The aim of present study was to determine whether IHT with lactate threshold workload intensity would enhance sea- level aerobic capacity and endurance performance in well-trained cyclists. The unique aspect of this research project included highly trained athletes and a well designed intensive training program. The most important finding from the present study is that the 3 week training program, associated with 3 IHT sessions per week (180min per week, where 90 - 120min per week corresponded to a workload equal to 95% of the lactate threshold), significantly improved aerobic capacity (VO2max by 4%) and endurance performance (time in TT by 2.6%) in well-trained cyclists at sea-level. However, only a few well-designed and well-controlled studies on trained subjects have reported increments in hemoglobin concentration or/and hematocrit value (Bonetti et al., 2006; Gore et al., 2006 Hamlin 2010), while other studies do not show significant changes in serum erythropoietin and erythrocyte count following IHE/IHT (Katayama et al., 2004; Marshall et al., 2008; Rodriguez et al., 2004; Roels et al., 2005). Efficiency of the oxygen transport system is most often evaluated by maximal oxygen uptake (VO2max). Theoretically, intermittent hypoxic training (IHT) may increase aerobic capacity and endurance performance at sea-level by several adaptive changes. However, research findings on IHT as an effective protocol for enhancing aerobic capacity and sport performance at sea-level are inconclusive. Few well-controlled studies support this theory (Dufour et al., 2006; Zoll et al., 2006). Dufour et al., 2006 observed a significant improvement in VO2max, and in running speed at the second ventilatory threshold (VT2), by 5% and 4%, respectively, after 6 weeks of intermittent hypoxic training, without changes in blood O2-carrying capacity. Moreover, the time in an all- out running test increased only in the experimental group, without significant modifications in VO2 kinetics. The subjects in the control and experimental groups continued their usual running training program with two additional sessions with intensity at the second ventilatory threshold. Athletes in the experimental group preformed these sessions in a hypoxic environment. In another study, Roels et al., 2005 also observed a significant improvement in values of VO2max after high intensive interval (IHT) sessions, but there were non-significant differences in mean power output during a 10- min cycle time trial and hematological variables after IHT. However, the IHT intensive interval sessions, as well as hypoxic exposure, were only twice a week (~115min per week). The interval training consisted of 6-8 reps of 2min duration at 100% peak power output (PPO) during the first 4 wk; then progressively increased to 5 reps of 5-6 min at 90% of PPO, followed by 4 reps of 8 min at 90% of PPO in the last week of training. It is difficult to pinpoint the exact causes of such training effects, yet they could have been affected by the short duration, as well as low overall volume, of interval work for well-trained athletes. In most available data, the overall volume of the hypoxic exposure compared to our study was significantly lower However, many studies do not confirm the ergogenic effects of IHT. The results of Roels et al., 2005 investigations are in accordance with those of Truijens et al., 2003, who found that 5 weeks of high-intensity training in a flume improved sea-level performance in well- trained swimmers, but there was no additional effect of hypoxic training (15.3% oxygen equivalent). Similarly, in a previous study, Vallier et al., 1996 found no significant increase in VO2max and maximal power output in five elite triathletes after IHT. During the experiment these subjects modified their usual training program and replaced three sessions of bicycling exercise with three sessions on a cycle ergometer in a hypobaric chamber simulating an altitude of 4000 m. However, the authors did not include a control group, so it is not possible to compare the relative effects of this program. Hendriksen and Meeuwsen, 2003 conducted an experiment in which they examined the effect of intermittent training in a hypobaric chamber on physical exercise at sea-level. During this study, subjects in the experimental group trained for 10 days, 2 h daily on a cycle ergometer placed in a hypobaric chamber at a simulated altitude of 2,500 m. Training intensity was at 60-70% of the heart rate reserve. The results indicated a significant (p < 0.05) increase in anaerobic capacity, but not in maximal oxygen uptake VO2max. These results were confirmed by recent study of Hamlin et al., 2010. During the experiment the authors used a very similar training protocol but the fraction of inspired oxygen (FIO2) was manually adjusted to allow a similar hypoxic stimulus for each subject. The SpO2 levels were 88% on days 1-2, 84% on days 3-4 and 82% on days 5-10 (the equivalent of 3200, 4000, and 4400m altitudes, respectively). Authors observed enhanced in main anaerobic power during a 30-s Wingate test, as well as found substantial increases in the hemoglobin concentration, hematocrit, and substantial reductions in serum iron and transferrin following IHT. However, there was a significant improvement in 20 km time trial. The lack of improved in aerobic capacity end endurance performance is this studies was most likely caused by hypoxia-induced low intensity efforts during the IHT workouts. In our opinion, intensity of 60-70% of the heart rate reserve is not a sufficient training stimulus, and will not lead to improvements in aerobic capacity. In our study the training load during the core element of practice sessions was significantly higher and reached on the average 250W while the HR ranged from 175 to 180 bpm. The results of our study are in accordance to those obtained by Dufour et al., 2006 and Zoll et al., 2006. We observed a significant (p < 0.05) increase in absolute and relative values of VO2max and VO2LT after the three weeks of IHT protocol. Additionally, a significant increase in WRmax and WRLT occurred, similarly to changes observed by Dufour et al., 2006. Moreover, the analysis of heart rate (HR) in our research indicated significant changes in exercising heart rates in group H. In this group, values of HRavg during the time trial were significantly lower after IHT, even though Pavg increased substantially. There was also a tendency