Why Sore Muscles After a Workout Doesn’t Mean They’re Growing Faster

sore muscles after a workoutIt’s common for many people, especially when they’re just starting out, to feel sore for a day or two after training.

Even Arnold Schwarzenegger was “feeling it” soon after finishing his first ever workout.

“The guys warned me that I’d get sore,” he writes in Arnold: The Education of a Bodybuilder. “But it didn’t seem to be having any effect. I thought I must be beyond that.”

“The next morning I couldn’t even lift my arm to comb my hair. Each time I tried, pain shot through every muscle in my shoulder and arm. I couldn’t hold the comb. I tried to drink coffee and spilled it all over the table. I was helpless.”

Most people think that sore muscles after a workout are a sign that you’ve stimulated growth, and that more soreness equals faster results.

But are the two really linked? What does muscle soreness have to do with muscle growth? Can you still build muscle without getting sore?

What causes sore muscles after a workout?

Well, it has nothing to do with lactic acid or lactate. In fact, most of the lactate is gone from your muscles soon after exercise.

A tough workout, or even just a single exercise that you haven’t done before, leads to a bout of inflammation — the same defense mechanism that causes swelling and pain if you cut your finger.

Inflammation is the way that your body handles an injury. And as part of the repair and recovery process, your body ramps up the production of immune cells.

These cells then produce substances that make certain nerve endings in your body more sensitive [1, 2]. When you move, these nerves send signals to the brain, which then creates the perception of soreness. In fact, pain appears to be an output constructed by the brain as opposed to an input to the brain as was once believed.

The nerve fibers that transmit pain are located mainly in the connective tissue found between muscle fibers, as well as the junction between the muscle and tendon. In other words, the source of the pain appears to be the connective tissue that helps to bind muscle fibers together, rather than the actual muscle fibers themselves [3].

Does muscle soreness mean that you had a good workout?

You went to the gym yesterday. Today, your muscles feel sore. That must mean your workout was effective, right?

Not necessarily. Exercise can cause damage to muscle fibers. But there’s very little evidence to show that muscle damage is a requirement for muscle growth.

Here’s how one group of researchers summarized the results of a study designed to test the theory that detectable damage is a necessary precursor for muscle growth [8]:

One group of participants experienced an initial bout of damaging exercise and the other had no detrimental symptoms of damage. Despite the different initial conditions, both groups experienced the same net increase in muscle size and strength. These results suggest that it is the total work done during training that impacts the final muscle remodeling, apparently independent of an initial triggering event.

That said, while muscle damage isn’t a requirement for growth, it may accelerate the process [9]. It’s also possible that muscle damage may become a much more important stimulus for growth the longer you’ve been training.

But even then, more damage won’t automatically mean faster growth. If it does exist, any dose-response relationship between muscle damage and muscle growth is likely to be shaped like a U, with a sweet spot found somewhere between “too much” and “not enough” damage.

Put differently, there’s going to be an optimal amount of damage, above and below which your gains will be compromised. This sweet spot may very well be a moving target, and will shift around depending on a number of factors, including how frequently you’re working each muscle group, your training volume, as well the exercises you’re doing.

Even if damage does help to accelerate growth, you can’t rely on muscle soreness to gauge the extent of the damage [4].

An increase in muscle soreness doesn’t necessarily reflect an increase in muscle damage. Conversely, a decrease in muscle soreness is not always indicative of less muscle damage.

When researchers compared voluntary with electrically-induced muscle contractions, the amount of muscle damage was considerably higher with the latter [6]. But there was no significant difference in muscle soreness between the two groups. Other studies report much the same thing, with only moderate levels of soreness associated with a high degree of damage [3].

In one study, a post-exercise bout of foam rolling led to a decrease in muscle soreness [7]. But contrary to what you might expect, this reduction in muscle soreness was accompanied by an increase in markers of muscle damage.

There is also a large degree of variability in the individual damage response to exercise. In fact, there seems to be a population of “high responders” to eccentric exercise. These people lose more strength after a workout, take longer to recover as well as experiencing a greater degree of muscle soreness.

Publishing their findings in the Journal of Applied Physiology, researchers from the University of Massachusetts looked at DNA from 157 untrained men and women following maximal eccentric exercise [10].

They found a link between variations in the CCL2 and CCR2 genes and the severity of exercise-induced muscle damage. With the exception of one individual, the presence of the rare alleles exacerbated strength loss, prolonged strength recovery, and elevated soreness.

