The responses to post-exercise water immersion and its use as a recovery tool following physical exercises have received special attention in the past few years. Based on previous studies, we hypothesized that post-exercise short-term water immersion following anaerobic exercise would result in increased aerobic energy expenditure, delaying the \({\dot{\text{V}}}_{{\text{O}}_{\text{2}}}\) kinetics and increasing EPOC especially during CWI. Furthermore, we expected that the other respiratory parameters would increase during immersion and that HR recovery would be accelerated during CWI and delayed during HWI. It was further anticipated that the recovery of blood [La-] would be accelerated during CWI and that the anaerobic mechanical power output would be decreased after CWI and increased after HWI. This randomized and controlled crossover experimental design demonstrated that recovery from anaerobic power exercise using water immersion at different temperatures compared to OWI: i) it provided increased aerobic energy expenditure and other respiratory parameters (including \({\dot{\text{V}}}_{{\text{O}}_{\text{2}}}\) kinetics and EPOC), a higher \({\dot{\text{V}}}_{\text{E}}\) response in HWI compared to CWI; ii) higher HR values during HWI and a similarity between CWI and OWI; iii) the slow recovery phase influenced the overall cardiorespiratory responses (AUC) more than the fast phase; iv) a similarity in the behavior and magnitude of blood [La-] between the three recovery methods; v) increased performance during WAnT2 carried out after HWI and decreased performance after CWI; vi) while the temperature in the CWI protocol in the present study falls outside of the range, this may still constitute CWI, as evidenced by the divergent power output parameters between OWI and HWI conditions, and vii) performance results which showed weak correlations with the blood [La-] and with other cardiorespiratory variable.
Kinetics Of Respiratory Variables
From a respiratory standpoint, the hypothesis of this study was confirmed through the observed increase in EPOC, \({\dot{\text{V}}}_{\text{C}{\text{O}}_{\text{2 AUC}}}\)and \({\dot{\text{V}}}_{{\text{E}}_{\text{ AUC}}}\). The effect of immersion temperature was significantly higher only in the \({\dot{\text{V}}}_{{\text{E}}_{\text{ AUC}}}\) during HWI. In general, the variables with higher area presented higher values of \(\text{τ}\) and asymp. A higher \(\text{τ}\) means a delay in the fast recovery phase, while a higher asymp means a delay in the slow recovery phase. Both conditions can impact the AUC, as it represents an integrative response between the behavior and magnitude of the respiratory variable and an oxidative metabolism more intense during recovery. The asymp was the parameter that exerted the greatest influence on the AUC in all cardiorespiratory variables.
In relation to \({\dot{\text{V}}}_{{\text{O}}_{\text{2}}}\)the CWI produced the greatest disturbance in EPOC accompanied by the highest values of \(\text{τ}{\dot{\text{V}}}_{{\text{O}}_{\text{2}}}\) and \({\dot{\text{V}}}_{{\text{O}}_{\text{2 asymp}}}\) (absolute and relative). These differences were significant only in relation to OWI. The EPOC presented a weak correlation coefficient with \(\text{τ}{\dot{\text{V}}}_{{\text{O}}_{\text{2}}}\) and a good coefficient with \({\dot{\text{V}}}_{{\text{O}}_{\text{2 asymp}}}\). This means that the slow phase of the recovery curve of \({\dot{\text{V}}}_{{\text{O}}_{\text{2}}}\)was the parameter that most influenced the magnitude of EPOC. A low correlation was found between and τ and asymp.