for lower HRmax values during the incremental test, but non-significant differences in values of this variable were caused by significant increases (6.6%) in WRmax. The changes in exercise HR (decreased at a set load) may be explained by increased stroke volume, what caused an improvement in values of oxygen pulse. These adaptive changes most likely allowed for a more effective work of the cardiovascular system. An increase in maximal oxygen uptake due to hypoxia is usually associated with an increase in hematocrit value and hemoglobin concentration. In the present study, improved VO2max after IHT cannot be explained by changes in blood variables, as no significant changes in hemoglobin concentration, hematocrit value and red blood cell distribution width were observed, yet the IHT showed a tendency for increased values of this variables. Statistical analysis showed only a significant increase (p < 0.05) in values of mean corpuscular volume (MCV) in H group. Not many well designed studies reported increments in hemoglobin concentration and/or hematocrit value (Bonetti et al., 2006; Gore et al., 2006; Hamlin 2010; Hamlin and Hellemans, 2007), while other studies showed no significant changes in serum erythropoietin and erythrocyte count following IHE/IHT (Katayama et al., 2004; Marshall et al., 2008; Rodriguez et al., 2004; Roels et al., 2005). These discrepancies related to the effectiveness of IHE/IHT are most likely caused by differences in the time course of the EPO response in humans, due to hypoxia. Knaupp et al., 1992 examined the relationship between the duration of normobaric hypoxic exposure and plasma EPO levels in healthy human subjects. No increase in EPO was seen after the 5- and 60-min exposures. However, a 50% increase was seen 240 min after the initiation of the 120-min hypoxic exposure (p < 0.01). Intermittent exposure resulted in an increase of EPO by 52%, 360 min after the onset of exposure (p < 0.05). They conclude that exposing humans continuously to an inspiratory O2 fraction of 0.105 for 120 min or intermittently for 240 min provides a sufficient stimulus to increased production of EPO. Since EPO blood concentration rises significantly after 90 minutes of continues exercise, the time of the exercise protocol seems fully justified. Additionally these adaptive changes require systematic frequent training stimulus with the volume ranging form 90 to 120 minutes. These findings were confirmed by Rodriguez et al., 2000, who stated that a single hypoxic (4000-5000 m) exposure of 90 min, three times per week for three consecutive weeks, significantly (p < 0.05) increases hematocrit value (HCT), hemoglobin concentration (HGB), the number of red blood cells (RBC) and reticulocytes. These authors suggest that a continuous exposure of 90 min represents the minimal stimulus to trigger an acute secretion of erythropoietin (EPO) (hypobaric chamber at 504 - 540 hPa). However, no significant differences were found in cycling exercise time or VO2max, and no normoxic control group was included. Moreover, Dufour et al. (2006), as well as Roels et al. (2005), observed improvements in VO2max without changes in blood O2-carrying capacity. It must be underlined, that the significant increase in values of VO2max and improvement in cycling performance observed also in our study after IHT is associated with non-hematological adaptive mechanisms due to hypoxia. The results of our and several well-controlled studies indicate that the improvement in aerobic capacity and endurance performance are caused by muscular and systemic adaptations, which are either absent or found to a lesser degree after training under normoxic conditions. (Dufour et al., 2006; Zoll et al., 2006). The systematic hypoxic condition during the training process may cause more drastic changes in muscle tissues than after traditional endurance training in normoxic conditions are related increased skeletal muscle mitochondrial density, capillary-to-fiber ratio, and fiber cross- sectional area, which were demonstrated in untrained individuals (Desplanches and Hoppeler, 1993; Vogt et al., 2001). These adaptive changes are associated with an increase hypoxia inducible factor-1α (HIF-1α), which is the global regulator of oxygen homeostasis and plays a critical role in the cardiovascular and respiratory responses to hypoxia (Semenza, 2004). In another three different studies (Green et al., 1999; Melissa et al., 1997; Terrados et al., 1990) that also used the IHT protocols have demonstrated significant (p < 0.05) increases in the activities of oxidative enzymes and in capillary density associated with VO2max improvement. There have been relatively few studies that have investigated changes in monocarboxylate transporters, MCT1 and MCT4, to altitude exposure (Clark et al., 2004; Gore, 2007; Zoll et al., 2006). Zoll et al., 2006 reported a significant increase in muscle mRNA concentration of MCT1 in nine well-trained runners after IHT, compared with a control group. The authors concluded that the increase in MCT1 mRNA allowed for an improved lactate exchange and removal, which may lead to a slower decline in pH at a given running velocity, thereby allowing the athletes to run longer (Zoll et al., 2006). These applications were confirmed in our study, where a significant increase (p < 0.05) in WRLT and decrease (p < 0.05) in ∆ LA0-20km during the time trial after IHT was noted. However, while values of LA0-30km and ∆ LAmax during the incremental test were significantly higher, this was associated and accountable due to much higher workloads in group H. In addition, transport of LA and H+, as well as the ability of skeletal muscle to buffer H+, are important for pH regulation, and changes in acid-base status have been proposed as a potential mechanism for improved performance after altitude exposure (Gore, 2007). Previous studies (Mizuno et al., 1990; Saltin et al., 1995) reported that training in a hypoxia environment may increase muscle buffering capacity in well- trained athletes. Despite that our results did not show significant changes in blood pH and acid- base balance at rest, during and after the incremental exercise, as well as the time trial, there were smaller disturbances in these variables at particular loads. Also there was a significant improvement in maximal and average generated power during TT after IHT. This may suggest that the buffering capacity was increased after IHT. |