Resting Done Right: Passive Rest or Active Recovery to Get the Most Out Of Your Workouts? Plus: How Do They Work?

Passive rest can be really enjoyable, but is it as productive?

An article by Alex Leaf (CPT)

In a typical training day, you may spend an hour in the gym training. Probably, you won't spend that whole hour pounding away at one muscle. Instead, you may focus on two or three muscle groups or perhaps even full-body with the burning desire to elicit a growth response that will take you one rep closer to your goals. From this perspective, the time you spend not training those muscles can be thought of as recovery time, and muscles need plenty of that. In fact, MacDougall, et al. (1995) found that muscle protein synthesis increases rapidly following resistance training (12 sets of 6- to 12-RM) and is nearly double baseline values at 24 hours post-exercise.

This was later expanded upon by Phillips, et al. (1997) who looked at both protein synthesis and protein breakdown following a session of resistance training (8 sets of 8RM) and found that the net protein synthesis was significantly elevated above baseline up to 48 hours following exercise. But exercise itself is catabolic, and to continuously strain your body will only diminish the potential for muscle growth and performance enhancement. So what to do during the recovery time? Eating right, getting adequate sleep, limiting life stressors are all great first steps and will undoubtedly help, but I’m talking activity wise.

Stetting the scene ⇒ Defining Terms

The idea of passive rest should be pretty straight forward: This is when you do nothing. You go about your normal day without doing much more than walking. When you think about it, passive rest is pretty much what the majority of the overweight and metabolically-impaired population is doing 24/7 x 365 years a day.

Passive rest vs. active recovery and rest between sets are two pairs of shoes. If you want to learn more about the latter, you may want to review Adel's True or False Article "True or False? Lower Rest Times Equate Lower Total Work Volume for a Given Workout. Plus: The Volume-Increasing Beauty of Progressive Exercise-To-Rest Ratios" | read more

In contrast, active recovery can be thought of as exercise performed at a reduced intensity and volume relative to the typical workout. It could be a light or easy day in the gym, or just being active in your leisure time. Context is key here, as a marathoner may just do a light jog, an Olympic lifter may do some technique work, and a totally unfit beginner exerciser may find anything beyond walking to be too stressful on the body to allow for recovery. The point is that active recovery should not be fatiguing and you should finish the workout or activity feeling better than when you started.

From Active Rest to Active Recovery

So what is the point of active recovery? There are at least three reasons why you and everyone else who is taking his or her training seriously may want to implement active recovery techniques into his or her training regimen - in a nutshell:

• Active recover may help you recover quicker and reduce soreness from the previous workout. 
• Depending on your goals and how you go about it, active recovery could also let you burn some calories and work on training technique. 
• And finally active recovery may serve some important psychological benefits not the least of which is that many people simply feel better when they exercise daily; movement is known to be able to elevate mood among other things. 

So with that in mind, let’s take a look at some of the actual pros and cons of active recovery.

• The main benefits of active recovery are actually a perfect example of where common sense and science get along: A light workout pumps some blood to the working muscles and can take advantage of this increased blood flow to deliver nutrients crucial for repair and growth while removing metabolic wastes.

Some may argue, though, that active recovery detracts from the recovery process through repartitioning nutrients towards fueling activity. In fact, Choi, et al. (1994) confirmed this: Light activity following a glycogen depleting workout does indeed lead to less net glycogen synthesis than passive rest and may even continue to lower glycogen levels if in a fasted state. And that last part is key.

Optimal glycogen repletion | more

How to counter the negative effects of active recovery on protein synthesis and glycogen repletion? Eat! Yes, it is as simple as eating beforehand. Performing light activity does not impede post-exercise glycogen resynthesis rates (Futre, et al. 1987), so whether you enjoy cycling away after a heavy leg session or playing some football with your friends the next day, just be sure to eat something first and reap the benefits of increased blood flow and nutrient delivery.

Although we possess the ability to partially recover glycogen stores via glycogenesis from both amino acids and lactate under fasting conditions (Fournier, et al. 2004), this is obviously not ideal and no one should hope to recover from intense training without eating. This is particularly true in view of the fact that fasting will limit the availability of nutrients that are necessary to enhance the protein synthetic response to exercise (Wolfe 2006).

