Sunday, October 20, 2013

DOMS - Delayed Onset Muscle Soreness: No Pain, No Gain? Is DOMS Necessary to Build Muscle?

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?
An arictle by Alex Leaf (CPT)

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
Through exercise, the former is accomplished and paves the way for the repair processes that require the latter to occur. In other words, without a need to increase muscle size and strength, hypertrophy will not happen. Likewise, even if there is a need, without proper nourishment hypertrophy simply cannot happen.

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 ;-).

Muscle Damage

Suggested Read: "Understanding Muscle Hypertrophy - Study Sheds More Light on Process of Satellite Cell Recruitment" | read more
The hypertrophy process begins with microtrauma and an ensuing accumulation of calcium within the damaged muscles (Sorichter. 1999). This is shortly followed by a rapid stimulation of satellite cells via hepatocyte growth factor (HGF) and nitric oxide (NO), both of which rely on the changes in calcium levels within the muscle tissue (Tatsumi, 2010), and satellite cells may even be activated by the calcium flux itself (Hara, et al., 2012).

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 IPart II
Just a reminder: This is a twp-part series on Delayed Onset Muscle Soreness. You can switch back and forth between part I "What Is DOMS & How Can It Be Managed? Science, Strategies, Supplements" & part II "No Pain, No Gain? Is DOMS Necessary to Build Muscle?" by clicking on the images to the left.
In their study, (Westing. 1991) measured the torque and EMG activity of the quadriceps muscle at different movement speeds between a knee angle of 30° and 70° on the leg extension for both the concentric and eccentric portions of the exercise. The participants were 14 highly trained athletes that were accustomed to performing maximally during training. As you can see in Figure 1, average torque of the eccentric activity was significantly greater than that of the concentric activity across all movement speeds, but the EMG activity was significantly lower and continued to lower as movement speed increased. The fact that the EMG values of the eccentric activity are below 100% shows that the activation during the concentric phase was higher, even at lower speeds and despite “maximal” effort.
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.
Actually, this gives support the idea that eccentric exercise is more damaging. It is hypothesized that neural drive to the working muscle is reduced under conditions of extreme muscle tension (i.e. less EMG but more torque) to protect the muscle from injury that could result if it became fully activated (Moore. 1984). Regardless, single bouts of eccentric contractions have been shown to increase the satellite cell content and activation status in Type II muscle fibers (Cermak. 2013).

Inflammation - Friend or Foe of Muscle Growth?

Learn more about eccentric training and satellite cell recruitment and how even fat cells can become muscle.
Once the damage has been done, the repair process may begin. As mentioned in "DOMS - Delayed Onset Muscle Soreness: What Is DOMS & How Can It Be Managed? Science, Strategies, Supplements" (read article), an acute inflammatory response follows microtrauma.

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.
    Insulin-like growth factor 1 (IGF-1) has also received much attention due to its ability to increase muscle mass via muscle protein and DNA augmentation (Chakravarthy, Davis and Booth 2000). These effects are at least in part attributed to the activation of satellite cells and increased protein synthesis within the muscle fibers (Barton-Davis, Shoturma and Sweeney 1999). And guess what? Damaging exercise increases IGF-1. A study by (Bamman, et al. 2001), for example, showed that eccentric exercise increased IGF-1 gene expression by 62% while decreasing inhibitory genes by 57%. Oh, and concentric exercise produced non-significant changes in the above markers, suggesting that it was indeed the structural damage responsible for the IGF-1 expression.
  • 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).
A final indirect notion of the importance of DOMS is the idea that NSAIDs – a common treatment method – reduce the hypertrophic response. Recall that both NO and HGF are responsible for activating satellite cells in the early stages of the repair process. This process appears to be partially regulated by the cyclooxygenase (COX)-2 pathway, which releases various prostaglandins known to stimulate satellite cells (Bondesen, et al. 2004). The problem is that NSAIDs inhibit this pathway and thus may impair the hypertrophic response (Schoenfeld 2012). Indeed, studies have shown NSAID usage following eccentric exercise reduced satellite cell activity for up to eight days (Mikkelsen, et al. 2009).
Summary: Hypertrophy involves a complex array of anabolic and catabolic processes working in a downstream manner to favor protein synthesis over degradation. DOMS is not necessary,  may however present itself during the early stages of exercise. What is necessary is a mechanical overload of the muscle resulting in microtrauma. So train hard, train smart, and may the growth be with you.
So is DOMS necessary? DOMS can be thought of as a sign of muscle damage, but it is the damage itself and the subsequent inflammatory response that are responsible for hypertrophy. DOMS is actually a rather poor indicator of muscle damage and will not always reflect the magnitude of the damage (Nosaka, et al., 2002). Nor will it always be present.

Studies have shown that even a single bout of eccentric exercise reduces and may negate DOMS in subsequent bouts (Nosaka. 2001), and these effects persist for at least several weeks (Clarkson. 1992). This would explain why soreness is common in the beginning of a new routine full of unaccustomed damaging exercise, but fades as time progresses. And in fact Flann (2011) showed that using a three week acclimation protocol prior to beginning an eight week eccentrically loaded leg press protocol significantly reduced DOMS and markers of muscle damage compared to beginning the routine cold turkey.
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