An Educational Biomechatronics Model of the Walk-Along Theory of Skeletal Muscle Contraction

Ziad O. Abu-Faraj ? §, Jad A. Al Salman §, Rafif I. Ghostine §, Elias G. Haddad §, Tatiana S. Khoury §, Jamil J. Jabali §, and Nabil N. Hamdan §

§ American University of Science and Technology, Department of Biomedical Engineering, Beirut, Lebanon

? Mebex Consultants, Beirut, Lebanon

First Published: January 2, 2021

ABSTRACT

Purpose: Despite the use of illustrations describing the Walk-Along theory of skeletal muscle contraction, the level of understanding by physiology students of this mechanism can be augmented by an original educational biomechatronics physiological model developed to better demonstrate this theory.

Methods: When the user initiates muscle contraction, a set of LEDs simulates the binding of ATP-molecules to the heads of cross-bridges on the myosin filament. Another set of LEDs simulates the rush of Ca++ ions from the sarcoplasmic reticulum towards the Troponin-C on the troponin-complex of the actin filament. A third-set of LEDs simulates troponin activation in conjunction with rotating-gears that displace the tropomyosin filaments exposing the binding sites on the actin filaments. Subsequently, ATP cleaves into ADP and Pi, energizing the myosin-heads and binding them to the activated sites of the actin filament. Servomotors simulate the resulting power-strokes due to the corresponding forward-tilting of the heads of the cross-bridges, and DC-motors advance the actin filaments towards the H-band of the sarcomere in a cyclic process of repeated power/recovery strokes.

Results: The model is validated using a group of 19 sophomore-students in two explanatory sessions—a standard explanation followed by another using the developed model. Each session concludes with a short descriptive assessment. The results reveal statistically significant changes between the two sessions in favor of the novel model introduced.

Conclusions: The explanation of complex physiological phenomena in Biomedical Engineering programs could be faithfully simplified by introducing low-cost interactive biomechatronics educational models constructed by students and faculty within these programs.

Keywords

Walk-Along Theory, Physiological Modeling, Technology-Enhanced Learning, Mechatronics Models, Ratchet Theory, Sliding-Filament Theory

Introduction

The Walk-Along theory of skeletal muscle contraction, also recognized as the Sliding Filament theory or the Ratchet Theory, was concurrently introduced and published in the same volume of Nature in 1954, by two independent research groups: i) Andrew F. Huxley and Rolf Niedergerke from the University of Cambridge; and, ii) Hugh Huxley and Jean Hanson from the Massachusetts Institute of Technology [1, 2]. This theory is used to describe the mechanism of skeletal muscle contraction at the molecular level [3]—it is elaborated later in the text. Despite the availability of anatomical and physiological illustrations and video animations that facilitate the description of this theory, the degree of understanding by the sophomore-level physiology student of the said intricate mechanism could be augmented through the introduction of a physical model that better demonstrates this theory. Accordingly, the aim of this study is to design and develop an original educational biomechatronics model of the Walk-Along theory of skeletal muscle contraction so as to provide an efficacious solution for the aforementioned problem. It is a comprehensive automated physiological model that integrates mechatronics and biomedical engineering techniques in order to faithfully reproduce the underlying mechanism of skeletal muscle contraction. The designed model serves as an educational tool in physiology classes for healthcare and biomedical engineering students. It sheds light on the importance of continuous development of technology in classrooms, and the role of technology-enhanced learning and modeling in revolutionizing the traditional educational methods and tools. The relevance of this study lies in its demonstration of how such low-cost interactive biomechatronics educational models and technologies could be introduced to Biomedical Engineering programs and constructed by students and faculty within these programs. Our research group has previously been involved in various scholarly activities in the fields of Biomedical Instrumentation [4, 5], Rehabilitation Engineering [6-8], and Biomedical Engineering Education [9, 10].

 Historical Background

The interest in muscle contraction and activity can be traced back to several centuries ago. During the ancient Greek civilization, Hippocrates (460 to 377 B.C.) studied the synergy between muscle function and motion, and published his findings in a manuscript entitled On Articulations [11]. Later, in a work entitled Animal Spirits [12], Aristotle (384 to 322 B.C.) performed a series of observations on the movement of animals and developed intuitive theories about the control of such movement [13]. However, the discovery of the contractile property of muscle is thought to be attributed to Erasistratus (310 to 250 B.C.), Aristotle’s grandson, who was both an anatomist and a physician [12]. The reverberation of the Greek exploration of muscle action was extended to the era of the Roman Empire that witnessed the actual birth of the anatomic period, and is attributed to Claudius Galenus, a.k.a. Galen of Pergamon, (130 to 210 A.D.), who was actually a Greek physician working for the Roman Emperor Marcus Aurelius [12]. Galen was able to classify exercise movements via a paradigm that incorporated the body segment, activity level, motion duration, and motion frequency [11]. Progress in this domain remained marginal till the fifteenth century when Leonardo da Vinci (1452 to 1519) showed particular interest in the structure of the human body, and conducted numerous anatomical studies relating to bones, muscles, and nerves through the dissection of cadavers. His work allowed him to portray the human body in various postures and activities [14]. Thereafter, Andreas Vesalius (1514 to 1564), who was an anatomist and a physician from Brussels–Habsburg Netherlands, is claimed by numerous historians as being the founder of modern human anatomy [15]. Vesalius published a seven-volume seminal manuscript entitled “De Humani Corporis Fabrica” translated as “On the Fabric of the Human Body”, in which accurate descriptions and detailed manifestations of anatomical figures are illustrated [16]. Figure 1 depicts one of Vesalius’s anatomical masterworks.

Figure 1. An anatomical figure from Andreas Vesalius’s text De Humani Corporis Fabrica. From Vesalius A. De Humani Corporis Fabrica, ca. 1543.

Later, Giovanni Alfonso Borelli (1608 to 1679), an Italian mathematician, currently recognized as the “Father of Biomechanics” [17], introduced mathematical principles to the study of movement, which was formerly based on experimental observation [12, 13]. Borelli’s investigation into biomechanics originated with the studies of animals as depicted in his seminal work, De Motu Animalium translated as On the Movement of Animals, and was published after his death [18]. Apparently, this title was borrowed from the Aristotelian treatise [14]. Using optical microscopy, Antonie van Leeuwenhoek (1632 to 1723) was able to describe myofibrils and cross-striations in muscle fibers in 1674 [19]. Later, between 1675 and 1680, William Croone (1633 to 1684) suggested that the sarcomeres could be the functional units of muscle contraction [20]. In 1771, Luigi Aloisio Galvani (1737 to 1798) demonstrated on animal muscle that muscle contraction could be triggered by the electrical stimulation of muscle tissue [21]. His work was published in 1792 in a manuscript entitled De Viribus Electricitatis in Motu Musculari Commentarius [22].

