Improved running economy and increased hemoglobin mass in elite runners after extended moderate altitude exposure

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1 Journal of Science and Medicine in Sport (2009) 12, Improved running economy and increased hemoglobin mass in elite runners after extended moderate altitude exposure P.U. Saunders a,, R.D. Telford b, D.B. Pyne a,b, A.G. Hahn a, C.J. Gore a,c a Department of Physiology, Australian Institute of Sport, Australia b Medical School, Australian National University, Australia c School of Education, Flinders University, Australia Received 18 January 2007; received in revised form 17 August 2007; accepted 18 August 2007 KEYWORDS Hypoxia; Red blood cells; and Elite athletes Summary There is conflicting evidence whether hypoxia improves running economy (RE), maximal O 2 uptake ( V O2 max ), haemoglobin mass (Hb mass ) and performance, and what total accumulated dose is necessary for effective adaptation. The aim of this study was to determine the effect of an extended hypoxic exposure on these physiological and performance measures. Nine elite middle distance runners were randomly assigned to a live high train low simulated altitude group (ALT) and spent 46 ± 8 nights (mean ± S.D.) at 2860 ± 41 m. A matched control group (CON, n =9) lived and trained near sea level ( 600 m). ALT decreased submaximal V O2 (L min 1 ) ( 3.2%, 90% confidence intervals, 1.0% to 5.2%, p = 0.02), increased Hb mass (4.9%, %, p = 0.01), decreased submaximal heart rate ( 3.1%, 1.8% to 4.4%, p = 0.00) and had a trivial increase in V O2 max (1.5%, 1.6 to 4.8; p = 0.41) compared with CON. There was a trivial correlation between change in Hb mass and change in V O2 max (r = 0.04, p = 0.93). Hypoxic exposure of 400 h was sufficient to improve Hb mass, a response not observed with shorter exposures. Although total O 2 carrying capacity was improved, the mechanism(s) to explain the lack of proportionate increase in V O2 max were not identified Sports Medicine Australia. Published by Elsevier Ltd. All rights reserved. Introduction There remains controversy about the magnitudes of change in maximal oxygen uptake ( V O2 max ), haemoglobin mass (Hb mass ) and exercise economy after altitude exposure in trained athletes. 1 Our Corresponding author. address: philo.saunders@ausport.gov.au (P.U. Saunders). laboratory has demonstrated a 3.3% improvement in running economy (RE) after 20 days moderate simulated live high train low (LHTL) altitude exposure in elite distance runners. 2 We have also consistently demonstrated only trivial changes in Hb mass after various altitude interventions in elite runners and cyclists of durations of days 2 7 ; in contrast with reports of 5 9% increases in red cell mass after altitude training in endurance athletes Those studies finding little change in /$ see front matter 2007 Sports Medicine Australia. Published by Elsevier Ltd. All rights reserved. doi: /j.jsams

2 68 P.U. Saunders et al. Hb mass after altitude exposure could be explained by either an insufficient altitude (< m) and/or an inadequate time at altitude (<3 4 weeks for >12 h day 1 ). 12 Several studies have demonstrated improved exercise economy after altitude acclimatization, 2,7,13 18 although this is strongly contested by others. 19 With the association between RE and performance well documented, 20 the ability to improve RE after altitude training is likely to lead to significant improvements in running performance. The present study aimed to test the hypothesis that a total of 400 h ( 50 days of 9hd 1 ) of LHTL simulated altitude exposure would enhance RE, Hb mass and V O2 max over and above that occurring with a similar exposure to a normoxic environment and to a greater extent than previously documented after exposures of a shorter duration. Methods Eighteen elite middle distance runners participated in this study with over half (n = 10) representing Australia at major international competitions (Table 1). Participants were informed of the experimental procedures and possible risks involved with participation before written consent was obtained. The Ethics Committee at the Australian Institute of Sport approved all testing procedures. Nine runners were randomly assigned to the LHTL simulated altitude group (ALT), consisting of 46 ± 8 nights (415 ± 75 h) at 2860 ± 41 m altitude; where values are mean ± standard deviation. During the 12-week period participants spent 5 days each week (9hd 1 ) in a normobaric hypoxic chamber and 2 days each week at the ambient altitude ( 600 m). The control group (CON) consisted of nine runners who lived and trained at the same location ( 600 m altitude) as ALT. The study was conducted during 2 6 month periods in consecutive years because of the limited space in the hypoxic chamber. Four participants in both the ALT and CON groups were tested in the first year and five in the second year. Prior to and within 2 days of completion of the intervention all participants performed testing under normoxic conditions in Canberra, Australia ( 600 m). RE was determined from submaximal oxygen consumption ( V O2 ) for 4 min at constant running speeds of 14, 16 and 18 km h 1 on a custom-built motorised treadmill. Ventilation ( V E ), respiratory exchange ratio, heart rate (HR) and blood lactate concentration [Lac-] were also measured. RE was defined as the V O2 during the last 60 s of each 4 min stage. V O2 max was measured during an incremental test to volitional exhaustion performed 2 min after the third submaximal effort. The treadmill and gas analysis procedures have been fully described previously. 21 The typical error of measurement (TE) established from pre- and post-tests on the CON participants in the current study were 1.8% for submaximal V O2 and 2.4% for V O2 max. Before and after the 3 months experimental period, participants underwent measurement of total Hb mass using the carbon monoxide rebreathing technique that we have described previously. 2 The TE for Hb mass from pre- and posttests on the CON participants in the current study was 1.2% when using capillary blood samples. Data were analysed in a spreadsheet for randomized controlled trials ( org/resource/stats) using unpaired t-tests with the natural logarithm of dependent variables used to reduce non-uniformity of error. Statistical significance was accepted at p < Measures of centrality and spread are shown as mean ± standard deviation. RE was analysed as pooled values of the three running speeds because differences from pre- to post-treatment were independent of speed. The magnitude of differences between change scores (pre versus post) was expressed as the effect of ALT compared to CON with the mean percentage change ± 90% confidence intervals. The percentage likelihood are expressed qualitatively (<1%, almost certainly not; <5%, very unlikely; <25%, unlikely or probably not; <50%, possibly not; >50%, possibly; >75%, likely or probable; >95%, very likely; >99%, almost certain) based on previous recommendations. 22 Effect sizes (ES) to represent the magnitude of the difference between two Table 1 Participant characteristics of the elite runners in both altitude and control groups (mean ± standard deviation) Variable Simulated altitude (n = 9) Control (n = 9) Age (year) 23.9 ± ± 5.5 Body mass (kg) 63.3 ± ± 7.6 V O2 max (ml min 1 kg 1 ) 71.0 ± ± 2.5 Training volume (km week 1 ) 127 ± ± 38

