During many movements, an eccentric muscle action occurs as a braking, or opposition, force in response to a concentric (shortening) action, in order to protect joint structures from damage. In an eccentric action, the muscle elongates under the tension caused when an opposing force (such as a weight) is greater than the force generated by the muscle.
Most of the classical muscle load studies in exercise physiology have focused on isometric (same length) and isotonic (shortening) contractions. One of the first research observations on eccentric muscle actions took place in 1882, when Adolf Fick discovered that a contracting muscle under stretch could produce a greater force than a shortening muscle contraction (Lindstedt, LaStayo & Reich 2001). About 50 years later, A.V. Hill (who became a Nobel laureate) ascertained that the body had a lower energy demand during an eccentric muscle action than during a concentric muscle action (Lindstedt, LaStayo & Reich 2001).
Lindstedt, LaStayo and Reich note that in 1953 researcher Erling Asmussen introduced eccentric exercise as “excentric,” with ex meaning “away from” and centric referring to “center,” thus giving the meaning of moving away from center. Lindstedt and colleagues further explain that when weight exceeds the force developed by the muscle, as in an eccentric muscle action, the exercise is referred to as negative work because the muscle is absorbing energy in this loaded motion.
Muscle is tension-producing tissue comprising small contractile units referred to as sarcomeres (see Figure 1). Each sarcomere contains thick (myosin) and thin (actin) myofilaments (muscle filaments or proteins), which overlap to allow for the formation of a cross-bridge bond (attachment). The cross-bridge (or sliding-filament) theory of muscle contraction states that the shortening of a muscle occurs as the myosin cross-bridges cyclically attach to actin and draw the actin across the myosin, thereby creating force and shortening (Herzog et al. 2008).
Herzog and colleagues add that each of the cross-bridge attachment and detachment cycles is powered by the splitting of one molecule of adenosine triphosphate (ATP). This shortening contraction cycle is referred to as a concentric action (or contraction). Examples of activities in which concentric muscle actions occur include walking on level ground, kicking a ball and picking up a weight.
An eccentric muscle contraction, on the other hand, is the stretching of a muscle in response to an opposing force on that muscle, when the opposing force (weight being lifted) is greater than the muscle’s current force production. Herzog and colleagues (2008) propose that when the myofilaments of a muscle fiber are stretched while contracting (i.e., doing an eccentric contraction), there may be a decreased rate of cross-bridge detachments (thus an increased percentage of cross-bridges remain attached), leading to greater force production on the eccentric bout. In addition, Herzog et al. state that there is an increase in the stiffness of the titin protein (see Figure 1) during an eccentric contraction. Titin adds a passive force enhancement (i.e., a tautness) to the muscle’s force production while being lengthened (under load).
Examples of activities in which eccentric muscle contractions occur include walking down a hill, and resisting the force of gravity while lowering a weight or object. Eccentric actions place a stretch on sarcomeres to the point where the myofilaments may experience sarcomere strain, or damage referred to as exercise-induced delayed-onset muscle soreness (DOMS).
All types of muscle contractions, especially in untrained individuals, can cause DOMS, but it is especially noticed after a bout of eccentric exercise. DOMS is typically characterized as the muscle soreness and swelling that become evident 8–10 hours after exercise and peak 24–48 hours after the activity (Balnave & Thompson 1993).
There are several theories explaining the multifactor causes of DOMS. One hypothesis is the connective-tissue theory, which emphasizes the disruption of noncontractile elements (i.e., connective tissue) in sarcomeres (such as the sarcoplasmic reticulum) and of connective tissue surrounding muscle proteins (i.e., sarcolemma) (McHugh et al. 1999).
Another hypothesis is a widely known cellular theory of DOMS that focuses on the irreversible strain placed on sarcomeres during an eccentric contraction, resulting in disruption of components within the sarcomeres (specifically the Z line and A band, shown in Figure 1) (McHugh et al. 1999).