Thereafter, Paul J. Barthez (1734 to 1806) postulated that a correlation exists between muscle function and body force [12]. Chabrier, circa 1820, verified the existence of the relationship between muscle function and the free and fixed lower extremities [12]. While significant, these contributions remained purely observational. Guillaume-Benjamin-Amand Duchenne (1806 to 1875) performed a set of experimentations on human subjects using electrical muscle stimulation [23]. In 1927, Richard Scherb (1880 to 1955) introduced a myokinesiographic technique for recording muscle action during gait [13]. His studies were conducted on individuals with gait pathologies, including hemiplegia, spastic paralysis, and poliomyelitis [24]. In 1849, the German physician and physiologist Emil du Bois-Reymond (1818 to 1896) discovered that the recording of the electrical activity generated during voluntary muscle contraction is possible [25, 26]. However, the term Electromyography (EMG) was introduced by the French Professor and Physiologist étienne-Jules Marey (1830 to 1904) in 1890 after performing the first actual recording of this activity [25, 26]. Since then, EMG has evolved to become a significant tool in neurophysiology and clinical medicine and rehabilitation. Edward H. Lambert (1915 to 2003)—recognized as the “Father of EMG”—was a neurologist who contributed to the development of various key concepts of muscle and nerve disorders [27]. Lambert’s seminal work in clinical neuromuscular physiology established EMG as an important subspecialty within the many areas of neurology [27]. Jacqueline Perry (1918 to 2013) was an orthopaedic surgeon, and a renowned expert on normal and pathological human gait analysis and the treatment of numerous neuromuscular and neurological conditions. Perry pioneered the application of fine-wire electromyography in clinical gait analysis [25, 26]. Her legacy was bestowed in a 1992 classical book titled Gait Analysis: Normal and Pathological Function [28]. John V. Basmajian (1921 to 2008) was a researcher and a practitioner in the field of Rehabilitation Science, specifically in the areas of Electromyography and Biofeedback; today, he is known as the father of Kinesiological Electromyography [15]. Basmajian, in the early 1970s, introduced “muscular feedback” as a tool applied to patients suffering from neuromuscular disorders so as to ameliorate the contractile function of weak muscles while reducing the activity of pathologically spastic muscles [15]. Currently, his techniques in biofeedback are implemented in various interactive routines that aim to rehabilitate individuals with neuromuscular disorders [15]. Basmajian’s text Muscles Alive – Their Functions Revealed by Electromyography stands as a testimony to his great scholarly activities [29].

Perhaps one of the most important findings in the quest for knowledge of muscle function was realized in the 1950s by the two unrelated Huxleys and their associates [1, 2]. AF Huxley, H Huxley, et al. realized that the sarcomeres of striated muscle contain overlapping sets of protein filaments that do not change much in length when sliding past one another as the muscle sarcomere shortens during muscle contraction [30]. This concept has become a fundamental part to the understanding of how muscles work [30].

Literature Review

Physiological models are physical, graphical, engineering, mathematical and other attempts to find simplified methods for precisely and accurately characterizing a physiological phenomenon or process. The literature contains a substantial number of studies that revolve around the Walk-Along theory of skeletal muscle contraction. The most relevant articles that relate to the current study are presented herein, in chronological order.

In 1977, Hatze reported on a myocybernetic control mathematical model of skeletal muscle [31]. Using motor unit recruitment and stimulation rate as parameters, the model was capable of describing the different contractile states that occur in a living muscle together with the force output. The model was validated using experimental data. In a 1998 Doctoral Dissertation, B.J.J.J. van der Linden described the functional behavior of skeletal muscle through several mechanical models [32]. The author began with a description of four classical models: Hill-type models; Huxley or Cross-Bridge models; Morphological models; and, Morpho-Mechanical models. He then examined the functional effects of muscle geometry on muscle contraction before proceeding with a delineation of the following models: i) a mechanical depiction of the unipennate skeletal muscle model; ii) simulation of concentric and isometric contractions using a finite element skeletal muscle model; and, iii) an experimental justification of various historical models of muscle contraction using a reduced cross-bridge model.

In 2001, Grazi and Cintio proposed that muscle contraction can be depicted as a chemo-osmoelastic transduction; whereby, during a power stroke, analysis of the energy partition requires consideration of both: osmotic and chemoelastic factors [33]. In a review article published in 2004, Cooke presented the evolution of the sliding filament model, from 1972 till 2004, which explains the mechanism of muscle contraction and the corresponding motor proteins that produce motility. The author stated that “these mechanisms were elucidated by innovations and technologies that largely were unimaginable in 1954” [34]. In a 2008 thesis, Marcucci presented a mechanical model of muscle contraction [35]. The author began by considering the two models of muscle contraction—Huxley’s model of 1957 and Huxley and Simmons model of 1971—as being complementary since the former delineates the attachment-detachment process and the events related to the “slow time scale”, while the latter delineates the power stroke process and the events related to the “fast time scale”. The author then examined the possibility of adjoining the two types of processes in a unified model which delineates the entire cross-bridge cycle from a mechanical engineering perspective, making use of the Brownian ratchets theory. In 2009, Squire presented a review of various imaging and modeling studies performed on the cores, crowns, and couplings of muscle myosin filaments [36]. The author stated that: while the quest to solve the ultrastructures of different myosin filaments was successful, there still remain some inaccuracies of their erroneous starts and false sidetracks. He then added that studies that were based on higher resolution should come up with the necessary answers.

In a 2012 Doctoral Dissertation, Bibó performed a mechanical modeling of motor protein myosin II [37]. Five objectives were addressed in this project: i) the different existing processes within the different functional sites of myosin II were modeled using a low degrees-of-freedom model; ii) continuous transitions between the different states of the system were set so as to minimize the effects of arbitrary influences on that system; iii) the model was designed to replicate the empirically observed properties of myosin II, including the four strokes of the Lymn-Taylor cycle; iv) the effects of thermal fluctuations were considered with an aim to answer whether the power stroke is an Eyring mechanism or a Kramers mechanism; and, v) to provide a justification for the inconsistency that exists between the values of stiffness acquired from single molecule experiments and the macroscopic efficiency measurements done on the muscle tissue. In 2015, Herzog et al. introduced a new paradigm for muscle contraction by hypothesizing that three filaments are involved in muscle contraction: actin, myosin, and titin [38]. The authors believe that titin plays a regulatory role on the force of attraction by: i) binding Ca++; and, ii) shortening of its spring length after binding to actin. In 2018, T. T. Dao and MC Ho Ba Tho published a holistic manuscript on 40 contemporary continuum models of skeletal muscles. The authors conducted a systematic review process and delineated the trends, limitations, and recommendations pertaining to these physiological models [39]. An elaborate review article by Caruel and Truskinovsky of the physics of muscle contraction was published in 2018 [40]. In this article, the authors highlight the latest attempts to use mechanics-based models of force generation in skeletal muscles to supplement the previously existing biochemically-based models.

In 2009, Jittivadhna et al. presented a hand-held model of a sarcomere that is used to demonstrate the mechanism of sliding filament during muscle contraction [41]. The efficacy of the educational effectiveness of this model was tested on 343 students who were previously exposed to the said concept, using textbook illustrations and computer graphics displays. The obtained results showed that the three-dimensional model was capable of dispelling some false conceptions maintained by these students from the two-dimensional illustrations. A faithful software animation model of the sliding filament theory of muscle contraction was released on YouTube in 2009 by Egner [42]. A hand-held manual sarcomere model is commercially available by Denoyer-Geppert, International (Skokie, IL, USA), and is sold for 1044.99 USD. Finally, a 2013 study by Preece et al. describes the advantages of a physical model over three-dimensional computer models and textbooks while studying imaging anatomy [43].