The delay observed in the recovery of \({\dot{\text{V}}}_{{\text{O}}_{\text{2}}}\) during CWI and HWI might be linked with a possible \({\text{O}}_{\text{2}}\) delivery limitation or an inadequate \({\text{O}}_{\text{2}}\) utilization. From the point of view of a \({\text{O}}_{\text{2}}\) delivery limitation, the blood redistribution triggered by immersion would have delayed the fast recovery phase of the \({\dot{\text{V}}}_{{\text{O}}_{\text{2}}}\) recovery phase by slowing down the restoration of muscle reserves of \({\text{O}}_{\text{2}}\), adenosine triphosphate (ATP) and creatine phosphate (CP) (Linnarsson 1974; Hughson 1990). The greatest \(\text{τ}{\dot{\text{V}}}_{{\text{O}}_{\text{2}}}\) during CWI would have been produced as a consequence of reduced peripheral blood flow resulting from convergent redistribution triggered by the hydrostatic pressure gradient and peripheral vasoconstriction (Alborelius et al. 1972; Echt et al. 1974; Risch et al. 1978b; Srámek et al. 2000). A reduction in \(\text{τHR}\) could also trigger a reduction in \(\text{τ}{\dot{\text{V}}}_{{\text{O}}_{\text{2}}}\), since an increase in \(\text{τHR}\) is associated with an increase in \(\text{τ}{\dot{\text{V}}}_{{\text{O}}_{\text{2}}}\) (Hughson and Morrisey 1983); however, this was not confirmed (Table 2). During HWI, the \(\text{τ}{\dot{\text{V}}}_{{\text{O}}_{\text{2}}}\) presented a delay of smaller magnitude with no differences from OWI. In this case, possible blood redistribution in divergent directions triggered by a hydrostatic pressure gradient and mainly peripheral vasodilation probably explain its lower values compared to CWI. The lower \(\text{τHR}\) also did not influence the \(\text{τ}{\dot{\text{V}}}_{{\text{O}}_{\text{2}}}\) during HWI. A \({\dot{\text{V}}}_{\text{E}}\) did not influence the \(\text{τ}{\dot{\text{V}}}_{{\text{O}}_{\text{2}}}\) in both situations, because its \(\text{τ}{\dot{\text{V}}}_{\text{E}}\) did not show differences between the retrieval methods. These results seem to confirm the data of Srámek and collaborators (2000) that attribute the early responses of the \({\dot{\text{V}}}_{{\text{O}}_{\text{2}}}\) during immersion in a liquid medium to vascular adjustments and the late responses to other thermoregulatory adjustments such as cardiorespiratory changes and increase in cellular metabolism.
In this sense, different from the fast recovery phase, the greater \({\dot{\text{V}}}_{{\text{O}}_{\text{2 asymp}}}\) would result from the increase triggered by the increase in cellular metabolism especially during CWI and cardiorespiratory changes during HWI. Considering that a greater heat gradient was produced during CWI recovery after intense exercise (Cannon and Keatinge 1960), it is possible to attribute the increased response of the \({\dot{\text{V}}}_{{\text{O}}_{\text{2 asymp}}}\) during CWI to the need for maintenance of cell temperature (Mekjavic and Bligh 1989), since, with the exception of \({\dot{\text{V}}}_{{\text{E}}_{\text{ AUC}}} ,\)the cardiorespiratory responses of CWI were not different from those of the OWI. Conversely, greater cardiorespiratory work was observed during HWI. Both the \({\dot{\text{V}}}_{{\text{E}}_{\text{ asymp}}}\) and \({\dot{\text{V}}}_{{\text{E}}_{\text{ AUC}}}\), as well as the \({\text{HR}}_{\text{ asymp}}\) and \({\text{HR}}_{\text{ AUC}}\), were higher during HWI in comparison to the other conditions. The incredible ventilatory increase observed during HWI would result from the need to provide heat energy loss, since the energy absorbed during warm immersion would hinder the loss of cellular heat energy produced during physical exertion (Gaudio and Abramson 1968). Despite the minor importance of heat exchange through respiration in thermoregulation in humans (Tsuji et al. 2012; Tsuji et al. 2016), it is likely that the elevation in body temperature contributed to the increase in ventilatory response. In addition, the increase seen in HR could result from a need to counterbalance the decrease in systolic volume caused by the vasodilation triggered by HWI (Keatinge and Evans 1961). In any case, these adjustments had repercussions in the increase observed in \({\text{HR}}_{\text{ AUC}}\) and \({\dot{\text{V}}}_{{\text{E}}_{\text{ AUC}}}\) and, consequently, in EPOC in relation to OWI.
