Trouble walking and climbing stairs has always been a badge of honor days after a grueling leg session. There’s nothing quite like your body telling you how messed up you are. Delayed onset muscle soreness (DOMS) has often been looked at as an indicator of the effectiveness of a single session session or training modality. Aside from telling you how hard you trained, what does DOMS tell us and what is the role of muscle damage in training for hypertrophy?
The Physiology of Muscle Damage
In this series’ last entry, we explored the anatomy of a muscle cell and discussed the mechanisms of fiber recruitment during a muscle action involving high amounts of tension. Although some of this textbook jargon may seem like review for some of you, I think it’s important to get down to the fiber level and physiology to help answer certain questions.
That being said, I want to touch on what happens following repeated bouts of heavy lifting on the fiber level. Exercise-induced muscle damage (EIMD) involves structural changes to the muscle cell including disruption of myofibrils and sarcomeres following high-intensity anaerobic training. The original thought process was that such a disruption may influence gene expression in an effort to strengthen muscle tissue to protect against further damage. The process of rebuilding may involve various regulatory mechanisms (e.g., hormonal, immune, and metabolic) (Haff, 2016). The muscle gets broken down, it gets rebuilt bigger and stronger…simple right?
Let’s go back to our example of the sarcomere from Part 1:
It was once thought an accumulation of lactic acid caused DOMS. But we know now that the disruption of the supporting structures, z-disks, is the primary culprit. Z-disks are a landmark structure in that they lay the boundaries of each sarcomere. The length from one z-disk to the next is considered a sarcomere. It is at this point where the actin filaments are anchored on. If the z-disk becomes damaged (in the way lifting weights causes), they are now much more permeable, meaning more fluids can enter and exit (especially the enzyme Creatine Kinase). In fact, elevated levels of Creatine Kinase (CK) in the blood is how we can measure muscle damage (Brancaccio et al. 2007). (Sidenote: Plasma CK levels are also one way heart attacks are diagnosed.)
This sequence of events following a training session results in an increased number of white blood cells (neutrophils especially) directed to the target area, triggering an inflammatory response (more blood is in the region). Other biomarkers including specific enzymes and increased myoglobinemia (oxygen-storage units that provide O2 to the desired muscle) are observed in conjunction.
The degree of muscle damage done will determine the necessary processes that follow (repair or regeneration for you Cell Bio folks). Starting regeneration, specific structures termed “satellite cells” will activate (Seale et al. 2003). If enough damage has accrued, a completely new fiber will need to be formed. Satellite cells will proliferate and differentiate. As a result, myoblasts are formed with the sole purpose of rebuilding muscle fibers. These myoblasts fuse to myofibrils and become the nuclei of the cell. (see figure below)
From there, satellite cells self-renew and are then set aside and ready to repeat the process. Again, depending on the amount of damage, the muscle cell will either need to be repaired or completely regenerated. In the case that only low amounts of damage occur, the fiber can repaired by replacing broken parts and keep the remaining structures. Regeneration of an entirely new fiber would be required if damage levels are high enough (Yang and Hu 2018).
Positive effects..? / Reasons to believe damage is causative of hypertrophy
As discussed in part 1 of this series, strength training causes an increase in muscle protein synthesis (MPS) and a proportionally smaller increase in muscle protein breakdown (MPB). Damaging exercise, especially heavy eccentric training, has been observed to increase the MPS rate more than traditional training (Evans and Cannon 1991). From part 1, we know that a positive protein balance (synthesis > breakdown) leads to muscle growth, and in most cases, an increase in synthetic rates or a decrease in breakdown rates is the way to more growth.
Furthermore, after applying what we now know about satellite cells, muscle damage would result in greater satellite cell differentiation and therefore, more nuclei in the muscle cell. With that said, a case could be made that the process of repair and regeneration becomes more efficient over time.
But, before you take that information and start doing heavy eccentric training every day, there are a few more points to consider…
A counter-argument / Reasons to believe damage is not causative of hypertrophy
Structurally, muscle fibers hypertrophy via an increase of proteins. That increase could result in:
- An addition of myofibrils* in parallel = increased diameter of the sarcomere
- An addition of myofibrils in series = increased length of the sarcomere
*composed of several proteins including actin and myosin
The process of laying new structures and repairing old ones occur completely independent of one another. Structurally speaking, a new myofibril, in it of itself, doesn’t have anything to do with an already existing damaged one. However, we must not neglect the fact that the specific resources used to clean up damage and the resources responsible for adaptation are one in the same. Foley et al. (1999) analyzed the effects of damage from eccentric training on muscle volume (extremely high amounts of damage). They observed a decrease in muscle volume can occur at high enough levels of damage.
