Why is eccentric training different? (strength is specific)

Reading time:

By Chris Beardsley, S&C Research columnist

In the last decade or so, there has been a surge of interest in eccentric training, which is training solely using the lowering phase of an exercise.

Much of this excitement surrounds the use of eccentric training for preventing or rehabilitating injuries. Even so, a key point is that strength gains after eccentric training are specific – they are greatest when measured with an eccentric test.

This is not surprising, as specificity of strength gains is one of the fundamental principles of strength training. It can be observed to varying degrees in relation to load, speed, range of motion, and external resistance type, as well as muscle action.

But why does it happen after eccentric training?

–

What do “eccentric” and “concentric” training mean?

When you lower a weight, it involves lengthening the prime mover muscles. This is called the eccentric phase. When you lift a weight, it involves shortening the prime mover muscles. This is called the concentric phase.

It is that simple, really.

Normal strength training comprises both lowering and lifting weights. This means both lengthening and shortening muscles under tension, usually directly in sequence. This sequence is called the stretch-shortening cycle (SSC).

Using solely the eccentric phase is very common in rehabilitation, but there are also reasons why it might help enhance sports performance, for reasons I will explain shortly.

Using solely the concentric phase is rarer, but does occur naturally as a result of the way in which some exercises are performed (such as the weightlifting derivatives, loaded carries, and sled pushing or dragging).

Sled pushing involves loading mainly in the concentric phase

Many literature review articles have been published about the unique properties of eccentric training (e.g. Brughelli & Cronin, 2007; Roig et al. 2009; Butterfield, 2012; Isner-Horobeti et al. 2013; Herzog, 2014; Vogt & Hoppeler, 2014; Kjaer & Heinemeier, 2014; Gluchowski et al. 2015; Duchateau & Enoka, 2016). There are also a number of good practical guides to eccentric training (e.g. Mike et a. 2015).

What can I say? It is a popular topic.

–

How do shortening and lengthening contractions differ?

To understand why eccentric training might produce specific strength gains, it is helpful to start with how shortening and lengthening contractions differ at the most basic (myofibrillar) level.

From a biomechanical point of view, muscles are structured of both active and passive elements. Importantly, the passive element has elastic properties.

When performed from a standing start (and ignoring the role of titin for a moment), shortening contractions can only make use of the active element.

Muscle shortening is driven (almost) entirely by chemical energy being converted into kinetic energy within individual sarcomeres, which make up the myofibrils inside the single fibers of a muscle. The thin (actin) and thick (myosin) myofilaments of the sarcomeres slide past one another, in a crossbridge cycle. The myosin myofilament drives this process, by detaching from actin, releasing ADP and rebinding with ATP, and binding to actin again further along the myofilament (Månsson et al. 2015).

In contrast, lengthening contractions make use of both active and passive elements. Also, the way in which the active element functions in lengthening contractions differs from the way it works in shortening contractions.

In lengthening contractions, the myosin crossbridges of the active elements are forcibly broken, detaching the myosin head from actin, without release of ADP and subsequent rebinding of ATP (Månsson et al. 2015). This is part of the reason why the energy requirement of lengthening contractions is quite low in comparison with shortening contractions.

In addition to the different way in which the active elements function during lengthening contractions, there is also a key role for passive elements: they resist lengthening. The passive elements include the three main extracellular matrix layers that surround the muscle fiber (the endomysium), the muscle fascicle (the perimysium), and the muscle itself (the epimysium), as well as the giant molecule titin, which lies parallel to the actin and myosin myofilaments.

Force production during muscle lengthening is therefore driven only partly by chemical energy being converted into kinetic energy within individual sarcomeres, as it is also partly supported by the elastic elements (Herzog, 2014).

This is a key point that differentiates lengthening and shortening contractions, and it has two very important implications.

–

Why is this important?

When exerting the same external force, lengthening contractions require less input from the active elements that drive muscle contraction, and they also require less energy.