Physiological Background

The Structural Organization of Skeletal Muscle

The skeletal muscle consists of striations of muscle fasciculi that are anatomically subdivided into the following hierarchical subunits: muscle fibers, myofibrils, and myofilaments, Figure 2 [3]. Each muscle fiber extends along the entire length of the muscle and is innervated by only one motor neuron. Also, each muscle fiber consists of hundreds to thousands of myofibrils. In turn, each myofibril consists of approximately 1500 neighboring myosin filaments surrounded by approximately 3000 actin filaments. The myosin and actin filaments are polymerized protein molecules that constitute the functional units in charge of the actual muscle contraction. At rest, the actin filaments partially interdigitate with the myosin filaments giving the myofibril a characteristic alternating light and dark bands. The light bands are named the I bands and represent only actin filaments. The dark bands are called the A bands and represent the myosin filaments and the portion of the actin filaments that overlap with the myosin filaments. Each myosin filament structurally contains tiny projections called cross-bridges from each of its sides except at its center—a region known as the H band. It is at this microscopic level that muscle contraction occurs due to the interaction between the cross-bridges of the myosin filaments with the active sites of the actin filaments. The ends of the actin filaments on each side of the associated myosin filaments are demarcated by a strong filamentous protein suture-like line known as the Z disc that extends crosswise within each myofibril and from one myofibril to another throughout the entire cross-section of the muscle fiber. Therefore, the light and dark bands are extrapolated from the myofibrils to the entire muscle fiber, giving the muscle fiber the same appearance in terms of these bands. Henceforth, the entire muscle possesses the same characteristic striated appearance. This anatomical phenomenon applies only to skeletal and cardiac muscles, but not to smooth muscles. The segment within each myofibril—ergo the entire muscle fiber—that is bounded between two consecutive Z discs is known as a sarcomere. When the muscle is relaxed, the sarcomere length is around 2.0 micrometers, and the actin filaments overlapping the myosin filament on each side are barely interdigitating with one another. During full muscle contraction, the sarcomere length is reduced to 1.6 micrometers, which is basically the length of the myosin filament.

Figure 2. The structural hierarchical organization of skeletal muscle. Adapted from Guyton, A.C. & Hall J.E. (2000). Contraction of skeletal muscle. In: Textbook of Medical Physiology. Tenth Edition. Philadelphia, PA, USA: W.B. Saunders Company, p. 68, 2000.

The myofibrils are suspended within the muscle fiber in an intracellular matrix named sarcoplasm. The latter essentially encompasses the normal intracellular constituents with a remarkable number of mitochondria lying parallel to the contracting myofibrils. The number of mitochondria is commensurate with the amount of energy required by these contractile elements, and is provided by adenosine triphosphate (ATP), which is produced by the mitochondria. The sarcoplasm also contains an elaborate sarcoplasmic reticulum that plays an important role in controlling the mechanism of muscle contraction.

 The Mechanism of Skeletal Muscle Contraction

The following ordered sequence of events delineates the initiation and execution of voluntary skeletal muscle contraction, Figures 3-4 [44]: i) an action potential propagates down a myelinated motor neuron towards its endings on the skeletal muscle fibers; ii) at each of these endings, the motor neuron releases a small volume of the neurotransmitter substance acetylcholine in a process of exocytosis; iii) the acetylcholine acts on a localized region of the skeletal muscle fiber membrane in order to open multiple acetylcholine-gated ligand channels via integral protein molecules within the membrane; iv) subsequently, large amounts of Na+ ions flow from the extracellular space down their concentration gradient towards the interior of the muscle fiber membrane, initiating an action potential within the muscle fiber; v) the generated action potential propagates along the membrane of the skeletal muscle fiber by depolarizing successive areas along the entire muscle; vi) concurrently, the action potential propagates in the transverse direction deeply within the muscle fiber, causing the sarcoplasmic reticulum to release copious amounts of Ca++ ions that have been initially stored within this reticulum when the muscle is at rest; vii) the Ca++ ions cause the contractile process to begin, whereby attractive forces between the actin and myosin filaments are initiated within each sarcomere, causing them to slide past each other; and, viii) after a few milliseconds, special Ca++ membrane pumps are used to pump back the Ca++ ions into the sarcoplasmic reticulum, and remain stored until the arrival of a new muscle action potential. This withdrawal of the Ca++ ions from the myofibrils causes the cessation of the muscle contraction.

Figure 3. The motor end plate in a longitudinal section. Adapted from Guyton A.C. & Hall J.E. (2000). Excitation of skeletal muscle: A. neuromuscular transmission and B. excitation-contraction coupling. In: Textbook of Medical Physiology. Tenth Edition. Philadelphia, PA, USA: W.B. Saunders Company, p. 81.

Figure 4. The release of acetylcholine at the neuromuscular junction. Adapted from Guyton A.C. & Hall J.E. (2000). Excitation of skeletal muscle: A. neuromuscular transmission and B. excitation-contraction coupling. In: Textbook of Medical Physiology. Tenth Edition. Philadelphia, PA, USA: W.B. Saunders Company, p. 81.

The Walk-Along Mechanism of Muscle Contraction

The Walk-Along or Sliding Filament Mechanism describes the process of Skeletal Muscle Contraction at the molecular level, namely the interaction between the myosin and actin filaments within a sarcomere [3]. When the muscle is relaxed, the extremities of the actin filaments extending from two adjacent Z discs slightly overlap one another, while concurrently encompassing the entire myosin filament. Moreover, the Z discs are spaced by 0.2 micrometer from each end of the myosin filament. When the muscle is fully contracted, the actin filaments are completely pulled inwards on both sides of the myosin filament, such that their ends overlap one another to a great extent. In this state, the Z discs abutt each end of the myosin filament whose length is about 1.6 micrometer.

The Walk-Along Mechanism is a result of the axial mechanical forces generated by the interaction between the cross-bridges extending from the myosin filaments with the active sites on the F-actin filaments. When the muscle is at rest, these forces are inhibited; however, when an action potential propagates over the membrane of the muscle fiber, it triggers the sarcoplasmic reticulum to release copious amounts of calcium ions that rapidly penetrate deep within its myofibrils. In turn, the released calcium ions actuate the forces between the myosin and actin filaments, initiating contraction. However, for the contractile mechanism to progress, energy needs to be expended. This energy is derived from the hydrolysis of high-energy bonds of adenosine triphosphate (ATP), which cleaves into adenosine diphosphate (ADP) to liberate the required energy in the form of inorganic phosphate (Pi). The hydrolysis of ATP is triggered by the myosin head, which acts as an ATPase enzyme.

