Peter Bärtsch

Individual variation in the erythropoietic response to altitude training in elite junior swimmers

Objectives: Inter-individual variations in sea level performance after altitude training have been attributed, at least in part, to an inter-individual variability in hypoxia induced erythropoiesis. The aim of the present study was to examine whether the variability in the increase in total haemoglobin mass after training at moderate altitude could be predicted by the erythropoietin response after 4 h exposure to normobaric hypoxia at an ambient Po2 corresponding to the training altitude. Methods: Erythropoietin levels were measured in 16 elite junior swimmers before and after 4 h exposure to normobaric hypoxia (Fio2 0.15, ∼2500 m) as well as repeatedly during 3 week altitude training (2100–2300 m). Before and after the altitude training, total haemoglobin mass (CO rebreathing) and performance in a stepwise increasing swimming test were determined. Results: The erythropoietin increase (10–185%) after 4 h exposure to normobaric hypoxia showed considerable inter-individual variation and was significantly (p<0.001) correlated with the acute erythropoietin increase during altitude training but not with the change in total haemoglobin mass (significant increase of ∼6% on average). The change in sea level performance after altitude training was not related to the change in total haemoglobin mass. Conclusions: The results of the present prospective study confirmed the wide inter-individual variability in erythropoietic response to altitude training in elite athletes. However, their erythropoietin response to acute altitude exposure might not identify those athletes who respond to altitude training with an increase in total haemoglobin mass.

International Olympic Committee consensus statement on thermoregulatory and altitude challenges for high-level athletes

Challenging environmental conditions, including heat and humidity, cold, and altitude, pose particular risks to the health of Olympic and other high-level athletes. As a further commitment to athlete safety, the International Olympic Committee (IOC) Medical Commission convened a panel of experts to review the scientific evidence base, reach consensus, and underscore practical safety guidelines and new research priorities regarding the unique environmental challenges Olympic and other international-level athletes face. For non-aquatic events, external thermal load is dependent on ambient temperature, humidity, wind speed and solar radiation, while clothing and protective gear can measurably increase thermal strain and prompt premature fatigue. In swimmers, body heat loss is the direct result of convection at a rate that is proportional to the effective water velocity around the swimmer and the temperature difference between the skin and the water. Other cold exposure and conditions, such as during Alpine skiing, biathlon and other sliding sports, facilitate body heat transfer to the environment, potentially leading to hypothermia and/or frostbite; although metabolic heat production during these activities usually increases well above the rate of body heat loss, and protective clothing and limited exposure time in certain events reduces these clinical risks as well. Most athletic events are held at altitudes that pose little to no health risks; and training exposures are typically brief and well-tolerated. While these and other environment-related threats to performance and safety can be lessened or averted by implementing a variety of individual and event preventative measures, more research and evidence-based guidelines and recommendations are needed. In the mean time, the IOC Medical Commission and International Sport Federations have implemented new guidelines and taken additional steps to mitigate risk even further.

Does ‘altitude training’ increase exercise performance in elite athletes?

The general practice of altitude training is widely accepted as a means to enhance sport performance despite a lack of rigorous scientific studies. For example, the scientific gold-standard design of a double-blind, placebo-controlled, cross-over trial has never been conducted on altitude training. Given that few studies have utilised appropriate controls, there should be more scepticism concerning the effects of altitude training methodologies. In this brief review we aim to point out weaknesses in theories and methodologies of the various altitude training paradigms and to highlight the few well-designed studies to give athletes, coaches and sports medicine professionals the current scientific state of knowledge on common forms of altitude training. Another aim is to encourage investigators to design well-controlled studies that will enhance our understanding of the mechanisms and potential benefits of altitude training.

Intermittent hypoxia at rest for improvement of athletic performance

Two modalities of applying hypoxia at rest are reviewed in this paper: intermittent hypoxic exposure (IHE), which consists of hypoxic air for 5–6 min alternating with breathing room air for 4–5 min during sessions lasting 60–90 min, or prolonged hypoxic exposure (PHE) to normobaric or hypobaric hypoxia over up to 3 h/day. Hypoxia with IHE is usually in the range of 12–10%, corresponding to an altitude of about 4000–6000 m. Normobaric or hypobaric hypoxia with PHE corresponds to altitudes of 4000–5500 m. Five of six studies applying IHE and all four well‐controlled studies using PHE could not show a significant improvement with these modalities of hypoxic exposure for sea level performance after 14–20 sessions of exposure, with the exception of swimmers in whom there might be a slight improvement by PHE in combination with a subsequent tapering. There is no direct or indirect evidence that IHE or PHE induce any significant physiological changes that might be associated with improving athletic performance at sea level. Therefore, IHE and PHE cannot be recommended for preparation of competitions held at sea level.

