's Forum Archives - General

Archive Home >> General(1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 26 27 28 29 30 31 32 33 34 35 36 )

Question on physiology/training.(16 posts)

Question on physiology/training.muncher
Apr 15, 2002 5:44 AM
On sat I ran for the first time since badly damaging my ankle in Jan (week on crutches, lots of physio).

I have been riding a lot in the meantime (only lateral stability was badly affected, so cycling has been fine for about 8 weeks luckily) and done some high-milage rides - 70 milesish - no probs.

However, despite a modest pace (7-8 min miles) over only 4-5 miles of mainly soft ground, and a very thorough warm up-down my thighs are completely shot, with a bad dose of the stiff, burning quads situation.

Question is - what causes this? Is it an internal brusing of the tissue of some kind? A build-up of some nasty stuff in the muscle fibre? Minute tearing of the muscle fibre?

Question 2 - is it avoidable by doing anything that I didn't do - or do you just have to grind through it?


Answers to physiology/training questions.speedisgood
Apr 15, 2002 6:21 AM
Even though you ran on soft ground, you still put 7-10 X your body weight on each leg as you run. That's a lot of stress. Plus, this stress is absorbed by the quads in an eccentric fashion, meaning that the quads contract but are lengthening at the same time. This eccentric muscle action creates the most delayed-onset muscle soreness (DOMS) by creating microscopic tears in the muscle cell walls and connective tissue holding the cells together.

Since you took 2 months "off" of running, your body "adapted" to the low-impact riding (or un-adapted to the pounding of running consistently.)

DOMS is usually present the day after hard/eccentric work, peaks the second day after, and goes away around four days after.

Can you avoid it? Sure. Don't run! If that's not an option, just accept that the soreness is gonna happen, ease gradually back into running (slower, less distance than normal), and massage and stretch well after the runs.

Good luck!
That's 100% correct...Wayne
Apr 15, 2002 7:01 AM
speedisgood has hit it on the nail. Running involves eccentric contractions of the quads which are much, much more damaging than concentric contractions. Cycling is almost a totally concentric movement for all the muscles involved. Thus, you can do hard efforts back to back to back, say for 21 days in July, but to level runners race maybe once or twice a week at the most.
I am no expert, butelviento
Apr 15, 2002 6:28 AM
Running uses muscles differently from riding so if you hadn't run in a few months and suddenly do a 5 miler, you are bound to have sore legs.
Neural RehabJon Billheimer
Apr 15, 2002 6:56 AM
In addition to "Speed's" commentary, your ankle is not fully rehabed neurologically yet, so the muscles of your upper leg are having to perform an even greater stabilizing function than they would normally. This produces an even greater eccentric workload, exacerbating the inevitable soreness. As mentioned, cut back on mileage. Run by feel: that is, if it hurts don't do it! Your body will adapt according to its own schedule. Another suggestion is to either buy or make a balance board and do 2 to 5 min practice on it every day. In another couple of months of this work your ankle proprioception should be back to normal. This will also help prevent re-injury.
Thanks for the responses. Oddly though...muncher
Apr 15, 2002 7:28 AM
My ankle was fine, save for a little initial soreness that passed about 5 mins into the run, and today "D+2", the other leg is the one that is stiffer - I guess it's down to favouring the other leg somehow.

Thanks for your resposes - I had never really considered the different muscle uses in that context - you learn something new every day.

To really push my knowledge envelope - anyone know why this problem disappears the more you build up the running - do the cells toughten up and become less prone to damage?

Embarrasing thing is that I work next to a guy who ran the London Marathon yesterday - and his legs are in far better shape than mine today...
Good point!speedisgood
Apr 15, 2002 8:23 AM
You can also work on proprioception by balancing on your bad leg and kicking the free lag forward, to the side, and backwards. Sounds easy but try to do it in 15x each direction w/o putting the good leg down to rest.