	Protein (g/kg bodyweight)	Carbohydrates (g/kg bodyweight)
Weight Training	0.3-0.5	0.3-1.5
Endurance Training	0.15-0.35	1.0-1.85
Table 1: Optimal post-workout nutrient intake for athletes (McDonald 2007).

As for metabolic waste, light activity following strenuous exercise has been shown to enhance blood lactate clearance (McLoughlin, McCaffrey and Moynihan 1991), and lower levels of creatine kinase (Gill, Beaven and Cook 2006). If the active recovery comes soon after the training session, then it may also serve as a cool-down that helps smooth the decline in body temperature, dampen nervous system activity, and strengthen the immune system (Reilly and Ekblom 2005).

Waste & Body Temperature, Mood & Psyche - Where Bro- & Proscience Unite

Waste removal an the normalization of the body temperature, together, may help reduce the likelihood of developing delayed-onset muscle soreness (DOMS). It is thus no wonder that not passive rest, but exercise has been shown to be one of the most effective means of reducing the symptoms of DOMS - at least termpoarily, as the pain usually returns upon cessation of the exercise (Cheung, Hume, & Maxwell, 2003; learn more in the "DOMS Series").

Part I	Part II

Just a reminder: For those of you who have not read Alex' two-part series on Delayed Onset Muscle Soreness this would be the ideal time to catch up on part I-II "What Is DOMS & How Can It Be Managed?" & "No Pain, No Gain? Is DOMS Necessary to Build Muscle?" of this series.

We should not forget the psychological benefits, either: Most people simply “feel better” after exercise (Berger and Owen 1998), and these benefits are seen almost immediately after just one bout of physical activity (Hansen, Stevens and Coast 2001). Moreover, low-intensity exercise following strenuous exercise has also been shown to enhance relaxation without adversely affecting physiological recovery (Suzuki, et al. 2004).

Beware of the Catch - Don't Turn Recovery Into Training Days!

Although active recovery may not deter from recovery or impact athletic performance (Andersson, et al. 2008), this assumes a relatively light workload. The only real downside to active recovery is that most people aren’t satisfied doing a short and easy workout (Halson and Jeukendrup 2004), and this is most noticeable in young athletes (Winsley and Matos 2001).

Illustration 1: The vicious circle of ever-increasing "recovery intensities" (Moussa. 2013)

With every 'recovery session' intensity and/or duration starts to climb, and what was supposed to be active recovery has turned into a full-blown training session. Light days become medium days, where the exercise is too hard to allow adequate recovery but not hard enough to stimulate fitness gains. Without adequate recovery, the normal hard training days start to become medium days as well and next thing you know the whole week ends up being in a dead-zone. This brings us to the main benefit of passive rest.

Passive Rest: A Safer Alternative?

Alex has written about the dangers of inactivity in Sean Casey's highly recommended CasePerformance newsletter | read more

The true benefit of passive rest is for people who have no self-control in the gym. Basically, if you are the type of person who must 'go hard or go home', then go home and stay out of the gym. Given the benefits of active recovery and lack of shortcomings aside from the above, there really is no reason to spend all day sitting around doing nothing, especially when you consider the downsides of inactivity outside the gym.

I have previously written about the dangers of being sedentary for most the day; and how there is even a new medical term associated with chronic inactivity: active couch potato syndrome, which is used to describe people who suffer from the same health risks as completely sedentary people despite doing moderate to vigorous daily workouts (Leaf. 2013).

That said, there is nothing wrong with taking a break when you need to, and it is not uncommon for many athletes to have at least one day of complete rest each week (usually Sunday).

Things to Remember - The Rules of Active Recovery: 

Understand the difference between recovery and training or you'll fall victim to the Athlete's Triad | more

Assuming you plan on doing active recovery and have the self-control necessary, I am going to give some guidelines that should provide the benefits stated.

1. The intensity should be about 40%-60% VO2 max for endurance exercise and a maximum of 75% the set RM for strength training.
2. The volume should be ½ the normal workout.
3. You should finish feeling better than you started.

So if you normally do 5x5 on squat, you would be doing 2x5 with 75% of your normal 5RM. If you normally run 8 miles, you would dial it back to 4 miles at half your typical heart rate.