In contrast, other studies have downplayed the importance of \({\text{O}}_{\text{2}}\) delivery limitation in determining the \({\dot{\text{V}}}_{{\text{O}}_{\text{2}}}\) kinetics responses and highlighting the influence of inadequate \({\text{O}}_{\text{2}}\) utilization at a peripheral level. This means that the increase or decrease in \({\text{O}}_{\text{2}}\) uptake, changes in blood flow or cardiorespiratory adjustments would not necessarily imply changes in the \({\dot{\text{V}}}_{{\text{O}}_{\text{2}}}\) kinetics (Grassi et al. 1998; Grassi 2000). In this sense, the delay of \(\text{τ}{\dot{\text{V}}}_{{\text{O}}_{\text{2}}}\) during immersion recovery could result from changes in tissue temperature on the enzymatic velocity and cellular metabolism, since similar responses were found in the on-transient pulmonary \({\dot{\text{V}}}_{{\text{O}}_{\text{2}}}\) kinetics after cooling during immersion (Ferretti et al. 1995; Stanley et al. 2014). In line with this reasoning, during CWI the decrease in tissue temperature could reduce hydrolysis (Ferretti et al. 1992) and ATP resynthesis (Blomstrand et al. 1984; Binzoni et al. 1990; Ishii et al. 1992) and the need to increase heat production suggests a decrease in cellular energy efficiency (Nedergaard et al. 2001; Cannon and Nedergaard 2011), producing a delay in the recovery curve of the \({\dot{\text{V}}}_{{\text{O}}_{\text{2}}}\) and an increase in EPOC. However, due to the short period of time, it is possible that the \(\text{τ}{\dot{\text{V}}}_{{\text{O}}_{\text{2}}}\) was not influenced by this mechanism, and it is more likely that only the slow phase of the recovery curve of \({\dot{\text{V}}}_{{\text{O}}_{\text{2}}}\) may be attributed (Mekjavic and Bligh 1989). As such, Choukroun and Varene (1990) verified a higher arteriovenous difference during immersion at rest at 25 ºC, in comparison to 34 ºC, without difference in cardiac output, reinforcing the effect of temperature on the extraction of \({\text{O}}_{\text{2}}\) by the tissue. It is also possible that the physiological shivering triggered by thermoregulation increases the cellular energy requirement (Golozoubova et al. 2001) contributing to the increase in \({\dot{\text{V}}}_{{\text{O}}_{\text{2 asymp}}}\) and EPOC; however, this phenomenon was observed in low intensity in only four athletes. In relation to HWI, it is likely that heat energy directly increased tissue temperature, elevated cellular enzymatic activity, and decreased cellular energy efficiency, because the \({\dot{\text{V}}}_{{\text{O}}_{\text{2}}}\) increased with the individual remaining at rest (Cannon and Keatinge 1960; Kingma et al. 2012). However, similarly to CWI, the \(\text{τ}{\dot{\text{V}}}_{{\text{O}}_{\text{2}}}\) was not influenced by this mechanism due to the short time frame (Mekjavic and Bligh 1989).
In this sense, although it was not the objective of the research to determine which parameters influenced the \({\dot{\text{V}}}_{{\text{O}}_{\text{2}}}\) kinetics, the factors related to the\({\text{O}}_{\text{2}}\) delivery limitation seem to explain the behavior of \({\dot{\text{V}}}_{{\text{O}}_{\text{2}}}\) at the beginning of immersion recovery, and the combination of both (\({\text{O}}_{\text{2}}\) delivery and \({\text{O}}_{\text{2}}\) utilization) seem to explain the late responses. Although the highest values of \({\dot{\text{V}}}_{{\text{O}}_{\text{2}}}\) were found during CWI, these responses were not significantly different from HWI. This result makes the issue complex, since the immersion temperature triggered different physiological responses, especially in relation to HR and \({\dot{\text{V}}}_{\text{E}}\). Research models associating these outcomes with different immersion temperatures and duration deserve to be developed.