If you have a therapy band (eg., Theraband or similar) attach it to your kicking leg to add a challenge. If that gets easy, try propping your heel (on the bad leg) up a couple of inches. An old phone book works well.
re: Question on physiology/training.netso
Apr 15, 2002 7:37 AM
1. Get a good Exercise Physiology text - read it well
2. Eccentric contractions appear to cause more soreness
3. With continued use, the capillarization in a muscle increases. This increases the blood flow, which in turn reduces the amount of Lactic Acid which is built up during exercise. The other theory of "muscle Tears" is not one I ascribe to, however it is used by some to describe muscle soreness.
Apr 15, 2002 8:07 AM
to some extent, that the muscle tears thing is not a proven fact but I doubt it has anything at all to do with lactic acid. Eccentric contractions consume less ATP than concentric contractions of the same force, so less energy metabolism is involved and I would think less lactic acid produced. Since the essential difference between eccentric and concentric contractions is in their mechanical nature most people buy into some sort of physical damage to the muscle rather than a metabolic explanation (which would probably actually favor the concentric contractions placing a greater demand on the muscle).
Also agree...speedisgood
Apr 15, 2002 8:34 AM
Plus, lactic acid from muscles is usually cleared out within an hour of intense, lactic acid producing activity. Any discomfort coming from acute lactic acidosis should also resolve in that time frame.

As far as I know, LA doesn't actually cause muscle damage itself.
Apr 15, 2002 8:42 AM
Owning a gym for over 20 years I always wondered why negatives (eccentric) movements caused so much soreness. However, Exercise Physiologists, including myself, cannot really give a good reason. I do know that in a bench press you can let down a heavier weight (controlled) than you can actually bench. Are more muscles used during an eccentric contraction? It seems as if you would use more fibers during concentric contractions.
I do know that even performing the same movement, like an incline bench, if you lay off for even a week, you get sore. Why?
Well, you asked..Wayne
Apr 15, 2002 9:11 AM
it's not 100% certain why eccentrics cause so much DOMS but like I said above most people subscribe to some kind of physical damage to the muscle.
Why can you produce more force during eccentrics than concentrics? The force a muscle is capable of producing is directly proportional to the number of attached cross-bridges.
During concentrics the actin and myosin are sliding past one another with the myosin head "ratcheting" and pulling itself along the actin filament, thus shortening the muscle and producing movement. But once it ratchets, it needs to let go, which requires an ATP molecule, and then bind to the next site as it moves by it, ratchet (produce force) and repeat the process. This is why the faster you move the less force you can produce. Think about pulling on rope that is moving through your hands in the same direction your pulling, the faster it's going the less force you can apply to it, before you need to let go and move your hands back along it's length so you can pull again. So at any given moment not all of the cross-bridges are producing force, some are hanging out with a bound ATP, detached waiting for the next oppurtunity to bind.
During eccentrics, you must have more active cross-bridges or you wouldn't produce more force. Think about a team in tug-of-war with each member representing one cross-bridge. In our above, concentric example, some of the team are going to be moving their hands forward to re-grip and pull, while others are pulling, etc. so only so many at any one point are going to be pulling (say 7 out of 10). Assume each is pulling 100% while they're pulling. Now in the eccentric case, you don't need to let go, either you're holding on and no movement is happening, or the rope is slipping through your hands, and you're immediately regripping. This is what happens in the muscle, once the ATP has been split, the myosin head stays in the "tightly bound state" even if it is forcibly pulled off of one actin binding site, it immediately binds to the next one. There is no binding of ATP, reattaching, ratcheting as in the concentric case, there is only reattaching. So at any given moment lets say on average 9 out of 10 team members have a strong grip on the rope. Thus you produce more force. Note there is no ATP required for this, so it's metabolically less demanding than concentric contractions.
Well, you asked..netso
Apr 15, 2002 10:00 AM
It sounds like my Perhydrocyclopentanophenanthrene ring answer. I still do not agree totally with your assessment.
However, you may be correct. Arthur Jones (Nautilus) was the first to really push negative movements. Boy, you really got sore. However, bodybuilders and powerlifters never really bought into his system. Not that he was wrong, it just was not popular with his audience. I do know that I could not do a 1000 lb. deadlift, but I could put it down. Why? Believe me I wish I knew. I have a Ph.D. in Physiology, and this area still baffles me. Strength is another one?
Well, this is fun stuff.Leisure
Apr 15, 2002 6:45 PM
One thing which is counterintuitive is that the ATP is actually consumed in RELAXING muscles, not contracting them! They've shown that actin and myosin strands in solution in the absence of ATP slide along each other just as in normal function. Beyond that my memory of the mechanism wanes, but I do know that this underlies why muscles exert more force in eccentric flexion. Under extension, the actin/myosin bonds have to be actively broken by the imposing load, but under contraction, ATP is required to open more length of available actin/myosin. Kinetics begins to take a role here, and contracting faster is harder to do with the same force because ATP consumption becomes rate-limiting in opening up actin/myosin units. I've seen graphs of how muscle strength varies with velocity; under eccentric loading across the entire velocity range tested, the muscle exerted almost twice what it would under static loading, but under regular contraction the force gradually fell off as the speed went up. When it was converted to power they showed where the muscle's max output was found. I'm tempted to think it corresponded quite nicely with our 60-90 rpm cadences, but it's been a few years.