And don’t forget about cross training, which is a great weigh to give the commonly used joints a rest. I commonly find myself cycling leisurely on a cycle ergometer for the length of a TV show following a working legs day. The show keeps me entertained and works as a timer; I may break a sweat, but I always finish feeling refreshed and anything but fatigued ⇔ Done correctly, active recovery is superior to passive rest, but only, I repeat, if done correctly.

References

• Andersson, H, T Raastad, J Nilsson, G Paulsen, I Garthe, and F Kadi. "Neuromuscular fatigue and recovery in elite female soccer: effects of active recovery." Medicine and Science in Sports and Exercise 40, no. 2 (2008): 372-380.
• Berger, B G, and D R Owen. "Relation of low and moderate intensity exercise with acute mood change in college joggers." Perceptual and Motor Skills 87, no. 2 (1998): 611-621.
• Cheung, K, P Hume, and L Maxwell. "Delayed onset muscle soreness : treatment strategies and performance factors." Sports Medicine 33, no. 2 (2003): 145-164.
• Choi, D, K J Cole, B H Goodpaster, W J Fink, and D L Costill. "Effect of passive and active recovery on the resynthesis of muscle glycogen." Medicine and Science in Sports and Exercise 26, no. 8 (1994): 992-996.
• Fournier, P A, T J Fairchild, L D Ferreira, and L Bräu. "Post-exercise muscle glycogen repletion in the extreme: effect of food absence and active recovery." Journal of Sports Science and Medicine 3, no. 3 (2004): 139-146.
• Futre, E P, T D Noakes, R I Raine, and S E Terblanche. "Muscle glycogen repletion during active postexercise recovery." The American Journal of Physiology 253, no. 3 Pt 1 (1987): E305-E311.
• Gill, N D, C M Beaven, and C Cook. "Effectiveness of post-match recovery strategies in rugby players." British Journal of Sports Medicine 40, no. 3 (2006): 260-263.
• Halson, S L, and A E Jeukendrup. "Does overtraining exist? An analysis of overreaching and overtraining research." Sports Medicine 34, no. 14 (2004): 967-981.
• Hansen, C J, L C Stevens, and J R Coast. "Exercise duration and mood state: how much is enought to feel better?" Health Psychology 20, no. 4 (2001): 267-275.
• Leaf, Alex J. "2013 March Newsletter Part I." CasePerformance. Edited by Sean Casey. April 26, 2013. http://www.caseperformance.com/157/2013-march-newsletter-part-i (accessed August 19, 2013).
• MacDougall, J D, M J Gibala, M A Tarnopolsky, J R MacDonald, S A Interisano, and K E Yarasheski. "The Time Course for Elevated Muscle Protein Synthesis Following Heavy Resistance Exercise." Canadian Journal of Applied Physiology 20, no. 4 (1995): 480-486.
• McDonald, Lyle. The Protein Book. 1st. 2007.
• McLoughlin, P, N McCaffrey, and J B Moynihan. "Gentle exercise with a previously inactive muscle group hastens the decline of blood lactate concentration after strenuous exercise." European Journal of Applied Physiology and Occupational Physiology 62, no. 4 (1991): 274-278.
• Phillips, S M, K D Tipton, A Aarsland, S E Wolf, and R R Wolfe. "Mixed muscle protein synthesis and breakdown after resistance exercise in humans." The American Journal of Physiology-Endocrinology And Metabolism 273, no. 1 (1997): E99-E107.
• Reilly, T, and B Ekblom. "The use of recovery methods post-exercise." Journal of Sports Sciences 23, no. 6 (2005): 619-627.
• Suzuki, M, T Umeda, S Nakaji, T Shimoyama, T Mashiko, and K Sugawara. "Effect of incorporating low intensity exercise into the recovery period after a rugby match." British Journal of Sports Medicine 38, no. 4 (2004): 436-440.
• Winsley, R, and N Matos. "Overtraining and elite young athletes." Medicine and Sport Science 56 (2001): 97-105.
• Wolfe, Robert R. "Skeletal Muscle Protein Metabolism and Resistance Exercise." The Journal of Nutrition 136, no. 2 (2006): 5255-5285.