This translates to both lower neural drive (as measured by EMG), and a smaller metabolic cost in sub-maximal lengthening contractions compared to shortening contractions, for the same external force (Bigland-Ritchie & Woods, 1976; Duchateau & Enoka, 2016).

Or to put it another way, you experience sub-maximal lengthening contractions as being easier than comparable shortening contractions.

This is because the passive elements contribute to the force production, which allows the active elements an easier ride.

Additionally, maximal force producing capability in lengthening contractions is definitively greater than in shortening contractions, despite what some strength coaches might claim. It is greater by around 50 – 80% when measuring single fibers in vitro, and by around 30 – 50% when measuring strength in live humans (Duchateau & Enoka, 2016).

Maximal force producing capability is greatest in lengthening contractions, because under these conditions, both active and passive elements can be made to contribute to their full extent at the same time, and the sum is much greater than just the active elements on their own.

–

Does eccentric training display specific strength gains?

In one of the first studies to compare eccentric and concentric training, Komi & Buskirk (1972) reported that eccentric training improved eccentric strength more than concentric training did, while both eccentric and concentric training groups improved concentric and isometric strength tests similarly.

Many later studies have confirmed that gains in eccentric strength are greater after eccentric training than after concentric training (Higbie et al. 1996; Hortobágyi et al. 1996; 2000; Miller et al. 2006; Nickols-Richardson et al. 2007).

Here is an illustration of what can happen:

Ratio changes calculated from Nickols-Richardson et al. (2007)

And this is not just a newbie phenomenon. In fact, we can see exactly the same effects in resistance-trained individuals.

Here is an example, also using elbow flexion exercise.

Ratio changes reported in Vikne et al. (2006)

As you can see from the charts, concentric training also displays strength specificity, although the effect is much less marked.

You can also see that eccentric training benefits concentric strength more than the other way around. The exact reasons for this are fairly obvious, but quite complex to explain. Put simply, titin is involved in displaying both eccentric strength and concentric strength, but the changes in titin that occur inside a muscle fiber are probably greater after eccentric training, than after concentric training.

(I will explain more about how titin is affected by eccentric training below).

In the meantime, what we can say is that after either eccentric or concentric training, the ratiosbetween eccentric and concentric strength, between eccentric and isometric strength, and between concentric and isometric strength are all changed (Hortobágyi et al. 1996; Vikne et al. 2006).

For example, in the study in trained subjects shown above, after elbow flexion training in resistance-trained subjects, the ratio of eccentric to concentric 1RM decreased from 1.30 to 1.20 after concentric training, but increased from 1.21 to 1.33 after eccentric training (Vikne et al. 2006).

So when we perform eccentric training, we are not just increasing strength, lengthening muscle fascicles, or altering injury risk, we are also altering the ratio of how much force we can produce while decelerating, compared to how much force we can produce while accelerating.

(This has important injury prevention implications. I will not say any more about it here, because I want to cover it properly in a later article).

But why does this ratio change?

–

Why are strength gains after eccentric training specific? 

So why are the gains in eccentric strength after eccentric training so much larger than gains in other forms of strength?

Although it has been extensively discussed whether eccentric training is superior to concentric training for hypertrophy (Roig et al. 2009), the answer probably lies in some of the other adaptations that occur after strength training, as hypertrophy should affect strength gains in all contraction modes in a relatively similar way.

Indeed, some of these changes in other features of the musculoskeletal system are very pronounced after eccentric training, while others are more obvious after concentric training. Some of the key changes are:

1. Muscle architecture
2. Muscle fiber type
3. Regional hypertrophy
4. Extracellular matrix and cytoskeleton
5. Tendon stiffness
6. Neural adaptations

Let’s take a look at each of these in turn.

–

#1. Muscle architecture

Strength training produces alterations in muscle architecture (muscle fascicle length and pennation angle), and these alterations differ in size depending on whether the contraction type used is predominantly eccentric or concentric.

Muscle fascicle length seems to increase by more after eccentric training, compared to after concentric training (Ema et al. 2016). Such changes probably occur through an increase in the number of sarcomere in series within the myofibrils of a muscle fiber (Brughelli & Cronin, 2007; Butterfield, 2012).

