Cycling performance requires high aerobic energy turnover and effective transfer of that energy to external power. Hence, the peak oxygen uptake (O_2peak) and gross efficiency (GE), defined as the ratio of work rate to metabolic rate, are two key determinants of performance (Joyner and Coyle, 2008). Exercise training interventions focusing on high-intensity training (HIT) in cyclists have repeatedly shown enhanced O_2peak as the main physiological adaptation (Lucia et al., 2000; Bacon et al., 2013) whereas GE has been reported to both be unaffected (Ronnestad et al., 2015) and improved (Hintzy et al., 2005; Hopker et al., 2009, 2010). However, the study of Ronnestad et al. (2015), where GE was unaffected, used an effort-based approach to control intensity, which likely induced higher intensity compared to the studies by Hopker et al. (2009, 2010) who regulated intensity by set blood lactate levels. The study by Hintzy et al. (2005) used a combination of moderate- and high-intensity, but the untrained participants in the study are a likely reason for the increased GE. Furthermore, sprint and strength training led to reduced oxygen cost of submaximal cycling (i.e., GE likely increased) (Paton and Hopkins, 2005), whereas low- and moderate-intensity training led to unchanged (Kristoffersen et al., 2014) or increased (Hopker et al., 2012) GE in cycling. Overall, the current literature indicates that both training intensity and fitness level influence the responses on GE.

It is generally believed that greater training loads, achieved through both volume of training and sufficient intensity, are required to trigger O_2peak or performance adaptations in individuals with high compared to low initial levels of O_2peak or performance. In previous studies, there has been reported an effect of initial level of O_2peak on the response to exercise (Saltin et al., 1969), but more recently no significant correlation between initial O_2peak and the response to a training intervention was reported (Kohrt et al., 1991; Skinner et al., 2001). However, these studies (Kohrt et al., 1991; Skinner et al., 2001) do not include any measures of performance, and the participants had a relatively low initial level of fitness (reported O_2peak < 31.8 mL kg^-1 min^-1). As such, inference to performance and/or more highly trained populations cannot be made based on these studies.

The interaction between O_2peak and GE adaptations in response to a training intervention requires further elucidation. An inverse relationship between O_2peak and GE has been found (Lucia et al., 2002) and also an inverse relationship between the change in GE and O_2peak following a training intervention (Santalla et al., 2009; Hopker et al., 2012). However, none of these interventions led to increased O_2peak at the group level.

Therefore, the purpose of the present study was to investigate how baseline characteristics of cycling performance, O_2peak and GE influence subsequent adaptations of these parameters and their interplay following a 12-week high-intensity intervention designed to increase O_2peak in competitive cyclists. We hypothesized that a large training load would lead to increased O_2peak and reduced GE, but there would be no influence of initial levels of O_2peak and GE.

Sixty-three male competitive cyclists (38 ± 8 year, O_2peak: 61 ± 6 mL kg^-1 min^-1) were recruited to take part in the current multicentre study, involving three test centers completing the same experimental trial. All participants were categorized as well-trained (Jeukendrup et al., 2000) with 9 ± 3 h of weekly training in the year prior to participation. All participants completed the intervention, however, three participants were excluded from the final analyses due to absence from post-testing. The study was approved by the ethics committee of the Faculty for Health and Sport Science, University of Agder, and registered with the Norwegian Social Science Data Services (NSD). All athletes gave their verbal and written informed consent prior to study participation. The present study is part of a larger research project and thus, the intervention period, testing procedures and instrument are described in brief. A detailed description of the intervention period, testing procedures, and instruments can be found in Sylta et al. (2016).

O_2peak ranged from 48 to 76 mL·kg^-1 min^-1 and GE from 16.5 to 20.8%. The average Power_40min ranged from 194 to 342 W and 2.3 to 4.6 W kg^-1 when expressed as absolute values and normalized to body mass, respectively. A plateau in O₂ occurred in 54 and 58 out of the 60 pre- and post-tests, respectively. Following the 12-week training intervention, there was a significant increase in O_2peak, PPO, and Power_40min but there was a decrease in GE (Table 1; all p < 0.05). The weekly training volume during the intervention was 10 ± 3 h, of which 97 ± 4% was endurance training. The mean power output during all HIT intervals was 310 ± 40 W and average blood lactate taken during the sessions was 8.7 ± 4.0 mmol L^-1. The overall intensity distribution for all training based on heart rate data is presented in Figure 2.