Enhanced myofiber recruitment during exhaustive squatting performed as whole-body vibration exercise.

Eckhardt, H, Wollny, R, Müller, H, Bärtsch, P, and Friedmann-Bette, B. Enhanced myofiber recruitment during exhaustive squatting performed as whole-body vibration exercise. J Strength Cond Res 25(4): 1120-1125, 2011-The purpose of the study was to test the hypothesis that myofiber recruitment is enhanced when whole-body vibration (WBV) is added to squat training. In a randomized cross-over design, 14 recreationally active men were subjected to 2 sessions consisting of 5 sets of 10 squats with external load, performed either on a vibration platform (whole-body vibration squatting [WBVS]) or conventionally without WBV (CON). Electromyographic (EMG) activity of the right vastus lateralis muscle was continuously recorded during WBVS and CON. The integrated EMG values were normalized to the EMG activity recorded during measurement of the maximal voluntary contraction force (MVC) on an isometric leg press at the beginning of each training session. Capillary lactate concentration was determined before and repeatedly after the squatting exercise. Overall mean normalized and integrated EMG (nIEMG) activity during WBVS (62 ± 4% MVC) was significantly (p < 0.001) higher compared with CON (47 ± 2% MVC). There was a tendency for nIEMG to increase during the 5 sets of 10 squats performed as WBVS (p = 0.089), whereas there was a significant (p < 0.001) decrease in nIEMG during CON. Whole-body vibration squatting induced a significantly (p < 0.001) larger increase in capillary lactate than CON (3.03 ± 0.32 vs. 1.60 ± 0.30 mmol·L−1, p < 0.001). The increased myoelectric activity and the enhanced exercise-induced increase in capillary lactate concentration during WBVS provide evidence for augmented recruitment of muscle tissue when WBV is added to exhaustive squatting exercise.

Missing correlation of retinal vessel diameter with high-altitude headache

The most common altitude‐related symptom, high‐altitude headache (HAH), has recently been suggested to originate from restricted cerebral venous drainage in the presence of increased inflow caused by hypoxia. In support of this novel hypothesis, retinal venous distension was shown to correlate with the degree of HAH. We quantified for the first time retinal vessel diameter changes at 4559 m using infrared fundus images obtained from a state of the art Spectralis™ HRA+OCT with a semiautomatic VesselMap 1® software. High‐altitude exposure resulted in altered arterial and venous diameter changes at high altitude, however, independent of headache burden.

Beta2-adrenergic stimulation blunts inhibition of epithelial ion transport by hypoxia of rat alveolar epithelial cells.

Hypoxia impairs alveolar fluid clearance by inhibition of Na+ reabsorption, and also impairs β 2 adrenergic signaling in alveolar epithelium. Since both are major rescue mechanisms preventing pulmonary edema, we studied whether acute and prolonged treatment with terbutaline would prevent hypoxic inhibition of ion transport. Short circuit currents (ISC) were measured on normoxic and hypoxic (1.5% O2; 24h) primary rat alveolar type II (ATII) cells in absence and presence of terbutaline (1 to 100 μM, 24h). Control and pre-treated cells were stimulated acutely with terbutaline. Transepithelial transport was measured as short circuit current (ISC) in Ussing chambers. Terbutaline induced a rapid decrease ISC (-20%) followed by a slow raise. The transient change in ISC was not inhibited by amiloride but was prevented after Cl- depletion indicating a Cl- current. The slow increase after this transient was amiloride-sensitive indicating a Na+ current. Total ISC, its amiloride-sensitive component, and the transient decrease upon terbutaline stimulation were decreased by hypoxia. 24h treatment with terbutaline stimulated these currents in normoxia and hypoxia, although stimulation was less in the latter. 24h treatment with terbutaline increased the capacity of Na+/K+-ATPase and ENaC as measured after permeabilization with amphotericin. These changes were not paralleled by altered mRNA expression. Acutely applied terbutaline induced a 4-fold increase in cAMP formation in normoxia; terbutaline-induced cAMP-formation was impaired by hypoxia (-20%). Pre-treatment with terbutaline for 24h decreased terbutaline-induced cAMP formation by 85%. Despite this desensitization, addition of terbutaline to terbutaline pre-treated cells caused a larger increase in Cl- and Na+ transport both in normoxia and hypoxia than in non pre-treated cells. These results indicate that β 2 adrenergic stimulation increased Na+- and Cl- transport in ATII cells even in hypoxia thus restoring normal reabsorption.