These increases may have advantages for fast movements, as longer fascicle lengths likely allow superior contraction velocities, as all the sarcomeres in a myofibril contract at the same time. They also seem to increase the joint angle for force production (to longer muscle lengths), which could be beneficial in some cases (Brughelli & Cronin, 2007). On the other hand, developing longer muscle fascicles seems to be bad for RFD, as longer fibers require more time to go from slack to taut, at the onset of a muscle contraction (Blazevich et al. 2009).

Since changing muscle fascicle length is essentially an increase in muscle size (Wisdom et al. 2015), it is hard to determine the effects on strength in isolation from hypertrophy, but the emphasis on increasing muscle fascicle length rather than pennation angle may be beneficial, in comparison with concentric training.

Indeed, muscle pennation angle seems to increase by more after concentric training, than after eccentric training (Ema et al. 2016). Increases in muscle pennation angle seem to be mainly a way to accommodate increases in muscle size, by packing more muscle tissue into the same space (Fukunaga et al. 1996), and since the angle of force production becomes less advantageous with increasing pennation angle, this involves a trade-off between more muscle tissue and a smaller component of force.

In any event, without a lot of extra analysis, there seems to be no obvious reason at the moment to assume that the different changes in muscle architecture (muscle fascicle length vs. pennation angle) are responsible for the specificity of strength gains after eccentric training.

–

#2. Muscle fiber type

One common suggestion is that eccentric training can produce greater, or preferential type II muscle fiber area growth than concentric training.

Indeed, there are some indications that this may be the case (Hortobágyi et al. 1996; Hortobágyi et al. 2000; Friedmann-Bette et al. 2010). But there are also an equal number of contrary reports that should make us pause before jumping on this idea (Mayhew et al. 1995; Seger et al. 1998; Vikne et al. 2006).

One explanation for this apparent phenomenon (assuming it is true) is that the size principle is breached, and eccentric training produces earlier recruitment of high threshold motor units, which are believed to correspond to type II muscle fibers (McHugh et al. 2002).

This explanation has two key flaws.

Firstly, a review of studies using careful methods has shown that the size principle is almost certainly not breached during eccentric training (Chalmers, 2008).

Secondly, although not widely-appreciated, the high threshold motor units that are recruited under situations of high demand do not actually correspond directly to type II muscle fibers anyway (Enoka & Duchateau, 2015).

Given the very conflicting evidence for preferential fiber type development from eccentric training compared to concentric training or SSC exercise, on top of the lack of a plausible mechanism, the jury is definitely out on whether this is a mechanism by which eccentric training could produce greater gains in strength.

Therefore, there is no obvious reason to assume that different rates of growth in muscle fibers of differing fiber types underpins the specificity of strength gains after eccentric training.

–

#3. Regional hypertrophy

Regional hypertrophy is a normal aspect of resistance training, and has been observed after various different programs, and in many muscles.

Even so, it has been argued that eccentric training might be particularly effective at producing regional hypertrophy, which is where certain parts of a muscle are more extensively developed than others (Hedayatpour & Falla, 2012). A large portion of the argument put forward here is dependent upon muscle fiber type differences and differences in their activation between lengthening and shortening contractions, which is an assumption that has recently been strongly challenged (see above).

Moreover, in the small number of studies that have actually compared the impact on regional hypertrophy between concentric and eccentric training, there have been no differences between the two training types (Smith & Rutherford, 1995; Blazevich et al. 2007).

So it seems very likely that regional hypertrophy does not differ between concentric and eccentric training, and therefore that this phenomenon is not responsible for the specificity of strength gains after eccentric training.

–

#4. Extracellular matrix and cytoskeletal adaptations

Around muscles, around muscle fascicles, and around muscles themselves is an extracellular matrix made of different types of collagen (the three main layers are called the epimysium, the perimysium, and the endomysium). Within each muscle fiber are myofibrils, supported by scaffolding-type structure, called the cytoskeleton. This cytoskeleton has longitudinal (parallel) and transverse (perpendicular) elements, and the most important longitudinal element is titin.

