The most common injuries in sports are not the catastrophic ones – the ruptured Achilles tendons, blown anterior-cruciate ligaments, or shattered tibias. What is most common is the overuse injury – a smaller-scale but none-the-less potentially devastating muscular disturbance produced when muscles are subjected to either extreme or prolonged stress. When a muscle is damaged by overuse, it can easily lose up to 40 to 50% of its normal strength, a decrement, which can impact performance in a profoundly negative way (“Muscle Function and Protein Metabolism Following Initiation of Eccentric Contraction-Induced Injury,” Journal of Applied Physiology, Vol. 79, pp. 1260-1270, 1995).
Almost every athlete has experienced an overuse injury – and its related loss of strength. As an example, a high-jumper might carry out an extremely strenuous strength-training session in the gym in the hope of building up functional strength and power in the quads and overall leg muscles. The day after such a workout, however, the high jumper notices soreness creeping into his/her quads, and his/her legs feel stiff. The scheduled jumping workout goes very poorly, and indeed jumping performance is worse – not better – for several days thereafter. Pain and stiffness peak after 48 hours and seem to ebb slowly. Although the high-jumper has no catastrophic injury, he/she in fact has a significant overuse injury and a relatively long-lasting impairment of muscle function.
The sad truth is that the recovery of strength following an overuse injury can often be a very slow process. In fact, the time required for complete recovery of strength after overuse can stretch to more than 30 days (“Dissociation of Force Production from MHC and Actin Contents in Muscles Injured by Eccentric Contractions,” Journal of Muscle Research and Cell Motility, Vol. 19, pp. 215-224, 1998). Other reports are even less sanguine, noting that in some cases only half of the lost strength associated with overuse is re-gained after five to six weeks (“Muscle Stiffness, Strength Loss, Swelling and Soreness Following Exercise-Induced Injury in Humans,” Journal of Physiology, Vol. 464, pp. 183-196, 1993). There would be no pain associated with this non-recovery, yet an athlete with such an incomplete recovery would be operating with muscles which were about 20 to 25% sub-par – five weeks after the major damage was done! Thus, it is imperative for athletes to plan workouts which are vigorous enough to enhance fitness without inducing the kind of overuse damage which would retard subsequent training and prevent fitness from increasing.
It is an imperfect world, however, and few athletes are able to create their programmes in such an optimal fashion. Thus, as exercise scientists have pointed out, it is important to understand exactly what causes the strength loss associated with overuse injury. With understanding, it may be possible to minimise or even prevent the losses in strength which occasionally occur.
Not surprisingly, there has been considerable debate in the exercise-science community about the actual source of the loss in strength associated with overuse. A traditional view has been that the loss in strength is solely due to damage to force-bearing structures within and outside muscle cells; inflammation associated with such damage has been believed to magnify the strength loss by further breaking down the force-bearing components of muscle tissue. However, some physiologists have suggested that other factors, including a net loss of protein from overused muscle, may be the paramount plummeter of muscular power. Recently, researchers at Georgia State University and the University of Minnesota took a close look at the processes, which contribute to strength loss after muscle injury (“What Mechanisms Contribute to the Strength Loss that Occurs During and in the Recovery from Skeletal Muscle Injury?” Journal of Orthopaedic & Sports Physical Therapy, Vol. 32, pp. 58-64, 2002). As they did so, they pointed out an important paradox: the largest strength loss that occurs after an injurious bout of exercise is present immediately, yet microscopic analysis of muscle tissue at that time reveals no troubles at all within the muscles; there is simply no visible sign of damage. The mayhem does not appear in the microscope until two to four days later, when white blood cells have invaded the troubled muscle. The obvious question, then, is: how can strength deficits be caused by damage to force-bearing structures, when the biggest deficit in strength occurs when the structures appear to be intact?