The purpose of the present study was to investigate how the initial characteristics of cycling performance, O_2peak, and GE, as well as their interplay, influences subsequent adaptations in these parameters following a 12-week HIT intervention in well-trained cyclists.

The training intervention led to an increase in performance and O_2peak but a decrease in GE. Furthermore, we found significant associations between the athletes’ initial levels of GE, O_2peak, and performance and subsequent adaptations of that same parameter. However, parameter specific initial levels explained only 4–18% of the variance in adaptations, and when we compared our four groups with combinations of high and/or low initial levels of GE and O_2peak, no differences in adaptations were found among groups. Overall, our study shows that the impact of initial characteristics of cycling performance, O_2peak, and GE on the subsequent responses to these parameters are relatively small, and the effect disappears if we investigate the relationship in groups based on initial GE and O_2peak characteristics in combination.

While the present study shows significant effects of initial performance and O_2peak on the subsequent adaptation to HIT in highly trained cyclists, the effect is only moderate. An effect of initial fitness on the O_2peak responses has also been reported previously in less trained individuals (Saltin et al., 1969), although other studies (Kohrt et al., 1991; Skinner et al., 2001) showed no effect. The HIT element in the present study had an overall positive effect on O_2peak and endurance performance, which differs from the previous studies that utilized a lower training intensity (e.g., 75% of O_2peak (Skinner et al., 2001)). Furthermore, the total training load added in our study seemed to be sufficient to elicit an overload stimulus and thereby trigger endurance adaptions in most of the athletes. This is exemplified by a recent study where further increasing the training load effectively elicited training adaptations in participants who were unresponsive to 180 min of moderate to high intensity exercise per week (Montero and Lundby, 2017). However, even in our study, the observed improvements were relatively modest, which may partly be due to differences in how optimal the added training load was for each individual participant. In addition, the subsequent recovery phase is of importance for adaptations, and e.g., subjects need to be healthy and avoid other factors which might negatively influence adaptations.

In contrast to the positive effects of the 12-week high intensity training intervention on O_2peak (∼5%), GE declined slightly following the intervention (∼2%), and there was a moderate association between initial level of GE and the subsequent response. However, there were no significant differences in adaptation between the groups with high and low GE. Previous literature examining changes in GE following high intensity training reported no effect (Ronnestad et al., 2015) or an increase in GE when utilizing an exercise intensity equivalent to five heart rate beats above the work rate eliciting 4 mmol⋅L^-1 of blood lactate (Hopker et al., 2010). However, previous studies in participants of a similar performance level to our participants, who utilized low- to moderate-intensity training, reported improved GE and a significant positive relationship between changes in GE and performance (Hopker et al., 2010, 2012).

A potential explanation for the different effect of training on GE between our study and others might be the HIT applied in our study, which primarily influenced performance via enhanced O_2peak (Sylta et al., 2016)). Previous studies (Hopker et al., 2010, 2012) have used a lower intensity compared to the present study, and a lower intensity may be more effective for enhancing GE at a submaximal work rate. In the present study, training was executed as HIT with the addition of ad libitum LIT. A possible influencing factor on the decline in GE in the present study may be the low amount of training as moderate-intensity exercise, which may be important for maintaining GE (Hopker et al., 2009; Kristoffersen et al., 2014).

Intensity in the present study was controlled utilizing an effort based approach where the participants are instructed to aim to achieve the highest possible average power output within each session (Seiler et al., 2013). This is the same approach used by Ronnestad et al. (2015) who demonstrated unchanged GE after HIT training. It is possible that the effort based intensity control leads to higher intensity, as shown through the high blood lactate levels during intervals in the present (i.e., average blood lactate of 8.9 mmol L^-1) and a previous study using intervals of 4 to 8 min duration (Seiler et al., 2013), compared to the approaches used by Hopker et al. (2010) who demonstrated increased GE with intensity based on absolute blood lactate levels of 4 mmol L^-1 + 5 heart rate beats per minute. Furthermore, Hopker et al. (2009, 2010) proposed that training at moderate intensity, eliciting less than 4 mmol L^-1 blood lactate, is important for maintaining GE. Hence, training at (very) high-intensity may lead to unchanged or declined GE, whereas training at lower intensity may have the opposite effect.