Other stuff: One reason muscles get less sore in future workouts is they build up more mitochondria to aerobically process whatever it is in the chain that precedes lactic acid (pyruvate, right?). I'm not completely sure about the muscle damage theory either, but I think something along those lines does happen. In my peak cycling condition I can cycle hard for hours and not get sore, but I can go jog a couple miles, not break a sweat, fatigue, or get my heart pounding, yet have miserable soreness the next day, just like muncher is describing. I already know I've got plenty of mitochondria, so I'd say impact is the key.
A couple of points...Wayne
Apr 16, 2002 5:33 AM
your right about a new ATP molecule being is required to "relax the muscle", really relaxing of the whole muscle is a cessation of the action potentials from the CNS, but a new ATP is required to break each actin-myoin cross-bridge. That's why rigor mortis happens when you die, no new ATP, calcium is leaking out of the sarcoplasmic reticulum, triggering cross-bridge binding, but no ATP to break them, so the muscles get stiff.
Your right that the primary determinate of contraction speed is the ATPase activity of the myosin head but that's probably not why there is an inverse relationship between concentric contraction speed and force. I think it really has to do with the number of bound cross-bridges that are in their "power-stoke" phase. To go back to my anology of the tug of war, if the rope is rapidly going through the hands of the people in the direction they're pulling, only those who have a grip and are pulling faster than the rope is moving can contribute to the force in that direction (equivalent to the ratcheting or power stroke of the myosin head following binding to the actin). Those that are in the process of moving their hands further along the rope to regrip or our just holding on will not contribute to the force. In the latter case because of momentum, the myosin and actin (or tug-of-war contestants hands) are passively sliding together with the rope, and therefore contributing little force. But in the case of eccentrics, or the rope being pulled out through the hands, the guys(or myosin heads) who are just hanging on do contribute to force in the opposite direction of the way the rope is moving, so you have more cross-bridges involved at any given instant in generating force, so you produce more force.
With aerobic exercise you build more mitochondria and enzymes of oxidation to oxidize fats and pyruvate. When ATP demands exceed the rate at which lactic acid can be converted to pyruvate and oxidized you start getting lactic acid accumulation as the glycolytic production of lactic acid continues to increase to supply the muscle's demand for ATP.
Nice response!Leisure
Apr 17, 2002 12:42 AM
I can see you're up on your bio. This stuff brings me back to all those physiology courses I took when I was premed. WAS is the key; I've been working in healthcare a while and don't think as much of the people in it as I used to. But as silly as it sounds the material was really cool to me.
As my memory comes back I realize you're right about ATP still being required to allow actin/myosin ratcheting to happen. I don't remember if it's really ATP or ADP or Phosphate in a high energy bond. What I was bringing up is that it doesn't directly contribute to the force created in that ratcheting action. Again, just like the rigor mortis deal. Just something I found interesting.
You could also be right about the rate-limiting being mostly due to the speed of the ratcheting action of actin/myosin cross-bridges; your tug-of-war analogy may be striking up vague memories from lectures long long ago in a galaxy far far away...;-). At the heart of it, it's a reaction rate limiting power output. Kinetics does apply, though perhaps not in as straight-forward a manner as I was thinking.