The amount of collagen within a muscle can increase as a result of exercise (Kjaer, 2004; Wisdom et al. 2015). While this is a bad thing for cattle breeders selling meat, it is usually a good thing for athletes. Collagen itself is very stiff and adding more collagen around the myofibrils increases the stiffness of the individual muscle fibers (Gillies & Lieber, 2011). This probably contributes to enhanced force production during lengthening contractions.

Similarly, the structure and content of the cytoskeleton within a muscle fiber can increase with training. Titin in particular seems to be affected. The number of titin filaments that surround each myosin filament can increase from 3 to 5 with training (Hidalgo et al. 2014; Krüger & Kötter, 2016). This almost certainly improves force generation during lengthening contractions (Lindstedt et al. 2001).

Eccentric exercise is particularly good at damaging both the extracellular matrix and the cytoskeleton, including titin (Friden & Lieber, 2001), and it triggers cellular signaling processes that interact with titin (Krüger & Kötter, 2016). This is almost certainly because eccentric training naturally relies more on these passive elements during contractions, and this greater loading in turn leads to more damage. Therefore, it is logical that eccentric exercise might produce greater adaptations in the passive elements than concentric training.

Unfortunately, very little work has been done to compare the effects of eccentric and concentric training types on adaptations in the extracellular matrix, the cytoskeleton, or titin (except for about a million studies looking at muscle damage).

Even so, it seems like a fairly safe bet that the specific gains in eccentric strength that are observed after programs of eccentric training are caused at least partly by changes in the extracellular matrix, in the cytoskeleton, and in titin.

–

#5. Tendon stiffness, and muscle stiffness

Stiffness is the extent to which an object resists being lengthened. A stiff spring only lengthens a little when you attach a weight to it. On the other hand, a compliant spring lengthens quite a long way.

Muscle-tendon units have both muscles and tendons in series (one after the other). So while we can look at the overall stiffness of the whole muscle-tendon unit, we can also assess the individual stiffness of both the muscle and tendon, separately.

Strength training leads to increased tendon stiffness, and although the effects are affected by load (higher loads are better), they do not differ between eccentric and concentric training (Bohm et al. 2015).

In contrast, while muscle stiffness probably increases slightly after concentric training, most likely because of increases in extracellular matrix and titin content (Gillies & Lieber, 2011) more recent research suggests that it actually decreases after eccentric training (Kay et al. 2016).

This seems strange.

If anything, we might expect that increases in muscle stiffness should be superior after eccentric training. Indeed, older research in animals using accentuated eccentric training, such as downhill running, has reported contrary results (Lindstedt et al. 2001). One possible explanation for this discrepancy could be the large increases in fascicle length that are produced by eccentric-only training.

After all, stiffness is stress (force per unit area) divided by strain (relative length change). So applying a stress to a long muscle fiber will result in a larger relative length change than the same stress applied to a shorter muscle fiber, all other things being equal. Consequently, increasing muscle fascicle length will lead you recording a lower value of stiffness, even if the individual muscle fibers are themselves now made of stiffer material.

Anyhow, what this means is that while muscle-tendon stiffness often increases with normal strength training or with concentric exercise, it does not necessarily increase after eccentric exercise (Kay et al. 2016). Increased muscle-tendon stiffness probably translates to greater joint stiffness, which could be desirable or not, depending on the goals of the athletes (Brazier et al. 2014).

Ultimately, what we can say is that since changes in tendon stiffness do not seem to differ between concentric and eccentric training, that changes in tendon stiffness are not responsible for the specificity of strength gains after eccentric training. The changes in muscle stiffness are less clear, but this might be because they are produced by a combination of variables.

–

#6. Neural adaptations

Over 20 years ago, a case was made that the neural control of lengthening contractions was different from shortening contractions, such that high threshold motor units were recruited earlier (Enoka, 1996). This would be in contradiction of the size principle.

More recently, this proposal was confirmed as rejected, and it is now believed that the size principle is maintained in both lengthening and shortening contractions (Duchateau & Enoka, 2016).

