Very little information on the physiological responses exists. Almost all the information available is related to heart rate (HR) adjustment and blood lactate (BLa) accumulation (Gobbi et al., 2005; D'Artibale et al., 2007; Konttinen et al., 2007).

One category of motorcycling is Enduro, where races are held on country roads, mule tracks, and public roads under ordinary traffic rules (Gobbi et al., 2005). Competitions last from 6 to 8 h and riders do not know the route and may face unexpected obstacles. Distances between checkpoints must be covered in established times (i.e., with a fixed average speed), from the cardiovascular point of view, Enduro causes acute and unpredictable variations in HR and possibly to other hemodynamic parameters (such as cardiac pre-load, inotropism and after-load) yet to be described. Moreover, the long duration of Enduro races, together with the clothing and equipment, can further stress athletes' cardiovascular systems because of heat and dehydration. The limited data available report that HR can reach values close to 190 bpm (Gobbi et al., 2005), thereby suggesting an increase in sympathetic tone which leads to cardiovascular activation. Moreover, Enduro requires the recruitment of the aerobic metabolism, which can be maintained at a level above that of the anaerobic threshold (AT) (Gobbi et al., 2005).

It is well-known that during exercise, cardiovascular adjustments are caused by the activation of the central command and by mechanical and metabolic muscle activity, which evoke the exercise pressor reflex (Nóbrega et al., 2014). These cardiovascular reflexes are supposed to be activated during Enduro since this activity causes motor cortex activation and mechanical and metabolic engagement at the muscle level (Gobbi et al., 2005). Considering these features, it is reasonable to hypothesize that the cardiovascular apparatus is subjected to stress during Enduro performances. Furthermore, the activation of both central command and exercise pressor reflex recruits myocardial inotropism (Nóbrega et al., 2014) which increases stroke volume (SV). The combination of increments in SV and HR induces elevation in cardiac output (CO). However, to the best of our knowledge, nobody to date has measured CO during motorcycle riding.

Furthermore, it is well known that changes in HR and SV may oppose each other (Higginbotham et al., 1986; Crisafulli et al., 2011), hence their combined effect should be investigated. Although SV is not easily measured, this parameter has been successfully assessed recently by means of a portable impedance cardiograph, which is able to gather hemodynamic data in extreme environments, such as during underwater diving (Tocco et al., 2013; Marongiu et al., 2015).

This investigation was devised to study acute hemodynamic adjustments induced by Enduro riding by using trans-thoracic impedance. In detail, we were interested in obtaining a complete hemodynamic picture by measuring HR, SV, and CO during a real Enduro session of short duration. The hypothesis was that isometric strains occurring during Enduro impaired venous return, thereby reducing cardiac pre-load, and increased after-load, which opposed cardiac emptying. This phenomenon would result in the impossibility to increase SV despite the Enduro-induced activation in central command and exercise pressor reflex activation. These two reflexes, together with HR increments, are supposed to recruit cardiac performance and pre-load (Crisafulli et al., 2009; Roberto et al., 2012; Marongiu et al., 2013; Milia et al., 2014; Nóbrega et al., 2014). Thus, if static effort prevailed over dynamic effort in Enduro, a reduction of, or a stable SV value throughout the race would be expected.

All Subjects Completed the Study Protocol. Figure 2 shows an example of the time course of HR, SV, and CO in one subject throughout the test. This picture shows that cardiovascular response was intermittently activated. Results from this observation look mainly at the SV time course, rather than at HR. In reality, whilst the HR level increased and almost stabilized, SV showed several peaks throughout the session.

Figures 3–5 show the statistics results applied to each variable. HR significantly increased from 96.5 ± 12.8 bpm at rest to 153.1 ± 17.7 bpm during the experimental trial. This parameter reached peaks of up to 200 bpm in some subjects. Recovery led to a reduction in HR but it did not return to pre-exercise levels (Figure 3A). SV increased from a level of 53.5 ± 14.1 ml at rest to 72.2 ± 22.1 ml during the Enduro session, showing peaks of up to 125 ml. During recovery SV returned to pre-exercise levels (Figure 3B). Likewise, CO increased during exercise as compared to rest (5.0 ± 1.1 vs. 10.9 ± 3.0 L·min⁻¹) to return to baseline during recovery (Figure 3C). In some subjects, CO reached a level of 20 L·min⁻¹ during riding.

VER was enhanced during the riding session and it returned to pre-exercise levels during recovery. The average VER levels during rest and riding were 192.9 ± 43.0 and 324.1 ± 83.6 ml·s¹ respectively, with peaks of up to 500 ml·s⁻¹ during the experimental trial (Figure 4A). VFR was augmented by Enduro riding with respect to rest (849.1 ± 309.8 vs. 141.1 ± 160.5 ml·s⁻¹). Peaks in VFR reached values of up to 1,500 ml·s⁻¹. During recovery, this variable returned to values similar to those at pre-exercise (Figure 4B). Figure 4C demonstrates that PEP decreased during riding with respect to rest and that this decrement was still present during recovery. VET (Figure 4D) decreased during riding, but it returned to values close to pre-exercise during recovery. Moreover DT (Figure 4E) was greatly reduced by ridding to return to a level similar to pre-exercise during recovery.