At the molecular level, the myosin molecule consists of a double helix of two heavy polypeptide chains constituting the tail, and two side-by-side light chains constituting the free heads that assist in controlling the myosin head during muscle contraction. The myosin filament consists of around 200 myosin molecules whose tails join in a bundle to form the body of the filament. Out of this bundle extends a part of every myosin molecule that serves as an arm that projects the head away from the body in a 120 degrees circumferential arrangement for every three consecutive myosin molecules. The myosin heads together with their protruding arms are named cross-bridges. It is believed that the cross-bridges within the same myosin filament operate independently of one another, such that the greater the number of cross-bridges involved in a muscle contraction, the greater is the force of contraction.

The actin filaments consist of actin, tropomyosin, and troponin protein complexes and are strongly attached at their bases to the Z discs. Two helical strands of F-actin proteins constitute the backbone of each actin filament. Every revolution within this strand contains 13 molecules of polymerized G-actin, each of which attracts one ADP molecule. It is hypothesized that the ADP molecules provide active sites on the F-actin strands for the cross-bridges of the corresponding myosin filament to interact with so as to produce muscle contraction. There exists one such active site on every 2.7 nanometers of the entire length of the actin filament, which is 1 micrometer in length. The tropomyosin is another protein that is helically wrapped around the F-actin strands. When the muscle is relaxed, the tropomyosin molecules cover the active sites of the F-actin helix. Accordingly, attraction between the myosin and actin filaments is inhibited. The tropomyosin molecules also carry complexes of proteins named troponin. Each troponin molecule consists of three loose subunits of proteins: i) troponin I, which possesses a strong affinity for actin; ii) troponin T, which possesses a strong affinity for tropomyosin; and, iii) troponin C, which possesses a strong affinity to calcium ions. It is believed that the interaction of troponin C with Ca++ is responsible for the initiation of the contractile process. Figure 5 depicts the actin filament and its subunits.

Figure 5. The actin filament and its subunits. Adapted from Guyton A.C. & Hall J.E. (2000). Contraction of skeletal muscle. In: Textbook of Medical Physiology. Tenth Edition. Philadelphia, PA, USA: W.B. Saunders Company, p. 71.

In order to initiate contraction, there should be an inhibition to the inhibitory effect produced by the troponin-tropomyosin complex of the actin filament. Such a feat is accomplished in the presence of Ca++; however, the exact mechanism behind which it occurs is yet to be discovered. It is hypothesized that when Ca++ binds with troponin C, the active sites of the actin filaments become exposed and attract the heads of the myosin cross-bridges for contraction to move forward. Such hypothesis, backed up with substantial evidence, is known as the “Walk-Along” theory or “ratchet” theory of contraction [3]. Figure 6 depicts the structure of the myosin and actin filaments within a sarcomere. Figure 7 depicts the Walk-Along mechanism of muscle contraction.

Figure 6. The structure of the myosin and actin filaments within a sarcomere. Adapted from Guyton A.C. & Hall J.E. (2000). Contraction of skeletal muscle. In: Textbook of Medical Physiology. Tenth Edition. Philadelphia, PA, USA: W.B. Saunders Company, p. 70.

Figure 7. The Walk-Along mechanism of muscle contraction. Adapted from Guyton A.C. & Hall J.E. (2000). Contraction of skeletal muscle. In: Textbook of Medical Physiology. Tenth Edition. Philadelphia, PA, USA: W.B. Saunders Company, p. 72.

Methods

An educational biomechatronics model of the Walk-Along theory of skeletal muscle contraction had been designed and developed in this study to provide an effectual solution that audio-visually describes this mechanism to sophomore-level students in health sciences and biomedical engineering. The developed model is a 350,000x magnification of the actual sarcomere, and dynamically reproduces the sequential physiological events that take place during a muscle contraction in a faithful manner.

The model is microcontroller-based and was designed to function as follows:

i) Before muscle contraction occurs, the sarcomere is in its relaxed state, and the heads of the myosin cross-bridges bind with ATP, which is immediately cleaved into ADP and Pi due to the ATPase activity of the myosin head. At this point, both ADP and Pi remain bound to the head which assumes a perpendicular position to the adjacent actin filament, however, without binding to the active sites of the latter due to their inactivation. The hydrolysis of ATP into ADP and Pi is simulated using light-emitting diodes (LEDs) of different colors associated with name tags placed onto the surface of the myosin heads. The inhibition of the active sites on the F-actin filaments is also carried out using LEDs in the OFF state with the associated label.

ii) When muscle contraction is initiated, the sarcoplasmic reticulum releases massive amounts of calcium ions that bind with the troponin-tropomyosin complex, resulting in the uncovering of the active sites of the F-actin filament and the subsequent binding of the myosin heads with these sites. This process is energized by the release of the inorganic phosphate (Pi) from the myosin head, and results in the formation of the cross-bridges between the myosin and actin filaments. This phase is modeled by flickering a set of LEDs to simulate the release of the Ca++ ions and their attachment to the troponin C. The activation of the active sites on the F-actin filaments is then carried out using LEDs in the ON state. The depletion of the Pi bond is carried out by switching its LED to the OFF state—after completing stage iii.

iii) As each myosin head binds with its corresponding active site on the actin filament, a conformational change occurs in the former that tilts it towards the arm of the cross-bridge. This process is called the power stroke and is energized by the earlier hydrolysis of the ATP molecule. The power stroke results in pulling the actin filaments on both sides of the myosin filament towards the H band at the center of the myosin filament in a step-wise manner. This step is modeled by using two sets of servo and dc motors: one for tilting the myosin heads and one for advancing the actin filaments, respectively.

iv) When the myosin head reaches its tilting limit of the power stroke, the ADP molecule is released and is substituted with a new ATP molecule. As a result, the myosin head is detached from the actin filament, and a recovery stroke is then produced. This process is modeled by switching OFF the LEDs, representing the ADP molecules as well as those representing the active sites of the actin filaments.

v) After the completion of the recovery stroke, the myosin head returns to its original position, whereby the ATP molecule cleaves to initiate the next cycle of contraction, resulting in a new power stroke. This stage is modeled by resetting the servo motors to their initial position, and switching OFF the LEDs representing the ATP molecules while switching the LEDs, representing the ADP and Pi back to the ON state.

As long as the Ca++ is still binding to the troponin C, the process is repeated in a cyclic manner of alternating power strokes and recovery strokes. This process of muscle contraction is continuously repeated until one of three conditions arise: a) the actin filaments pull the Z discs all the way towards the ends of the myosin filaments; b) until the load carried by the muscle becomes excessively large that the muscle sarcomeres cannot perform the sliding mechanism anymore; or, c) the subjects voluntarily decides to relax the muscle which results in the withdrawal of Ca++ ions back to the sarcoplasmic reticulum.

The detailed mechanism of the Walk-Along theory of skeletal muscle contraction explained herein is provided in an audio playback feature for the student in synchrony with the actual mechanical operation of the mechatronics model which faithfully delineates the cycle of voluntary skeletal muscle contraction in a slowed-down mechanism that takes less than a minute to complete. Figure 8 depicts the functional prototype of the Biomechatronics Model of the Walk-Along Theory of Skeletal Muscle Contraction.

Figure 8. The functional prototype of the Biomechatronics Model of the Walk-Along Theory of Skeletal Muscle Contraction during testing.