3 Running economy, hemoglobin mass and hypoxia 69 groups in terms of standard deviations, were calculated from the log-transformed data by dividing the change in the mean by the average of the standard deviations of the repeated analysis. A modified scale to interpret ES was established as trivial, <0.2%; small, %; moderate, %; large, >1.2%. 23 Results The pre- and post-test scores and the corresponding percentage changes for all physiological variables are shown in Table 2. The decrease in submaximal V O2 was present at all three running speeds (Fig. 1) and the increase in Hb mass was present in eight of the nine runners in ALT (Fig. 2). There was only a trivial relationship between change in V O2 max and change in Hb mass (r = 0.04) in ALT. ALT undertook 11% more training than CON (p = 0.42, ES = 0.42, small Figure 2 Individual changes in hemoglobin mass (Hb mass ) pre and post 46 ± 8 d intervention period in (A) control (CON, n = 9) and (B) altitude (ALT, n = 9) groups. The group means ± standard deviations are shown in heavy grey with a slight offset for clarity. effect). The coefficient of variation (CV) for performance over 1500 m of the athletes during this period was 1.7% with a range of % (ALT 1.8%, %; CON 1.6%, %), which are similar to the CV previously reported for well-trained to elite runners ( % in cross-country and road runs, 2.7% and 4.2% in half marathons, and 2.6% in marathons). 24 Discussion Figure 1 Percentage change in submaximal V O2 at the three running speeds from pre- to post-intervention in (A) control (CON, n = 8) and (B) altitude (ALT, n = 9) groups. The group means ± standard deviations are shown in heavy grey with a slight offset for clarity. Negative values indicate a decrease in V O2 and improved running economy. The major finding of the present study was that sleeping at moderate simulated altitude for 400 h during a 3 months period and training near sea level was sufficient to substantially increase Hb mass compared to a matched control group, which contrasts previous reports from our laboratory using hypoxic exposures of a shorter duration ( h). Nevertheless, the current study elicited a similar magnitude of improvement in RE to those studies with shorter durations of hypoxia. 2,7,13 16,18

4 Table 2 Physiological characteristics pre- and post-altitude training intervention for simulated altitude (ALT, n = 9) and control (CON, n = 8 except Hb mass where n = 9) groups Variable ALT CON Effect Likelihood P-value Pre-mean ± S.D. Post-mean ± S.D. Pre-mean ± S.D. Post-mean ± S.D. % (90% CI) % Qualitative descriptor Submaximal V O2 (L min 1 ) 3.38 ± ± ± ± ( 1.0, 5.2) 95 very likely 0.02 V E (L min 1 ) 94.0 ± ± ± ± ( 3.0, 3.5) 18 unlikely 0.92 RER ratio 0.94 ± ± ± ± ( 0.7, 5.0) 76 likely 0.03 HR (b min 1 ) ± ± ± ± ( 1.8, 4.4) 92 likely 0.00 [Lac-] (mm) 2.3 ± ± ± ± (2.9, 26.1) 72 possibly 0.04 Maximal V O2 (L min 1 ) 4.53 ± ± ± ± ( 1.6, 4.8) 61 possibly 0.41 V E (L min 1 ) ± ± ± ± (1.3, 10.2) 96 very likely 0.04 RER ratio 1.15 ± ± ± ± ( 4.7, 1.0) 71 possibly 0.26 HR (b min 1 ) ± ± ± ± ( 2.6, 0.6) 51 possibly 0.28 [Lac-] (mm) 11.1 ± ± ± ± ( 10.6, 38.2) 78 likely 0.40 Hb mass (g) 951 ± ± ± ± (2.3, 7.6) 97 very likely 0.01 Values are means and standard deviations, and effects as percentages along with the lower and upper 90% confidence intervals. Submaximal results are for pooled data from three running speeds (14, 16, 18 km h 1 ). No variable was significantly different between groups at pre. V O2, oxygen consumption; V E, minute ventilation (BTPS); RER, respiratory exchange ratio; HR, heart rate; [Lac-], concentration of blood lactate; Hb mass, haemoglobin mass. 70 P.U. Saunders et al.