Similar to EPOC, the response of \({\dot{\text{V}}}_{\text{C}{\text{O}}_{\text{2 AUC}}}\) revealed higher values during immersion, with no difference between temperatures. Therefore, immersion did not cause important changes in RER, keeping values higher than 1.0 throughout the period for the three recovery methods. This result can be attributed to the high blood [La-] oxidation that exhibiteed similar behavior and magnitude during the recovery period for the three experimental conditions (Scott 1998; 2000). As the EPOC and a \({\dot{\text{V}}}_{\text{C}{\text{O}}_{\text{2 AUC}}}\) were higher during immersion, and blood [La-] levels were similar, it is possible to speculate that a longer recovery period might reveal differences in blood [La-] levels. A longer recovery time might also reveal differences in aerobic energy recovery highlighting the effect of non-shivering and/or shivering thermogenesis, reduced energy efficiency, or possible modifications in RER between the methods (Srámek et al. 2000).
Heart Rate Kinetics
From the cardiac point of view, the hypothesis of this study was that the recovery temperature would trigger antagonistic responses in HR. HR recovery during CWI would be accelerated, presenting reduced levels during recovery, while during HWI, there would be a delay and elevation in its values. CWI accelerated and maintained HR recovery only after WAnT2, while its values of \({\text{HR}}_{\text{ asymp}}\) and \({\text{HR}}_{\text{AUC}}\) values did not present the expected decrease, being little different from that observed during OWI. The lower values of \(\text{τHR}\) during CWI may be attributed to a faster withdrawal of sympathetic tone and a faster reactivation of parasympathetic tone (Al Haddad et al. 2010) as an effect of immediate immersion. We know that the baroreflex stimulation generated by immersion triggers a reduction in HR and a decrease in muscle sympathetic nerve activity (MSNA) (Mano et al. 1991). These effects are potentiated in immersions below the thermoneutral temperature, being interrupted at very low immersion temperatures (Srámek et al. 2000), and proportional to the HR values measured before the individual entered the water (Kruel et al. 2014). However, this mechanism does not seem to have influenced the slow recovery phase of HR. An \({\text{HR}}_{\text{ asymp}}\) was similar between CWI and OWI, which may be attributed to late thermoregulatory responses due to the need to maintain body temperature observed during prolonged immersions at or below 20ºC related to increased sympathetic activity (Srámek et al. 2000). Unlike other studies that verified such responses at immersion temperatures below 20ºC (Srámek et al. 2000), the occurrence in this study could be justified because the design consisted of recovery from a high-intensity physical test. Thus, we suggest that thermoregulatory responses could occur at immersion temperatures above 20ºC due to physiological stress prior to immersion.
Conversely, the lower values of \(\text{τHR}\) during HWI do not seem to represent a more accelerated recovery, but a mathematical consequence of the rise of its asymptote \(({\text{HR}}_{\text{ asymp}}\)) and the reduction in the amplitude of the variable recovery response (\({A}_{1}\)). A \({\text{HR}}_{\text{ asymp}}\) during HWI was between 10 to 17 bpm higher than the other recovery methods and this contributed to the elevation of its values of \({\text{HR}}_{\text{AUC}}\). These results seem to be related to hemodynamic responses resulting from vasodilation triggered by thermoregulation to heat and stimulation of cardioaccelerator centers due to likely elevation of core body temperature (Becker et al. 2009). In this sense, it is likely that prior exercise intensity, type of environment, temperature, and immersion time may modify HR behavior during recovery. In this study, the environment and the effect of immersion temperature were tested. These factors may influence the monitoring of the recovery period if HR is used as an evaluation parameter.
Lactate Kinetics
Contrary to the initial hypothesis, the increased aerobic energy expenditure following CWI had no influence on blood [La-] responses. We could verify that the sum of all blood [La-] values throughout the recovery was not different between various recovery methods. Individual blood [La-] values showed significant differences between time measurements without dependence on the recovery method. There was a cumulative effect of blood [La-] between WAnT1 and WAnT2 so that the recovery values of WAnT2 were higher than those of WAnT1. With the exception of \({\dot{\text{V}}}_{{\text{E}}_{\text{ AUC}}}\), weak correlations were found between blood [La-]overall values and the other physiological and performance variables.