A newer theory spotlights disruption of the excitation-contraction (E-C) coupling mechanism of the myosin cross-bridges attaching to actin proteins as an additional contributor to DOMS (Proske & Allen 2005). Lamb (2009) explains that the sarcoplasmic reticulum is “stretched” significantly during an eccentric contraction, resulting in an uncontrolled release of calcium ions (from the sarcoplasmic reticulum) into the cell fluid (sarcoplasm) (see Figure 2). According to Lamb, this event results in a disruption of the voltage-regulating sensors in the sarcomeres (which regulate neural input in the muscle) and also contributes to DOMS occurring from the eccentric exercise (Lamb 2009).
With the numerous theories about what causes DOMS, it is safe to say that there is still much to be learned through research, although all the theories clearly indicate that exercise-induced DOMS is a multifactor event in muscle (see Figure 3).
One area of research that has much promise in relation to DOMS and eccentric exercise is the repeated-bout effect (RBE) (see Figure 4). One of the only ways, it seems, to prevent or lessen DOMS from eccentric exercise (or to hasten recovery from it) is to eccentrically stimulate the muscles about 1 week (or more) prior to the eccentric training bout (Pettitt et al. 2005). The reduced DOMS response to eccentric resistance, after the prior eccentric exposure, is referred to as the RBE.
Several studies have shown that performing a bout of exercise leading to DOMS and then repeating the eccentric bout of exercise several days (and/or up to 6 months) later results in significantly lower levels of DOMS; reduced levels of circulating creatine kinase (a marker of muscle damage); increased range-of-motion recovery; and enhanced strength recovery after the repeated eccentric workout (Pettitt et al. 2005; Balnave & Thompson 1993).
Performing two, six or 10 maximal eccentric contractions has been shown to provide a protective effect for a subsequent repeated bout of 24–50 maximal muscular contractions weeks later (McHugh 2003). The mechanism that causes the RBE has not been conclusively determined; however, different theories suggest neural input to the muscle, connective tissue restructuring in the muscle and cellular adaptations (an increase in sarcomeres) as possible explanations (McHugh 2003; McHugh et al. 1999).
Older men are not as susceptible as their younger counterparts to the muscle damage caused by eccentric exercise.
Lavender and Nosaka (2006) investigated the responses of older (average age = 70) and younger (average age = 19) males to 6 sets of 5 eccentric-exercise reps (at 40% of one-repetition maximum, or 1-RM) targeting the elbow flexors. The younger men experienced more DOMS and showed higher metabolic markers of DOMS (i.e., increased levels of creatine kinase) after the eccentric training. The authors proposed that slight decreases in range of motion (due to age-related changes in muscles) might partially explain the lower levels of DOMS in the older group. In addition, with aging there is a propensity for loss or atrophy (decrease in size) of fast-twitch muscle fibers, which are particularly challenged (leading to DOMS) in eccentric training (Lavender & Nosaka 2006).
Lavender and Nosaka hypothesize that the older adults may instinctively have developed neural inhibitory mechanisms to avoid exercise-induced muscle damage. With females, Ploutz-Snyder et al. (2001) found no difference in DOMS between older women (66 years) and younger women (23 years) in either concentric or eccentric strength training in a 12-week study evaluating knee extension strength.
As discussed previously, eccentric loading leads to DOMS, especially if the loading occurs in an unaccustomed condition and/or at maximal or near-maximal intensities. During traditional resistance training workouts, the loads of the lifts are typically submaximal (i.e., some percentage of 1-RM). To compare the DOMS effects following maximal versus submaximal eccentric training, Nosaka and Newton (2002) measured muscle damage (of the elbow flexors) in untrained males after completing maximal eccentric exercise bouts (3 sets of 10 repetitions at 100% of 1-RM) with one arm and submaximal eccentric exercise bouts (3 sets of 10 repetitions at 50% 1-RM) with the other arm, 4 weeks apart.
Findings indicated that in untrained subjects performing eccentric exercise, muscle damage was significantly less and muscles recovered significantly faster after submaximal (50%) loading than after maximal loading. The finding is meaningful to personal trainers in that it shows that too much intensity can cause greater DOMS, which may lead to a drop-off in exercise adherence among these clients.
