• Introduction
  • The basics of the length-tension relationship
  • Active vs passive tension
  • Training implications of the length-tension relationship
  • Final thoughts
  • Acetylcholine (ACh): neurotransmitter that binds at a motor end-plate to trigger depolarization
  • Actin: thin myofilaments found in the sarcomeres of a muscle fiber.
  • Action potential: a rapid shift in the voltage across a membrane.
  • Active tension: the force created when actin and myosin filaments slide past each other inside a sarcomere.
  • Active insufficiency: decreased tension when multi-joint muscles are shortened across one or more of its joints.
  • Excitation-contraction coupling: sequence of events from motor neuron signaling to the contraction of the fiber’s sarcomeres.
  • Fascicle: bundle of muscle fibers surrounded by the perimysium.
  • Muscle architecture: the structural design of a skeletal muscle, including the arrangement of the muscle fibers, muscle units, and connective tissue within and around which they are embedded.
  • Myofibril: long, cylindrical organelles that extend in parallel columns along the length of the muscle fiber. Contains the sarcomeres.
  • Myosin: thick myofilaments found within a sarcomeres of a muscle fiber.
  • Passive tension: tension produced by connective tissue as the muscle lengthens.
  • Passive insufficiency: increased tension when a multi-joint muscle is lengthened to its fullest extent at both joints.
  • Sarcomere: the smallest contractile unit of a muscle fiber consisting of actin and myosin filaments.
  • Sarcolemma: the plasma membrane surrounding a skeletal muscle fiber.
  • Sarcoplasm: cytoplasm of a muscle fiber.


Skeletal muscles are composed of cylindrical, multinucleate cells called muscle fibers. Each muscle fiber is comprised of myofibrils, which are long filaments that run parallel to each other. Myofibrils are surrounded by the sarcolemma (plasma membrane of the muscle cell), which contains invaginations called transverse tubules (T-tubules) that project deep into the cell. Each myofibril contains contractile proteins, actin (thin) and myosin (thick) filaments. These filaments are arranged longitudinally into sarcomeres – the basic contractile units of muscle fibers (myocytes).

A muscle fiber contraction begins when an action potential propagates along the motor neuron’s axon towards the neuromuscular junction. Once the action potential reaches the axon terminal, a neurotransmitter acetylcholine (ACh) is released from the synaptic vesicles in the axon terminal. The released ACh then diffuses across the synaptic cleft, causing a the depolarization of the sarcolemma. This, in turn, stimulates the release of Ca2+ from the sarcoplasmic reticulum, which initiates a muscle contraction. Muscles contract according to the sliding filament theory, which states that actin and myosin filaments must slide past each other in order to shorten the sarcomere.

This post explains the basics of the length-tension relationship and how it affects force production and human movement.

The basics of the length-tension relationship

The length-tension relationship describes the amount of force generated by a sarcomere in relation to its length. However, this should not be confused with the length-tension relationship of an entire musculotendinous unit. Active tension is generated by the overlap between two contractile filaments, actin (thin) and myosin (thick), found within the sarcomere. Several studies have shown that the number of cross-bridges (the attachment of myosin with actin within the muscle cell) formed by these two myofilaments is directly proportional to the contractile force the muscle fiber produces. 

The greatest amount of tension is produced when sarcomeres are at resting length, providing an optimal overlap between actin and myosin filaments. This gradually decreases when the muscle is shortened or stretched in relation to its resting length. As the muscle shortens, the filaments become crowded and tension is reduced. Similarly, active tension is reduced when muscle is stretched due to less overlap between actin and myosin filaments. Therefore, fewer cross-bridges are formed. This relationship between sarcomere length and the tension produced is observed via the length-tension curve.