STATISTICS

Nineteen sophomore-level students enrolled in the Introduction to Physiology course, in the Health Sciences and Biomedical Engineering Programs of the American University of Science and Technology, Beirut, Lebanon, were recruited to participate in the validation process of the model developed in this study, Figure 9. Subjects (17 males and 2 females) ranged in age between 18.0 and 21.5 years (Mean ± S.D. = 19.2 ± 1.0 years), and were free from any learning disabilities as examined by the university’s clinician. An agreement of consent for research subjects form approved by the Institutional Review Board was signed by each study participant prior to the testing phase.

The experimental protocol of this study consisted of two stages:

i) The study participants were gathered in the Quantitative Medical Physiology Laboratory which is free of any external distractions, and the course instructor explained the Walk-Along theory of skeletal muscle contraction in a classical manner that involved two-dimensional illustrations, for a time period of 30 minutes. Subsequently, the students were asked to sit for a 30-minute objective exam that delineates the aforementioned process in 10 major randomly shuffled stages. This exam requires each student to arrange the stages in the correct order. Subsequently, each correct stage is given one point over 10 (Appendix A).

ii) The study participants were then given a 15-minute resting period after which they were exposed to the Biomechatronics Model of the Walk-Along Theory of Skeletal Muscle Contraction for 10 minutes. Subsequently, the students were asked to sit again for the same 30-minute objective exam that delineates the aforementioned process in 10 major shuffled stages. The exam also requires each student to arrange the stages in the correct order; each correct stage is given one point over 10 (Appendix A).

In order to quantify the changes between the two study-exams, a Wilcoxon Signed Rank Test was implemented via Sigma Stat? statistical software (Systat Software Inc., San Jose, CA, USA) with a confidence interval of 95%. The study used the Signed Rank Test procedure since it is a nonparametric method that does not require assuming normality or equal variance. Such method is best suitable i) when determining if the effect of a single treatment on the same subjects is significant, and ii) when the treatment effects are not normally distributed with the same variances. These two conditions correlate well with the possible existence of inter-subject variability in the response to the effect of the educational audio-visual Biomechatronics Model of the Walk-Along Theory of Skeletal Muscle Contraction. Accordingly, the Wilcoxon Signed Rank Test was implemented in this work with the null-hypothesis that the said model has no effect on the students. Comparisons between the two objective exams were carried-out by running a paired-difference test on the investigated study metric with n = 19, where n is the size of the series signifying the correct scores obtained for each stage by the study participants in each exam. Accordingly, if the computed p-value from the two test comparisons is less than or equal to 0.05, the changes in test scores are then considered statistically significant.

Figure 9. The group of sophomore-level students participating in this study.

Results and Discussion

The results obtained from the two aforementioned assessment tests are shown in Tables 1 and 2. Each table delineates the assessment key for the corresponding 10 stages. In Table 1, subjects were anonymously labeled as n1-n19, whereas, in Table 2, subjects were anonymously labeled as N1-N19. Subjects 1-19 in Tables 1 and 2 were randomly shuffled such that subject n1 does not necessarily correspond to subject N1. Correct answers in each table were shaded in black, while incorrect answers were kept in alphabetical annotation so as to further analyze where the majority of miscomprehensions exist, and subsequently address these shortcomings in both methods of explanation. It is imperative to recognize that the subjects did not have any prior knowledge of the Walk-Along theory of skeletal muscle contraction, and that the explanation of the said mechanism using the classical approach followed by the developed Biomechatronics Model was ad hoc; moreover, the two tests were successively completed without any preparation or revision on behalf of these subjects. This fact suggests why some of the individual scores were very low—a shortcoming that is worthwhile investigating.

Table 1. Assessment results of exam 1 where the Walk-Along theory of skeletal muscle contraction was explained in a classical manner that involved two-dimensional illustrations.

Table 2. Assessment results of exam 2 where the Walk-Along theory of skeletal muscle contraction was demonstrated using the developed Biomechatronics Model.

A Shapiro-Wilk test was conducted to determine the nature of the distribution of the scores pertaining to the 10 stages of each of the two exams. The normality test failed with a value of P < 0.050, which indicates that the data in both series significantly deviate from a normal distribution, Table 3. Such finding justifies the suitability of using the Wilcoxon Signed Rank Test for this study. Moreover, Figure 10 compares the outcomes for each of the ten stages in both objective exams, namely the explanation of the Walk-Along theory of skeletal muscle contraction in a classical manner and using the Biomechatronics Model.

Table 3. Data distribution of the two study exams. Series 1 represent the scores of the 10 stages obtained from the classical explanation of the Walk-Along theory of skeletal muscle contraction. Series 2 represent the scores of the 10 stages obtained from the developed Biomechatronics Model.

Figure 10. Comparison of the two teaching methods of the Walk-Along theory of skeletal muscle contraction. The red bars indicate the scores of the 10 stages using the classical method of teaching, whereas the green bars represent the scores of the stages using the developed Biomechatronics Model.

The results obtained in this comparison reveal notable differences between the different stages of the two objective exams. These outcomes were consistent in all study participants. The comparison of group results between the two tests show statistically significant variations between the two exams in favor of the novel model introduced (P = 0.004). Hence, the change that occurred between these two trials is greater than would be expected by chance.

These results confirm the hypothesis behind this work, namely that the educational comprehensive biomechatronics automated physiological model introduced in this work better demonstrates the Walk-Along Theory of Skeletal Muscle Contraction. These results agree with those reported by Preece et al. who stated that “physical models may hold a significant advantage over alternative learning resources in enhancing visuospatial and 3D understanding of complex anatomical architecture” [43]. The results also agree with those reported by Jittivadhna et al. who posited that the “3D hand-held sarcomere model has proven to be quite efficacious in dispelling some alternative conceptions held by students previously exposed to only 2D textbook illustrations” [41].

Our future work will continue to advocate technology-enhanced learning by developing other educational physiological models that would facilitate the comprehension of the intricate underlying mechanisms required to be mastered by students of different levels and related majors. The aim of these technology-based projects is to introduce required material in a simplified audio-visual interactive manner.

Conclusions

Visual learning techniques often assist pupils to grasp concepts easily by affecting their cognitive capabilities and stimulating their imagination. Despite the use of anatomical and physiological illustrations and video animations that describe the Walk-Along theory of skeletal muscle contraction, the level of understanding by the physiology student of this intricate mechanism can be significantly augmented using technology-enhanced learning. In this regard, this study presents an Educational Biomechatronics Model of the Walk-Along Theory of Skeletal Muscle Contraction that has undergone four stages of development, namely: i) concept proof; ii) engineering prototype; iii) production prototype; and, iv) validation testing. Validation results revealed statistically significant variations—favoring the novel model introduced—within a study group who underwent two lectures and exams pertaining to the mechanism in question: i) using the classical method of teaching; and, ii) using the developed model. These results confirm the hypothesis behind this work, namely that the educational comprehensive biomechatronics automated physiological model introduced in this work better demonstrates the Walk-Along Theory of Skeletal Muscle Contraction. The developed model sheds light on the importance of continuous development of technology in classrooms, and the role of technology-enhanced learning and modeling in revolutionizing the traditional educational methods and tools.