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 I	Part 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.

References

• Bamman, M M, et al. "Mechanical load increases muscle IGF-I and androgen receptor mRNA concentrations in humans." American Journal of Physiology - Endocrinology and Metabolism 280, no. 3 (2001): E383-E390.
• Banfi, G, A Colombini, G Lombardi, and A Lubkowska. "Metabolic markers in sports medicine." Advances in Clinical Chemistry 56 (2012): 1-54.
• Barton-Davis, E R, D I Shoturma, and H L Sweeney. "Contribution of satellite cells to IGF-I induced hypertrophy of skeletal muscle." Acta Physiologica Scandinavica 167, no. 4 (1999): 301-305.
• Bischoff, R. "Chemotaxis of skeletal muscle satellite cells." Developmental Dynamics 208, no. 4 (1997): 505-515.
• Bondesen, B A, S T Mills, K M Kegley, and G K Pavlath. "The COX-2 pathway is essential during early stages of skeletal muscle regeneration." American Journal of Physiology - Cell Physiology 287, no. 2 (2004): C475-C483 .
• Bruunsgaard, H, H Galbo, J Halkjaer-Kristensen, T L Johansen, D A MacLean, and B K Pedersen. "Exercise-induced increase in serum interleukin-6 in humans is related to muscle damage." The Journal of Physiology 499, no. Pt 3 (1997): 833-841.
• Cermak, N M, et al. "Eccentric exercise increases satellite cell content in type II muscle fibers." Medicine and Science in Sports and Exercise 45, no. 2 (2013): 230-237.
• Chakravarthy, M V, B S Davis, and F W Booth. "IGF-I restores satellite cell proliferative potential in immobilized old skeletal muscle." Journal of Applied Physiology 89, no. 4 (2000): 1365-1379.
• Chargé, S B, and M A Rudnicki. "Cellular and molecular regulation of muscle regeneration." Physiological Reviews 84, no. 1 (2004): 209-238.
• Chazaud, B. "Dual effect of HGF on satellite/myogenic cell quiescence." American Journal of Physiology - Cell Physiology 298, no. 3 (2010): C448-C449.
• Clarkson, P M, K Nosaka, and B Braun. "Muscle function after exercise-induced muscle damage and rapid adaptation." Medicine and Science in Sports and Exercise 24, no. 5 (1992): 512-520.
• Faulkner, J A, S V Brooks, and J A Opiteck. "Injury to Skeletal Muscle Fibers During Contractions: Conditions of Occurrence and Prevention." Physical Therapy 73 (1993): 911-921.
• Flann, K L, P C LaStayo, D A McClain, M Hazel, and S L Lindstedt. "Muscle damage and muscle remodeling: no pain, no gain?" The Journal of Experimental Biology 214 (2011): 674-679.
• Furmanczyk, P, and L S Quinn. "Interleukin-15 increases myosin accretion in human skeletal myogenic cultures." Cell Biology International 27, no. 10 (2003): 845-851.
• Goldberg, A L, J D Etlinger, D F Goldspink, and C Jablecki. "Mechanism of work-induced hypertrophy of skeletal muscle." Medicine and Science in Sports 7, no. 3 (1975): 185-198.
• Hara, M, et al. "Calcium influx through a possible coupling of cation channels impacts skeletal muscle satellite cell activation in response to mechanical stretch." American Journal of Physiology - Cell Physiology 302, no. 12 (2012): C1741-C1750.
• Jennische, E, S Ekberg, and G L Matejka. "Expression of hepatocyte growth factor in growing and regenerating rat skeletal muscle." The American Journal of Physiology 265, no. 1 Pt 1 (1993): C122-C128.
