(Introduction: The Blog Experiment is primarily to help me overcome my writer's block. I write free-lance articles on fitness, sports and biology and have been working on a book project. But I have suffered a serious case of the infamous Writer's Block (TM) over the last four months. I was inspired to write this recently.)
Doomed by DOMS
My forearms ache; I can’t grip or squeeze. Typing makes me wince.
Yesterday they were sore, today I’m doomed; doomed by DOMS.
What is DOMS? No, it’s not a demented onset mental state. Delayed Onset Muscle Soreness is what most athletes and Weekend Warriors experience after participating in a new exercise, a long marathon, or the first weekend of the season in the garden. Generally, 12-48 hours later, muscles are typically tight and sore, joints are stiff, and some swelling may occur. This time lapse is why it was named “Delayed Onset Muscle Soreness, or DOMS. The severity and duration depends on the individual’s basic conditioning and the nature and intensity of the activity.
Although I am a recreational and competitive weight lifter, I have a bad case of DOMS in my forearms, lats and traps. But not from picking up a loaded barbell. Instead I spent five+ hours stabilizing a tractor PTO-driven auger to drill holes in Texas clay soil. Then rocking it back and forth and helping to pull the auger up out of the bottom of the hole after it cratered itself. The two of us were exhausted after 28 holes.
As a scientist that researches skeletal muscle biology and pathology and a weight lifter, my interest in DOMS could pass as borderline obsessive. What causes it and why? Why are some athletes always sore while others rarely experience soreness? What mechanism(s) reduce soreness from subsequent bouts of activity? How does all this relate to adaptations in strength, endurance and size? Is there a gender difference in DOMS?
Over many years, these questions prompted me to read as much literature on DOMS as I could find, starting with the first hypotheses and models proposed by several authors during the 1980’s and ‘90’s. An accepted ‘theory’ was considered the classical model for DOMS: damage to the cell membrane (sarcolemma) and to the contractile units (called sarcomeres), followed by a series of events that ultimately result in tissue regeneration.
Leakage of proteins from injured cells into the immediate areas outside the cells and into the circulation induces the next stage, inflammation. Immune cells invade damaged cells, clean up debris and also release chemical signals. Thus starts the cascade of steps that repair and regenerate damaged tissue.
The sensation of soreness is thought to be caused by several factors. First, some of these various chemical signals sensitize and activate nearby pain receptors. Secondly, fluid leaks into the damaged area and causes the tissue to swell. Blood is pumped into the tissue, all increasing the volume of the muscle inside its surrounding cocoon of connective tissue. Thirdly, connective tissue also has pain receptors. When tendons and ligaments are traumatized, even stretched too much, it hurts. These all contribute to the soreness sensation upon palpitation and use of the muscle.
Because of misinterpretations of earlier studies (especially extrapolation from animal models), this ‘theory’ has been stretched to fill in holes lacking answers associated with muscle and exercise adaptations to stresses.
“Increases in muscle size occur only when the muscle cell is necrotic (dead) or severely damaged.”
“Damage to the muscle membrane is a prerequisite for increases in muscle cross-sectional area [size].”
“People should not train or exercise again until they are no longer sore.”
“Soreness means poor recovery.”
“A weight trainee will gain more strength and size if he/she lifts to fatigue at every workout.”
“Train ‘till you are sore! No pain, no gain!”
Interpretation: The messenger must be injured or killed in order for the message to be delivered and read.
In many cases, the classical DOMS theory has served as a thumb stuck in a dam in which a crack allows unanswered questions to leak out. But it doesn’t seal the crack. With several recently published studies, specifically from two research groups, that thumb is being extracted and good silicon caulking is being used to seal the crack.
I’ve always had my doubts about the validity of this accepted hypothesis ( I was skeptical despite its universal acceptance, so I always referred to it as a ‘hypothesis’ rather than a ‘theory’. It’s all relative to my Reality, right?)
Imagine my excitement when I read, and reread five papers and a PhD thesis over the weekend that challenges this model and the reductionist interpretations and conclusions in dozens of exercise studies. All while my forearms and lats are stiff and sore.
A series of published studies from labs in Sweden and Denmark demonstrate that muscle cell damage is NOT a prerequisite for muscle cell regeneration and adaptation. These elegant imunohistological and immunocytological studies demonstrate that satellite cells and the contractile ultrastructure are activated and increased, respectively, without necrosis, inflammation, and membrane damage. Satellite cells, the muscle cell precursors required for muscle repair and regeneration of muscle tissue, proliferated after mechanical stress in the absence of cellular damage after one bout. Even after 210 repetitions of lengthening contractions, considered the most damaging to muscle tissue, there was no membrane damage. An extensive series of histology and cytology studies demonstrated that new proteins are synthesized and incorporated into the cells’ contractile machinery in the absence of cell damage. The authors propose that the term ‘remodeling’ be used to replace the historical ‘damage’ based on the lack of evidence for the latter. These studies also offer mechanistic evidence for the Repeated Bout Effect (the observation that muscle soreness is alleviated and eventually disappears during sequential bouts of the same activity).
This is indeed exciting!
Regardless, many questions remain:
How does this relate to total and myofibrillar protein synthesis and degradation? New contractile-associated proteins are incorporated into the additional sarcomeres, but does this correlate with hypertrophy (increase in muscle cell size)?
These studies were performed in subjects unaccustomed to the exercise stress. Does training status alter this process in trained subjects?
In relation to the previous question, what is the temporal nature of this process during and after subsequent bouts of the same stressor?
What chemical signals are involved?
Do protein level changes correlate with those of their corresponding mRNA?
Is this process the same across all exercise modes: resistance and endurance?
All these studies used lengthening contractions only compared to shortening contractions. Is this process altered in movements that involve both types of contractions, which better reflects the ‘real world’ of athletes and recreationally active people?
What is the threshold intensity where morphological damage is induced and how does the same process compare to lower intensity or volume with no myofiber damage?
Can we extrapolate anything useful from this to the loss of muscle tissue in denervation and atrophy?
Oh, so many more questions. Perhaps we have only traded thumbs.
Meanwhile, I’d like to be the smallest nanoparticle equipped with a miniature video injected into my forearm muscle to watch and record what happens over time.
And if I eat my spinach, will I have forearms like Popeye?