Effects of active recovery on muscle H+ and lactate concentration Pcr and Glycogen
The effects of active recovery on blood lactate removal are well documented. However, a limited number of studies have used muscle biopsies to examine the changes of muscle lactate and other metabolites or substrates such as PCr and muscle glycogen, during active compared to passive recovery following repeated exercise bouts (Spencer et al., 2006, 2008; McAinch et al., 2004; Bangsbo et al., 1994; Fairchild et al., 2003; Choi et al., 1994; Peters-Futre et al., 1987). The changes in the rate of recovery of selected metabolites may have an impact on performance during short or long duration sprints. This impact may be different (positive or negative) depending on the intensity or the duration of active recovery. Following a sprint, muscle lactate will increase while muscle glycogen, pH and PCr will decrease. The magnitude of these changes is related to sprint duration, the number of sprints as well as the interval between sprints. Whatever the case, despite a fast PCr resynthesis, muscle pH, muscle lactate and muscle glycogen restoration may take several minutes or hours. Active or passive recovery after a sprint may change the rate of replacement of these metabolites.
Muscle pH and Lactate after Active and Passive Recovery
The muscle homeostasis has been shown to recuperate faster as a response of active recovery (Sairyo et al., 2003) although this has not observed in all studies (Bangsbo et al., 1993, 1994). These studies used leg extension (Bangsbo et al., 1993, 1994) or wrist flexion (Sayrio et al., 2003) as exercise modes (different from commonly used human locomotory activities) and measured changes of muscle pH with muscle biopsies and magnetic resonance spectroscopy respectively. Nevertheless, their findings are in contrast, since muscle pH after active compared to passive recovery was unchanged during leg extension but increased during wrist flexion exercise (Bangsbo et al., 1994; Sayrio et al., 2003). Furthermore, any comparison between studies is difficult because different active recovery modes were used (progressively decreased intensity, constant intensity). While there is no strong evidence for a faster muscle pH restoration, this fact cannot be excluded.
Muscle lactate has been shown to decrease after 10 minutes of active compared to passive recovery (Bangsbo et al., 1994). However, there arereports of higher (Peters-Futre et al., 1987) or unchanged (Choi et al., 1994; McAinch et al., 2004; Fairchild et al., 2003) muscle lactate concentration following long duration of active recovery (15 to 60 min). Higher muscle lactate after active recovery has been reported following repeated short duration sprints (Spencer et al., 2006). Although the results concerning the muscle lactate and pH changes after active recovery are limited, it is obvious that this issue is critical for performance on a subsequent exercise bout and needs further examination.
PCr Resynthesis after Active and Passive Recovery
Restoration of PCr is of vital importance for performance in a subsequent sprint (Bogdanis et al., 1995). The PCr resynthesis starts immediately after the cessation of a sprint bout and is dependent on a number of factors (for review see McMahon and Jenkins 2002). Briefly, PCr resynthesis is an oxygen dependent process (Haseler et al., 1999) which is also affected by muscle H+ concentration (Sahlin et al., 1979). Therefore, any factor that may interfere with oxygen availability and muscle pH will affect the rate of PCr resynthesis.
It has been shown that active recovery decreases muscle oxygenation (decreased oxygen contend of myoglobin) and leads to increased levels of deoxyhaemoglobin (Dupont et al., 2007; Buchheit et al., 2009). In this case, it is not surprising that a lower percentage of PCr was restored immediately after and 21 s later following a set of 6x4 s sprints (Spencer et al., 2006).
Immediately after the sprint repetitions, only 32% of PCr was resynthesized following active recovery while 45% of PCr was restored following passive recovery. Twenty-one seconds after the end of the last sprint, PCr was 55% of the resting levels when recovery was active compared to 72% when recovery was passive. Although these differences were not statistically significant, they showed a trend towards an impairment of PCr resynthesis after active recovery (Spencer et al., 2006). It is likely that the mitochondrial oxygen demand during active recovery decreases the oxygen available for PCr resynthesis.
Notably, PCr stores are lower after active recovery compared to passive recovery not only after short duration but also after long interval duration (McAinch et al., 2004).
