Altering body posture from sitting to standing and engaging the muscle mass of the lower legs as a recovery strategy following a simulated hockey shift was found to be effective for maintaining Q and slowing the precipitous drop in Q that occurs with the abrupt cessation of exercise. This paper presents novel evidence that standing and pacing on the bench between shifts may represent an easily adopted and viable alternative to light skating to “cool down” slowly between shifts, when a player must leave the ice. This may have important implications for the high-performance athlete and aging recreational hockey player alike, both of whom face potential challenges that stem from insufficient Q between shifts while the body attempts to recover from a previous bout of stressful activity.
The current data supported our hypothesis regarding the overall effects on Q; however, the hypothesized mechanisms of this elevation were not fully supported, as elevations in SV did not reach significance. As can be observed from the graphical representation of data in Fig. 2, the elevated response of SV and HR in the active recovery condition was temporally similar; however, the larger variance around the measure of SV compared to HR almost certainly played a role in reducing the chances of reaching statistical significance (p = 0.06). In the current investigation, blood pressure was used to calibrate the ICG unit; however, a continuous BP signal was not recorded throughout exercise or recovery owing to the “field-based” nature of data collection, which is a limitation worth noting. Alterations in HR for time points 45–120 s, which significantly differed between active and passive recovery conditions, had a mean difference of 12 ± 3 bpm. At the matched time points, the mean alteration in SV was 12 ± 6 mL/beat, thus suggesting that the change in SV actually represented a slightly greater relative deviation from baseline at 8.8 % compared to HR at 7.5 %. Notably, alterations did not occur within the first 30 s of recovery, which likely reflects the time necessary for the cardiovascular system to adjust to the changing exercise demands. By 180 s, difference between the active and passive conditions started to disappear, and this likely relates to the fact that the young, fit hockey players used in the current investigation were conditioned to recover in approximately 3–4 min of rest. This effect may be amplified (at both the beginning and end of the rest period) in less fit athletes, or by altering the intensity of the active recovery condition, which was intentionally light in the current investigation.
Cardiovascular Implications for Performance
There is convincing evidence from cycle ergometry models demonstrating significant decrements in repeated sprint ability when athletes recover passively between work bouts, as opposed to engaging in a light “active” recovery [22, 23]. It is suggested that this effect is primarily driven by ATP repletion and pH recovery, both of which are affected by Q/blood flow  through alterations in O2 delivery and the maintenance of metabolite (H+) gradients between the passing blood and local muscle tissue [24, 25]. Corresponding to the temporal demands of a hockey shift, evidence clearly demonstrates that sprints of 15–30-s duration, separated by rests of 3–4 min, show benefits to mechanical power output when light activity is substituted for passive rest, particularly in the first 10–15 s [22, 23]. As such, it would appear that competitive athletes may benefit from improved performance as a result of better recovery, but direct tests of skating speed, power, and longer term in-game adoption of this strategy are warranted.
Cardiovascular Implications for Health
By contrast, blood flow may have different, yet equally important, implications for the older recreational hockey player given the effects on central, rather than peripheral, circulation. Despite the well-accepted understanding that the risk reward of exercise greatly favors participation , it is undeniable that exercise can act as a trigger for a myocardial infarction or sudden cardiac death in the susceptible myocardium [12, 26]. Among the factors that might act to trigger these events in-game, or immediately after exercise, are the decrease in Q and relatively slow compensatory vasoconstriction of leg vasculature [27, 28]. This in turn can affect venous return, Q, and coronary perfusion, particularly in the vulnerable heart wherein supply and demand mismatches may be exacerbated. Prolonged intense exercise in particular (as often occurs in many recreational hockey games wherein there are suboptimal numbers of players per team to offer regular shift changes) can worsen these effects. If this type of prolonged vigorous play also leads to significant heat stress and dehydration , the associated reductions in blood plasma, coagulatory factors, and thermoregulatory fluid shifts have the potential to further compound the supply and demand imbalance through a reduction in stroke volume and compensatory increase in heart rate . Prolonging an elevated Q further into recovery may be beneficial for promoting recovery of the working skeletal muscles and also avoiding venous pooling and reduced myocardial perfusion, particularly in persons with compromised coronary artery flow.
For the high-performance athlete, the mechanism for maintaining an increased Q may be of little consequence, as perfusion of the working muscles is augmented nonetheless, and improvements in blood flow-driven blood/tissue gradients (for the transfer of O2, nutrients, and waste products) are established regardless of the underlying hemodynamic alterations. However, for the aging hockey player with a potentially susceptible myocardium, the observed mechanisms supporting an elevated Q could be further optimized for avoiding a supply and demand imbalance. This may be of greater importance for some individuals more than others given the clearly divergent responses in SV evident in the large variability in individual response, but it should be noted that the current population comprised exclusively of young ostensibly healthy men, who were of high fitness. The response of older potentially susceptible participants may be more homogenous in its response . In practice, myocardial supply would be enhanced by reductions in HR, which would prolong diastolic filling time during which coronary arteries supply oxygenated blood to the cardiac tissue itself . A current trend in sports performance apparel includes the wearing of compression garments to improve both performance and recovery through alterations in blood flow. If external compression devices are capable of promoting improved venous return , there may be a yet unexplored role for such garments in helping to bridge the gap between the benefits of activity for promoting long-term health and fitness and the acute risk posed during a given exercise session in a potentially at-risk population. External compression combined with light activity could also potentially alter the effective time-course of the observed recovery effects and should be further explored.