General Adaptation and Supercompensation

The general adaptation syndrome describes a decline in an often undefined y-axis variable during exercise and recovery after exercise. The recovery does not return to baseline but rather overshoots it. This overshooting of baseline is termed supercompensation. Supercompensation is a term you hear a lot in the strength based lifting community with the idea that you train hard for 4-6 weeks and then deload so that your numbers supersede what you have been doing in the gym. Anecdotally I have not seen this done with great success which makes me think that this mechanism is not truly at play due to its very big lack of replication in real time.

I often feel like there is a buildup of fatigue when not managed appropriately and once that fatigue is high it can start to create issues with one’s ability to perform at the same high level they did when they were fresh. I don’t think this is due so much to the muscles ability to recover appropriately although it can be part of the problem but rather I think this is due to the perceived effort of the exercises and the constant battle for progression. Adding that with all the other variables like sleep, life stress, and nutrition and they all play a role in someone’s ability to truly express themselves in the desired sport. I have seen athlete’s start to stall in progression and instead of retooling their program, we added in a few more hours of sleep and some stress relief practices and they were back hitting PR’s. Being able to surpass your baseline is far more complicated and requires a lot more thought than a predictive model such as general adaptation because we are far from a predictable model and it is a constant swing of stress reduction and fatigue management.

Paper 1

In Conchola’s study they observed a lack of recovery of RTD up to 30-min post fatigue. That time course was not the same for all markers though PT took 15 mins to recover after the TISV protocol and 7 minutes to recover after the LIFV protocol. This showcases that it is not an exact predictable time course and some things are more fatigue resistant than others and some protocols create a different amount of fatigue than others. He states in his paper that early RFD is a function of calcium ion activation. Given the impairments of calcium release may occur as a result of low-frequency fatigue from repetitive muscular contractions, calcium impairment kinetics may be a mechanism contributing to the decreased early RFD found in the present study. This is what we saw when looking at muscle damage and as we know muscle damage can lead to a decrease in force production among other things.

What this study showcases and what he talks about is that time course are very dependent on the protocols. The higher volume protocols elicit higher rates of fatigue for longer time course. In the literature we have seen that the CNS through afferent feedback from III and IV neurons have resulted in fatigue with higher volume protocols. So between the calcium release and the down regulation of the CNS through higher volume protocols it would make sense not to see a similar RTD following exercise and once those cellular mechanisms heal and function properly again you will see a return to proper firing and if the exercise protocol was progressive in nature you will see a slight bump in performance but to say that is general adaptation would be a bit of a stretch because it is not an exact time course.

Paper 2

In the Bjornsen paper they concluded that there was a supercompensation effect due to the overreaching that the first block put their subjects through and it did not fully showcase until after the second block with 3-20 days of rest. To say it was a supercompensation may be a bit of a stretch and some of the reasons for that were referenced within the paper. They speculated in the paper that previous studies observed that phosphorylation of hypertrophy-associated signaling proteins are suppressed during the repeated bouts after exercise and that the responses can be resynthesized after 10 days of detraining. This would go in line with their supercompensation idea. In this paper they saw a decrease in MFA in the type I muscle fibers during training but an increase in CSA. This would lend itself to the thought of cell swelling and an influx of inflammation and edema being the cause of the initial surge is CSA and not muscle growth as we saw the MFA decrease until the swelling went down. During the rest week after the first block the CSA area decreased leading into the second block which again points to not real CSA gain because of muscle growth. Damas et al. (2017) has found very similar findings and stated that they did not see actual muscle growth until the damage was repaired and that the initial increase in CSA was due to damage and swelling.

We also know that when muscles are severely damaged they are compromised in their ability to produce force, in this study they took untrained subjects and put them through an intense first block of training so much so that one subject had to quit and use crutches to walk. Based on the extremely high levels of CK they found as well tells me that the protocol was so intense that the subjects were not able to fully showcase any real growth or strength until they were fully recovered. The problem with the study because of this is that they compared the drop-in baseline strength to the recovery strength, instead of comparing the baseline strength to the end strength which was a modest gain of 4kg which would be expected in an untrained population if not more with a more appropriate training program. They saw a reduction in MFA and they saw an upregulation of p21 which is a sign of muscle atrophy. They did an incredible amount of work in their first 3 sessions compared to the Neilson study they tried to replicate in a 2:1 ratio and I think that is what caused the issues and because they didn’t have a control group it is hard to compare. They saw a down regulation of MFA and strength during training due to the volume being too high and training to failure which can cause psychological stress as well.

This is why there were so many discrepancies between the two papers. Perceived exertion was through the roof, muscle damage and soreness were high, and fatigue in both the PNS and CNS would be high as well so of course the subjects underperformed during the blocks of training and only because of the repeated bout effect where they able to start to see some progress because that can help attenuate those other response. I don’t think it was so much that they saw a supercompensation effect although it can look like it from a time course perspective. I think they just followed a poorly designed program that created a lot of damage, unnecessarily, and until that damage repaired itself the subjects were not fully able to express their progress. It would have been nice to see a control group who matched overall volume but it was spread out over the rest week so they could not create so much damage would they have progressed more. I think that if the athletes were able to train in an uncompromised manner they would have made far more progress in strength. The study was set-up in a way to showcase supercompensation but the idea of we have to make our athletes worst in order for them to get better does not apply in the real world. Did this paper so supercompensation, yes from an outsider’s perspective looking in it matches the time course of training, digging a hole, and recovering to supersede previous gains but we know from the research that the hole does not need to be dug and by doing so creates more risk than reward. It is far more complex than just saying here is the model because the model does not actually explain the all the mechanisms at play here.

 

References:

Damas F, Libardi CA, Ugrinowitsch C. The development of skeletal muscle hypertrophy through resistance training: the role of muscle damage and muscle protein synthesis. Eur J Appl Physiol. 2018 Mar;118(3):485-500. doi: 10.1007/s00421-017-3792-9. Epub 2017 Dec 27. PMID: 29282529.

 

Bjørnsen T, Wernbom M, Løvstad A, Paulsen G, D'Souza RF, Cameron-Smith D, Flesche A, Hisdal J, Berntsen S, Raastad T. Delayed myonuclear addition, myofiber hypertrophy, and increases in strength with high-frequency low-load blood flow restricted training to volitional failure. J Appl Physiol (1985). 2019 Mar 1;126(3):578-592. doi: 10.1152/japplphysiol.00397.2018. Epub 2018 Dec 13. PMID: 30543499.

 

Conchola, Eric C.1; Thiele, Ryan M.1; Palmer, Ty B.1; Smith, Doug B.1; Thompson, Brennan J.2 Acute Postexercise Time Course Responses of Hypertrophic vs. Power-Endurance Squat Exercise Protocols on Maximal and Rapid Torque of the Knee Extensors, Journal of Strength and Conditioning Research: May 2015 - Volume 29 - Issue 5 - p 1285-1294

doi: 10.1519/JSC.0000000000000692