This chapter concentrates on mechanical aspects of muscle contraction occurring at the level above the sarcomere. The “intrasarcomere” mechanisms, such as the actin–myosin interaction, are mentioned only in passing. It is assumed that the readers are familiar with these mechanisms from courses in muscle physiology.
The chapter deals with two main issues: mechanical phenomena occurring in the muscle during muscle contraction (section 3.1) and the so-called functional relations (section 3.2). After brief comments on experimental approaches used in studies on muscle mechanics (section 3.1.1), the chapter starts with a description of the muscle transition from rest to activity (i.e., muscle activation; section 3.1.2).
3.1 Muscle Force Production and Transmission
This section addresses the force production and transmission within a muscle. It also describes some intramuscular effects of muscle force changes.
3.1.1 Experimental Methods
The existing knowledge of muscle mechanics was gained from experiments performed on whole muscles, single-fiber preparations, and isolated myofibril preparations. Experiments on whole muscles were conducted in vivo (within a living body), in situ (in the original place but with partial isolation), or in vitro (isolated from a living body). To perform experiments on excised muscles or muscle fibers, the investigator must keep them alive. The muscles (fibers, myofibrils) should be bathed in physiological solution with osmotic pressure and ionic composition similar to those in the tissue fluids in the animal’s body. Usually muscles contain plenty of sources of energy, mostly glycogen, that allow them to work for long periods without additional supply of food substances. The crucial issue is adequate oxygen supply. Mammalian muscles have a high metabolic rate. To supply them with oxygen, intact blood circulation has to be preserved. Due to this requirement, experiments on mammalian muscles in vitroare not performed.
In experiments, muscles are typically activated by electric stimuli applied to muscle surface or to the nerve innervating the muscle. If the strength of a single stimulus exceeds a certain threshold, the muscle responds by a brief period of contraction followed by relaxation (twitch). If the stimuli are repeated at a sufficiently high frequency, summation occurs and a smooth tetanus is observed. Smooth tetanus is characterized by force levels higher than the maximal twitch force. When single fibers (i.e., muscle cells) of mammalian skeletal muscles are stimulated, the fibers follow the all-or-nothing law: the response to any suprathreshold stimulus is maximal and cannot be increased by increasing the strength of the stimulus. In contrast, when the whole muscle is stimulated, the response is graded; with an increasing strength of the stimulus, the muscle force increases because of the increased number of activated fibers. To obtain reproducible results, investigators usually use supramaximal stimuli, which are expected to induce contraction of all the fibers at each presentation.
3.1.2 Transition From Rest to Activity
Representative publications: Hill 1949a, 1949b, 1950; Buller and Lewis 1965
Starting from the arrival of a neural stimulus to a muscle, the muscle needs time to become active, develop force, and start shortening. The period between stimulus arrival and muscle force increase and shortening is known as the latent period (figure 3.1).
• • • Physiology Refresher • • •
Muscle activation involves a complex sequence of events that can be considered at two levels: (1) individual muscle fibers and (2) the entire muscle. Only a brief, simplified overview of these processes is provided here.
At the level of the individual muscle fibers, the process involves the following:
- Neuromuscular transmission: the excitation propagates from the motor axon to the muscle fibers. At the neuromuscular junction, the incoming neural impulse opens the calcium channels, which cause local increase of Ca2+ ions and release of acetylcholine. The associated events trigger an action potential on the muscle fiber membrane that propagates along its entire length.
- Excitation–contraction coupling: excitation propagates from the fiber membranes inside the fibers via the transverse tubular system leading to release of Ca2+ ions from the sarcoplasmic reticulum. With an increasing intracellular Ca2+ concentration and Ca2+ ion–troponin binding along the thin (actin) filaments, the myosin heads establish links (called crossbridges) between the myosin and actin filaments. Muscle contraction begins.
At the level of the entire muscle, the process involves the activation (recruitment) of individual motor units and their muscle fibers. The desired level of muscle force is controlled by recruiting various numbers and types of motoneurons and associated muscle fibers and by changing the frequency of motoneuronal firing (rate coding). A motor unit consists of a motoneuron and the muscle fibers it innervates. Motor units possess different properties and are classified as Type I (slow, fatigue resistant, their motoneurons are relatively small), Type IIA (fast but fatigue resistant), and Type IIX (fast with low resistance to fatigue). Fast motor units have motoneurons of relatively large size. During natural contractions, the recruitment follows the size principle: with gradually increasing neural drive to a motoneuronal pool, small motoneurons are activated before large ones because of lower activation thresholds. Hence the activation progresses from small to large motoneurons and consequently from the slow to the fast motor units. For a muscle involved in a specific motion, the recruitment order of motor units is relatively fixed.
We first consider the mechanical aspects of muscle activation (excitation–activation coupling) in experimental conditions and then force development in humans. Excitation (or neural excitation) refers to the motoneuron action potentials or electric stimuli transmitted to the muscle; the term activation (or muscle activation) designates the set of events linking the excitation with the contractile machinery and resulting in force production. The excitation–contractile machinery linkage is mediated by calcium release (the amount of Ca2+ ions released inside the fibers) and its binding to the troponin at the thin (actin) filaments. In vivomuscle excitation is a function of the number of recruited motor units and their firing frequency.
■■■ From the Literature ■■■
Modeling Neural Control of Gradation of Muscle Force (Neural Excitation)
Source: Tax, A.A., and J.J. Denier van der Gon. 1991. A model for neural control of gradation of muscle force. Biol Cybern 65(4):227-234
A model is presented that relates neural control signals linearly to muscle force. The model allows for different relative contributions from the two force-grading mechanisms—the recruitment of motor units and the modulation of their firing frequency. Consider a motoneuron pool that receives input from a nerve bundle. A weighted sum of activities in a nerve bundle I is
where I is the control signal of the motoneuron pool, ei is the firing frequency of action potential traveling along each nerve fiberin the bundle, and ui is the synaptic weight of a nerve fiber i projecting to a motoneuron (in the model, it is assumed that synaptic weights for all motoneurons are equal). When some commonly accepted physiological facts were incorporated into the model (e.g., different recruitment density of the small and large motor units), a linear relation between the control signals I and the muscle force was elucidated. Hence, the control signal I is proportional to the muscle force and can be interpreted as an internal representation of muscle force. The model confirms an intuitive notion that a weighted sum of activities in a nerve bundle can directly represent an externally controlled variable, which in this case is exerted muscle force.