Robert F. Chapman

Defining the “dose” of altitude training: how high to live for optimal sea level performance enhancement

Chronic living at altitudes of ∼2,500 m causes consistent hematological acclimatization in most, but not all, groups of athletes; however, responses of erythropoietin (EPO) and red cell mass to a given altitude show substantial individual variability. We hypothesized that athletes living at higher altitudes would experience greater improvements in sea level performance, secondary to greater hematological acclimatization, compared with athletes living at lower altitudes. After 4 wk of group sea level training and testing, 48 collegiate distance runners (32 men, 16 women) were randomly assigned to one of four living altitudes (1,780, 2,085, 2,454, or 2,800 m). All athletes trained together daily at a common altitude from 1,250-3,000 m following a modified live high-train low model. Subjects completed hematological, metabolic, and performance measures at sea level, before and after altitude training; EPO was assessed at various time points while at altitude. On return from altitude, 3,000-m time trial performance was significantly improved in groups living at the middle two altitudes (2,085 and 2,454 m), but not in groups living at 1,780 and 2,800 m. EPO was significantly higher in all groups at 24 and 48 h, but returned to sea level baseline after 72 h in the 1,780-m group. Erythrocyte volume was significantly higher within all groups after return from altitude and was not different between groups. These data suggest that, when completing a 4-wk altitude camp following the live high-train low model, there is a target altitude between 2,000 and 2,500 m that produces an optimal acclimatization response for sea level performance.

Impairment of 3000-m Run Time at Altitude Is Influenced by Arterial Oxyhemoglobin Saturation

UNLABELLEDnThe decline in maximal oxygen uptake (ΔVO(2)max) with acute exposure to moderate altitude is dependent on the ability to maintain arterial oxyhemoglobin saturation (SaO2).nnnPURPOSEnThis study examined if factors related to ΔVO(2)max at altitude are also related to the decline in race performance of elite athletes at altitude.nnnMETHODSnTwenty-seven elite distance runners (18 men and 9 women, VO(2)max = 71.8 ± 7.2 mL·kg(-1)·min(-1)) performed a treadmill exercise at a constant speed that simulated their 3000-m race pace, both in normoxia and in 16.3% O2 (∼2100 m). Separate 3000-m time trials were completed at sea level (18 h before altitude exposure) and at 2100 m (48 h after arrival at altitude). Statistical significance was set at P ≤ 0.05.nnnRESULTSnGroup 3000-m performance was significantly slower at altitude versus sea level (48.5 ± 12.7 s), and the declines were significant in men (48.4 ± 14.6 s) and women (48.6 ± 8.9 s). Athletes grouped by low SaO2 during race pace in normoxia (SaO2 < 91%, n = 7) had a significantly larger ΔVO(2) in hypoxia (-9.2 ± 2.1 mL·kg(-1)·min(-1)) and Δ3000-m time at altitude (54.0 ± 13.7 s) compared with athletes with high SaO2 in normoxia (SaO2 > 93%, n = 7, ΔVO(2) = -3.5 ± 2.0 mL·kg(-1)·min(-1), Δ3000-m time = 38.9 ± 9.7 s). For all athletes, SaO2 during normoxic race pace running was significantly correlated with both ΔVO(2) (r = -0.68) and Δ3000-m time (r = -0.38).nnnCONCLUSIONSnThese results indicate that the degree of arterial oxyhemoglobin desaturation, already known to influence ΔVO(2)max at altitude, also contributes to the magnitude of decline in race performance at altitude.

Altitude training considerations for the winter sport athlete

Winter sports events routinely take place at low to moderate altitudes, and nearly all Winter Olympic Games have had at least one venue at an altitude >1000 m. The acute and chronic effects of altitude can have a substantial effect on performance outcomes. Acutely, the decline in oxygen delivery to working muscle decreases maximal oxygen uptake, negatively affecting performance in endurance events, such as cross‐country skiing and biathlon. The reduction in air resistance at altitude can dramatically affect sports involving high velocities and technical skill components, such as ski jumping, speed skating, figure skating and ice hockey. Dissociation between velocity and sensations usually associated with work intensity (ventilation, metabolic signals in skeletal muscle and heart rate) may impair pacing strategy and make it difficult to determine optimal race pace. For competitions taking place at altitude, a number of strategies may be useful, depending on the altitude of residence of the athlete and ultimate competition altitude, as follows. First, allow extra time and practice (how much is yet undetermined) for athletes to adjust to the changes in projectile motion; hockey, shooting, figure skating and ski jumping may be particularly affected. These considerations apply equally in the reverse direction; that is, for athletes practising at altitude but competing at sea level. Second, allow time for acclimatization for endurance sports: 3–5 days if possible, especially for low altitude (500–2000 m); 1–2 weeks for moderate altitude (2000–3000 m); and at least 2 weeks if possible for high altitude (>3000 m). Third, increase exercise–recovery ratios as much as possible, with 1:3 ratio probably optimal, and consider more frequent substitutions for sports where this is allowed, such as ice hockey. Fourth, consider the use of supplemental O2 on the sideline (ice hockey) or in between heats (skating and Alpine skiing) to facilitate recovery. For competitions at sea level, the ‘live high–train low’ model of altitude training can help athletes in endurance events to maximize performance.