• Mikkelsen, U R, et al. "Local NSAID infusion inhibits satellite cell proliferation in human skeletal muscle after eccentric exercise." Journal of Applied Physiology 107, no. 5 (2009): 1600-1611.
• Miyazaki, M, and K A Esser. "Cellular mechanisms regulating protein synthesis and skeletal muscle hypertrophy in animals." Journal of Applied Physiology 106, no. 4 (2009): 1367-1373.
• Moore, J C. "The Golgi tendon organ: a review and update." American Journal of Occupational Therapy 38, no. 4 (1984): 227-236.
• Nosaka, K, K Sakamoto, M Newton, and P Sacco. "The repeated bout effect of reduced-load eccentric exercise on elbow flexor muscle damage." European Journal of Applied Physiology 85, no. 1-2 (2001): 34-40.
• Nosaka, K, M Newton, and P Sacco. "Delayed-onset muscle soreness does not reflect the magnitude of eccentric exercise-induced muscle damage." Scandinavian Journal of Medicine & Science in Sports 12, no. 6 (2002): 337-346.
• Pedersen, B K, K Ostrowski, T Rohde, and H Bruunsgaard. "The cytokine response to strenuous exercise." Canadian Journal of Physiology and Pharmacology 76, no. 5 (1998): 505-511.
• Pedersen, B K, T C Akerström, A R Nielsen, and C P Fischer. "Role of myokines in exercise and metabolism." Journal of Applied Physiology, 2007: 1093-1098.
• Schoenfeld, B J. "Does exercise-induced muscle damage play a role in skeletal muscle hypertrophy?" Journal of Strength and Conditioning Research 26, no. 5 (2012): 1441-1453.
• Schoenfeld, B J. "The use of nonsteroidal anti-inflammatory drugs for exercise-induced muscle damage: implications for skeletal muscle development." Sports Medicine 42, no. 12 (2012): 1017-1028.
• Serrano, A L, B Baeza-Raja, E Perdiguero, M Jardí, and P Muñoz-Cánoves. "Interleukin-6 is an essential regulator of satellite cell-mediated skeletal muscle hypertrophy." Cell Metabolism 7, no. 1 (2008): 33-44.
• Sorichter, S, B Puschendorf, and J Mair. "Skeletal muscle injury induced by eccentric muscle action: muscle proteins as markers of muscle fiber injury." Exercise Immunology Review 5 (1999): 5-21.
• Tatsumi, R. "Mechano-biology of skeletal muscle hypertrophy and regeneration: possible mechanism of stretch-induced activation of resident myogenic stem cells." Animal Science Journal 81, no. 1 (2010): 11-20.
• Tatsumi, R, J E Anderson, C J Nevoret, O Halevy, and R E Allen. "HGF/SF is present in normal adult skeletal muscle and is capable of activating satellite cells." Developmental Biology 194, no. 1 (1998): 114-128.
• Toigo, M, and U Boutellier. "New fundamental resistance exercise determinants of molecular and cellular muscle adaptations." European Journal of Applied Physiology 97, no. 6 (August 2006): 643-663.
• Vierck, J, et al. "Satellite Cell Regulation Following Myotrauma caused by Resitance Exercise." Cell Biology International 24, no. 5 (2000): 263-272.
• Westing, S H, A G Cresswell, and A Thorstensson. "Muscle activation during maximal voluntary eccentric and concentric knee extension." European Journal of Applied Physiology and Occupational Physiology 62, no. 2 (1991): 104-108.
• Yamada, M, et al. "High concentrations of HGF inhibit skeletal muscle satellite cell proliferation in vitro by inducing expression of myostatin: a possible mechanism for reestablishing satellite cell quiescence in vivo." American Journal of Physiology - Cell Physiology 298, no. 3 (2010): C465-C476.