The sliding filament theory provides an explanation to the tension produced by concentrically and isometrically activated muscles. However, the theory has failed to explain the residual force enhancement observed during eccentric muscle actions. It has been proposed that a structural protein titin works alongside actin and myosin filaments to provide passive force when the sarcomeres become over-stretched. However, it is not clear to what extent titin contributes to passive tension. Regardless of the exact mechanism, it is understood that muscle tension (amount of force built up in a muscle) is a result of both active (contractile) and passive (non-contractile) mechanisms within the muscle. The sum of both active and passive tension is referred to as total tension.

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The Length-Tension Relationship

Describes the amount of force produced by a sarcomere in relation to its lengthHighest amount of force is produced at resting (optimal) lengthForce production decreases when the muscle is lengthened or shortened

Active vs passive tension

Active tension is created when actin and myosin filaments slide past each other inside a sarcomere. This requires the constant formation of cross-bridges (cross-bridge cycling) – a process that relies on adenosine triphosphate (ATP) to function. Passive tension refers to the force created when the connective tissue elements inside the muscle-tendon unit are stretched. Some studies have indicated that titin content was the most important contributor to passive tension, whereas the collagen and elastin of the endomysium contributed only minimally. Although active length-tension properties are consistent between sarcomeres, the passive length-tension properties of muscle fibers and muscles are less consistent and less known.

Interestingly, passive tension can reach significantly higher forces than active muscle tension. It is therefore considered the main limitor of movement in extreme ends of a joint’s range of motion (ROM). The increase in passive tension can occur either by passively stretching a muscle, or when an antagonist muscle contracts and causes the antagonist to lengthen. The increase in passive tension is especially evident in multi-joint exercises where muscles are stretched to their limits at all the joints they cross, preventing the full ROM of one or more joints (passive insufficiency). Conversely, if a multi-joint muscle shortens over two or more joints, the muscle creates too much slack and is unable to produce tension (active insufficiency).

Passive tension does not contribute to the muscle’s force production during movements in the middle range of joint motion. However, it plays an important part in low-force exercises and movements closer to the end of a joint’s range of motion. At maximal lengths, tension (resistance to further lengthening of the muscle) is virtually all passive.

Passive tension also allows for the ”pre-stretch” to occur in the stretch-shortening cycle. Thus, helping the muscle produce more force in the concentric phase of a movement.

Training implications of the length-tension relationship

Mechanical loading is considered to be the greatest physiological driver of hypertrophy (muscle growth). When muscle fibers produce contractile force and the passive structures are able to contribute to force production, the overall mechanical tension of the muscle fiber is increased. This added passive tension is due to presence of titin, which increases tension when the muscle is stretched to long lengths as well as when the muscle lengthens while activated (eccentric muscle actions).

During strength training, muscles experience higher tension at longer muscle lengths (larger ranges of motion) as well as during eccentric muscle actions. When the muscle lengthens while contracting, it allows titin to produce tension even at short muscle lengths. This happens because titin’s elastic segment cannot elongate when the muscle is active, forcing its stiff segments to stretch instead. Without muscle activation, titin’s stiff segment elongates only when the elastic segment has already stretched (occurs at long fiber lengths).

When muscle fibers contract at longer lengths, their passive structures (titin and collagen) are already elongated when the contraction takes place. This allows them to participate in force production, and thus, increase mechanical tension of the muscle fiber (up to 30% more than the equivalent concentric muscle action). The increased tension is also why training at long muscle lengths (traditional strength training or isometric training) often result in greater hypertrophy and increased fascicle length than training at short muscle lengths.

To achieve the highest tension possible, a combination both active and passive tension is likely beneficial. This means choosing exercises that allow for high amounts of active tension (plateau region) and high amounts of passive tension (close to the end of their range of motion).

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Final thoughts

The length-tension relationship describes the amount of force produced by a sarcomere or an entire muscle in relation to its length. Total muscle tension is the sum of both active (contractile elements) and passive (connective tissue) mechanisms found in a muscle. 

According to studies, maximal force is produced at resting length when the overlap between actin and myosin filaments is the highest. When the muscle shortened or elongated, its capacity to produce force is reduced. 

Did you learn anything new about the length-tension relationship? Let us know in the comments.


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