Acknowledgements

This work was supported in part by funds from the Lebanese Industrial Research Achievements Program of the Lebanese Ministry of Industry and the Research Council of the American University of Science & Technology (AUST, Beirut, Lebanon).

Professor Ziad O. Abu-Faraj and the co-authors thank Mrs. Henriette Skaff in the Department of Languages and Translation at AUST for proof-reading this article.

About the Authors

Jad A. Al Salman holds a B.S. (2019) in Biomedical Engineering from the American University of Science and Technology, Lebanon. He is currently pursuing his higher education in Biomedical Engineering—Information Bioengineering at the Politecnico di Milano, Milan, Italy. He aims to employ his academic knowledge and practical experience to help designing novel approaches in the management of healthcare systems, through the integration of modern information technology and clinical assessment techniques.

Rafif I. Ghostine holds a B.S. (2019) in Computer and Communications Engineering with minors in Biomedical Engineering and Biomedical Sciences from the American University of Science and Technology, Lebanon. She is pursuing her Master’s degree in Telecommunication Engineering—Data Communication at the Politecnico di Milano, Milan, Italy. Her future plan is to expand her knowledge in the telecommunication field in two specific areas: design and research & development.

Elias Haddad holds a B.S. (2019) in Biomedical Engineering from the American University of Science and Technology, Lebanon. He aims to pursue his higher education in the same field. He strives to formulate strategic healthcare solutions that have direct positive impact on global cultures, societies, environment, and economy.

Tatiana S. Khoury holds a B.S. (2019) in Computer and Communications Engineering with minors in Biomedical Engineering and Biomedical Sciences from the American University of Science and Technology, Lebanon. She is currently pursuing her Master’s degree in Computer and Communications Engineering at the American University of Science and Technology, Lebanon. She strives to formulate strategic solutions that have direct impact on the betterment of human life.

Jamil J. Jabali holds a B.S. (2019) in Biomedical Engineering from the American University of Science and Technology, Lebanon. He is currently working as a Mechatronics Service Engineer with specialization in ATM hardware and software. He aims to pursue his higher education in Software and Systems Engineering, and strives to become an entrepreneur in the field of Systems Engineering.

Nabil N. Hamdan holds a B.S. (2019) in Biomedical Engineering from the American University of Science and Technology, Lebanon. He is currently working in a medical services company specialized in medical and laboratory equipment. He strives to become an entrepreneur in the field of Biomedical Engineering.

Ziad O. Abu-Faraj, Ph.D. is a Full-Professor of Biomedical Engineering. He received the B.E. degree in Electrical Engineering from the American University of Beirut-Lebanon in 1988. Specializing in Organ Investigation, Biomedical Instrumentation, and Biomechanics/Biomaterials, he obtained the M.S. and Ph.D. degrees in Biomedical Engineering from Marquette University-USA in 1991 and 1995, respectively. During 1995-1997, he served a Post-Doctorate Research Fellowship in Pediatric Motion Analysis at Shriners Hospital for Children-Chicago.

Professor Abu-Faraj is the Editor of a comprehensive two-volume research handbook in Bioengineering/Biomedical Engineering entitled “Handbook of Research on Biomedical Engineering Education and Advanced Bioengineering Learning: Interdisciplinary Concepts”, published by IGI-Global, Hershey, PA, USA in 2012 [9]. He is the lead author of a reputable number of research articles in several areas of Biomedical Engineering. His research interests are in: Humanities and Social Sciences: Sustainable Development, Science Technology and Innovation, and Fourth Industrial Revolution [45]; Epidemiology: COVID-19 [46-48]; Biomedical Science and Biomedical Engineering Education [10, 49-56]; Kinesiology and Orthopaedic Biomechanics: Physical Activity, Exercise Physiology, Human Movement Analysis, Postural Stability, Measurement of Human Performance, and Plantar Pressure Analysis [5, 8, 57-75]; Rehabilitation Science and Engineering [6-7, 76-80]; Neuroscience and Neural Engineering [81-84]; Biomedical Instrumentation and Control: Portable Microprocessor-Based Data Acquisition Systems, Biosensors, and Biocontrol Systems [4, 85-97]; Biometrics [98]; Biomedical Informatics and Biomedical Computing: Biosignals and Systems, Biostatistical Analysis, and Modeling of Physiological Systems [99-101]; Electroencephalography [100-102]; and Public Safety [103].

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[48]      Abu-Faraj ZO. Was COVID-19 used as a Litmus paper for testing 5G capabilities? LinkedIn Pulse. May 29, 2020. Available online: https://www.dhirubhai.net/pulse/covid-19-used-litmus-paper-testing-5g-capabilities-abu-faraj-1f/

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[51]      Abu-Faraj ZO. A premier comprehensive curriculum in biomedical engineering within the Middle East and Northern African region. Proceedings of the 27th Annual International Conference of the IEEE Engineering in Medicine and Biology Society, Shanghai, People Republic of China. September 1-4, 2005. 4 pp. DOI: 10.1109/IEMBS.2005.1616418

[52]      Abu-Faraj ZO. A recommended model of an undergraduate biomedical engineering curriculum for the MEDA region. Proceedings of the International Medical Informatics and Biomedical Engineering Symposium, Amman, Jordan. March 20-22, 2006:14-20.

[53]      Abu-Faraj ZO. Career development in bioengineering/biomedical engineering: A student's roadmap. Proceedings of the 30th Annual International Conference of the IEEE Engineering in Medicine and Biology Society, Vancouver, British Columbia, Canada. August 20-24, 2008:1564-1567. DOI: 10.1109/IEMBS.2008.4649469

[54]      Abu-Faraj ZO. Project Alexander the Great: A study on the world proliferation of biomedical engineering education. Proceedings of the 30th Annual International Conference of the IEEE Engineering in Medicine and Biology Society, Vancouver, British Columbia, Canada. August 20-24, 2008:2873-2876. DOI: 10.1109/IEMBS.2008.4649802

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[63]      Abu-Faraj ZO, Harris GF, Smith PA. Plantar pressure-based quantitative assessment of subtalar arthrodesis in the rehabilitation of planovalgus foot deformity. In: Harris GF and Smith PA; Editors. Foot and Ankle Motion Analysis: Clinical Treatment and Technology, First Edition, CRC Press - Taylor & Francis Group, Boca Raton, Florida, USA. 2008. pp. 105-129. ISBN: 9780849339714 - CAT# 3971

[64]      Abu-Faraj ZU, De La Fuente EK, Marx K, Montgomery S, Riedel S, Harris G. Assessment of pull-to-stand joint reactions in human subjects: Biomechanical analysis. Proceedings of the IEEE Engineering in Medicine & Biology Society, Paris, France. October 29 - November 1, 1992;14(4):1164-1165.

[65]      Harris GF, Smith PA, Abler J, Abu-Faraj Z, Millar EA. Biomechanical evaluation of the planovalgus foot in cerebral palsy: a microprocessor-based insole system. Proceedings of the 8th Annual East Coast Clinical Gait Laboratory Conference, Mayo Clinic, Rochester, MN, USA. 1993. pp. 125-126.