DOMS - Delayed Onset Muscle Soreness: What Is DOMS & How Can It Be Managed? Science, Strategies, Supplements

Whether the text on this photo is actually true or not will be discussed in part II of this series, for now we are going to restrict ourselves to an analysis of the underlying reasons of DOMS and means to prevent that the pain becomes unbearable.

An article by Alex Leaf (CPT)

If you train regularly I’m sure you’re well aware of it, especially the morning following a heavy training session. Delayed onset muscle soreness (DOMS) is the sensation experienced upon waking the next morning and lasting upwards of 72 hours after a heavy exercise session.

It is most commonly brought about through unaccustomed eccentric muscle action causing a disruption of connective and/or contractile tissue (Cheung. 2003). It is not a singular mechanism but rather a result of several mechanisms beginning with microtrauma followed by an inflammatory response (Lewis. 2012).

Does DOMS influence exercise performance?

Although DOMS may make you rethink taking the stairs the next day, its effect on exercise is minimal. This assumes, of course, that you aren’t training the same muscles the very next day. It’s been shown that DOMS impairs force output for up to 24 hours following exercise and even alters the agonist-antagonist muscle activity through reducing motor unit discharge rates (Vila-Chã, Hassanlouei, Farina, & Falla, 2012).

A word of caution: The regular use of NSAIDs as a means to counter delayed onset muscle damage is not a sustainable strategy for any athlete who cares about the health of his intestinal tract and liver. So you better make sure to stick to occasional use, only.

The latter could be attributed to a self-protection mechanism to prevent further damage, as DOMS has also been shown to alter walking and running biomechanics (Paschalis, et al., 2007). But like I said, this only matters if you are training the same muscles the very next day. Assuming you have a rest day or are on some form of a split-routine, DOMS is not a contributor to perceived exertion (Haddad, et al., 2013).

What can be done to prevent or diminish DOMS?

Numerous treatment strategies have been investigated to help alleviate DOMS and restore maximal function to the muscles (Cheung, Hume, & Maxwell, 2003).

• 

  Figure 1: Disruption, inhibition, proteolysis and inflammation - these are the tree main phases trough which you will be going after a hard workout. The "thing" that hurts, though, is the inflammation in step three - the "onset" part in "DOMS" ;-)

  Nonsteroidal anti-inflammatory drugs have shown dosage-dependent effects with little reason to believe that the occasional use will negatively affect muscle growth (Ticchi, 2009). However, given their reported impairment of satellite cell activity, longer-term NSAID use may well be detrimental (Schoenfeld, 2012).
• Warm water immersion (Hassan, 2011) but not cryotherapy (Howatson & Van Someren, 2003) has also demonstrated alleviating effects in the majority of respective trials.
• Similarly, massage has shown varying success that is probably attributable to the type and timing of the massage. Stretching, which is also recommended as a means to prevent or even counter DOMS, on the other hand, has no science to support its effectiveness as an effective DOMS killer (Torres. 2012).

And then of course there is exercise, which has shown to be one of the most effective means of reducing the symptoms of DOMS, although the pain relief is temporary and will resume again following the cessation of exercise (Cheung, Hume, & Maxwell, 2003). More than likely this is due to the break-up and removal of waste products within the muscles via increased blood flow, and also due to an increased endorphin release during exercise (Hough, 1900).

Remember: Irrespective of whether or not DOMS may be necessary for muscle growth (this will be explicitly discussed in part II of this article), some researchers believe that the use of large amounts of anti-oxidant supplements can counter some the beneficial health effects of exercise (Peterneli & Coombes, 2011), (Ristow & Schmeisser, 2011)

What about foods, nutrients and supplements?

Suggested Read: "Pre-regeneration with a warm bath!?" | read more

The best supplement for reducing DOMS isn’t a supplement per se, but rather supplementing the workout with nutrients. Consuming milk or a milk-based carbohydrate/protein supplement immediately post-workout has been shown to limit reductions in muscle performance and symptoms of DOMS 24 and 48 hours later (Cockburn, Stevenson, Hayes, Robson-Ansley, & Howatson, 2010), and these benefits can be achieved with a mere 500 mL – roughly two cups – of milk (Cockburn, Robson-Ansley, Hayes, & Stevenson, 2012).

The reductions in muscle soreness are more than likely do to the high-quality protein of the milk rather than the carbohydrates or fats (Flakoll, Judy, Flinn, Carr, & Flinn, 2004). One study using BCAAs found that about 5g taken before a high volume squat exercise had significantly reduced levels of DOMS and preservation of power output 48 hours post-exercise compared to an isocaloric carbohydrate placebo (Shimomura, et al., 2006).  Five grams of BCAAs is the equivalent of just under 700mL – three cups – of milk, which just so happens to be the amount used in another study that found chocolate milk to reduce DOMS more so than an isocaloric carbohydrate drink (Gilson, et al., 2010). And if you aren’t a fan of milk, all this is about 20 to 25 grams of milk protein around training sessions.

