Hypobaric (HH) as well as normobaric hypoxia (NH) are well-described situations and several authors have shown this impact on exercise performance and related physiological variables (Angermann et al., 2006; Friedmann et al., 2007; Petrassi et al., 2012). Differences in physiological responses of HH and NH are reported in an actual paper (Girard et al., 2012). Some papers showed a linear reduction of exercise performance and oxygen uptake with increasing altitude (Benoit et al., 1997; Grataloup et al., 2007; Mollard et al., 2007a). The decrease in maximal exercise performance under hypoxic conditions was shown to be dependent on maximal exercise performance in normoxia even this relationship is not always reported as linear (Faiss et al., 2014; Wehrlin and Hallen, 2006). Performance at submaximal parameters such as the anaerobic threshold was shown to be significantly reduced by hypoxia, but the reliability and validity of different thresholds in normoxia and normobaric hypoxia have not been investigated yet.
Additionally, the impact of chronic hypoxia on the human body and its adaptation processes have been investigated extensively; however, only a few papers were found about the impact of acute normobaric hypoxia (Benoit et al., 2003; Calbet et al., 2003; Fukuda et al., 2010; Gallagher et al., 2014; Richard and Koehle, 2012; Soroko et al., 2012).
A better understanding of the typical acute responses in these conditions could be essential for training supervision as well as for medical purposes (McKenzie, 2012). Skinner and McLellan had already described a three-phase behaviour of selected physiological variables during incremental exercise in 1980 (Hofmann et al., 1997; Skinner and McLellan, 1980; Smekal et al., 2012). This concept has been adapted and may be seen as the standard model to describe exercise performance (Hofmann and Tschakert, 2011). The concept is based on the lactate shuttle theory (Brooks, 1986; 2009) which implies three specific phases of energy supply and consequently two turn points namely the first ([LTP.sub.1]) and the second ([LTP.sub.2]) lactate turn point (Hofmann et al., 1994a; 1997; 2001). They were shown to be objective markers of performance to describe defined metabolic conditions and the maximal lactate steady state (Hofmann et al., 1994a; Smekal et al., 2012; Wonisch et al., 2002). However, no studies were found to investigate these lactate turn points in hypoxic conditions.
Several authors showed contrary outcomes for the impact of acute hypoxia on selected physiological variables and thresholds. One of the reasons for these differences could be the use of different test protocols and the application of different fractions of oxygen in the air (Fi[O.sub.2]) (Angermann et al., 2006; Calbet et al., 2003; Friedmann et al., 2004). Some authors reported a loss of power output and a reduced maximal heart rate in acute hypoxia (Angermann et al., 2006; Grataloup et al., 2007; Mollard et al., 2007b). In addition, some authors reported a higher reduction in power output in trained athletes compared to untrained participants. However, other authors reported no reduction of maximal heart rate in hypoxia (Fukuda et al., 2010; Lawler et al., 1988; Peltonen et al., 2001). Some authors showed that the maximal lactate concentration in both hypoxia and normoxia was the same (Angermann et al., 2006; Benoit et al., 1997; Mollard et al., 2007b) while Marees reported higher lactate concentration in hypoxia than in normoxia at the same submaximal power output (Marees, 2003). This author also reported an increase of the tidal volume in hypoxia whereas no differences were found by Mollard et.al. (2007b). Rathat et al suggested a test to identify high risk subjects for high altitude diseases (Rathat et al., 1992). Discrepancies were also shown for minute ventilation, where Marees (2003) claimed an increasing minute ventilation volume in hypoxia while other authors reported no differences (Marees, 2003; Grataloup et al., 2007; Orhan et al., 2010). All authors agreed that the [VO.sub.2max] is clearly lower in hypoxia while the [O.sub.2]-uptake at rest was higher in hypoxia compared to normoxia (Hofmann et al., 1994b; Mollard et al., 2007b). These effects were more pronounced in trained than in untrained participants. Furthermore, Friedmann et al. reported a higher maximal respiratory exchange ratio (RER) in hypoxia, while Fukada et al. could not find RER differences in hypoxic conditions (Friedmann et al., 2004; Fukuda et al., 2010). Additionally, the so-called lactate paradox at high altitudes was discussed by several authors (West, 2007; van Hall, 2007). However, comparison of data is difficult as most authors applied a different [O.sub.2]-concentration (FI[O.sub.2] 8-17%) and pressure mode (normobaric vs. hypobaric).
The aim of this study is therefore to determine and compare the lactate turn points to standard ventilatory turn points and the heart rate turn point in normoxia and normobaric hypoxia. According to our hypothesis, the maximal and the turn point variables were suggested to be not significantly different in relative and absolute terms independent of the environmental conditions.
The study was designed as a single-blinded randomized case control study. Ten moderately trained participants underwent two maximal incremental exercise tests under normoxic and normobaric hypoxic conditions (FI[O.sub.2] = 0.14 [O.sub.2] according to an altitude of 3500 m above sea level) in a hypoxic chamber. Air temperature and humidity were the same in both conditions. For inclusion, participants had to be at the age of 20-35, athletically active, healthy, and without any medication. The study was approved by the local ethics committee and meets the re quirements of ICH-GCP as well as the requirements of the actual Declaration of Helsinki.
Both incremental exercise tests were performed on an electronically braked cycle ergometer (Ergoline ergometrics 800s, Ergoline, Germany) in a random order applying the following protocol. After 3 minutes without physical workload in a sitting position (R1) on the cycle ergometer, participants started to cycle at a workload of 40 watt for additional 3 minutes (W1), followed by an increase of 20 watt per minute up to voluntary exhaustion. The cycling cadence was set at 70 rpm. After completion of the maximal work load ([P.sub.max]), participants worked at 40 W for 3 min. again (W2) and subsequently passively rested for additional 3 min. sitting on the cycle ergometer (R2). Between the first and the second exercise test participants had a break of 7 days for optimal recovery. The tests were performed by all participants at the same day and time. All participants were instructed to avoid any strenuous exercise the day before the tests and were allowed to pre-acclimatize in the altitude chamber 30 min before performing the test in both conditions. [N.sub.2]-generators were running in both conditions to keep participants blinded for hypoxia. Submaximal turn points for blood lactate concentration ([LTP.sub.1], [LTP.sub.2]), ventilation ([VETP.sub.1], [VETP.sub.2]), and heart rate (HRTP) were calculated by means of linear regression break point analysis as shown previously (Binder et al., 2008; Hofmann et al., 1994b; Hofmann and Tschakert, 2011). The determination was performed within the same defined regions of interest for all selected variables.
Blood lactate concentration (La) was determined from capillary blood samples (Biosen S_line...