Contrary to our results, Connelly et al. (1990) found that both blood [La-] and blood catecholamine levels returned more rapidly to pre-exercise values after recovery in water. This effect was attributed to a reduction in sympathetic activity triggered by baroreflex stimulation during immersion. However, lower levels of these two variables had already been observed in the last two stages of the physical test, since the test was performed in the liquid medium and this would have influenced its recovery. Nakamura and co-workers (1996) also verified lower levels of blood [La-] during recovery in immersion, and the lowest values were found at lower immersion temperatures (30ºC vs 38ºC vs OWI). The authors attribute these results to redistribution of blood flow as a response to thermoregulation. This phenomenon would cause the diversion of blood located in the skeletal muscles to the splanchnic region, providing increased blood supply to organs that perform blood [La-] oxidation, such as the liver, kidneys and heart (Rowell et al. 1966; Belcastro and Bonen 1975). This hypothesis, together with the expectation that immersion would provide a significant decrease in MSNA (Mano et al. 1991), decreasing noradrenaline levels (Grossman et al. 1992), and accelerating post-exercise parasympathetic reactivation (Al Haddad et al. 2010), would justify the use of immersion for blood [La-] removal after exercise. Furthermore, the elevation of EPOC and \({\dot{\text{V}}}_{\text{E}}\) during HWI and CWI would strengthen this justification. Increased activity of respiratory muscles, especially the diaphragm (Cooper et al. 1976), is related to higher blood [La-] oxidation (Romer et al. 2002).
However, the results did not confirm these expectations. The increase in \({\text{O}}_{\text{2}}\) delivery, \({\dot{\text{V}}}_{{\text{O}}_{\text{2}}}\), \({\dot{\text{V}}}_{\text{E}}\) and HR reduction during CWI or HR elevation during HWI did not modify exthe removal of blood [La-] during the evaluated period. The alteration of these factors did not accelerate blood [La-] removal under the conditions of this study or they are not as important as the consumption of limbs skeletal muscles (Gaesser and Brooks 1984; Scott 1998; Thomas et al. 2005). The immersion temperature used might not have been low enough to provide changes. However, very low temperatures may hinder blood [La-] recovery as both blood catecholamines and HR increase during immersions below 20°C (Srámek et al. 2000). Another possibility is that the athletes performed two supramaximal tests with an insufficient recovery period to generate changes in the blood [La-]. However, favorable results were found during the same recovery period: Bastos and collaborators (2012) verified a reduction of blood [La-] from the 4th to the 8th minute in supine positions out of water, after 6 min of immersion at 11 ºC, after treadmill running until exhaustion in maximal aerobic speed. Nakamura and collaborators (1996) verified a decrease of blood [La-] out of water after 10 min in immersion at 30 ºC after pedaling at 80% of \({\dot{\text{V}}}_{{\text{O}}_{\text{2 max}}}\). A common aspect in these studies is that the reduction of blood [La-] was verified only out of water, after the immersion period. In any case, if the recovery conditions were insufficient to generate changes in the blood [La-], they were sufficient to modify subsequent physical performance. Although blood [La-] is still used today as a parameter in determining physiological exercise intensity (Lundby and Robach 2015), metabolic pathway, (Gladden 2001) and recovery from exercise (Thomas et al. 2005), its importance as a triggering mechanism of fatigue has been widely questioned (Gladden 2004; Robergs et al. 2004), and the results of this study contribute to this discussion.
Anaerobic Mechanical Performance After Cold And Hot Water Imersion Recovery
Confirming the hypothesis of this study, the anaerobic mechanical power output decreased after CWI and increased after HWI. With the exception of the fatigue index, HWI increased all the variables of physical performance, being higher than those obtained after CWI. Absolute and relative mean power output were higher after HWI compared to CWI and OWI, and lower after CWI compared to OWI.
