Effect of prior exercise on the \(\dot{V}{\text{O}}_{{2}}\)-plateau incidence
Gordon et al. (
2012) described in a group of 12 cyclists a significant increase in the plateau incidence from 50 to 100% after a prior exercise at 50% of the difference between
PGET and
Pmax. Furthermore, they found a trend towards an increase from 50 to 82% after a prior exercise at 80% of the difference between
PGET and
Pmax. Although we used a comparable prior exercise, which also comprised a 6-min exercise bout at 50% of the difference between
PGET and
Pmax as well as a subsequent 6-min active recovery, the plateau incidence was mostly unaffected in our study.
In addition to this outcome, we also found a significant reduction in
\(\dot{V}{\text{O}}_{{{\text{2max}}}}\) and
Pmax in the primed compared with the unprimed ramp test. According to previous prior exercise studies, this indicates that the recovery between the prior exercise and the subsequent ramp test was too short, which results in an impaired anaerobic capacity and a reduced exercise tolerance (Ferguson et al.
2007; Bailey et al.
2009; Wittekind et al.
2012). Since the occurrence of a
\(\dot{V}{\text{O}}_{{2}}\)-plateau has been related to anaerobic capacity (Gordon et al.
2011), the absence of an increase in the plateau incidence may be caused by a too fatiguing prior exercise or insufficient recovery. However, even in the participants with a mostly similar
Pmax (± 10 W) in the unprimed and primed ramp test (
n = 9) we did not find an increase in the plateau incidence (
n = 5 and 4 in the unprimed and primed ramp test, respectively). Therefore, an insufficient recovery of anaerobic capacity and the resulting reduction in
Pmax may not be the sole cause for the absence of an increase in the plateau incidence.
Another potential reason for the divergent findings may be the procedure of
\(\dot{V}{\text{O}}_{{2}}\)-plateau determination. We accepted a plateau when the
\(\Delta \dot{V}{\text{O}}_{{2}} /\Delta P\) of the final 50 W was less than 5.0 ml min
−1 W
−1. As recently shown (Niemeyer et al.
2020), this definition enables to detect a plateau with a risk of false plateau diagnoses below 5%. Gordon et al. (
2012) determined the
\(\dot{V}{\text{O}}_{{2}}\)-plateau from the difference between the last and next-to-last 30 s of a ramp test with an incremental rate of 30 W min
−1. They accepted a plateau when the difference was less than 2.1 ml min
−1 kg
−1. Since the mean workload of two consecutive 30 s intervals differs by about 15 W, the expected mean increase in
\(\dot{V}{\text{O}}_{{2}}\) in the submaximal intensity domain is ~ 150 ml min
−1 (assuming a
\(\Delta \dot{V}{\text{O}}_{{2}} /\Delta P\) of 10 ml min
−1 W
−1). Because the average body mass in the study by Gordon et al. (
2012) was 69 kg, their mean cut-off was in fact set at 145 ml min
−1, which is only 5 ml min
−1 below the expected increase in
\(\dot{V}{\text{O}}_{{2}}\), if no plateau occurs. If the plateau definition of Gordon et al. (
2012) is applied to our data, the plateau incidence in the unprimed and primed ramp tests increases to 80 and 65%, respectively. It is therefore very likely that the findings of Gordon et al. (
2012) are affected by a high frequency of false-positive plateau diagnoses (Niemeyer et al.
2020).
Effect of prior exercise on \(\Delta \dot{V}{\text{O}}_{{2}} /\Delta P\)
Contrary to our hypothesis, we found a comparable
\(\Delta \dot{V}{\text{O}}_{{2}} /\Delta P\) in the
S1 and even a reduction in the
S2 and ST intensity domains, as shown in Fig.
1 and Table
2. Previously, an increase in
\(\Delta \dot{V}{\text{O}}_{{2}} /\Delta P\) after a prior exercise has been described. However, the findings are inconsistent. Jones and Carter (
2004) described an increase in the
S2 and ST intensity domains, whereas Boone et al. (
2012) found an increase in the
S1 and a reduction in the
S2 domain. Marles et al. (
2006) and Ferguson et al. (
2007) did not find any change of
\(\Delta \dot{V}{\text{O}}_{{2}} /\Delta P\) after an intensive prior exercise.
