The initial aim of the present study was to examine the effects of BCAA supplementation on indices of muscle damage in resistance-trained volunteers. The principle findings show BCAA can reduce the negative effects of damaging exercise by attenuating CK efflux, reducing residual muscle soreness and improving recovery of muscle function to a greater extent than a placebo control.
The protocol successfully induced muscle damage, which was evident from the significant time effects for all dependent variables. This supports the efficacy of the protocol as a model to induce muscle damage in a sport specific manner [27, 28]. Additionally, the data presented here support previous literature suggesting BCAA as an effective intervention to reduce the negative effects of damaging exercise [15–18] and more specifically from damaging resistance exercise [14, 20, 21]. The novel information offered by these data demonstrate that BCAA can be used as an effective intervention to ameliorate the negative effects EIMD precipitated from a sport specific damaging bout of resistance exercise in trained participants.
Creatine kinase, a surrogate index of muscle damage, is more indicative of damage or gaps in the sarcolemma and hence causing the cytosolic enzymes to ‘leak’ from the cell in to the blood . However, the cell membrane is likely to have undergone some degree of lipolysis as a result of an imbalance in calcium homeostasis , almost certainly from the exercise insult. The damage literature often shows a high degree of inter-subject variability in CK and other cytosolic markers of EIMD, however, variability in the current study was relatively small, partly attributable to the trained status of the volunteers. The greater conditioning of these participants has almost certainly led to a repeated bout effect , whereby, a conditioning bout of exercise (in this case prior training) leads to a decrease in damage indices on subsequent bouts [4, 31, 32]. This is further supported by the low CK response seen in both groups following the exercise, when compared to the damage responses seen in untrained volunteers [19, 20]. Despite this relative homogeneity, the CK response was less in the BCAA group suggesting the membrane integrity was maintained to greater extent than the placebo group. The damage response is known to be bi-phasic in nature; a primary response caused by the mechanical stress of the exercise, followed by a secondary, transient inflammatory response over the following hours and days . The subsequent inflammatory response increases protein uptake necessary for use as an energy source and/or pathways responsible for cell signaling and subsequent muscle remodeling [14, 33]. Although we cannot definitively support this postulate, it seems plausible that the greater bioavailability provided by BCAA facilitated this response and thereby decreased secondary damage to the muscle.
Our data concur with previous studies that show a peak in soreness at 48 h post-exercise [27, 32]. Furthermore, the group effects support previous data [20, 21, 34] showing a reduction in muscle soreness following a damaging bout of exercise with BCAA supplementation. Although the mechanism surrounding muscle soreness following a damaging bout of exercise is not well understood, it seems likely to be related to inflammation, particularly to the connective tissue elements  that sensitise nociceptors in muscle and hence increase sensations of pain . However, previous work  demonstrating a reduction in soreness following BCAA supplementation also measured the acute inflammatory response (interleukin-6, a pro-inflammatory cytokine) and showed no difference between the BCAA and placebo groups. Jackman et al.  suggested that the increase in food or feeding per se, particularly amino acids, might be related to reductions in soreness. Although this idea is somewhat speculative and has no supporting evidence or proposed mechanism, we show similar trends in our data, but it is not possible to support or refute this theory. Based on the reductions in CK, it makes the expectation tenable that the secondary damage phase is reduced by the aforementioned uptake of BCAA for protein synthesis, thus, limiting the extent of damage and hence reducing the precipitation of soreness.
Whilst there was no difference in vertical jump performance and limb girth, the most notable finding is that reductions in MVC were attenuated and recovery of MVC was accelerated following BCAA supplementation. This study demonstrated an effect on function and is in contrast to other work  that used untrained participants in a similar experimental design showing no benefits in the recovery of force production with BCAA. Interestingly, other studies [21, 37] using non-resistance-trained student populations have shown some benefit in the recovery of muscle function. These data should be treated with caution however, as both studies [21, 37] used a cross-over design which suffers the limitation of the repeated bout effect (RBE). The RBE refers to a protective effect or attenuation of damage indices when the exercise is repeated [4,31,32]. Although up to 11 weeks was given between damaging bouts, the RBE has been previously shown to accelerate the recovery of muscle function for between 6 and 9 months following the initial damaging bout .