The deterioration of physical performance due to adverse environmental conditions, such as when the athlete feels cold or wet (pre-immersion), has been observed in other studies, especially during exercises executed at high intensity (Bergh and Ekblom 1979; Howard et al. 1994; Schniepp et al. 2002). Contrary to these results, Marsh and Sleivert (1999) found an increase in power after performing pre-immersion for 30 min at a temperature between 12 ºC and 18 ºC. However, this study performed pre-immersion only of the trunk, with the legs out of the water, and the individuals performed a 10-min warm-up before starting the 70-second anaerobic power test in a cycloergometer.
The main factor explaining the decrease in power after pre-immersion in CWI has been the decrease in muscle temperature that may be triggered by the conduction of the heat and consequent decrease in muscle blood flow (Suzuki et al. 1980; Blomstrand and Essen-Gustavsson 1987; Bonde-Petersen et al. 1992). For these reasons, changes in energy metabolism may occur (Blomstrand et al. 1984; Ferretti et al. 1992; Perini et al. 1998) or in the balance of agonist-antagonist electromyographic activity of the muscle (Oksa et al. 1995). The reduction of blood flow added to the \({\text{O}}_{\text{2}}\) demand during exercise may intensify the dependence on anaerobic metabolism for ATP resynthesis and increase acidosis (Schniepp et al. 2002). For example, Beelen and Sargeant (1991) found higher peak blood [La-] when muscles exercised at 70% of \({\dot{\text{V}}}_{{\text{O}}_{\text{2max}}}\) had been previously submitted for water cooling at 12 ºC for 45 min. However, in the present study, even though peripheral vasoconstriction occurred, it seems that it was not enough to modify lactic metabolism, and physical performance was independent of blood [La-] response in the three recovery methods.
The reduction in muscle temperature could also be related to the decrease in ATP resynthesis due to the decrease in enzymatic activity in glycolytic and oxidative reactions (Blomstrand et al. 1984; Binzoni et al. 1990; Ishii et al. 1992) and the decrease in ATP hydrolysis rate (Ferretti et al. 1992). These factors, besides reducing the energy supply to the muscle, decrease the rate of cross-bridge disconnection (Ferretti et al. 1992), leading to greater muscle stiffness and, consequently, greater mechanical resistance in cooled muscles (Faulkner et al. 1990). The reduction in muscle temperature may also generate deterioration in the activation of motor units caused by the decrease in nerve impulse frequency (Vangaard 1975). Oksa and collaborators (1995) verified that, under conditions of muscle cooling, there was a decrease in the electromyographic signal integral (iEMG) of the agonist muscle and an increase in the iEMG of the antagonist muscle. The authors highlighted that in high-speed situations, a slight alteration in the agonist/antagonist balance can impair the coordination of movements and hinder an adequate production of force. Bergh and Ekblom (1979), on the other hand, did not find alterations in the EMG signal during exercise in cycloergometer after muscular cooling from 38 ºC to 30 ºC; however, they verified a decrease of 4–6% in the power produced for each 1 ºC of reduction in the muscular temperature. In this sense, muscle cooling seems to impair performance, especially at high velocities of muscle contraction (Ferretti et al. 1992) by reducing pedaling frequency.
In contrast, the performance improvement seen after HWI could be attributed to the increase in muscle temperature through heat conduction and by peripheral vasodilation, contributing to faster restoration of energy stores and acceleration of the rate of cross-bridge disconnection (Stienen et al. 1996; He et al. 2000). Although confirmed only when associated with water movement at thermoneutral temperatures (Sato et al. 2014; Sato et al. 2015), stimulation of peripheral thermoreceptors during immersions at 40°C could contribute to increased performance by virtue of increased corticospinal excitability, decreased intracortical inhibition and increased intracortical facilitation (Sato et al. 2015). All these factors could explain the increase in muscle contraction speed. As the braking force was the same between the recovery methods, the increase in mechanical work was a result of the increase in pedaling frequency and, consequently, of the total distance traveled. The WAnT2 performed after HWI recovery obtained an increase in two pedal rotations, approximately 15 m of the travel distance, at an average rhythm of 2.13 Hz, while after CWI, there was a reduction of close to one rotation, approximately 5 m, at an average rhythm of 2.03 Hz. The difference between the methods was slightly higher than three rotations or 20 m in 30 s of testing (Table 2). This difference was observed in both the total and average values assessed during the test (Fig. 7 and Table 2).