Classic research in this area has uncovered some surprising findings. One study found that in mouse muscles, which were displaying a 50% loss in strength, only 5% of the muscle cells showed any signs of damage. Either that small group of cells was producing most of the strength, or else something besides the breakdown of force-bearing structures was creating the loss in force. In another study, mouse muscles exhibiting strength losses of 38, 60, and 84% possessed deterioration in only 5, 21, and 34% of the muscle cross-sectional areas (“Characteristics of Lengthening Contractions Associated with Injury to Skeletal Muscles,” Journal of Applied Physiology, Vol. 61, pp. 293-299, 1986). Muscle strength is normally directly proportional to muscle cross-sectional area, so the strength loss in this study was roughly from three to eight times greater than one would have predicted from the extent of muscular damage.
“One of the key events in the process of getting a muscle cell to contract is the release of calcium ions within the muscle cell”
If damage to force-bearing structures is not producing the loss in strength after overuse, what is? To answer this question, we need to think briefly about how muscle cells actually produce force. As you are probably aware, one of the key events in the process of getting a muscle cell to contract is the release of calcium ions within the muscle cell. What actually happens is this. The nerve cell (motor neuron) which controls a muscle fibre releases a chemical called acetylcholine at the “neuromuscular junction” (the meeting point between the controlling nerve cell and the controlled muscle cell). The acetylcholine then “excites” the muscle-cell membrane, and a wave of excitement (actually an electrical de-polarisation) passes deep into the muscle cell via very tiny, hollow structures called t-tubules. As the tubules are depolarised, the t-tubules’ associated “voltage sensors” undergo a conformational change which induces a special, membranous structure within the muscle cell called the sarcoplasmic reticulum to release calcium ions into the interior of the fibre!
This release of calcium causes key protein structures (actin and myosin) within the cell to slide past each other, et voila!, the muscle produces force. This entire sequence of events is sometimes called the “excitation-contraction coupling pathway”, a useful term to introduce into conversation at your next dinner party. The phrase simply refers to the fact that an excitation (originally from the motor nerve but then passing into the muscle cell) is coupled with a contraction of the muscle fibre.
As an aside, the preceding paragraph in effect outlines a reason why caffeine is a viable ergogenic aid. One of the physiological effects of caffeine is to increase calcium levels inside muscle fibres by opening up the sarcoplasmic-reticulum’s calcium-release channels (“Excitation Failure in Mouse Soleus Muscle Injured by Eccentric Contractions,” Journal of Physiology, Vol. 468, pp. 487-499, 1993). When caffeine is present in a physiological sufficient amount within muscle cells, muscular force production loses its dependence on acetylcholine release at the neuromuscular junction, depolarisation of the muscle-cell membrane, and the link between depolarisation and the release of calcium from the sarcoplasmic reticulum. Caffeine can make these steps non-limiting by making the sacrcoplasmic reticulum really leaky.
As you might have guessed already, experimental manipulations of the excitation-contraction coupling pathway might help us understand why muscles lose strength following overuse injury. Specifically, exercise scientists could put overused muscle cells into a “broth” containing supramaximal levels of calcium ions and then induce the cells to contract. Any deficits in strength exhibited by the muscles could then not be the result of problems in the events leading up to contraction (excitation, depolarisation, floods of calcium, etc), since there would be overabundant calcium within the cells. The deficits would almost have to be the outcome of damaged force-generating structures within the cells (basically, the sliding actin and myosin proteins, along with their associated micro-structures).
“Damage to the force-bearing structure within the muscle could account – at best – for only half of the muscle’s loss of strength”
As you might expect, those kinds of experiments have been done, and in one important study in which overused muscle cells received a nice bath of supramaximal calcium, their overall strength was down by 34%, compared with before the overuse (“Eccentric Contraction-Induced Injury in Normal and Hindlimb-Suspended Mouse Soleus and EDL Muscles, Journal of Applied Physiology, Vol. 77, pp. 1421-1430, 1994). However, the actual overall strength of the muscle (calculated when the cells were not brimming with calcium) was decreased by 69%. The lesson? Damage to the force-bearing structures within the muscle could – at best – account for only half of the muscle’s loss of strength. In fact, this 50% figure is probably an overestimate, since the calcium-bath studies were carried out with single muscle cells, and in a whole muscle (containing lots of cells), there can be lateral force transmission from “neighbour to neighbour”.