It would seem that differences between our findings and those of Jackman et al.  might lie largely with the participant populations; Jackman et al.  chose untrained participants, whereas the current study recruited resistance-trained volunteers. This is evident in the group familiar with resistance exercise at 72 h (> 90% recovery of MVC) in comparison to the untrained population  that were only ~60% recovered at the same time point. The other obvious difference between the current investigation and previous literature is the amount of BCAA administered. Historically, previous literature [21, 34] examining recovery from damaging resistance exercise has only used a single bolus of ~5 g BCAA, finding small positive effects, particularly on muscle soreness. Interestingly, Jackman et al.  fed participants considerably more BCAA than this previous work, consisting of 88 g in total over the test period (with no loading phase), whereas the present study gave 280 g total over the test period. Our supplementation procedure included a 7 day loading phase (20 g per day) and 20 g per day during the subsequent recovery phase. Furthermore, we provided a 20 g dose immediately before and after the bout of exercise, which is when the biggest discrepancy in BCAA feeding occurred between studies. Previous work  has shown that timing of a protein based recovery strategy is important and immediately following a damaging bout of exercise can be most beneficial in accelerating recovery. Whist Jackman et al.  did supplement with BCAA after the damaging bout, there was a delay of at least 1 h that may also account for the positive effect found in the present study, which fed immediately after the bout of damaging exercise. Previous work  showed BCAA to rise in plasma within 15 min and peak 30 min after ingestion, which means the bioavailability of BCAA post-exercise in our investigation was at least 1 h earlier than that of Jackman et al. ; therefore, it seems plausible that early feeding post-damaging exercise increased the efficacy of the intervention. This is somewhat conjectural and would serve as an interesting question for future research to ascertain the optimal strategy for BCAA supplementation.
Regardless of whether the loading phase and timing of the supplementation post-exercise was effective in increasing the bioavailability of BCAA, there is still a stark difference in the total supplementation volume (88 vs. 140 g). The larger quantity of BCAA we provided might partly account for the difference between studies in damage indices (MVC and CK). We based our supplementation regimen on previous work that showed a positive effect [16, 26] and propose that positive effects beyond attenuation of muscle soreness (i.e., recovery of muscle function) may need a more immediate bioavailability and greater quantity of BCAA than those used previously.
There are two limitations from the study, which need to be acknowledged. Firstly the lack of specific dietary control might have led to discrepancies in caloric and, more specifically, protein ingestion between the groups. Although we attempted to control this by asking participants to record food intake during the loading phase and replicate this following the damaging exercise, an approach that has been previous used [11, 21], there was no specific control between groups. Conceivably discrepancies in protein intake can affect the bioavailability of the substrate and hence affect protein turnover and ultimately influence the outcome of these data. The second limitation is that we used an artificial sweetener with little or no calorific value was used, which will certainly alter the energy balance by around 80 kcal/day, and may be problematic if the placebo group were in energy deficit, but based on the food record sheets this does not seem likely. Although the current investigation has a good degree of external validity, future research might like to consider more rigorous dietary control measures such as; 1) asking participants to weigh food and accurately log food intake; or 2) providing a pre-determined menu for the participants to ensure no discrepancies between and within groups, although this still relies on participant adherence outside the laboratory. Finally, 3) although difficult to facilitate, participants could be housed in an environment where dietary behavior can be imposed and thereby strictly controlled.
In summary, these data offer novel information on the application of BCAA supplementation. A 20 g/day supplementation regimen administered 7 days prior to (with additional 20 g immediately before and following the damaging exercise) and for 4 days after a damaging bout of eccentric biased exercise reduced soreness and the plasma level of intramuscular enzymes. Most importantly, BCAA attenuated reductions in muscle function and accelerated recovery post-exercise in a resistance-trained population.