Thus, it is possible that both HWI and CWI modified the force-velocity (F-V) relationship of the muscles, which can be observed through the alteration of total pedal rotations during test time (Fig. 7). During WAnT2, the previous elevation of temperature increased the contraction velocity and pedaling frequency, while the decrease of temperature reduced the contraction velocity and pedaling frequency for the same braking force. In study with skinned fibers, conditions of low pH and high inorganic phosphate levels, the force and velocity of contraction are reduced for both fast and slow muscle fibers, independent of blood [La-]. However, muscle temperature can alter these effects: fast fibers are more sensitive at low temperatures, whereas at temperatures close to thermoneutral, slow fibers are more reduced (Fitts 2008). On the other hand, high temperatures increase maximum velocity (V0) and maximum force of contraction (P0) in both fiber types and reduce their curvature (a/P0 ratio) of F-V relationship (see Fig. 5 in Fenn and Marsh 1935; Driss and Vandewalle 2013; Alcazar et al. 2019). Added to the previously mentioned factors, these effects can be explained by the altered sensitivity to Ca++ during muscle contraction: decreased at low temperatures and increased at high temperatures (Fitts 2008). In vivo studies have confirmed similar effects of the temperature dependence of the F-V relationship (De Ruiter and De Haan 2000), even at temperatures higher (39ºC) than the thermoneutral (Binkhorst et al. 1977). Despite not characterizing a fatigue situation (see OWI in Fig. 6), the present study found an interaction effect (recovery method vs test) on pedaling speed and mechanical power for the same braking force after HWI, even after previous physiological stress (WAnT1), contrary to other studies that found a greater reduction of performance in fatigue condition after immersion in thermoneutral temperatures (De Ruiter and De Haan 2000; 2001). Unlike the in vivo studies cited above, the present research was conducted during a multi-joint exercise.
The immersion temperature was responsible for the increase of 2.2% in mean power output after HWI and the reduction of 2.4% after CWI when compared to OWI, and for the decrease of about 3% in peak power output after CWI when compared to HWI (Fig. 8). Analyzing the power-velocity (P-V) relationship, the elevation of muscle temperature seems to increase both the speed of maximum power (Pmax) and its value, the opposite happening with the reduction of muscle temperature (De Ruiter and De Haan 2000). In this study a similar behavior was observed in mean power output, while in peak power output this effect was significant only after cooling. It is important to remember that these values represent only one point of the P-V relationship (Fig. 8). Although this is not in consensus due to different methods of determination, the braking force of 7.5% BW seems to be adequate and close to the optimal intensity of Pmax during WAnT for expert endurance cyclists (Dotan and Bar-Or 1983; Driss and Vandewalle 2013). Similar repercussions of temperature in the P-V relationship have been seen both in skinned fibers (Fitts 2008) and in vivo studies, especially at high muscle contraction velocities (Sargeant 1987). The athletes in this study were instructed to pedal as powerfully as possible.
It is interesting that despite the increase in performance, the HWI was the recovery method considered by most athletes as having produced the worst subjective sensation, including two cases of nausea and malaise after performing the protocol. Conversely, CWI was considered by most to provide the best subjective sensation, despite being associated with decreased performance. In general, both conditions produced greater physiological disturbance in comparison to OWI; however, they differed antagonistically in relation to performance and subjective sensation. As such, according to the model used in this study, a better physiological recovery (considering a faster return and lower values) was not associated with the best physical performance nor with the best subjective sensation, and the best physical performance was not influenced by the physiological and subjective parameters analyzed.