MAP was higher during recovery than during pre-exercise, while SVR did not show any difference between pre-exercise and recovery (Figures 5A,B respectively). Finally, BLa significantly accumulated during recovery with respect to pre-exercise levels, reaching values higher than 6 mmol•L⁻¹, with peaks of about 10 mmol•L⁻¹ (Figure 5C).

The hemodynamic scenario obtained from the present study reveals that during Enduro a substantial increase in CO occurs. On average, this parameter doubled during riding from about 5 to 10 L·min⁻¹ as compared to rest. This CO response was the consequence of a significant increase in both HR and SV. It should to be underscored that athletes performed not a real race. Instead, it was a short training, without the psychological stress imposed by a real race. Moreover, the riders performed the test alone, without rivals. Thus, any bias due to psychological stress can be ruled out.

Whilst an increment in HR is a well-known phenomenon during racing, and was expected, the increment in SV is an important new finding. To the best of our knowledge, this is the first time this parameter has been investigated during motocross riding. In detail, SV increased from an average pre-exercise level of 53 to 72 ml during riding, i.e., an increment of about 35%. This increment occurred notwithstanding the fact that motocross is primarily considered an activity where isometric actions prevail over dynamic actions (Konttinen et al., 2007). It is well-known that static exercise causes a reduction in SV, although conflicting results have been reported in the literature (Shoemaker et al., 2007; Elstad et al., 2009; Toska, 2010). Our hypothesis was that isometric strains impaired venous return, thereby reducing cardiac pre-load and SV. Furthermore, isometric strains caused an increase in after-load, which opposed ventricular emptying. Our reasoning was that if static effort prevailed over dynamic effort in Enduro, a reduction of, or a stable SV value throughout the race would have been expected. However, this was not observed in this study.

Several factors may explain this phenomenon. Firstly, it is possible that dynamic muscle contractions were as frequent as the isometric contractions during Enduro. Dynamic muscle activity facilitates venous return by squeezing peripheral veins, especially in the lower limbs (Carter et al., 1999; Crisafulli et al., 2004). Hence, we speculate that in our setting, the presence of dynamic muscle contractions counteracted the isometric activity, thereby improving cardiac filling and pre-load. This fact recruited the Frank-Starling mechanism and supported the SV response. Secondly, it must be remembered that venous return and cardiac pre-load also depend on the sympathetic activity. Indeed, during exercise, sympathetic-mediated venous-constriction takes place in order to centralize blood volume and to support SV when the mechanical and the metabolic arm of the exercise pressor reflex is activated, i.e., during eliciting of the so-called mechano-metaboreflex (Crisafulli et al., 2009; Nóbrega et al., 2014; Milia et al., 2015). This reflex, provides continuous feedback on the mechanical and metabolic status of contracting muscles and is stimulated by both isometric and dynamic exercise. Hence, it is possible to hypothesize that muscle activity occurring during Enduro activated the mechano-metaboreflex, thereby leading to a sympathetic-mediated venous constriction, which in turn, enhanced venous return and cardiac pre-load. This resulted in the augmented SV observed in the present investigation. This occurrence is supported by the findings that VFR was substantially increased during the riding period. This parameter is the measure of the filling rate of ventricles and is an expression of the global capacity of the circulatory system to support pre-load during diastole (Gledhill et al., 1994; Crisafulli et al., 2000; Marongiu et al., 2013; Milia et al., 2014). It is to be noticed that this mechanism was very effective since diastole shortened more than ejection time, thereby reducing the time available for ventricular filling. Actually, the increase in VFR was greater than that in VER.

Another phenomenon that could explain the SV response was the enhanced cardiac performance, as testified by VER behavior. This parameter is the rate of ventricle emptying is correlated to cardiac performance (Tanaka et al., 1986; Concu and Marcello, 1993; Gledhill et al., 1994). Our finding of an enhancement of VER during riding demonstrates that an increase in myocardial performance takes place during Enduro and this fact, along with the increased VFR, further supports the rise in SV found in the present investigation. Two phenomena can account for the improved myocardial performance: (i) the recruitment of the Frank-Starling mechanism by the augmented cardiac pre-load due to the sustained VFR; and (ii) the sympathetic-mediated increase in inotropism.

The hypothesis that the sympathetic tone was elevated during Enduro is supported by HR time course, which showed a mean group level of 153 bpm, with peaks of up to 200 bpm in some individuals. The sympathetic activation was likely the consequence of the recruitment of both the central command and the exercise pressor reflex, which are operative during exercise even at mild levels (Nóbrega et al., 2014; Crisafulli et al., 2015).

Taken together, data from the present study support the concept that Enduro is a challenging activity from a cardiovascular point of view. Actually, substantial hemodynamic activation occurred during the 10 min of riding utilized in the present study. Thus, we can speculate that this hemodynamic engagement would have been even higher if riding sessions had been longer. Moreover, it also emerged that the cardiovascular apparatus was intermittently activated. Figure 2 shows that SV and CO peaked several times throughout the race, whereas this phenomenon was not evident looking at the HR time course alone. Another outcome that deserves attention is that substantial metabolic engagement was also present, as is supported by the BLa level gathered immediately after the races.

IS, VP, RM, and AC conceived the study, conducted experiments, designed and wrote the paper. GM, SR, and SO conducted experiments, designed and wrote the paper. All authors read and approved the final version of the manuscript.