However, the decline in GE may also be influenced by the fact that it was calculated at a moderate intensity (i.e., the average of 125, 175, and 225 W) and might not reflect what occurs at higher workloads (i.e., training intensity average interval work rate of 310 W). Additionally, since 225 W exceed 60% of PPO, there is a possibility that the O₂ slow component influence our measurements slightly, which could have led to an overestimation of the decline in GE from pre- to post-test. However, since there was no difference in the change in GE for the three work rates used for GE calculation and the corresponding RER measurements were below 1.0, a possible influence would be minor.

As expected, we found a positive relationship between change in cycling performance and change in O_2peak. In contrast, change in GE was not related to a change in performance. This inverse relationship between the change in GE and O_2peak (Figure 5) corresponds with previous findings (Lucia et al., 2002; Hopker et al., 2012). However, in contrast to previous studies which have shown an increase in GE and small changes in O_2peak (Lucia et al., 2002; Hopker et al., 2012), we show the same inverse relationship when the average GE decreases and the average O_2peak increases.

Also contrary to previous findings (Hopker et al., 2012) is an increased performance despite a decrease in GE. Although the 12-week HIT intervention led to a large increase in O_2peak that positively influenced cycling performance, it appears that cycling efficiency is slightly reduced, especially in those with large O_2peak improvements. However, it is important to keep in mind the relatively short duration of the intervention executed in this study. As demonstrated by the findings in this study, the decrease in GE over a relatively short period where the objective of training is to increase O_2peak was not detrimental to performance due to the improved O_2peak. However, in general, long-term decreases in GE can be detrimental to performance. Since studies using low- and moderate-intensity training, as well as sprint and strength training (Paton and Hopkins, 2005; Hopker et al., 2012) have shown increases in GE, cyclists should likely use a combination of different training intensities to optimize their long-term performance development. This also represents a typical training pattern over a season for elite cyclists, where a combination of intensities and periods with different focus is employed (Lucia et al., 2000; Hopker et al., 2009). Although different types of training influence GE and O_2peak differently, both high and moderate intensity training may be necessary for optimal performance increases during a competitive season. Additionally, the long-term effect on GE and O_2peak is potentially different from the effects seen in this relatively short 12-week intervention compared to the effect on performance.

We believe the finding of a small effect of baseline level has important practical implications and demonstrates that if an appropriate training stimulus is administered, the initial physiological characteristics have little effect on the training adaptation in a large cohort of well-trained athletes. It demonstrates that an appropriate training stimulus can further enhance performance, independent of the initial physiological characteristics of even well-trained athletes. A known limitation of the present arises from the baseline characteristic and change following the intervention are not independent measurements, we violate the assumption of independence in the correlation analyses. This may lead to an effect known as regression to the mean (Altman and Bland, 1994) which ultimately would lead to an overestimation of the correlation. When calculated using Oldham’s correction to minimize the effect, the correlations in the present study were weakened. The additional finding that the groups based on differences in baseline characteristics show no difference in the adaptation to the training intervention also supports our interpretation. Although the groups in the present study where comprised of only eight athletes which limit statistical power with multiple comparisons, however, the group size is comparable to similar studies on training adaptation.

In conclusion, the present study demonstrates statistically significant, but practically trivial effects of initial levels of O_2peak and performance on subsequent adaptations following a 12-week HIT intervention in well-trained cyclists. In contrast to the improvements in performance and O_2peak following this intervention, GE was reduced and the changes in GE negatively correlated with changes in O_2peak. However, when comparing adaptations between groups with different levels of O_2peak and/or GE, we found no differences. Overall, this study indicates that the effects of initial level of performance and physiological capacities on subsequent adaptations are relatively small, and the effect disappears if we investigate the relationship in groups based on GE and O_2peak characteristics.

KS, ØSa, ET, JD, BR, and ØSy contributed in conceptualization the study. KS, ØSa, DH, and JD contributed in data collection. KS, ØSa, DH, and ØSy contributed in data handling and statistical analysis. KS, ØSa, ET, DH, JD, SS, BR, and ØSy contributed in preparing the manuscript.

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.