[66]      Abu-Faraj ZO, Sampath G, Smith PA, Harris GF. A clinical system for the analysis of three-dimensional pediatric foot and ankle motion. Proceedings of the IEEE Engineering in Medicine & Biology Society, Chicago, IL, USA.  October 30-November 2, 1997;19:1831-1834. DOI: 10.1109/IEMBS.1997.757087

[67]      Sampath G, Abu-Faraj ZO, Smith PA, Harris GF. Clinical validation of a system for the analysis of pediatric foot and ankle kinematics during gait. Proceedings of the IEEE Engineering in Medicine & Biology Society, Hong Kong. October 29-November 1, 1998;20:2418-2421. DOI: 10.1109/IEMBS.1998.744918

[68]      Abu-Faraj ZO, Harris GF, Smith PA. Quantitative assessment of the effects of subtalar arthrodesis on the planovalgus foot using three-dimensional motion analysis and plantar pressure measurements. Proceedings of the 8th Annual Meeting of the Gait and Clinical Movement Analysis Society, Wilmington, DE, USA. May 7-10, 2003. pp. 145-146.

[69]      Abu-Faraj ZO, Akar HA, Assaf EH, Al-Qadiri MN, Youssef EG. Evaluation of fall and fall recovery in a simulated seismic environment: A pilot study. Proceedings of the 32nd Annual International Conference of the IEEE Engineering in Medicine and Biology Society, Buenos Aires, Argentina. August 31-September 4, 2010. pp. 3954-3957. DOI: 10.1109/IEMBS.2010.5627696

[70]      Abu-Faraj ZO, Faraj YT, Mohtar KH, Rammal MM. Characterization of plantar pressures in visually impaired individuals: A pilot study. Proceedings of the 6th International IEEE EMBS Conference on Neural Engineering, San Diego, CA, USA. November 6-8, 2013. pp. 1549-1553. DOI: 10.1109/NER.2013.6696242

[71]      Mattar R, Diab J, Wehbe S, Merhej C, and Abu-Faraj ZO. Normative plantar pressure distribution in asymptomatic adult subjects: A pilot study. Proceedings of the Third International Conference on Advances in Biomedical Engineering, Hadat-Beirut, Lebanon. September 16-18, 2015. pp. 230-233.

[72]      Abu-Faraj ZO, Abdul-Al MM, and Al-Deeb RA. Leg length discrepancy: A study on in-shoe plantar pressure distribution. Proceedings of the 8th International Conference on BioMedical Engineering and Informatics (BMEI 2015), Shenyang, China. October 14-16, 2015. pp. 381-385. DOI: 10.1109/BMEI.2015.7401534

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[74]      Abu-Faraj ZU, Wertsch JJ, Wervey RA, Abler JH, Harris GF. Plantar pressure during stair climbing and descending. Archives of Physical Medicine and Rehabilitation. 1995;76(1):1074. DOI: 10.1016/S0003-9993(95)81318-7

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[77]      Abu-Faraj ZO, Hassani S, Harris GF. Gait analysis: A rehabilitative interdiscipline. In: Kumar S, Editor. Perspectives in Rehabilitation Ergonomics, First Edition, Taylor & Francis Ltd. Publishers, London, UK; 1997, Chapter 7, pp. 166-195. ISBN: 0 7484 0673 5

[78]      Abu-Faraj ZO, Mashaalany MJ, Bou Sleiman HC, Heneine JLD, and Al Katergi WM. Design and development of a low-cost eye tracking system for the rehabilitation of the completely locked-in patient. Proceedings of the 28th Annual International Conference of the IEEE Engineering in Medicine and Biology Society, New York City, NY, USA.  August 30-September 3, 2006. pp. 4905-4908. DOI: 10.1109/IEMBS.2006.260280

[79]      Abu-Faraj ZO, Jabbour E, Ibrahim P, Ghaoui A. Design and development of a prototype rehabilitative shoes and spectacles for the blind. Proceedings of the 5th International Conference on BioMedical Engineering and Informatics, Chongqing, People Republic of China. October 16-18, 2012. pp. 683-687. DOI: 10.1109/BMEI.2012.6513135

[80]      Boustany G, Itani AED, Youssef R, Chami O, and Abu-Faraj ZO. Design and development of a rehabilitative eye-tracking based home automation system. Proceedings of the Third Middle East Conference on Biomedical Engineering (MECBME’16), Beirut, Lebanon. October 6-7, 2016. pp. 30-33. DOI: 10.1109/MECBME.2016.7745401

[81]      Abu-Faraj ZO, Abou Rjeily DM, Bou Nasreddine RW, Andari MA, and Taok HH. A prototype retinal prosthesis for visual stimulation. Proceedings of the 29th Annual International Conference of the IEEE Engineering in Medicine and Biology Society, Lyon, France. August 23-26, 2007. pp. 5774-5777. DOI: 10.1109/IEMBS.2007.4353659

[82]      Parks TJ, Wertsch JJ, Abu-Faraj ZU. Repeatability of transcarpal median and ulnar short segment latencies: considerations in delta determination. Muscle and Nerve. 1994;17(9):1083. DOI: 10.1002/mus.880170920

[83]      Parks TJ, Roberts MM, Abu-Faraj ZU, Wertsch JJ. Premotor potentials in the normal elderly. Muscle and Nerve. 1994;17(9):1083. DOI: 10.1002/mus.880170920

[84]      Ackman JD, Abu-Faraj Z, Chambers C, Phillips B, Davids J, Hood J. Botulinum toxin treatment of dynamic deformities in an ambulatory spastic cerebral palsy population: A multi-center study.  Gait & Posture. 1998;7(2):167. DOI: 10.1016/S0966-6362(98)90245-4

[85]      Abu-Faraj ZO. A Holter type system for recording plantar pressures: Development and clinical applications. Ph.D. Dissertation, Marquette University, Milwaukee, WI, USA, 1995, 150 p., Publication Number: AAT 9600843.

[86]      Harris GF, Abu-Faraj ZU, Wertsch JJ, Abler JH, Vengsarkar AS. A Holter type system for study of plantar foot pressures. Journal of Biomedical Engineering. 1994;1:233-239. Also in Biomedical Engineering - Applications, Basis & Communications. 1995;7(4):409-415.