More specific supplements

While it may help with DOMS, n-acetyl-cystein (NAC) is also one of the likely candidates that could theoertically blunt the exercise induced inflammation to a degree that would actually hamper the adaptive processes that's at the heart of strength, mass and performance gains (read more & learn about hormesis)

These classics these classics, there is evidence from peer-reviewed randomized controlled trials that all of the following supplements can help ameliorate / prevent DOMS, as well:

• 1,800mg of the antioxidants EGCG and N-acetyl-cysteine taken pre-exercise were associated with less muscle soreness the next day (Kerksick. 2010),; 
• 2g of L-carnitine L-tartrate daily (Volek. 2002), and 
• 8g of citrulline malate prior to training (Pérez-Guisado. 2010) 

The usual suspects, vitamins C and E show mixed results, at best (McGinley, Shafat, & Donnelly, 2009). Moreover, super-dosing antioxidants may blunt the beneficial effects of exercise via interfering with important physiological processes (Peterneli & Coombes, 2011).

Part I	Part II

Just a reminder: This is a two-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.

Other supplements may even increase DOMS. The most effective naturally occurring statin, Red Yeast Rice, contains lovastatin which has been shown to increase markers of muscle damage following exercise (Thompson, et al., 1997). Diuretic compounds (Cleary, Sitler, & Kendrick, Dehydration and Symptoms of Delayed-Onset Muscle Soreness in Normothermic Men, 2006) and thermogenic agents (Cleary, Sweeney, Kendrick, & Sitler, 2005) may also exacerbate DOMS if fluid intake is not adequate.

There is still one important question to answer:  We have learned that delayed onset muscle soreness is an almost inevitable consequence of microscopic muscle damage, but usually does not affect athletic performance or perceived exertion if you are not training the same muscles the next day. We also analyzed a variety of treatment strategies and supplements that may reduce DOMS. So I suppose the only question left to answer is:

Is DOMS necessary for muscular hypertrophy?

I mean, it’s “No pain, no gain…” - isn’t it? Come back to next Sunday for Part II of this two-part series and find out!

Take home messages: Let's just briefly recapitulate what we've learned already in today's first installment of this two-post series on delayed onset muscle soreness:

• DOMS is a result of exercise induced microtrauma.
• Eccentric and unaccustomed exercises are particularly prone to induce DOMS.
• DOMS will impair the muscular force production immediately after a workout
• Unless you train the same muscle group on subsequent training days, its effects on athletic performance or perceived exertion are negligible

Measures to counter DOMS include NSAIDs, warm-water immersion, massage and light exercise to mobilize the muscle. Supplements to prevent / ameliorate DOMS include (milk) protein and BCAA supplements, n-acetyl-cysteine, l-carnitine tartrate, citrulline and green tea (EGCG). Statins and statin-like OTC supplements such as red yeast rice, but also diuretics and some thermogenic agents can increase DOMS.