However, that does not mean that other aspects of neural control (that do not violate the size principle) cannot differ between lengthening and shortening contractions.

So it is interesting to observe that after programs of unilateral exercise, eccentric training produces a greater cross-over of strength gains from the trained limb to the untrained limb than concentric training (Hortobágyi et al. 1997; Seger et al. 1998; Nickols-Richardson et al. 2007; Kidgell et al. 2015). Kidgell et al. (2015) suggested that this occurs because of greater reductions in corticospinal inhibition following eccentric training, compared to after concentric training.

Consequently, it seems probable that the specific gains in eccentric strength that are observed after programs of eccentric training are caused at least partly by different neural changes, including greater reductions in corticospinal inhibition.

–

Conclusions

Lengthening contractions involve lower metabolic cost, and require lower neural drive than shortening contractions for the same external force production. Maximal eccentric force is around 30 – 50% greater than maximal concentric force, and could be even higher in athletes.

Compared to concentric training, eccentric training seems to produce greater increases in muscle fascicle length, greater increases in the stiffness of passive structures (extracellular matrix and titin), and greater reductions in corticospinal inhibition.

The specific gains in eccentric strength observed after programs of eccentric training are probably caused by increased extracellular matrix and titin content, which increase passive force production, and by elevated corticospinal excitability. Fiber type, regional hypertrophy, tendon stiffness, and muscle architecture seem to be less important.

What do you think? Tell us on Facebook!