[87]      Abu-Faraj ZO, Harris GF, Abler JH, Smith PA, Wertsch JJ. A Holter-type microprocessor-based rehabilitation instrument for acquisition and storage of plantar pressure data in children with cerebral palsy. IEEE Transactions on Rehabilitation Engineering. 1996;4(1):33-38, March 1996. DOI: 10.1109/86.486055

[88]      Abu-Faraj ZU, De La Fuente EK, Marx K, Montgomery S, Riedel S, Harris G. Assessment of pull-to-stand joint reactions in human subjects: Design and instrumentation of an integrated system. Proceedings of the IEEE Engineering in Medicine & Biology Society, Paris, France.  October 29 - November 1, 1992;14(4):1162-1163. DOI: 10.1109/IEMBS.1992.5761972

[89]      Sampath G, Abu-Faraj ZO, Smith PA, Harris GF. Design and development of an active marker based system for analysis of 3-D pediatric foot and ankle motion. Proceedings of the IEEE Engineering in Medicine & Biology Society, Hong Kong.  October 29-November 1, 1998;20:2415-2417. DOI: 10.1109/IEMBS.1998.744916

[90]      Abu-Faraj ZU, Harris GF, Wertsch JJ, Woodbury WM, Vengsarkar AS. A data-acquisition system for monitoring skin surface temperature during nerve conduction studies. Proceedings of the IEEE Engineering in Medicine & Biology Society, San Diego, CA, USA. October 28-31, 1993;15(2):1030-1031. DOI: 10.1109/IEMBS.1993.978990

[91]      Abu-Faraj ZO, Hamdan TF, Wehbi MR, Khalil GA, and Hamdan HM. Design and development of an earthquake-simulated environment for the study of postural stability. Proceedings of the International Conference on Biomedical and Pharmaceutical Engineering, Republic of Singapore. December 11-14, 2006. pp. 188-193. ID: 9705574

[92]      Abu-Faraj ZU, Harris GF, Wertsch JJ, Abler JH, Vengsarkar AS. Holter system development for recording plantar pressures: Design and instrumentation. Proceedings of the IEEE Engineering in Medicine & Biology Society, Baltimore, MD, USA. November 3-6, 1994;16:934-935. DOI: 10.1109/IEMBS.1994.415220

[93]      Vengsarkar AS, Abler JH, Abu-Faraj ZU, Harris GF, Wertsch JJ. Holter system development for recording plantar pressures: software development. Proceedings of the IEEE Engineering in Medicine & Biology Society, Baltimore, MD, USA. November 3-6, 1994;16:936-937. DOI: 10.1109/IEMBS.1994.415221

[94]      Wervey RA, Abler JH, Abu-Faraj ZU, Harris GF, Wertsch JJ. Data preview software for interactive review of Holter type plantar pressure data. Proceedings of the IEEE Engineering in Medicine & Biology Society, Montréal, Canada. September 20-23, 1995;17:2 pp. DOI: 10.1109/IEMBS.1995.579681

[95]      Harris GF, Smith PA, Abu-Faraj ZO, Hassani S. Pediatric gait analysis: Instrumentation requirements and clinical data interpretation. Proceedings of the International Conference on Biomedical Engineering (BME '96), Hong Kong. June 3-5, 1996. pp. L9-L11.

[96]      Abu-Faraj ZO, Al Chamaa W, Al Hadchiti A, Sraj Y, and Tannous J. Design and development of a heart attack detection steering wheel. Proceedings of the 11th International Conference on BioMedical Engineering and Informatics (BMEI 2018), Beijing, China. October 13-15, 2018. 6 pp. DOI: 10.1109/CISP-BMEI.2018.8633210

[97]      Abu-Faraj ZO, Sampath G, Smith PA, Hassani S, Harris GF. A clinical system for analysis of pediatric foot and ankle motion. Abstract: Gait & Posture. 1997;5(2):149. DOI: 10.1016/S0966-6362(97)83368-1

[98]      Abu-Faraj ZO, Atie A, Chebaklo K, Khoukaz E. Fingerprint identification software for forensic applications. Proceedings of the 7th IEEE International Conference on Electronics, Circuits and Systems, Kaslik, Lebanon. December 17-20, 2000. 4 pp. DOI: 10.1109/ICECS.2000.911541

[99]      Abu-Faraj ZO, Barakat SS, Chaleby MH, Zaklit JD. A SIM card-based ubiquitous medical record bracelet/pendant system: A pilot study. Proceedings of the 4th International Conference on BioMedical Engineering and Informatics, Shanghai, People Republic of China. October 15-17, 2011. pp. 1914-1918. DOI: 10.1109/BMEI.2011.6098724

[100]    Abu-Faraj Z. Characterization of the Electroencephalogram as a Chaotic Time Series. Master Thesis Marquette University, Milwaukee, WI, USA, 1991, 115 pp.

[101]    Abu-Faraj Z, Ropella K, Myklebust J, Goldstein M. Characterization of the electroencephalogram as a chaotic time series. Proceedings of the Annual International Conference of the IEEE Engineering in Medicine and Biology Society, Orlando, FL, USA. October 31-Novemer 3, 1991;13(5):2228-2229. DOI: 10.1109/IEMBS.1991.684975

[102]    Abu-Faraj ZO. Is the term paradoxical sleep a misnomer? LinkedIn Pulse. June 17, 2020. Available online: https://www.dhirubhai.net/pulse/term-paradoxical-sleep-misnomer-prof-ziad-abu-faraj

[103]    Abu-Faraj ZO. Shattered glass is allegedly blamable for most of the victims of Beirut’s blast. LinkedIn Pulse. August 26, 2020. Available online: https://www.dhirubhai.net/pulse/shattered-glass-allegedly-blamable-most-victims-blast-abu-faraj

Appendix A

Arrange the following sentences in the correct order so as to accurately delineate the Walk-Along Mechanism of Muscle Contraction.

a)  The power stroke results in pulling the actin filaments on both sides of the myosin filament towards the H band at the center of the myosin filament in a step-wise manner.

b)  When muscle contraction is initiated, the sarcoplasmic reticulum releases massive amounts of calcium ions that bind with the troponin-tropomyosin complex, resulting in the uncovering of the active sites of the F-actin filament and the subsequent binding of the myosin heads with these sites.

c)  This process of muscle contraction is continuously repeated until one of three conditions arise: a) the actin filaments pull the Z discs all the way towards the ends of the myosin filaments; b) until the load carried by the muscle becomes excessively large that the muscle sarcomeres cannot perform the sliding mechanism anymore; or, c) the subjects voluntarily decides to relax the muscle which results in the withdrawal of Ca++ ions back to the sarcoplasmic reticulum.

d)  Before muscle contraction occurs, the sarcomere is in its relaxed state, and the heads of the myosin cross-bridges bind with ATP, which is immediately cleaved into ADP and Pi due to the ATPase activity of the myosin head.

e)  This process is energized by the release of the inorganic phosphate (Pi) from the myosin head, and results in the formation of the cross-bridges between the myosin and actin filaments.

f)   At this point, both ADP and Pi remain bound to the head which assumes a perpendicular position to the adjacent actin filament, however, without binding to the active sites of the actin filament due to their inactivation.

g)  After the completion of the recovery stroke, the myosin head returns to its original position, whereby the ATP molecule cleaves to initiate the next cycle of contraction, resulting in a new power stroke.

h)  When the myosin head reaches its tilting limit of the power stroke, the ADP molecule is released and is substituted with a new ATP molecule. As a result, the myosin head is detached from the actin filament, and a recovery stroke is then produced.

i)   As each myosin head binds with its corresponding active site on the actin filament, a conformational change occurs in the myosin head that tilts it towards the arm of the cross-bridge. This process is called the power stroke and is energized by the earlier hydrolysis of the ATP molecule.

j)   As long as the Ca++ is still binding to the troponin C, the process is repeated in a cyclic manner of alternating power strokes and recovery strokes.