|Are stretch, tear and DOMS what makes concentration curls an effective biceps builder? Can we use the soreness as a gauge for the efficiency of our training?|
In last Sunday's first installment of our discussion on delayed onset muscle soreness (DOMS), we looked at what causes DOMS as well as treatment methods and supplements for relieving its symptoms. This led us to today’s big question: Is DOMS necessary for muscular adaptations to exercise? No pain, no gain, right?
Before we can discern whether DOMS may benefit muscle growth, we need to look at what muscle growth is and what causes it, so that we may see if DOMS is in fact a piece of the puzzle.
Taking a Second Look at Muscular Hypertrophy
During muscle fiber hypertrophy, contractile proteins proliferate, and the muscle fibers enlarge to support this growth (Vierck. 2000). While there are many factors regulating this process, from gene expression to hormones and other growth factors, the two necessities for hypertrophy are some form of increased muscular tension, damage, or stress (Goldberg. 1975), and a positive net protein synthetic response with adequate energy availability (Miyazaki & Esser. 2009).
|Beware of too much "good" ROS scavengers. NAC will effectively block the recruitment of new satellite cells | learn more|
So with exercise being the trigger and nutrition the ammo, what is left to play the gun? Skeletal muscle does not undergo significant cell replacement once mature (Chargé & Rudnicki. 2004), and thus a repair mechanism for any microtrauma is essential.
This medic is the satellite cell, a type of stem cell found only within mature muscle tissue. After microtrauma, satellite cells activate, proliferate, and ultimately fuse to one another and existing muscle fibers to form new myofibrils (Toigo & Boutellier. 2006).
All parts of this regenerative weapon rely on one another. The satellite cells mediate the hypertrophic process, but without a need (the exercise) they will not start, and without the nourishment (energy availability) they cannot function. All else that impacts the accuracy of the gun can be thought of as the factors influencing satellite cell efficiency. Hormones could be wind speed, gene expression the user’s accuracy, and perhaps DOMS is the distance to the target (or not ;-).
|Suggested Read: "Understanding Muscle Hypertrophy - Study Sheds More Light on Process of Satellite Cell Recruitment" | read more|
Furthermore, HGF secretion is proportional to the extent of the muscle damage (Tatsumi, et al., 1998). Therefore, it seems plausible that greater muscle damage leads to greater satellite cell recruitment, especially since the activation of satellite cells is exclusive to the fiber that has become damaged and satellite cells of one muscle fiber will not respond to injury of adjacent muscle fibers (Chargé & Rudnicki, 2004).
As it just so happens, DOMS inducing eccentric contractions disrupts muscle integrity more so than concentric or isometric contractions (Faulkner, 1993). What may seem odd, however, is that EMG activity has been shown to be lower in eccentric loading compared to concentric loading (Westing. 1991), suggesting less fiber recruitment.
|Part I||Part II|
|Figure 1: Exemplary data from Westing (1991) showing the mean and SEM torque- and EMG-velocity relationships during the eccentric (open symbols) and concentric (filled symbols) tests.|
Inflammation - Friend or Foe of Muscle Growth?
|Learn more about eccentric training and satellite cell recruitment and how even fat cells can become muscle.|
This is also the time that DOMS normally makes it move. During this time, the damaged muscle releases several cytokines, while white blood cells such as neutrophils and macrophages invade the damaged tissue and release several growth factors, all of which may regulate satellite cell activity (Toigo & Boutellier. 2006). Creatine kinase, for example, is a standard indirect measurement of muscle damage (Banfi. 2012).
As stated above, several cytokines and growth factors are involved in the anabolic response to muscle damaging exercise. The list is quite extensive but a few notable players are:
- The cytokine interleukin-6 (IL-6) appears to be an essential regulator of satellite cell mediated hypertrophy, and genetic loss of IL-6 blunts the hypertrophic response (Serrano, et al. 2008). There also appears to be a close association between cytokine concentrations and muscle damage (Pedersen, Ostrowski, et al. 1998), with (Bruunsgaard, et al. 1997) showing that IL-6 concentration is higher after eccentric cycling compared with concentric cycling. Likewise, interleukin-15 (IL-15) is another highly anabolic player in the inflammatory response to muscle damage (Furmanczyk and Quinn 2003), and is elevated following resistance exercise but not treadmill running, suggesting a need for microtrauma in its stimulation (Pedersen, Akerström, et al. 2007).
Learn more about the different splice variants of IGF-1 and how they figure in the process of muscle hypertrophy and why systemic measures may mislead us.
- Lastly, the aforementioned HGF acts as a chemo-attractant for satellite cells (Bischoff 1997), effectively stimulating satellite cells to migrate to the place of injury, where it then has a direct effect on satellite cell proliferation and differentiation (Vierck, et al. 2000). Oddly enough, abnormally elevated concentrations of HGF actually inhibit muscle regeneration via up-regulation of myostatin (Yamada, et al. 2010). Since HGF is secreted by regenerating muscles for the first three days following injury (Jennische, Ekberg and Matejka 1993), its accumulation could act as a regulatory “stop” mechanism that marks the end of muscle repair via satellite cells (Chazaud 2010).
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