If damage to force-bearing structures is not the key event in overuse-related loss of muscle strength, what is the main player, and how can the major mechanism be controlled and/or minimised? As it turns out, there is strong evidence that the “bad guy” might be excitation-contraction (E-C) coupling. In one study in which overused muscle cells were bathed in caffeine (see above discussion of caffeine’s effects), the overused muscle cells exhibited just as much strength as “control” muscles, even though maximal isometric strength in the overall muscle had dropped by 43%. If a simulated restoration of E-C coupling could completely restore muscle strength, then loss of E-C coupling must be the source of lost strength after overuse, the experimenters in this investigation reasoned. In another study in which maximal muscular strength was down by about 50% three days after overuse injury, researchers were able to show that intramuscular calcium levels were also reduced by up to 45% (“E-C Coupling Failure in Mouse EDL Muscle after in Vivo Eccentric Contractions,” Journal of Applied Physiology, Vol. 85, pp. 58-67, 1998).
As you might have already surmised, this kind of research, corroborated by several other studies, also suggests that the site of the E-C coupling failure is above the calcium-release channel in the sarcoplasmic reticulum, since that channel works perfectly well if its beloved caffeine is present. Thus, the onus must fall on activities at the neuromuscular junction, the resulting membrane-depolarisation process (including the depolarisation of the t-tubules), the voltage sensors, or else the dialogue which occurs between the voltage sensors and the sarcoplasmic reticulum.
For various reasons, the Georgia-State and Minnesota researchers believe the problem must reside within the voltage sensors or else their mysterious communications with the sarcoplasmic reticulum, but what can be done about it? Unfortunately, the bad news is that the current answer to this question is “nothing” (more optimistically, one might say that the answer would be that athletes need to learn to train in ways which keep their voltage sensors out of trouble). However, there is also good news: the loss in strength after muscular overuse is actually a two-part process, and something can be done about the second part of the process.
Here’s the basic story. For the first three days after overuse, the big problem for muscles is their deficits in E-C coupling, as described above. After that, however, things change. At approximately three days post-overuse, protein degradation in overused muscles reaches a peak. As a result, there is an actual loss of contractile protein within the overused muscles. The truly odd thing is that even though contractile-protein content continues to dip for the next several days (after the third day), muscular strength actually begins to recover! The reason for this is that the E-C problems are becoming increasingly minor after three days, allowing overused muscles to regain some of their strength.
So, let’s set the scenario. It’s now three days after an overuse injury, and your muscles are beginning to recover their strength, primarily because your voltage sensors or their connections to your sarcoplasmic reticula are humming again. However, there is one little thing going on which will slow your strength restoration: protein degradation, although beginning to slow down, is still going on, and the actual contractile protein content of your muscles is continuing to dip. After 14 days, your entire decrement in strength (remember that after a rough bout of overuse it can take 28 to 35 days to get your strength back) is associated with your contractile-protein deficit. Furthermore, the recovery in strength from two weeks on exactly parallels the recovery in contractile protein content, suggesting a nice causal relationship between the two factors during that time frame.
The lesson, of course, is that minimising protein-degradation rate and maximising the restoration of contractile-protein content after strenuous training are the paramount factors in getting muscle strength back to 100% as quickly as possible (remember that not much can be done about the loss which occurs over the first three days after overuse, but after that the power pick-up becomes more and more a contractile-protein-content story). Fortunately, there are some strategies athletes can utilise to get their contractile proteins up to par quickly; we outline those strategies in the following article.
Overall, the clearest recommendations we can make for athletes are as follows: