In accordance with previous studies, RBF during exercise produced a marked reduction in VE. VE measured at the end of exercise was 49% lower in B10 than SB (Figure 1). With a similar breathing frequency reduction during cycle ergometry, Yamamoto et al., 1987 and Sharp et al. (1991) obtained a smaller reduction of VE. However, different testing protocols and intensities of exercise with RBF were used in these studies. Yamamoto et al., 1987 showed a reduction of 30% in VE during an interval test with RBF (30 s of exercise at 210 W with RBF alternating with 30 s rest intervals with spontaneous breathing). Sharp et al. (1991) measured a reduction of 25% in VE during 8 min of exercise at an intensity above the lactate threshold due to RBF. In the studies of RBF during front crawl swimming, a similar reduction in VE, as it was obtained in the present study, was observed with taking a breath every sixth (Town and Vanness, 1990) or eighth (West et al., 2005) stroke cycle as compared to taking a breath every second stroke cycle. However, after cessation of B10, when spontaneous breathing was allowed, VE dramatically increased to a peak in the 20th s of recovery. Thereafter, it decreased to the resting values. In contrast, VE immediately began to decrease to the resting values after cessation of exercise with SB. During the initial 20 s of recovery after B10, the subjects breathed an average 26.4 liters of air compared to 20.5 liters after exercise with SB. This marked hyperventilation influenced changes in other respiratory and blood parameters. As expected, at the end of exercise, RBF resulted in lower PETO2, SaO2 and PO2, when compared to spontaneous breathing during exercise (Figure 2 and 4, Table 3). These data were in accordance with previous studies, which measured these parameters during different cycling exercises with RBF (Kapus et al., 2007; Sharp et al., 1991; Yamamoto et al., 1987). Due to different testing protocols, Yamamoto et al., 1987 and Kapus et al., 2007 reported higher values of SaO2 than that were measured at the end of B10. The intensity (subject’s peak power output) and duration (exercise to exhaustion) of B10 were maximal for each subject. Considering that, low values of SaO2 (83% (8%)) at the end of exercise with RBF were expected in the present study. The results confirmed severe hypoxia during B10. However, hyperventilation after the cessation of B10 induced a rapid recovery of PETO2, SaO2, and PO2. Lower values of O2 were detected only during the initial 16 s and 20 s after B10 in comparison to SB, measured by SaO2 (Figure 4) and PETO2 (Figure 2) respectively. However, there were no significant differences in PO2 between SB and B10 measured immediately after the exercise (Table 3). The delay between the subjects’s cessation of the exercise and the first measurement did not exceed 15 s. Nonetheless, this delay was apparently too long to detect hypoxia with measurement of PO2 after B10. According to our experience, this delay is longer for field testing such as swimming tests in the swimming pool. Considering that, the time of measurement may be the reason why previous studies failed to demonstrate a reduction in PO2 due to RBF during swimming (Kapus et al., 2002; 2003). In accordance with previous studies (Dicker et al., 1980; Kapus et al., 2007; Peyrebrune et al., 2002; Sharp et al., 1991; Town and Vanness, 1990; West et al., 2005, Yamamoto et al., 1987), RBF produced hypercapnia, as evidenced by higher PETCO2 and PCO2 in B10 than during SB. Yamamoto et al., 1987 found that arterial partial pressure of carbon dioxide (PaCO2) and hydrogen ion concentration ([H+]) continuously increased to the end of an interval test with RBF. Using 8 min of exercise with RBF at an intensity 10 % above lactate threshold workload, Sharp et al., 1991 reported similar results. They concluded that RBF during exercise caused respiratory acidosis at exercise intensities that were not associated with [H+] disturbance during unreduced VE. Considering that, it was suggested that the combination of severe hypercapnia, respiratory acidosis and metabolic acidosis was the possible reason for earlier fatigue during exercise at higher intensities, when RBF was used (Kapus et al., 2003). During recovery from exercise, PETCO2 remained elevated in the B10 trial compared to the SB trial (Figure 4), even after PETO2 had normalized (Figure 2). Lee et al., 1990 reported a reduction in VCO2 during exercise with RBF, and a subsequent increase during recovery. They suggested that CO2 was retained in muscle, plasma and erythrocytes during exercise with RBF and that it was released from these stores during recovery. It seemed that despite hyperventilation during recovery, hypercapnia could be detected by measuring blood gas parameters within 15 s after the exercise with RBF. Possible study limitations: Ideally blood gases should be obtained in arterial blood. However, indwelling arterial catheters for sampling arterial blood are not always feasible and desirable. Considering that, some indirect methods were used to assess blood gases in the present study. Therefore, the degree to which the actual measurements provide an accurate proxy for arterial measures should be considered. Arterial blood gases (PaO2 and PaCO2) during exercise could be estimated by using arterialized earlobe blood samples (PO2 and PCO2). Some previous studies found that arterialized earlobe blood samples are in good agreement with arterial blood samples for partial pressure of carbon dioxide, but not for partial pressure of oxygen (Dall´Ava-Santucci, 1996; Fajac et al., 1998; McEvoy and Jones, 1975). During exercise, PO2 was lower than PaO2 on average 0.23 kPa (McEvoy and Jones, 1975), 0.63 kPa (Fajac et al., 1998) and 1.2 kPa (Dall´Ava-Santucci, 1996). The main cause of underestimation of PaO2 in earlobe samples could be insufficient arterialization of blood due to venus admixture. The earlobe method requires adequate blood flow in the earlobe to enable a sufficient volume of blood to be sampled without additional external pressure during sampling. This was the reason for the delay of up to 15 s between the subject’s cessation of the exercise and the first measure in the present study. In addition, measurement of end-tidal pressure of carbon dioxide (PETCO2) has been used to estimate PaCO2 at rest and during exercise. Most comparative studies have concluded that PETCO2 provides good index of PaCO2 at rest (Jones et al., 1979, Williams and Babb, 1997). However, during exercise, the differences between PETCO2 and PaCO2 were 0.3 kPa (0.3 kPa) (Williams and Babb, 1997) and 0.4 kPa (0.3 kPa) (Robbins et al., 1990). These differences increased at a higher workload and with increasing tidal volume (Jones et al., 1979). Ear pulse oximeters are often used to provide a non-invasive, continuous estimate of the oxyhemoglobin saturation of arterial blood (SaO2). In most previous validation studies, ear pulse oximeter estimates during exercise have been shown to be accurate predictors of SaO2 at least when saturation is above 85% in non-smoking subjects (Mengelkoch et al., 1994, Smyth et al., 1986, Powers et al., 1989, Martin et al., 1992). Considering ear pulse oximeters of Datex-Ohmeda, differences between estimated and measured (via blood sampling) SaO2 values were 0.87 % (2.6 %), 0.59 % (2.4 %) (Martin et al., 1992) and -0.57 % (1.78 %) (Powers et al., 1989). Thus, the error in the pulse oximeter is not likely greater than 1 %, while significant differences between SB and B10 in SaO2 were between 5 and 10 % during the initial 16 s of recovery. |