OK, went for a run Sunday, first time in forever. So, of course, my quads are really sore. I understand DOMS (delayed onset muscle soreness) I jsut don’t understand why the negative action is worse than the positive. It hurts more sitting down and going down stairs than standing up or going up stairs. Is this just due to the different muscles used? Or is somethign else at work?
Muscle fibers can only do one thing: contract. When you’re doing a negative rep (like in a bench press where you let the weight down slowly) the tendons and ligaments actually do all the work. These tend to be what gets sore after you run or lift, hence the onset of DOMS.
That doesn’t jibe with what I know, but I’d welcome a cite saying I’m wrong.
Muscle fibers can contract and uncontract. In an eccentric motion (lowering a weight), the fibers have to uncontract slowly, which creates a lot of tension. Hence DOMS.
ultrafilter-
Each muscle in the body has an opposition muscle. The biceps in the upper arm, for example, have the triceps. Since the biceps can not “uncontract” the triceps have to contract in order for the biceps to relax.
From here:
Emphasis mine.
Hmmm, so what you’re saying, ultrafilter, is that because the eccentric (need to look this term up as it relates to kinesiology and not as it relates to moment) motion is slower, that’s why it hurts more to go down stairs rather than up? It actually occurred to me last night that maybe the speed was an factor so I experimented trying to make sure I went up or down a step at the same rate. But are you saying that the eccentric motion is inherently slower than the positive action?
OK, I just cross-posted with Lord Ashtar. So tendons and ligaments can cause DOMS? I thought that DOMS was due to microscopic tears in the muscle tissue.
That’s probably not quite right. Come to think of it, I’m not quite sure why eccentric activity causes much more damage. I’ll find out, though.
And now on to Lord Ashtar:
As you may note, the emphasized portion contradicts the rest of the paragraph: a muscle fiber contracts either completely or not at all, but any given muscle is only completely contracted when 100% of the fibers are contracted.
That’s not what I wanted the cite for. I was looking for confirmation of this statement:
The correct medical terminology is: a mucle can only contract or relax, it cannot “uncontract”, in the sense of expanding.
I’m a physician, so I’m afraid any sources I’d cite would be medical or biochemical (most of the the lay stuff makes no sense to me, or makes me tear out my hair. I don’t have enough hair to dare look at it). Google >actin myosin “muscle contraction”< if you want more info
The reason a muscle can only contract has to do with the way the actin and myosin fibers work: a myosin fiber is covered in little arms that grab the actin fibers, much like a person pulling themselves along a pipe using a rope tied to the far end… Some arms 'let go" and reach up, grab the myosin and flex (as others arm “hold on” to keep the muscle form stretching) Then a new set or arms goes from holding to flexing, as the old ones hold on.
The flexing is a specific molecular bending. It involves a reaction with ATP, a cellular fuel molecule. The ATP breaks down to ADP + Pi, releasing energy. If you tried to reverse the reaction, you’d have to combine ADP+Pi to form ATP – which would absorb energy, not release it, so you can’t extract work by pushing with myosin.
Think of it this way: you can pull youself though a pipe with a rope that’s tied at the far end, but you can push yourself backwards using that rope. No matter how much rope you push, you can’t get any work done. Rope is good for pulling, lousy for pushing.
All the skeletal muscles in the body are organized in opposing pairs or complementary sets: some of them relax when others contract. To reverse the motion, the pairs switch, and formerly contracting muscles relax. Actually, even the relaxing muscles contract slightly to kelp maintain control.
That may be why your muscles hurt doing things you’d think would be easy on them. Some fibers activate before others,a nd as you need more force, you ‘recruit’ more fibers. (partly the order of recruitment is wiring, partly it’s ‘habit’, meaning that a muscle can ‘learn’ to recruit fibers differently, with practice)
When a muscle is pulling, it’s using a lot of its fibers. When it’s controlling the motion of the opposing muscle, it’s only using a few fibers – its “favorites” if you will. Maybe these favorites are the fibers most likely to be injured, since they get the most use (that’s just a guess) Certainly there is a known effect where X complaining fibers create less perceived pain when they contract with 5000 otehr fibers than if they are contacting with only 50. It’s like galley slaves on a Roman trireme or Viking boat: if a few guys scream in pain and the whole crew is rowing, you don’t hear it as much. Also, when there are only a few rowers doing a precision maneuver, you listen more carefully to each of them.
Patients often encounter more trouble during controlled relaxation of an injured muscle than with full contraction. You may have noticed that you work harder doing a controlled let-down of a weight than you do during the lift.
I don’t know the precise mechanism for what you call DOMS (I don’t recall that term being used when I was in school) but you should be aware that there are many more pain receptors in muscles (including tendon attachment points) than there are in tendons. Also, the Delay sounds like an effect of muscle repair/growth - tendons are much slower metabolically. If DOMS begins in a day or two and resolves in several days (which is the effect I’m thinking of) it’s a muscle thing, not a tendon thing. Tendons can take weeks or even months to fully repair.
Muscle repair pain has many causes: the fibrils thicken during growth, but they also thicken when the contract, so things can get squashed in their connective tissue sleeves (god, that’s such an over simplification). Small tears in capillaries release blood, with is an irritant.Also, the connective tissues and fibers have to be partly torn down to be remodelled. It’s not in the best operating condition.
I’ve had to simplify a great deal. I hope I didn’t suck all the meaning out of it, along with the scientific elegance. Most of what I’ve said is analogy. Please treat it as such.
Oh, to address a misconception I saw above:
Tendons (which connect muscles to bone), ligaments (which connect bone to bone, e.g. around joints) and other fascia (connective tissue) don’t “do any work”. They don’t actively contract or expand. They are like ropes, leather straps or bungie cords. They tie things together, and provide shock cushioning. They do house sensors that feedback signals through the spinal cord, so the muscle knows how much force it’s exerting, but aside from that and the ability to repair themselves, they are surprisingly inert. That’s why they heal so slowly, compared to muscle, when they are injured.