There are also large differences in the ability of various exercises to create soreness. Certain movements, particularly those involving high levels of muscle activation at long rather than short muscle lengths, are more likely to create muscle soreness than others [5, 11].

This “length-dependent component” is the reason why Romanian deadlifts (high levels of muscle activation at a long muscle length) lead to so much soreness, while the lateral raise (high levels of muscle activation at a short muscle length) doesn’t.

In his excellent review of the subject, New Zealand personal trainer and coach Matt Perryman points out that many of the assumptions regarding soreness and growth are just plain wrong.

“There’s no link between muscle soreness and protein synthesis; no link between muscle soreness and long-term growth; and no link between muscle soreness and muscle fiber damage.”

“Muscle soreness happens when you create enough total damage to aggravate the connective tissues,” he adds. “This will sometimes correlate with a muscle-stimulating, growth-inducing workout. But just as often, it has nothing to do with muscle stimulation.”

Muscle soreness is nothing more than a sign that you did something your body wasn’t used to, or performed an exercise that just so happens to trigger more soreness than others.

In other words, the fact that you’re not sore doesn’t mean your muscles aren’t growing. Likewise, sore muscles don’t necessarily translate into faster growth.

“Being sore, stiff, and exhausted might feel good,” Perryman concludes. “But it’s not a replacement for training intelligently.”

If you enjoyed this post, there’s a good chance you’ll also like Truth and Lies about Building Muscle: 10 Muscle Myths Debunked By Science.

It's a FREE 20-page special report (PDF) I put together to debunk 10 popular myths that are still widely believed, despite all the evidence to the contrary. You can download a copy here.


SHAMELESS PLUG: Muscle Evo wraps up all my best ideas and advice into a complete science-based training program that you can use to get the "lean, strong and athletic" look without spending unnecessary hours in the gym. Click here to learn more about Muscle Evo.

SEE ALSO

 

About Christian Finn

Christian FinnChristian Finn holds a master's degree in exercise science, is a certified personal trainer and has been featured on BBC TV and radio, as well as in Men's Health, Men's Fitness, Fit Pro, Zest, and Perfect Body magazine. You can contact Christian using Facebook, Twitter, Google+ or via e-mail.

References
1. Armstrong RB. (1984). Mechanisms of exercise-induced delayed onset muscular soreness: a brief review. Medicine and Science in Sports and Exercise, 16, 529-538
2. Basbaum AI, Bautista DM, Scherrer G, Julius D. (2009). Cellular and molecular mechanisms of pain. Cell, 139, 267-284
3. Lauritzen F, Paulsen G, Raastad T, Bergersen LH, Owe SG. (2009). Gross ultrastructural changes and necrotic fiber segments in elbow flexor muscles after maximal voluntary eccentric action in humans. Journal of Applied Physiology, 107, 1923-1934
4. Nosaka K, Newton M, Sacco P. (2002). Delayed-onset muscle soreness does not reflect the magnitude of eccentric exercise-induced muscle damage. Scandinavian Journal of Medicine and Science in Sports, 12, 337-346
5. Newham DJ, Jones DA, Ghosh G, Aurora P. (1988). Muscle fatigue and pain after eccentric contractions at long and short length. Clinical Science, 74, 553-557
6. Crameri RM, Aagaard P, Qvortrup K, Langberg H, Olesen J, Kjaer M. (2007). Myofibre damage in human skeletal muscle: effects of electrical stimulation versus voluntary contraction. Journal of Physiology, 583, 365-380
7. Macdonald GZ, Button DC, Drinkwater EJ, Behm DG. (2014). Foam rolling as a recovery tool after an intense bout of physical activity. Medicine and Science in Sports and Exercise, 46, 131-142
8. Flann KL, LaStayo PC, McClain DA, Hazel M, Lindstedt SL. (2011). Muscle damage and muscle remodeling: no pain, no gain? Journal of Experimental Biology, 214, 674-679
9. Schoenfeld BJ. (2012). Does exercise-induced muscle damage play a role in skeletal muscle hypertrophy? Journal of Strength and Conditioning Research, 26, 1441-1453
10. Hubal MJ, Devaney JM, Hoffman EP, Zambraski EJ, Gordish-Dressman H, Kearns AK, Larkin JS, Adham K, Patel RR, Clarkson PM. (2010). CCL2 and CCR2 polymorphisms are associated with markers of exercise-induced skeletal muscle damage. Journal of Applied Physiology, 108, 1651-1658
11. Jones DA, Newham DJ, Torgan C. (1989). Mechanical influences on long-lasting human muscle fatigue and delayed-onset pain. Journal of Physiology, 412, 415-427