitude were not different from pre-altitude. The season-long comparison indicated that no clear advantage was obtained by swimmers who completed altitude training. Both Classic and LHTL elicited ~4% increases in tHb. Although altitude training induced erythropoeisis, this physiological adaptation did not transfer directly into improved competitive performance in elite swimmers.

“Live high–train low” using normobaric hypoxia: a double-blinded, placebo-controlled study

The combination of living at altitude and training near sea level [live high-train low (LHTL)] may improve performance of endurance athletes. However, to date, no study can rule out a potential placebo effect as at least part of the explanation, especially for performance measures. With the use of a placebo-controlled, double-blinded design, we tested the hypothesis that LHTL-related improvements in endurance performance are mediated through physiological mechanisms and not through a placebo effect. Sixteen endurance cyclists trained for 8 wk at low altitude (<1,200 m). After a 2-wk lead-in period, athletes spent 16 h/day for the following 4 wk in rooms flushed with either normal air (placebo group, n = 6) or normobaric hypoxia, corresponding to an altitude of 3,000 m (LHTL group, n = 10). Physiological investigations were performed twice during the lead-in period, after 3 and 4 wk during the LHTL intervention, and again, 1 and 2 wk after the LHTL intervention. Questionnaires revealed that subjects were unaware of group classification. Weekly training effort was similar between groups. Hb mass, maximal oxygen uptake (VO(2)) in normoxia, and at a simulated altitude of 2,500 m and mean power output in a simulated, 26.15-km time trial remained unchanged in both groups throughout the study. Exercise economy (i.e., VO(2) measured at 200 W) did not change during the LHTL intervention and was never significantly different between groups. In conclusion, 4 wk of LHTL, using 16 h/day of normobaric hypoxia, did not improve endurance performance or any of the measured, associated physiological variables.

Reproducibility of Performance Changes to Simulated Live High/Train Low Altitude

Elite athletes often undertake multiple altitude exposures within and between training years in an attempt to improve sea level performance. To quantify the reproducibility of responses to live high/train low (LHTL) altitude exposure in the same group of athletes. Sixteen highly trained runners with maximal aerobic power (VO2max) of 73.1 +/- 4.6 and 64.4 +/- 3.2 mL x kg(-1) x min(-1) (mean +/- SD) for males and females, respectively, completed 2 x 3-wk blocks of simulated LHTL (14 h x d(-1), 3000 m) or resided near sea level (600 m) in a controlled study design. Changes in the 4.5-km time trial performance and physiological measures including VO2max, running economy and hemoglobin mass (Hb(mass)) were assessed. Time trial performance showed small and variable changes after each 3-wk altitude block in both the LHTL (mean [+/-90% confidence limits]: -1.4% [+/-1.1%] and 0.7% [+/-1.3%]) and the control (0.5% [+/-1.5%] and -0.7% [+/-0.8%]) groups. The LHTL group demonstrated reproducible improvements in VO2max (2.1% [+/-2.1%] and 2.1% [+/-3.9%]) and Hb(mass) (2.8% [+/-2.1%] and 2.7% [+/-1.8%]) after each 3-wk block. Compared with those in the control group, the runners in the LHTL group were substantially faster after the first 3-wk block (LHTL - control = -1.9% [+/-1.8%]) and had substantially higher Hb(mass) after the second 3-wk block (4.2% [+/-2.1%]). There was no substantial difference in the change in mean VO2max between the groups after the first (1.2% [+/-3.3%]) or second 3-wk block (1.4% [+/-4.6%]). Three-week LHTL altitude exposure can induce reproducible mean improvements in VO2max and Hb(mass) in highly trained runners, but changes in time trial performance seem to be more variable. Competitive performance is dependent not only on improvements in physiological capacities that underpin performance but also on a complex interaction of many factors including fitness, fatigue, and motivation.

Influence of Intermittent Hypobaric Exposure on SOD and TBARS Levels in Trained Rats

Live high train low (LHTL) is a well-known training model for preparation of competitions. In this study, the thiobarbituric acid reacting substances (TBARS) levels and superoxide dismutase (SOD) activity were determined in heart, lung and muscle tissues of rats. They were intermittently exposed to hypobaric pressure of 523 mmHg, corresponding to an altitude of 3,000 m, and they performed swim training at sea level. Two groups of male rats were trained to swim for thirty minutes a day and 4 days a week, lasting 9 weeks. Two groups were exposed to hypobaria for 120 min a day and 4 days a week for 9 weeks in pressure cabin. In heart tissue, TBARS levels of normobaric trained (NbT) group was higher (P < 0.05) than those of the normobaric sedentary (control) group. TBARS levels of hypobaric trained (HbT) group was higher than those of the control and hypobaric sedentary (Hb) groups (P < 0.001; P < 0.01, respectively). TBARS levels of lung tissue of HbT group was also higher than those of the same groups (control; P < 0.01, Hb; P < 0.05, respectively). In muscle tissue, TBARS levels of HbT group was higher than those of the sedentary groups (control; P < 0.001, Hb; P < 0.05, respectively). SOD activity of heart tissue of HbT group was higher (P < 0.001) than that of the other groups. In lung tissue, SOD activity of control group was lower than that of the other groups (HbT; P < 0.001, NbT; P < 0.01, Hb; P < 0.01, respectively). In muscle tissue, SOD activity of HbT group was higher (P < 0.01) than that of the control group. The results of this study suggest that intermittent hypobaric exposure may augment exercise-induced oxidative stress in heart, lung and muscle of trained rats.

