China 
Africa 
Explore chapters and articles related to this topic
Force Generation Mechanism of Skeletal Muscle Contraction
Published in Yuehong Yin, Biomechanical Principles on Force Generation and Control of Skeletal Muscle and their Applications in Robotic Exoskeleton, 2020
T-tubule transfers excitation from sarcolemma to the deeper part of muscle fiber through the connecting point of T-tubule and SR. The T-tubule with the SR (longitudinal tubule) on its two sides is called the thribble structure. The T-tubule connects with SR terminal cisterna through the coupling structure of dihydropyridine (DHPR) and ryanodine receptor (RyR) (tetramer) [19]. Tetramer is actually an electrically and mechanically coupled L-type Ca2+ channel. When the AP on T-tubule reaches the terminal cisterna, DHPR will take conformational change when the potential rise is detected. Then it drives RyR to move from SR to open the channel so that the high-concentration Ca2+ in SR could be released to cytoplasm. It can be seen that the tetramer channel acts like a molecular stopper. The motion of the stopper is controlled by the potential of T-tubule. The structure of tetramer is illustrated in Figure 1.12b. Each group of RyR is arranged like a parallelogram, corresponding to the four DHPRs, respectively. Through the electrically and mechanically coupled L-type Ca2+ channel, the AP spreading on sarcolemma is able to control [Ca2+] in sarcoplasm to activate muscle contraction.
Electromyography in ergonomics
Published in Kumar Shrawan, Mital Anil, Electromyography in Ergonomics, 2017
The technique of electromyography is based on the phenomenon of electromechanical coupling in muscle. Electrical signals generated in the muscle eventually lead to the phenomenon of muscle contraction through intermediate processes. Briefly, as a single or a train of action potentials sweep the muscle membrane (sarcolemma), these electrical potential differences travel deep into the muscle cells through- t-tubules. The t-tubules are invaginations of the muscle membrane inside the muscle cells. Such invaginations are numerous and occur at the junctions of the light and dark bands of the myofibrils where they surround it as a ring on a finger. These rings are interconnected with the rings of neighboring myofibrils making an extensive system of tubules. Such structural organization allows the electrical potential to travel to the deepest parts of the muscle almost instantly as it sweeps the surface. These action potentials trigger the release of Ca2+ ions from the sarcoplasmic reticulum into the muscle cytoplasm. These calcium ions are responsible for facilitating the muscle contraction which in turn manifests itself in the motion of body members and generation of force. Thus, though there is an electromechanical coupling in the muscle, it is mediated through biochemical means. The latter, therefore, does modify this coupling differently in different conditions, such as, motion, duration, geometrical configuration, and fatigue, etc. These considerations will be discussed later in the section on ‘analysis and interpretation’ (see Winter, Chapter 4).
Measurement of Electrical Potentials and Magnetic Fields from the Body Surface
Published in Robert B. Northrop, Non-Invasive Instrumentation and Measurement in Medical Diagnosis, 2017
To ensure that all of the deep contractile apparatus in the center of the muscle fiber is stimulated to contract at the same time and with equal strength, many transverse, radially directed tubules penetrate into the center of the fiber along its length. These T-tubules are open to the extracellular fluid space, as is the surface of the fiber, and they are connected to the surface membrane at both ends. The T-tubules conduct the muscle action potential into the interior of the fiber in many locations along its length.
Sprint start performance: the potential influence of triceps surae electromechanical delay
Published in Sports Biomechanics, 2022
Evan D. Crotty, Kevin Hayes, Andrew J. Harrison
Mapping and measuring the sequence of physiological and mechanical delays is important for a precise understanding of the SSRT. Research to date has demonstrated that SSRT is dependent on several factors: the time taken for the start signal stimulus to arrive at the sensory organ, the delay for conversion by the sensory organ to a neural signal, the delays for neural transmissions and processing, activation of the muscles, soft tissue compliance and selection of the external measurement parameter used to detect the response (Komi, Ishikawa, & Salmi, 2009). Signal processing time encompasses the delays between the stimulus onset and muscle activation. Following the presentation of the stimulus, a delay exists before the athlete hears the signal, this is estimated to be 3 ms for each metre the sound has to travel. Generally successful attempts have been made to reduce this delay period by ensuring speakers are positioned behind the athlete’s blocks (Dapena, 2005). From the ear, the stimulus travels through the brain stem to the auditory cortex and then the motor cortex. A further delay exists between the stimulus arriving at the motor cortex, through the reticulospinal tract of the spinal cord, to its arrival at the muscles, i.e. the electromyographic (EMG) activity onset (Winter & Brookes, 1991). EMD is the delay between the onset of EMG activity and joint motion. EMD can be subdivided into two distinct time periods; force development time representing the delay between muscle activation and the onset of muscle tension, and elastic charge time, representing the delay between muscle tension onset and movement (Winter & Brookes, 1991). EMD contains several components: the conduction of an action potential through the T-tubule system, calcium release from the sarcoplasmic reticulum, the cross-bridge formation of actin and myosin filaments, and the development of tension in the contractile component. The main determinant of the EMD is the time taken for the muscle-tendon unit to stretch in vivo. This period is determined by the elastic properties of the muscle-tendon unit and its capability to remove inherent series elastic ‘slack’ (Cavanagh & Komi, 1979; Viitasalo & Komi, 1981). More precisely, this ‘slack’ refers to the time required to stretch the series elastic component and initiate movement of the joint following contraction in the sarcomeres (Muraoka, Muramatsu, Fukunaga, & Kanehisa, 2004).