Health risk for athletes at moderate altitude and normobaric hypoxia

Altitudes at which athletes compete or train do usually not exceed 2000–2500 m. At these moderate altitudes acute mountain sickness (AMS) is mild, transient and affects at the most 25% of a tourist population at risk. Unpublished data included in this review paper demonstrate that more intense physical activity associated with high-altitude training or mountaineering does not increase prevalence or severity of AMS at these altitudes. These conclusions can also be extended to the use of normobaric hypoxia, as data in this paper suggest that the severity of AMS is not significantly different between hypobaric and normobaric hypoxia at the same ambient pO2. Furthermore, high-altitude cerebral or pulmonary oedema do not occur at these altitudes and intermittent exposure to considerably higher altitudes (4000–6000 m) used by athletes for hypoxic training are too short to cause acute high-altitude illnesses. Even moderate altitude between 2000 and 3000 m can, however, exacerbate cardiovascular or pulmonary disease or lead to a first manifestation of undiagnosed illness in older people that may belong to the accompanying staff of athletes. Moderate altitudes may also lead to splenic infarctions in healthy athletes with sickle cell trait.

Increased hepcidin levels in high-altitude pulmonary edema.

Low iron availability enhances hypoxic pulmonary vasoconstriction (HPV). Considering that reduced serum iron is caused by increased erythropoiesis, insufficient reabsorption, or elevated hepcidin levels, one might speculate that exaggerated HPV in high-altitude pulmonary edema (HAPE) is related to low serum iron. To test this notion we measured serum iron and hepcidin in blood samples obtained in previously published studies at low altitude and during 2 days at 4,559 m (HA1, HA2) from controls, individuals with HAPE, and HAPE-susceptible individuals where prophylactic dexamethasone and tadalafil prevented HAPE. As reported, at 4,559 m pulmonary arterial pressure was increased in healthy volunteers but reached higher levels in HAPE. Serum iron levels were reduced in all groups at HA2. Hepcidin levels were reduced in all groups at HA1 and HA2 except in HAPE, where hepcidin was decreased at HA1 but unexpectedly high at HA2. Elevated hepcidin in HAPE correlated with increased IL-6 at HA2, suggesting that an inflammatory response related to HAPE contributes to increased hepcidin. Likewise, platelet-derived growth factor, a regulator of hepcidin, was increased at HA1 and HA2 in controls but not in HAPE, suggesting that hypoxia-controlled factors that regulate serum iron are inappropriately expressed in HAPE. In summary, we found that HAPE is associated with inappropriate expression of hepcidin without inducing expected changes in serum iron within 2 days at HA, likely due to too short time. Although hepcidin expression is uncoupled from serum iron availability and hypoxia in individuals developing HAPE, our findings indicate that serum iron is not related with exaggerated HPV.

Inhaled budesonide does not prevent acute mountain sickness after rapid ascent to 4559 m

Recent studies showed that inhaled budesonide (200 µg twice per day) reduced the incidence of acute mountain sickness (AMS) after passive ascent to 3700 and 3900 m [1, 2]. These findings raised the possibility that mediators released from the hypoxic lung transmit signals to the brain which contribute to the cerebral processes leading to AMS [3]. Because neither of these studies reflect alpine-style climbing, the present study was performed to test whether inhalation of budesonide at two different doses (200 and 800 µg twice per day) prior to active and rapid ascent (<20 h) to 4559 m prevents AMS in this high-risk setting. Prophylactic inhalation of budesonide does not prevent acute mountain sickness after rapid ascent to high-altitude http://ow.ly/Bc9p30dOz46