Timing of return from altitude training for optimal sea level performance

While a number of published studies exist to guide endurance athletes with the best practices regarding implementation of altitude training, a key unanswered question concerns the proper timing of return to sea level prior to major competitions. Evidence reviewed here suggests that, altogether, the deacclimatization responses of hematological, ventilatory, and biomechanical factors with return to sea level likely interact to determine the best timing for competitive performance.

Using Deception to Establish a Reproducible Improvement in 4-Km Cycling Time Trial Performance.

We investigated whether performance gains achieved with deception persisted after the deception was revealed, and whether pacing strategy changed. 14 trained cyclists completed 4 simulated 4-km time trials (TT) on a cycle ergometer comprising familiarization and baseline trials (BAS), followed by unaware (of deception, UAW) and aware (of deception, AW) trials on separate days. In the UAW trial, participants competed against an on-screen avatar set at 102% of their baseline trial mean power output (Pmean) believing it was set at 100% of BAS Pmean. 24u2009h prior to the AW trial, participants were informed of the deception in the UAW trial. 4 participants did not improve in the UAW trial compared to BAS. 10 participants improved time to completion (TTC) and Pmean in the UAW and AW trials compared to BAS (p<0.03) with no significant differences between UAW and AW (p=1.0). Pacing strategy (at 0.5-km intervals) and RPE responses were unchanged (p>0.05) for these participants. In summary, deception did not improve performance in all participants. However, participants whose time trial performance improved following deception could retain their performance gains once the deception was revealed, demonstrating a similar pacing strategy and RPE response.

The role of inspiratory muscle training in the management of asthma and exercise-induced bronchoconstriction.

ABSTRACT Asthma is a pathological condition comprising of a variety of symptoms which affect the ability to function in daily life. Due to the high prevalence of asthma and associated healthcare costs, it is important to identify low-cost alternatives to traditional pharmacotherapy. One of these low cost alternatives is the use of inspiratory muscle training (IMT), which is a technique aimed at increasing the strength and endurance of the diaphragm and accessory muscles of respiration. IMT typically consists of taking voluntary inspirations against a resistive load across the entire range of vital capacity while at rest. In healthy individuals, the most notable benefits of IMT are an increase in diaphragm thickness and strength, a decrease in exertional dyspnea, and a decrease in the oxygen cost of breathing. Due to the presence of expiratory flow limitation in asthma and exercise-induced bronchoconstriction, dynamic lung hyperinflation is common. As a result of varying operational lung volumes, due in part to hyperinflation, the respiratory muscles may operate far from the optimal portion of the length-tension curve, and thus may be forced to operate against a low pulmonary compliance. Therefore, the ability of these muscles to generate tension is reduced, and for any given level of ventilation, the work of breathing is increased as compared to non-asthmatics. Evidence that IMT is an effective treatment for asthma is inconclusive, due to limited data and a wide variation in study methodologies. However, IMT has been shown to decrease dyspnea, increase inspiratory muscle strength, and improve exercise capacity in asthmatic individuals. In order to develop more concrete recommendations regarding IMT as an effective low-cost adjunct in addition to traditional asthma treatments, we recommend that a standard treatment protocol be developed and tested in a placebo-controlled clinical trial with a large representative sample.

Commentaries on Viewpoint: Time for a new metric for hypoxic dose?

TO THE EDITOR: The proposal by our well-respected colleagues (2) to introduce a new metric—incorporating the altitude elevation and the total exposure duration, termed “kilometer hours”—for better describing the “hypoxic dose” is decidedly a step forward. By only quantifying the “external” stress, this metric presents several limitations: It suggests a linear relationship between altitude elevation and saturation decrease [but the Fick curve is curvilinear (3)] or that it applies to all athletes irrespectively of their training background [but elite endurance athletes suffer the largest decrease in V̇O2max (1)], altitude experience [but elite athletes who have had previous hypoxic exposure better adapt to hypoxic condition (4)], or type of hypoxia [but hypobaric vs. normobaric hypoxia induces larger desaturation (5)]. The large intersubject variability in the physiological responses to a given “hypoxic dose” implies that the magnitude of the stimulus rather than the altitude elevation should instead be considered. We therefore propose a new metric based on the sustained duration at a given arterial saturation level. Hence, desaturation levels in normoxia (exercise-induced arterial hypoxemia) or in hypoxia (3) predict the decrement in V̇O2max in hypoxia and therefore the ̇amplitude of the “hypoxic stimulus.” This metric termed “saturation hours” is defined as %·h (98/s 1) h 100, where s is the saturation value (in %) and h the time (in hours) sustained at any second level. Practically, with the development of new sport gears incorporating the oximeter inside the textile, this metric will readily be measured without any disturbances to individuals.