References

• Cheung, K., Hume, P., & Maxwell, L. (2003). Delayed onset muscle soreness : treatment strategies and performance factors. Sports Medicine, 33(2), 145-164. 
• Cleary, M. A., Sitler, M. R., & Kendrick, Z. V. (2006). Dehydration and Symptoms of Delayed-Onset Muscle Soreness in Normothermic Men. Journal of Athletic Training, 41(1), 36-45.
• Cleary, M. A., Sweeney, L. A., Kendrick, Z. V., & Sitler, M. R. (2005). Dehydration and symptoms of delayed-onset muscle soreness in hyperthermic males. Journal of Athletic Training, 40(4), 288-297. 
• Cockburn, E., Robson-Ansley, P., Hayes, P. R., & Stevenson, E. (2012). Effect of volume of milk consumed on the attenuation of exercise-induced muscle damage. European Journal of Applied Physiology, 112(9), 3187-3194.
• Cockburn, E., Stevenson, E., Hayes, P. R., Robson-Ansley, P., & Howatson, G. (2010). Effect of milk-based carbohydrate-protein supplement timing on the attenuation of exercise-induced muscle damage. Applied Physiology, Nutrition, and Metabolism, 35(3), 270-277.
• Flakoll, P. J., Judy, T., Flinn, K., Carr, C., & Flinn, S. (2004). Postexercise protein supplementation improves health and muscle soreness during basic military training in marine recruits. Journal of Applied Physiology, 96(3), 951-956
• Gilson, S. F., Saunders, M. J., Moran, C. W., Moore, R. W., Womack, C. J., & Todd, M. K. (2010). Effects of chocolate milk consumption on markers of muscle recovery following soccer training: a randomized cross-over study. Journal of the International Society of Sports Nutrition, 7(19).
• Haddad, M., Chaouachi, A., Wong, d. P., Castagna, C., Hambli, M., Hue, O., & Chamari, K. (2013). Influence of fatigue, stress, muscle soreness and sleep on perceived exertion during submaximal effort. Physiology & Behavior, 119, 185-189..
• Hassan, E. S. (2011). Thermal therapy and delayed onset muscle soreness. The Journal of Sports Medicine and Physical Fitness, 51(2), 249-254. 
• Hough, T. (1900). ERGOGRAPHIC STUDIES IN MUSCULAR FATIGUE AND SORENESS. Journal of the Boston Society of Medical Sciences, 5(3), 81-92. 
• Howatson, G., & Van Someren, K. A. (2003). Ice massage. Effects on exercise-induced muscle damage. The Journal of Sports Medicine and Physical Fitness, 43(4), 500-505. 
• Kerksick, C. M., Kreider, R. B., & Willoughby, D. S. (2010). Intramuscular adaptations to eccentric exercise and antioxidant supplementation. Amino Acids, 39(1), 219-232.
• Lewis, P. B., Ruby, D., & Bush-Joseph, C. A. (2012). Muscle soreness and delayed-onset muscle soreness. Clinics in sports medicine, 31(2), 255-262. 
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• Paschalis, V., Giakas, G., Baltzopoulos, V., Jamurtas, A. Z., Theoharis, V., Kotzamanidis, C., & Koutedakis, Y. (2007). The effects of muscle damage following eccentric exercise on gait biomechanics. Gait & Posture, 25(2), 236-242
• Pérez-Guisado, J., & Jakeman, P. M. (2010). Citrulline malate enhances athletic anaerobic performance and relieves muscle soreness. Journal of Strength and Conditioning Research, 24(5), 1215-1222.
• Peterneli, T. T., & Coombes, J. S. (2011). Antioxidant supplementation during exercise training: beneficial or detrimental? Sports Medicine, 41(12), 1043-1069.
• Ristow, M., & Schmeisser, S. (2011). Extending life span by increasing oxidative stress. Free Radic Biol Med, 51(2).
• Schoenfeld, B. J. (2012). The use of nonsteroidal anti-inflammatory drugs for exercise-induced muscle damage: implications for skeletal muscle development. Sports Medicine, 42(12), 1017-1028.
• Shimomura, Y., Yamamoto, Y., Bajotto, G., Sato, J., Murakami, T., Shimomura, N., . . . Mawatari, K. (2006). Nutraceutical effects of branched-chain amino acids on skeletal muscle. The Journal of Nutrition, 136(2), 529S-532S. 
• Thompson, P. D., Zmuda, J. M., Domalik, L. J., Zimet, R. J., Staggers, J., & Guyton, J. R. (1997). Lovastatin increases exercise-induced skeletal muscle injury. Metabolism, 46(10), 1206-1210.
• Ticchi, S. J. (2009). The effect of nonsteroidal anti-inflammatory drugs on muscle recovery and strength after injury. The University of Toledo
• Torres, R., Ribeiro, F., Alberto Duarte, J., & Cabri, J. M. (2012). Evidence of the physiotherapeutic interventions used currently after exercise-induced muscle damage: systematic review and meta-analysis. Physical Therapy in Sport, 13(2), 101-114. 
• Vila-Chã, C., Hassanlouei, H., Farina, D., & Falla, D. (2012). Eccentric exercise and delayed onset muscle soreness of the quadriceps induce adjustments in agonist–antagonist activity, which are dependent on the motor task. Experimental Brain Research, 216(3), 385-395.
• Volek, J. S., Kraemer, W. J., Rubin, M. R., Gómez, A. L., Ratamess, N. A., & Gaynor, P. (2002). L-Carnitine L-tartrate supplementation favorably affects markers of recovery from exercise stress. American Journal of Physiology - Endocrinology and Metabolism, 282(2), E474-E482.