5 Running economy, hemoglobin mass and hypoxia 71 The modest increase in Hb mass in the current study contrasts to those of our earlier studies with LHTL exposures ranging from 12 to 23 days (9 11 h d 1 ) that failed to elicit a substantial increase in Hb mass. 2 5,7 Although the increase in Hb mass in ALT was small, its magnitude is substantially above the 1.2% TE for this method in our hands, indicating that the increase is unlikely to be measurement error. The increase in Hb mass in the current study was less than that (7 9%) determined by others using a similar altitude stimulus and duration. 8,9 One explanation for such discrepancies is that increases in Hb mass after altitude exposure may be an artefact of experimental error, with methods used to determine red cell mass or volume differing between laboratories. 25 For instance, a study of Nordic skiers reported a 9.5% reduction in red cell volume (from 2.87 to 2.62 L, p = 0.08) of a control group that may be attributable to errors in the baseline values rather than a real decrease. 26 Failure of many investigators to routinely report their TE makes it difficult to interpret confidently the magnitude of reported changes. The current finding supports the contention of Rusko et al. 12 that the inability of studies to elicit an increase Hb mass after altitude exposure may be attributable to an inadequate duration or severity of hypoxia. Rusko et al. 12 recommend >12 h d 1, for >3 weeks, at altitudes > m for an accelerated erythropoiesis. The current study totalled 415 h during 12 weeks at 2860 m simulated altitude, supporting the theory that the total duration of hypoxic exposure (h d) provides the overall stimulus to increase Hb mass rather than any single parameter. The current findings challenge the recommendations from Rusko et al. 12 by obtaining an increase in Hb mass using only 9 h d 1, 3h less than the recommended >12 h d 1. We propose that the total duration of hypoxia over an extended period is probably the primary consideration for the prescription of altitude exposure. However, there appears to be a threshold of daily exposure to hypoxia because there were minimal change in Hb mass after 3 h d 1 simulated altitude of m, 5 d week 1 for 4 weeks 27. Although the current altitude exposure substantially increased Hb mass, there was not a corresponding increase in V O2 max. The lack of increase in V O2 max after the LHTL exposure suggests that although total O 2 carrying capacity is improved there may be a parallel reduction in cardiac output ( Q ), vascular regulation or some other mechanism. The current study adds credence to the proposed impairment in vascular regulation and reduced Q after altitude training, 28 with a non-significant 1% reduction in maximal HR during the V O2 max test for ALT compared with CON. A gradual decrease in maximal HR is related to changes in myocardial -adrenergic and myocardial receptor density after hypoxic exposure and may account for a decreased Q 28. Our findings are consistent with a growing number of studies that have demonstrated that various altitude exposures can reduce submaximal V O2 by 3 10%, hence improving exercise economy. 2,7,13 18 Others have demonstrated that submaximal V O2 at sea level remains largely unchanged after altitude exposure. 19 However, it is our view that in elite runners, days of LHTL exposure to moderate simulated altitude substantially improves RE. Plausible mechanisms for improved RE after a period of altitude exposure include an increase in ATP production per mole of O 2 used, 14 a decrease in the ATP cost of muscle contraction, 29 and/or a decrease in the cardiorespiratory cost of O 2 transport. 13 The latter mechanism is supported by the reduced HR at the three submaximal running speeds after simulated altitude in the ALT group compared to CON. In conclusion, the current study demonstrated that 400 h of simulated LHTL altitude ( 2900 m) substantially improved RE, decreased submaximal HR and increased Hb mass in elite runners. A trivial increase in V O2 max was unrelated to the increase in Hb mass possibly due to a decrease in Q and/or decrease in vascular regulation. Improved RE and increased Hb mass are likely to contribute to improve race performance giving credence to the use of extended LHTL altitude training in the lead up to competitions. A potential limitation of the study was the extra training undertaken by ALT, although not significant, and our belief is that the groups were well matched and the differences were due to the hypoxic exposure. Practical implications Sleeping at moderate altitude for approximately 400 hours increases total body haemoglobin, allowing a greater oxygen carrying capacity. Extended altitude exposure results in elite runners being more economical at typical training speeds. Altitude exposure in the lead up to major competitions appears worthwhile in improving running performance in elite runners. Acknowledgements The technical and financial support from BOC Gases Australia is gratefully acknowledged, as is the funding from the Australian Sports Commission.

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