Epo production at altitude in elite endurance athletes is not associated with the sea level hypoxic ventilatory response

The level of circulating erythropoietin (EPO) in response to a fixed level of hypoxia shows substantial inter-individual variability, the source of which is undetermined. Arterial PO(2) at altitude is regulated in part by the hypoxic ventilatory response, which also shows a wide inter-individual variability. We asked if the ventilatory response to hypoxia is related to the magnitude of EPO release at moderate altitude. Twenty-six national class US distance runners (17 M, 9 F) participated in a test of isocapnic hypoxic ventilatory response (HVR) at sea level, 2-7 days prior to departure to altitude. EPO measures were obtained at sea level and after 20 h at 2500 m. HVR for all subjects was 0.21±0.16 L min⁻¹ %SaO₂⁻¹ (range 0.01-0.61 L min⁻¹ %SaO₂⁻¹), with no significant difference between men and women. EPO was significantly increased from pre-altitude (8.6±2.6 ng ml(-1), range 4.0-14.6 ng ml⁻¹) to acute altitude (16.6±4.4 ng ml⁻¹, range 5.0-27.0 ng ml⁻¹), an increase of 92.2±70.1%. There was no significant sex difference in the EPO increase. ΔEPO for all subjects was not correlated with HVR (r=-0.17). Similarly, a statistically or physiologically significant correlation was not present between ΔEPO and HVR within the group of men (r=-0.22) or women (r=-0.19). The variability in the acute EPO response to moderate altitude is not explained by differences in peripheral chemoresponsiveness in elite distance runners. These results suggest that factors acting downstream from the lung influence the magnitude of the acute EPO response to altitude.

Comparative Effects of Caffeine and Albuterol on the Bronchoconstrictor Response to Exercise in Asthmatic Athletes

The main aim of this study was to evaluate the comparative and additive effects of caffeine and albuterol (short-acting beta (2)-agonist) on the severity of EIB. Ten asthmatic subjects with EIB (exercise-induced bronchoconstriction) participated in a randomized, double-blind, double-dummy crossover study. One hour before an exercise challenge, each subject was given 0, 3, 6, or 9 mg/kg of caffeine or placebo mixed in a flavored sugar drink. Fifteen minutes before the exercise bout, an inhaler containing either albuterol (180 microg) or placebo was administered to each subject. Pulmonary function tests were conducted pre- and post-exercise. Caffeine at a dose of 6 and 9 mg/kg significantly reduced (p<0.05) the mean maximum % fall in post-exercise FEV (1) to -9.0+/-9.2% and -6.8+/-6.5% respectively compared to the double-placebo (-14.3+/-11.1%) and baseline (-18.4+/-7.2%). There was no significant difference (p>0.05) in the post-exercise % fall in FEV (1) between albuterol ( PLUS CAFFEINE PLACEBO) (-4.0+/-5.2%) and the 9 mg/kg dose of caffeine (-6.8+/-6.5%). Interestingly, there was no significant difference (p>0.05) in the post-exercise % fall in FEV (1) between albuterol ( PLUS CAFFEINE PLACEBO) (-4.0+/-5.2%) and albuterol with 3, 6 or 9 mg/kg of caffeine (-4.4+/-3.8, -6.8+/-5.6, -4.4+/-6.0% respectively). Similar changes were observed for the post-exercise % fall in FVC, FEF (25-75%) and PEF. These data indicate that moderate (6 mg/kg) to high doses (9 mg/kg) of caffeine provide a significant protective effect against EIB. It is feasible that the negative effects of daily use of short-acting beta (2)-agonists by asthmatic athletes could be reduced simply by increasing caffeine consumption prior to exercise.

Inspiratory loading and limb locomotor and respiratory muscle deoxygenation during cycling exercise

The aim of this study was to determine the effect of inspiratory loading on limb locomotor (LM) and respiratory muscle (RM) deoxygenation ([deoxy (Hb+Mb)]) using NIRS during constant-power cycling exercise. Sixteen, male cyclists completed three, 6-min trials. The intensity of the first 3-min of each trial was equivalent to ~80% V(O(2max)) (EX(80%)); during the final 3-min, subjects received an intervention consisting of either moderate inspiratory loading (Load(mod)), heavy inspiratory loading (Load(heavy)), or maximal exercise (Load(EX)). Load(heavy) significantly increased LM [deoxy(Hb+Mb)] from 12.2±9.0 μm during EX(80%) to 15.3±11.7 μm, and RM [deoxy(Hb+Mb)] from 5.9±3.6 μm to 9.5±6.6 μm. LM and RM [deoxy(Hb+Mb)] were significantly increased from EX(80%) to Load(EX); 12.8±9.1 μm to 16.4±10.3 μm and 5.9±2.9 μm to 11.0±6.4 μm, respectively. These data suggest an increase in respiratory muscle load increases muscle deoxy(Hb+Mb) and thus may indicate a reduction in oxygen delivery and/or increased oxygen extraction by the active muscles.