In a related article, Chris Beardsley discussed research that introduced an alternative proposal by Butterfield, 2010. In this study, they found calcium to have a contributory role in muscle damage. With every muscle contraction comes a release in calcium ions and that a build up of intracellular calcium (and white blood cells) can degrade the inside of the muscle fiber. Through blocking the influx of extracellular calcium into the muscle, they observed a reduced amount of damage to the cytoskeleton.
This is a very unique finding, and it may explain the increase in MPS following exercise induced damage – the need to repair degradation. However, we know that calcium ions are released on both concentric and eccentric phases of muscle contraction. Now, the amount released during each probably differs, but I think more research needs to be done before we can say this is the biggest contributor to muscle damage.
My Anecdotes and Observations
With everything in this field, we can’t get in a black or white/good or bad mindset. We don’t quite have a full picture of how hypertrophy occurs and we may never have a concrete answer on all mechanisms inducing growth. Due to the current state of the literature, there are some things that we just have to conduct our own n = 1 experiments and rely on experience and anecdotes. Soreness and damage is one of them.
Take your own personal experience in the gym for example. What kind of things usually result in soreness? For me, its things like:
- Increased training volumes
- Using heavier loads than previously used to
- Training at close proximity to failure
- A stretch under load/eccentric dominant exercises (like an RDL)
I would imagine your list is pretty similar. The point being is, the things that cause damage and make you sore are the things that cause the most growth. So what does that tell us? Well, whether muscle damage is causative of growth or not, it has to be correlated to some degree (or at least correlated to the training that maximizes hypertrophic adaptations). All five of those are only benefit us in moderation, and because of that, there is more than likely a ‘goldilocks zone’ of just enough soreness and not too much.
In addition and on a simplistic note, what else does soreness tell us? It can be useful feedback on our technique. If you’re getting sore in the desired muscle, that means you’re targeting that muscle to a considerable degree. If you’re getting sore (primarily) in other synergistic muscles and other connective tissues (i.e., low back soreness/knee pain from squats but not in the Quads) and not in the prime movers, it means your technique could probably use some work. It could also help guide you in exercise selection with that same feedback. Soreness can also tell you whether or not you’re training with too much volume.
Likewise, if you’re so sore that you start seeing a drop in performance (or even perceptual difficulty) you’re definitely doing more harm than good. With that in mind, consider the point(s) where you’re most sore. For most people, it comes at the beginning of a new training block – where volume and intensity are significantly higher (post deload or break) with new movements potentially introduced. So how can we combat this? The key here is to use an introductory period of 1-2 weeks training with approximately 70-75% of volumes you plan to reach in that mesocycle. Intensities can also see a drop in a few RPE points. Doing so will significantly combat unnecessary amounts of damage right out of the gate and will put you in a better position to have a productive mesocycle. On the flipside, if your training never makes you sore, there’s a really good chance you can do more and push harder.
The idea of lactic acid accumulation causing soreness is outdated. Exercise-Induced Muscle Damage, the damage to structural landmarks of the muscle cell is the primary contributor of delayed onset muscle soreness. Getting sore should not be the hallmark of a good workout, nor should we be chasing soreness. As it is a commonly misunderstood concept, there are cases for and against muscle damage. From anecdotes and experience with manipulating training variables, there is a good chance an optimal amount of damage exists even if it does not make any significant contribution to hypertrophy. Muscle damage can occur at various degrees and can be helpful in designing a program and giving feedback on exercise execution. Whether EIMD is causative of hypertrophy or not, it is definitely correlated.
- Haff, G., & Triplett, N. T. (2016). Essentials of strength training and conditioning. Champaign, IL: Human Kinetics.
- Brancaccio, P., Maffulli, N., & Limongelli, F. M. (2007). Creatine kinase monitoring in sport medicine. British Medical Bulletin, 81-82(1), 209–230.
- Seale P, Polesskaya A, Rudnicki MA (2003). “Adult stem cell specification by Wnt signaling in muscle regeneration”
- Yang, W., & Hu, P. (2018). Skeletal muscle regeneration is modulated by inflammation. Journal of Orthopaedic Translation, 13, 25–32.
- Evans, W. J., & Cannon, J. G. (1991). 3 The Metabolic Effects of Exercise-Induced Muscle Damage. Exercise and Sport Sciences Reviews, 19(1).
- Foley, J. M., Jayaraman, R. C., Prior, B. M., Pivarnik, J. M., & Meyer, R. A. (1998). Mr Measurements Of Muscle Damage And Adaptation After Eccentric Exercise. Medicine & Science in Sports & Exercise, 30(Supplement), 69.