These contradictory findings are potentially caused by methodological differences in terms of the protocol of the prior exercise and the subsequent recovery. The aim of the present study was to test whether the described increase in the
\(\dot{V}{\text{O}}_{{2}}\)-plateau incidence after an intensive prior exercise (Gordon et al.
2012) is caused by a higher
\(\Delta \dot{V}{\text{O}}_{{2}} /\Delta P\), which results in faster attainment of
\(\dot{V}{\text{O}}_{{{\text{2max}}}}\) and therefore contributes to the development of a
\(\dot{V}{\text{O}}_{{2}}\)-plateau despite a similar
Pmax. Thus, we chose a very similar experimental design as described by Gordon et al. (
2012). In contrast to our study and the study of Gordon et al. (
2012), Jones & Carter (
2004), as well as Boone et al. (
2012) used incremental ramp tests as prior exercises. Since these ramp tests were performed up to exhaustion, it is likely that the priming interventions were more intensive than in our and the Gordon et al (
2012) study. However, the BLC
BSL immediately before the start of the primed ramp test in our study was very similar compared to the corresponding values reported by Jones and Carter (
2004) and Boone et al. (
2012). Furthermore, it has been shown that even a priming exercise in the heavy intensity domain, which goes along with much lower BLC values, led to speeding of
\(\dot{V}{\text{O}}_{{2}}\) kinetics (Burnley et al.
2000,
2006). Consequently, it seems to be rather unlikely that the intensity of the prior exercise was too low to induce a speeding of
\(\dot{V}{\text{O}}_{{2}}\) overall kinetics and a corresponding increase in
\(\Delta \dot{V}{\text{O}}_{{2}} /\Delta P\).
In accordance with the study of Gordon et al. (
2012), we chose a 6-min active recovery between the prior exercise bout and the primed ramp test. Thus, the recovery protocol of our study was slightly different from the studies of Jones and Carter (
2004) and Boone et al. (
2012), which used a 10-min active recovery (Jones and Carter
2004) or a 3-min rest followed by a 3-min active recovery (Boone et al.
2012). It seems to be possible that the duration or kind of recovery (rest vs. low-intensity cycling) affects the
\(\dot{V}{\text{O}}_{{2}}\)-ramp test kinetics.
As shown in Table
2 and Fig.
1,
\(\dot{V}{\text{O}}_{{2}}\) at baseline-cycling preceding the ramp tests was significantly elevated in the primed condition. A potential explanation for this may be an increased activation of less efficient type 2 muscles fibers (Han et al.
2003). However, this explanation is rather unlikely because the EMG signal did not differ between the primed and the unprimed ramp test. Instead, it seems to be likely that the elevated
\(\dot{V}{\text{O}}_{{2}}\) at baseline-cycling and the beginning of the ramp test results from an elevated
\(\dot{V}{\text{O}}_{{2}}\) demand, which is caused by the same mechanisms that are responsible for the excess post-exercise oxygen consumption (EPOC) (Børsheim and Bahr
2003). The EPOC leads to an increase in
\(\dot{V}{\text{O}}_{{2}}\) not only at rest but also at subsequent low-intensity exercise (Bangsbo et al.
1994; Børsheim and Bahr
2003). The EPOC decreases exponentially with time (Børsheim and Bahr
2003). Therefore, with respect to the rather short recovery duration used in our study, it is possible that a potential increase in
\(\Delta \dot{V}{\text{O}}_{{2}} /\Delta P\) in the
S1 and ST domain is superimposed by the EPOC kinetics. Furthermore, the reduction in EPOC with time is much more pronounced during rest compared to active recovery, as described by Bangsbo et al. (
1994). This may explain why Boone et al. (
2012) found an increase in
\(\Delta \dot{V}{\text{O}}_{{2}} /\Delta P\) in the
S1 domain, despite using a recovery duration of 6 min also. Therefore, a passive and/or longer recovery phase may be more suitable to induce an increase in
\(\Delta \dot{V}{\text{O}}_{{2}} /\Delta P\). However, the effect of the recovery mode or duration on the change of ramp tests kinetics after a priming exercise has never been examined.