Strength and power athletes extensively focus on 1-RM as a way to gauge and measure strength increases and decreases. A higher 1-RM allows an exerciser to have a higher relative submaximal training volume—and thus the potential to improve submaximal muscle performance. In a study conducted by Doan et al. (2002), researchers found that 1-RM could be acutely increased by applying a supramaximal load (i.e., 105% of 1-RM) on the eccentric phase of the lift. This acute increase (5% greater than 1-RM) in eccentric loading improved 1-RM concentric performance by 5–15 pounds for all subjects.
Theories as to why strength increases occur following eccentric loading include enhanced neural stimulation to and within muscle, higher stored elastic energy in muscle and increases in muscle hypertrophy. Neural stimulation within muscle from eccentric exercise causes a greater muscle spindle stretch. The muscle spindle is a stretch receptor in muscle that lies parallel to the contractile proteins (actin and myosin). It is responsive to stretch and speed of stretch. A greater stretch of the muscle spindles activates an increase in firing motor nerves to the muscle, potentially boosting the concentric force of contraction in the muscle fibers (Dietz, Schmidtbleicher & Noth 1979).
Doan and colleagues suggest that supramaximal eccentric training is an excellent tool to have athletes and clients complete in order to break through training plateaus. Interestingly, Hortobágyi et al. (1996) note that in a 12-week study of isokinetic concentric versus isokinetic eccentric training, subjects experienced more fatigue with the concentric training regimen. The authors conclude that these findings advocate the importance of integrating eccentric training into recreational settings.
Anterior cruciate ligament reconstruction (ACL-R) rehabilitation continues to be a challenging area of research. Safe and effective methods are constantly being researched. Careful, progressive overloading of the muscle early after surgery is essential to an effective recovery.
Gerber and colleagues (2009) found that patients performing a 12-week eccentric training program (along with functional rehabilitation exercises) beginning 3 weeks after surgery showed greater improvements in quadriceps femoris and gluteus maximus muscle volume and overall function than patients performing a standard rehabilitation protocol of weight-bearing exercise, resistance exercise and functional training. At a 1-year follow-up, the eccentric exercise group had a 50% greater improvement in quadriceps femoris and gluteus maximus muscle volume. Additionally, improvement in overall function was significantly greater in this group than in the standard rehabilitation control group.
Another common injury (especially in athletes) treated in rehabilitation settings is patellar tendinopathy (jumper’s knee). Jumper’s knee occurs frequently in high-level volleyball, basketball and soccer players. Using a 12-week eccentric rehabilitation intervention, Bahr et al. (2006) found no measurable differences between a surgical intervention and eccentric exercise rehabilitation for jumper’s knee in a combined athlete and nonathlete group of predominantly men.
With the prevalence of fitness enthusiasts pushing themselves to compete in recreational sports, it is helpful for personal trainers to realize that eccentric training is a viable intervention to use with clients needing postrehabilitation conditioning.
Research has found that doing exercise with an eccentric emphasis can acutely and meaningfully raise the resting energy expenditure (REE) of both trained and untrained individuals after a total-body multiset workout (Hackney, Engels & Gretebeck 2008). Hackney and colleagues found that performing a full-body workout with an eccentric emphasis (1-second concentric and 3-second eccentric on all exercises) elevated REE approximately 9% after the workout. The REE from resistance exercise is likely caused by recovery and repair factors associated with DOMS, the overall muscle repair process and the energy costs associated with protein synthesis (Hackney, Engels & Gretebeck 2008).
Eccentric muscle exercise provides many unique features of conditioning. The challenge to fitness professionals is to recognize the potential of this power-generating training method and to structure effective workouts that will benefit clients. Go negative!
1. With a concentric action, the myosin cross-bridges attach and draw the actin proteins toward each other, shortening the sarcomere.
2. With an eccentric action, the myosin cross-bridges attach and the actin proteins move away from each other (as the weight is greater than the force of the muscle), lengthening the sarcomere.
The sarcoplasmic reticulum surrounds muscle proteins and contains calcium ions. It may be overstretched from an eccentric contraction, causing a substantial release of calcium ions, which it contains. Calcium ions, which have a double-positive electrical charge, may then disrupt the voltage-regulating sensors in the muscle, contributing to DOMS.
Source: Adapted from Proske & Allen 2005.
Source: Adapted from McHugh et al. 1999.
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