The effects of different intensities of active recovery were studied following the experimental protocol described previously (i.e. 6x4 s sprints with 21 s interval; Spencer et al, 2008). Unfortunately muscle biopsies were not taken after passive recovery; nevertheless, both active recovery intensities which were studied corresponded to 20 and 35% of VO2max and showed the same changes in PCr content following the 6x4 s sprints (Spencer et al., 2008).
In addition, it should be noticed that muscle oxygenation was not different when active recovery of 20 or 40% of VO2max was used during a short interval period of 15 s between sprints (Dupont et al., 2007). The absence of differences between active recovery-intensities may be attributed to the lower efficiency observed during cycling at very low workloads (Smith et al., 2006; Ettema and Lorås 2009). Thus, a lower efficiency at very low intensities used for active recovery may mask any effect of active recovery-intensity on the PCr content. Furthermore, it is likely that the rate of PCr resynthesis is slower in type II compared to type I muscle fibers (Casey et al., 1996) and type II
fibers are depleting the PCr stores faster than the type I fibers (Greenhaff et al., 1994). Because of these differences between fiber types, it is likely that type II fibers may be more prone to the impairment of PCr resynthesis. These fibers are mainly activated during short duration sprints performed with fast rate of muscle actions, such as those performed in the above-mentioned studies. However, this hypothesis has not been tested after active recovery. A possible concurrent use of oxygen for lactate oxidation and for muscle contractions during active recovery may prevent the oxygen needed for a fast PCr resynthesis. Under these conditions, PCr may be lower after active compared to passive recovery of short or long duration. This may affect type II more than type I muscle fibers and probably will decrease performance when a short interval is provided.
Muscle Glycogen after Active and Passive Recover
A significant reduction of muscle glycogen occurs after single and repeated high intensity sprints of short or long duration (Gaitanos et al., 1993, Bogdanis et al., 1995, Hargreaves et al., 1998). The replenishment of muscle glycogen starts after a sprint and an increased rate of muscle glycogen restoration has been reported after cessation of exercise following passive recovery (Pascoe and Gladden 1996). Muscle glycogen can be partly replenished during the recovery period, without the availability of any exogenous carbohydrate source (i.e. fluids or food), using the lactate as a substrate. Glycogen can be replenished either using lactate directly as a source or after conversion of lactate to glucose (Fournier et al., 2004). The rate of refilling of glycogen stores is higher after high intensity compared to low intensity exercise probably because of the higher lactate availability following high intensity exercise.
The lactate during recovery is either converted to glycogen or oxidized during active recovery (Hermansen and Vaage 1977, Brooks and Gaesser 1980). However, the fate of lactate following active recovery may be an important issue, since an increased rate of lactate oxidation, which probably takes place during active recovery, may reduce the substrate availability for glycogen replenishment within the muscle. Early reports have shown no different rates of muscle glycogen replenishment after 45 min of active or passive recovery following high intensity exercise (5x90 s bouts at intensity of 120% VO2max; Peters-Futre et al., 1987). Later studies observed a decreased
rate of glycogen restoration when the participants followed partially active (30 min active plus 30 min passive recovery) compared to 60 min of passive recovery (Choi et al., 1994). These findings were confirmed by recent studies, however, the decreased muscle glycogen restoration was limited to the slow type I muscle fibers, while the fast contracting type II fibers were not affected (Fairchild et al., 2003).
It should be considered that the impaired muscle glycogen restoration was observed following long duration active recovery periods (i.e. 30-45 min; Choi et al., 1994; Fairchild et al., 2003). It is uncommon to use such a long duration of active recovery during training or following a training session. The duration of active recovery commonly used in practice (i.e. about 15 min) may not impair muscle glycogen replenishment. For example, no difference on muscle glycogen content was observed when active recovery at intensity 40% of VO2 peak was applied for a period of 15 min (McAinch et al., 2004) or after 10 minutes of one leg active recovery (Bangsbo et al., 1994). Coaches are advised to follow shorter than 15 min of low intensity active recovery in order to avoid any decrement in the rate of glycogen resynthesis. A fast glycogen resynthesis is important to maintain a high glycogen content before the start of the next high intensity event or training session.