At the first glance, the priming-induced reduction in
\(\Delta \dot{V}{\text{O}}_{{2}} /\Delta P\) in the
S2 intensity domain seems to be caused by a reduced slow component of
\(\dot{V}{\text{O}}_{{2}}\)-kinetics. Especially in ramp tests with low incremental rates (< 30 W min
−1), a slightly upward deflection of the
\(\dot{V}{\text{O}}_{{2}}\)–workload-relationship has been reported at workloads above
PGET (Boone and Bourgois
2012). This upward deflection has been related to the same mechanisms that are responsible for the slow component of
\(\dot{V}{\text{O}}_{{2}}\)-kinetics (Grassi et al.
2015). It is well known that a priming exercise in the heavy or severe intensity domain reduces the magnitude of the slow component (Bailey et al.
2009; Burnley et al.
2000;
2006). However, this reduction is not based on a lower
\(\dot{V}{\text{O}}_{{2}}\) at the end of a constant load bout, which would indicate a lower gain of overall
\(\dot{V}{\text{O}}_{{2}}\)-kinetics (i.e., a higher delta-efficiency). Instead, the reduction in the slow component is caused by a higher amplitude of the primary/fast component of
\(\dot{V}{\text{O}}_{{2}}\)-kinetics (Bailey et al.
2009; Burnley et al.
2000,
2006). Thus, an increase in the fast component amplitude and a resulting speeding of
\(\dot{V}{\text{O}}_{{2}}\) overall kinetics should lead to an increase in
\(\Delta \dot{V}{\text{O}}_{{2}} /\Delta P\) in the
S2 and ST intensity domains (Wilcox et al.
2016), as demonstrated by Jones and Carter (
2004). Reasons for our contrary findings are unclear and must be examined in subsequent studies.
Effect of prior exercise on ∆RMS/∆P
In the study of Boone et al. (
2012), the increase in
\(\Delta \dot{V}{\text{O}}_{{2}} /\Delta P\) in the S1 intensity domain was accompanied by a steeper increase in the integrated EMG-signal of the left vastus lateralis. This indicates that the higher
\(\Delta \dot{V}{\text{O}}_{{2}} /\Delta P\) is caused by elevated muscle fiber activation. Despite recording the EMG-signal from VL, VM and GM of each leg, we did not find any changes in ∆RMS/∆P. Since we also did not find an increase in
\(\Delta \dot{V}{\text{O}}_{{2}} /\Delta P\) in the
S1 intensity domain, the similar ∆RMS/∆P in the unprimed and primed ramp test does not challenge the finding that the priming-induced increase in
\(\Delta \dot{V}{\text{O}}_{{2}} /\Delta P\) is caused by elevated muscle fiber recruitment (Boone et al.
2012).
The reasons for these different findings are unclear. Unlike our study, Boone et al. (
2012) used a ramp exercise bout as a priming intervention. This approach enables to measure muscle fiber activation of the primed and unprimed ramp test within the same electrode application. However, we tagged the position of the electrodes with an indelible marker to ensure the same position despite the ramp tests being performed on different days. Furthermore, the RMS signal was normalized to the mean RMS of the last minute of the 50 W-baseline cycling. Therefore, it is unlikely that the divergent findings are caused by changes in the electrode applications.
As described above, the recovery protocol of our study was slightly different compared to the study of Boone et al. (
2012). Therefore, it cannot be excluded that the absence of an increase in ∆RMS/∆P in our study is caused by the use of a 6-min active recovery instead of a 3-min rest followed by a 3-min baseline-cycling at 50 W, as performed by Boone et al. (
2012).