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.

Improved Race Performance in Elite Middle-Distance Runners After Cumulative Altitude Exposure

We quantified the effect of an extended live high-train low (LHTL) simulated altitude exposure followed by a series of training camps at natural moderate altitude on competitive performance in seven elite middle-distance runners (Vo2max 71.4 +/- 3.4 mL.min-1.kg-1, mean +/- SD). Runners spent 44 +/- 7 nights (mean +/- SD) at a simulated altitude of 2846 +/- 32 m, and a further 4 7- to 10-d training at natural moderate altitude (1700-2200 m) before racing. The combination of simulated LHTL and natural altitude training improved competitive performance by 1.9% (90% confidence limits, 1.3-2.5%). Middle-distance runners can confidently use a combination of simulated and natural altitude to stimulate adaptations responsible for improving performance.

Sea-Level Exercise Performance Following Adaptation to Hypoxia

Adaptation to living or training in hypoxic environments (altitude training) continues to gain interest from sport scientists and endurance athletes. Here we present the first meta-analytic review of the effects on performance and related physiological measures following adaptation to six protocols of natural or artificial hypoxia: live-high train-high (LHTH), live-high train-low (LHTL), artificial LHTL with daily exposure to long (8-18 hours) continuous, brief (1.5-5 hours) continuous or brief (<1.5 hours) intermittent periods of hypoxia, and artificial live-low train-high (LLTH). The 51 qualifying studies provided 11-33 estimates for effects on power output with each protocol and up to 20 estimates for effects on maximal oxygen uptake (VO2max) and other potential mediators. The meta-analytic random-effect models included covariates to adjust for and estimate moderating effects of study characteristics such as altitude level and days of exposure. Poor reporting of inferential statistics limited the weighting factor in the models to sample size. Probabilistic inferences were derived using a smallest worthwhile effect on performance of 1%. Substantial enhancement of maximal endurance power output in controlled studies of subelite athletes was very likely with artificial brief intermittent LHTL (2.6%; 90% confidence limits+/-1.2%), likely with LHTL (4.2%; +/-2.9%), possible with artificial long continuous LHTL (1.4; +/-2.0%), but unclear with LHTH (0.9; +/-3.4%), artificial brief continuous LHTL (0.7%; +/-2.5%) and LLTH (0.9%; +/-2.4%). In elite athletes, enhancement was possible with natural LHTL (4.0%; +/-3.7%), but unclear with other protocols. There was evidence that these effects were mediated at least partly by substantial placebo, nocebo and training-camp effects with some protocols. Enhancing protocols by appropriate manipulation of study characteristics produced clear effects with all protocols (3.5-6.8%) in subelite athletes, but only with LHTH (5.2%) and LHTL (4.3%) in elite athletes. For VO2max, increases were very likely with LHTH (4.3%; +/-2.6%) in subelite athletes, whereas in elite athletes a 'reduction' was possible with LHTH (-1.5%; +/-2.0%); changes with other protocols were unclear. Effects on erythropoietic and other physiological mediators provided little additional insight into mechanisms. In summary, natural LHTL currently provides the best protocol for enhancing endurance performance in elite and subelite athletes, while some artificial protocols are effective in subelite athletes. Likely mediators include VO2max and the placebo, nocebo and training-camp effects. Modification of the protocols presents the possibility of further enhancements, which should be the focus of future research.

Interactions between exposure to hypoxia and the training-induced autonomic adaptations in a “live high–train low” session

The autonomic and cardiovascular adaptations to hypoxia are opposite to those resulting from aerobic training. We investigated (1) whether exposure to hypoxia in a live high-train low (LHTL) session limits the autonomic and cardiovascular adaptations to training, and (2) whether such interactions remain 15 days after the end of the LHTL. Eighteen national swimmers trained for 13 days at 1,200 m, living (16 h day(-1)) either at 1,200 m (live low-train low, LLTL) or at a simulated height of 2,500-3,000 m (LHTL). Subjects were investigated at 1,200 m before and at the end of the training session, and after the following 15 days of sea-level training. Cardiovascular parameters and the autonomic control assessed by spectral analysis of R-R and diastolic blood pressure (DBP) variability were obtained in the resting supine position and in response to an orthostatic test. At the end of the 13-day training, resting heart rate (HR) and sympathetic modulation on heart decreased in LLTL (-10.1% and -25.4%, P<0.01, respectively) but not in LHTL (-5.8, -15.5%, respectively). Total peripheral resistance (TPR) and DBP became higher in LHTL than in LLTL (P<0.05). Stroke index decreased in both groups during the tilt test, counteracted by an increase in HR and sympathetic modulation to the heart and vasculature, and a decrease in vagal modulation to the heart. After the following 15-day sea-level training, differences in TPR and DBP between groups disappeared. During an LHTL session, adaptations to hypoxia interacted with the autonomic and cardiovascular adaptations to training. However, these interactions did not limit the adaptations to the following sea-level training.

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.

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

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

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

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