–

References

1. Bigland-Ritchie, B., & Woods, J. J. (1976). Integrated electromyogram and oxygen uptake during positive and negative work. The Journal of Physiology, 260(2), 267.
2. Blazevich, A. J., Cannavan, D., Coleman, D. R., & Horne, S. (2007). Influence of concentric and eccentric resistance training on architectural adaptation in human quadriceps muscles. Journal of Applied Physiology, 103(5), 1565-1575.
3. Blazevich, A. J., Cannavan, D., Horne, S., Coleman, D. R., & Aagaard, P. (2009). Changes in muscle force–length properties affect the early rise of force in vivo. Muscle & Nerve, 39(4), 512-520.
4. Bohm, S., Mersmann, F., & Arampatzis, A. (2015). Human tendon adaptation in response to mechanical loading: a systematic review and meta-analysis of exercise intervention studies on healthy adults. Sports Med Open, 1(1), 7.
5. Brazier, J., Bishop, C., Simons, C., Antrobus, M., Read, P. J., & Turner, A. N. (2014). Lower extremity stiffness: Effects on performance and injury and implications for training. Strength & Conditioning Journal, 36(5), 103-112.
6. Brughelli, M., & Cronin, J. (2007). Altering the length-tension relationship with eccentric exercise.Sports Medicine, 37(9), 807-826.
7. Brughelli, M., & Cronin, J. (2008). Influence of running velocity on vertical, leg and joint stiffness.Sports Medicine, 38(8), 647-657.
8. Butterfield, T. A. (2010). Eccentric exercise in vivo: strain-induced muscle damage and adaptation in a stable system. Exercise & Sport Sciences Reviews, 38(2), 51-60.
9. Chalmers, G. R. (2008). Can fast-twitch muscle fibres be selectively recruited during lengthening contractions? Review and applications to sport movements. Sports Biomechanics, 7(1), 137-157.
10. Duchateau, J., & Enoka, R. M. (2016). Neural control of lengthening contractions. Journal of Experimental Biology, 219(2), 197-204.
11. Ema, R., Akagi, R., Wakahara, T., & Kawakami, Y. (2016). Training-induced changes in architecture of human skeletal muscles: Current evidence and unresolved issues. The Journal of Physical Fitness and Sports Medicine, 5(1), 37-46.
12. Enoka, R. M. (1996). Eccentric contractions require unique activation strategies by the nervous system. Journal of Applied Physiology, 81(6), 2339-2346.
13. Enoka, R. M., & Duchateau, J. (2015). Inappropriate interpretation of surface EMG signals and muscle fiber characteristics impedes understanding of the control of neuromuscular function.Journal of Applied Physiology, 119(12), 1516-1518.
14. Friedmann-Bette, B., Bauer, T., Kinscherf, R., Vorwald, S., Klute, K., Bischoff, D., & Bärtsch, P. (2010). Effects of strength training with eccentric overload on muscle adaptation in male athletes.European Journal of Applied Physiology, 108(4), 821-836.
15. Fukunaga, T., Kawakami, Y., Kuno, S., Funato, K., & Fukashiro, S. (1997). Muscle architecture and function in humans. Journal of Biomechanics, 30(5), 457-463.
16. Friden, J., & Lieber, R. L. (2001). Eccentric exercise‐induced injuries to contractile and cytoskeletal muscle fibre components. Acta Physiologica Scandinavica, 171(3), 321-326.
17. Gillies, A. R., & Lieber, R. L. (2011). Structure and function of the skeletal muscle extracellular matrix. Muscle & Nerve, 44(3), 318-331.
18. Gluchowski, A., Harris, N., Dulson, D., & Cronin, J. (2015). Chronic Eccentric Exercise and the Older Adult. Sports Medicine, 45(10), 1413-1430.
19. Herzog, W. (2014). Mechanisms of enhanced force production in lengthening (eccentric) muscle contractions. Journal of Applied Physiology, 116(11), 1407-1417.
20. Hedayatpour, N., & Falla, D. (2012). Non-uniform muscle adaptations to eccentric exercise and the implications for training and sport. Journal of Electromyography and Kinesiology, 22(3), 329-333.
21. Hidalgo, C., Saripalli, C., & Granzier, H. L. (2014). Effect of exercise training on post-translational and post-transcriptional regulation of titin stiffness in striated muscle of wild type and IG KO mice. Archives of Biochemistry and Biophysics, 552, 100-107.
22. Higbie, E. J., Cureton, K. J., Warren, G. L., & Prior, B. M. (1996). Effects of concentric and eccentric training on muscle strength, cross-sectional area, and neural activation. Journal of Applied Physiology, 81(5), 2173-2181.
23. Hortobágyi, T., Hill, J. P., Houmard, J. A., Fraser, D. D., Lambert, N. J., & Israel, R. G. (1996). Adaptive responses to muscle lengthening and shortening in humans. Journal of Applied Physiology, 80(3), 765.]
24. Hortobágyi, T., Lambert, N. J., & Hill, J. P. (1997). Greater cross education following training with muscle lengthening than shortening. Medicine & Science in Sports & Exercise, 29(1), 107.