Practical Implications
The use of immersion in a liquid medium for short periods of recovery from anaerobic exercises is a method that needs to be used with caution. Except for some parameters, immersion delays the recovery of cardiorespiratory variables and increases aerobic energy expenditure without generating advantages in relation to blood removal [La-]. The anaerobic performance increases after recovery in warm water and may decrease after recovery in cold water. While small, the changes in performance may be relevant from a competitive point of view, because a similar intervention before a test or track cycling race, for example, could have an impact on your final result. Although recovery in cold water provides improvement in a subjective sensation during recovery, its use for short recovery intervals between series or competitive trials increases aerobic energy expenditure and reduces later anaerobic performance. On the other hand, recovery in warm water increases posterior anaerobic performance, despite subjective discomfort and increased energy expenditure. Another issue is that most previous studies implementing CWI as a recovery modality used temperatures ranging from 5 to 15°C (Higgins et al. 2017; Stephens et al. 2017). While the temperature in the CWI protocol in the present study falls outside of the range, this may still constitute CWI, as evidenced by the divergent power output parameters between OWI and HWI conditions. In contrast to other studies that describe their water immersion recovery without providing a detailed description of temperature control and maintenance, in this study, we developed an equipment capable of controlling and maintaining a constant temperature in a 250 L tank during the recovery period. If reaching and maintaining a constant immersion temperature close to 10°C is difficult, maintaining a temperature of 20°C is easier and approaches the limited conditions that a coach or athlete has in their area of expertise. In this regard, reaching and maintaining water at 20°C in training or competition places is easier and less expensive. Moreover, in addition to causing physiological shivering, very low (as well as high) temperatures impair human comfort.
The choice of WAnT and a short recovery period is justified in order to provide a high anaerobic demand in a short time to perform two tests in sequence, significantly increasing the response of lactate and cardiorespiratory variables and thus potentiating the effect of the recovery method in both physiological responses and subsequent performance. This research model is appropriate for competition and training situations where the recovery time between batteries or series is very short, as well as providing experimental evidence on the effect of environmental conditions on the EPOC and VO2 kinetics response and their relationship with anaerobic performance.
Study Limitations.
A limitation of the calculation of the recovery kinetics of physiological variables was the existence of transition times between the end of the WAnT and the beginning of the recovery evaluation. The athlete's displacement and the procedures (removal of sneakers) were standardized in order to maintain similar transition times between the three recovery methods. Although small, differences in transition time were found between immersed and OWI recovery after WAnT1. The first seconds of rapid recovery phase are important for the calculation of \(\text{τ}\). To mitigate this limitation, the transition time was inserted as a covariate in the statistical model in the variables that presented significance. A positive aspect is that, with the exception of \(\text{τHR}\text{, }\)the variables of the rapid phase were not influenced by the test factor, since after the WAnT2, the differences in transition time between the methods were suppressed (Table 2). Another question was the 10 min recovery period’s. This fact may have influenced the effect of immersion on the behavior of blood [La-]. It is possible that a longer period of recovery might have revealed different blood [La-] actions between the recovery methods and consequently influenced the physical performance. However, variations of performance were observed independently of the blood [La-] results and other physiological variables. Moreover, the recovery period did not allow the physiological variables to return to pre-exercise conditions. Despite this, the athletes were able to repeat the performance after OWI. For this reason, the increase in performance verified after HWI, and the deterioration after CWI, justifies the protocol of this study and proves the effect of immersion temperature during recovery on anaerobic performance. Recovery during OWI served as the control condition in this crossover design, and performance after OWI was not significantly modified. This result helps to refute any suggestion that the thermal effect of HWI could have enhanced performance by virtue of not performing warm-up prior to WAnT. Although it is not a consensus (Inbar et al. 1996), there is evidence that warming up performed before WAnT does not improve its performance (Hawley et al. 1989). Finally, although the physiological variables analyzed in this study do not include all the relevant adaptive responses (for example muscle oxygenation using NIRS and EMG to assess muscle activation), they are widely used in the evaluation of physical tests, control of training and monitoring of recovery periods during both applied and laboratory conditions.