Okay, I admit it. The cite I offered above is lousy. I was just about to leave work and in a hurry.
Also, I misspoke when I said the tendons and ligaments “do all the work”. What I meant was that they bear most of the load, since the muscles are relaxing and not contracting.
Thanks KP, that explanation makes a lot of sense. In a nutshell, you use fewer muscles to control the rate of muscle relaxation (what body builders call the negative action) so, if the muscles are sore from previous activity, the fewer muscle fibers being used will hurt more.
Hmmmm, I wonder how this squares with the popular body building belief that a slow negative action (such as, during bench pressing, taking two seconds to lift the wieght and four seconds to lower the weight) increases strength and muscle size more rapidly. Maybe a slow negative only increases soreness and gives the impression of being more effective.
BTW, DOMS is the current popular term among athletes for the muscle soreness you get a day or two after working out and sounds like the same pain you’re talking
The more you beat the hell out of those fibers, the more they have to adapt to compensate.
In an eccentri contraction, the muscles ARE contracting. DOMS has nothing to do with tendons or ligaments, it is due to a lactic acid build up in the muscles. Think about the motion of taking a drink…as you raise the cup to your mouth, that is a “positive” muscle contraction(biceps, for instance)…as you lower it back to the table, you are NOT contracting the triceps…you are contracting the biceps muscle as it lenthens (a negative, or eccentric contraction). The explanation above about myosin heads is easiest to visualize as a series of ratcheting heads, that grab the actin fiber, pulls itself up, releases, and grabs again over and over, shortening the muscle fibers.
You may see people at a gym doing “negative” reps…a spotter helps them lift a weight that they could not normally lift, and then they lower it as slowly as possible…the muscle is contracting with all of its force, yet is still lenthening…the myosin heads tear away against their will, which causes more soreness.
It is true that muscles only contract and relax, however, they CAN contract and lengthen as they do so.
I don’t remember if the myosin heads tearing away against their will causes more lactic acid build up, or if it is a seperate cause for soreness…maybe someone who remembers the chemistry of muscle fiber building better than me can help here.
To restate what I’m sure you meant, muscles will increase in length, even if some or all of its fibers are contracting, if sufficient external opposing force is applied. They don’t ‘lengthen’ appeciably on their own. In arm-wrestling, the loser’s near-maximally contracted muscles are forced to lengthen against his will. As you lower your coffee cup, the weight of the cup and your arm oppose your biceps contraction. If you tried the same motion by primarily contracting the triceps, you’d shatter the cup against the table.
BTW, your rachet analogy for myosin heads is excellent.
Muscle pain is actually a very complex phenomenon. The question of what irritants or stimuli cause the pain isn’t always as simple as it sounds, and the raw signals are co-processed in the spinal cord and brain with other signals from the tissue, psychological factors, etc.
Lactic acid buildup is a result of anerobic respiration. The first part (glycolysis) of the pathway that turns blood sugar to energy can run for a while when the cell has insufficient oxygen. Glycolysis only produces a tiny fraction of the ATP you’d get from going all the way through oxidation (4 ATP-equivalent per glucose vs. 36-40 for the full cycle, depending on the organism, IIRC) In humans, this process breaks the glucose into two pyruvates, which can’t enter the next stage (the famous Krebs cycle) when the cell is short on oxygen.
Enzymes are catalysts. They only speed up things that would happen anyway. When too much pyruvate builds up, it becomes hard to “pump against the gradient” (high pyruvate concentrations make the reaction run backwards as much as it runs forward, -like a sewer backup, with a seronet effect). The solution is to convert the pyruvate to a similar but distinct compund to get it out of the way - ideally, in a reversible manner, so you don’t permanently waste the remaining energy, but can recover it when you have sufficient oxygen. Some microbes convert the pyruvate to alcohol, a few to acetate, etc. We convert it to lactate.
If you feel the need to genetically engineer yourself to produce alcohol when you exercise anerobically, knock yourself out. (It’s inevitable.) Either fitness will become much more fun than it ever was, or you’ll end up with a beerbelly that grows with exercise 
)
(I should probably distinguish between cellular lactate and tissue lactate. They’re the same chemical, but lactate inside the cell is rapidly reconverted to pyruvate when sufficient oxygen is available, while lactate that escapes into the tissues or blood can persist considerably longer - but generally only on the order of minutes, not days. A lot of things said about lactate, even by physical therapists, chiropractors, etc., don’t make any sense to me, even though I was a molecular biologist before medical school.)
The only reasons I can think of for damage to myosin to increase lactate are a) damage to cellular respiration (e.g. mitochondrial damage), which is very unlikely to be significant; and b) the increased cellular workload of replacing damaged myosin protein, but even this shouldn’t keep a cell in lactate-producing anaerobic respiration when you’re resting (and good thing too: if a muscle cell runs anerobically for too long, it ‘suffocates’ and dies)
Damaged myosin still takes up space, and is still capable of exerting force with its remaining heads, so I imagine that such damage may be more beneficial for ‘fast bulk-up’ than increased strength, but this added bulk might be lost in weeks if training stops, as the cellullar housekeeping breaks down the damaged myosin. (Over the long term, weight training result in more and larger muscle fibers with more actin chains to accomodate more myosin chains, resulting in a more lasting change, but I’m not up to date on the specifics of cellular housekeeping in myocytes in such conditions)
I know that, in physical therapy and rehab, what you call ‘negative action’ is at least as valuable [because it helps improve control) as primary full contraction (which tends to increase peak strength)