25. Hortobágyi, T., Dempsey, L., Fraser, D., Zheng, D., Hamilton, G., Lambert, J., & Dohm, L. (2000). Changes in muscle strength, muscle fibre size and myofibrillar gene expression after immobilization and retraining in humans. The Journal of Physiology, 524(1), 293-304.
26. Ishøi, L., Sørensen, C. N., Kaae, N. M., Jørgensen, L. B., Hölmich, P., & Serner, A. (2015). Large eccentric strength increase using the Copenhagen Adduction exercise in football: A randomized controlled trial. Scandinavian Journal of Medicine & Science in Sports.
27. Isner-Horobeti, M. E., Dufour, S. P., Vautravers, P., Geny, B., Coudeyre, E., & Richard, R. (2013). Eccentric exercise training: modalities, applications and perspectives. Sports Medicine, 43(6), 483-512.
28. Kay, A. D., Richmond, D., Talbot, C., Mina, M., Baross, A. W., & Blazevich, A. J. (2016). Stretching of Active Muscle Elicits Chronic Changes in Multiple Strain Risk Factors. Medicine & Science in Sports & Exercise.
29. Kidgell, D. J., Frazer, A. K., Rantalainen, T., Ruotsalainen, I., Ahtiainen, J., Avela, J., & Howatson, G. (2015). Increased cross-education of muscle strength and reduced corticospinal inhibition following eccentric strength training. Neuroscience, 300, 566-575.
30. Kjaer, M. (2004). Role of extracellular matrix in adaptation of tendon and skeletal muscle to mechanical loading. Physiological Reviews, 84(2), 649-698.
31. Kjaer, M., & Heinemeier, K. M. (2014). Eccentric exercise: acute and chronic effects on healthy and diseased tendons. Journal of Applied Physiology, 116(11), 1435-1438.
32. Krüger, M., & Kötter, S. (2016). Titin, a central mediator for hypertrophic signaling, exercise-induced mechanosignaling and skeletal muscle remodeling. Frontiers in Physiology, 7.
33. Lindstedt, S. L., LaStayo, P. C., & Reich, T. E. (2001). When active muscles lengthen: properties and consequences of eccentric contractions. Physiology, 16(6), 256-261.
34. Månsson, A., Rassier, D., & Tsiavaliaris, G. (2015). Poorly understood aspects of striated muscle contraction. BioMed Research International, 2015.
35. Mayhew, T. P., Rothstein, J. M., Finucane, S. D., & Lamb, R. L. (1995). Muscular adaptation to concentric and eccentric exercise at equal power levels. Medicine & Science in Sports & Exercise, 27(6), 868-873.]
36. McHugh, M. P., Tyler, T. F., Greenberg, S. C., & Gleim, G. W. (2002). Differences in activation patterns between eccentric and concentric quadriceps contractions. Journal of Sports Sciences, 20(2), 83-91.
37. Mjølsnes, R., Arnason, A., Østhagen, T., Raastad, T., & Bahr, R. (2004). A 10-week randomized trial comparing eccentric vs. concentric hamstring strength training in well-trained soccer players.Scandinavian Journal of Medicine & Science in Sports, 14(5), 311.
38. Mike, J., Kerksick, C. M., & Kravitz, L. (2015). How to Incorporate Eccentric Training Into a Resistance Training Program. Strength & Conditioning Journal, 37(1), 5-17.
39. Miller, L. E., Pierson, L. M., Nickols-Richardson, S. M., Wootten, D. F., Selmon, S. E., Ramp, W. K., & Herbert, W. G. (2006). Knee extensor and flexor torque development with concentric and eccentric isokinetic training. Research Quarterly for Exercise and Sport, 77(1), 58-63.
40. Nickols-Richardson, S. M., Miller, L. E., Wootten, D. F., Ramp, W. K., & Herbert, W. G. (2007). Concentric and eccentric isokinetic resistance training similarly increases muscular strength, fat-free soft tissue mass, and specific bone mineral measurements in young women. Osteoporosis International, 18(6), 789-796.
41. Roig, M., O’Brien, K., Kirk, G., Murray, R., McKinnon, P., Shadgan, B., & Reid, D. W. (2009). The effects of eccentric versus concentric resistance training on muscle strength and mass in healthy adults: a systematic review with meta-analyses. British Journal of Sports Medicine, 43(8), 556.
42. Seger, J. Y., Arvidsson, B., Thorstensson, A., & Seger, J. Y. (1998). Specific effects of eccentric and concentric training on muscle strength and morphology in humans. European Journal of Applied Physiology and Occupational Physiology, 79(1), 49-57.
43. Smith, R. C., & Rutherford, O. M. (1995). The role of metabolites in strength training. European Journal of Applied Physiology and Occupational Physiology, 71(4), 332-336.
44. Vikne, H., Refsnes, P. E., Ekmark, M., Medbø, J. I., Gundersen, V., & Gundersen, K. (2006). Muscular performance after concentric and eccentric exercise in trained men. Medicine & Science in Sports & Exercise, 38(10), 1770-1781.
45. Vogt, M., & Hoppeler, H. H. (2014). Eccentric exercise: mechanisms and effects when used as training regime or training adjunct. Journal of Applied Physiology, 116(11), 1446-1454.
46. Wisdom, K. M., Delp, S. L., & Kuhl, E. (2015). Use it or lose it: multiscale skeletal muscle adaptation to mechanical stimuli. Biomechanics and Modeling in Mechanobiology, 14(2), 195-215.