Musculoskeletal System for the DAT
/Learn key DAT concepts related to muscle types, contraction, bone structure, and skin structure, plus practice questions and answers
everything you need to know about the musculoskeletal system for the dat
Table of Contents
Part 1: Introduction to the musculoskeletal system
Part 2: Types of muscle
Part 3: Muscle contraction
Part 4: Additional connective elements
a) Bone structure
b) Bone maintenance
c) Ossification
d) Tendons, ligaments, cartilage, and joints
Part 5: Skin
a) Structure
b) Glands
c) Homeostasis
Part 6: High-yield terms
Part 7: Questions and answers
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Part 1: Introduction to the musculoskeletal system
Understanding the musculoskeletal system is pivotal as it both sustains the body and enables movement. A comprehensive grasp of its structure and the typical mechanisms of muscle contraction is essential. This guide will teach you all you need to know for the DAT. In order to retain content, make note of any bolded terms.
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Part 2: Types of muscle
The body houses diverse muscle types, each with distinct characteristics and functions. We'll explore three main types: skeletal, cardiac, and smooth muscle.
Skeletal muscle drives voluntary movement, controlled consciously by the somatic nervous system. Identified by their striated appearance and multiple nuclei, these muscles contain two fiber types—slow-twitch (type I) and fast-twitch (type II). These fiber types differ in their contractile velocity, or how quick they can contract to produce movement. Slow-twitch fibers, rich in myoglobin and mitochondria, contract slowly but resist fatigue. Conversely, fast-twitch fibers contract rapidly but fatigue quickly due to lower myoglobin levels.
Fatigue in skeletal muscles arises from oxygen debt, a mismatch between oxygen required for ATP energy production and available oxygen through breathing.
Skeletal muscle contractions facilitate fluid movement, aiding blood and lymph circulation by 'squeezing' surrounding vessels.
The fundamental unit of skeletal muscle, the sarcomere, comprises thick (myosin) and thin (actin) protein filaments. These thick and thin filaments interweave with each other in what is called the contractile apparatus. Troponin and tropomyosin assist actin and myosin in muscle contraction. Sarcoplasmic reticulum, housing Ca²⁺ ions, plays a crucial role in this process.
FIGURE 1: LABELED SARCOMERE
Smooth muscle—regulated by the autonomic nervous system—operates involuntarily and lines essential organs like the digestive tract, bladder, uterus, and blood vessels. Smooth muscle facilitates material transport through peristalsis. Unlike skeletal muscle, smooth muscle lacks the organized sarcomeres of myosin and actin fibers. Remarkably, it exhibits myogenic activity, meaning it contracts without nervous system input. This myogenic activity often gives rise to the notion of a "second brain" in the gut. Additionally, smooth muscles lack striations and have a single nucleus at their core.
In contrast, cardiac muscle is unique to the heart and shares attributes with both skeletal and smooth muscle. It's striated and comprised of sarcomeres similar to skeletal muscle, yet it functions involuntarily, with each cell housing a single nucleus. The interconnectedness of cardiac muscle cells through intercalated discs, packed with gap junctions, allows rapid ion flow and swift propagation of action potentials. This unique feature promotes synchronized contraction, unlike neuron action potentials that require sequential signal propagation.
Cardiac muscle cells also exhibit myogenic activity that governs the heart's rhythm independently of the brain. This rhythmic activity originates from a distinct cluster of specialized cells located at the heart's apex, termed the sinoatrial node (SA node). From here, electrical signals spread across the heart, initiating muscle contractions. Progressing through the atrioventricular (AV) node and the Bundle of His, these signals finally disseminate via the Purkinje fibers, situated within the ventricular walls, thereby prompting the contraction of cardiac muscle.
FIGURE 2: FLOW OF ELECTRICITY THROUGH THE HEART
| Skeletal | Smooth | Cardiac |
|---|---|---|
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Part 3: Muscle contraction
Muscle fibers house both thin and thick filaments, also known as actin and myosin, which drive skeletal muscle contractions through the actin-myosin crossbridge cycle.
Before this cycle begins, a signal from the somatic nervous system travels through motor neurons to the junction between the nerve terminal and the muscle fiber, known as the neuromuscular junction's motor endplate.
At this junction, the nervous system's motor neurons interact with muscles through a chemical synapse. Activation of an axon in the somatic nervous system prompts the release of acetylcholine into the synaptic cleft. Acetylcholine binds to the sarcolemma of the receiving muscle cell, initiating ion channel opening, depolarization, and subsequent action potential propagation through T-tubules. These actions facilitate the release of stored Ca²⁺ ions from the sarcoplasmic reticulum.
At rest, actin and myosin in muscle cells typically interact with additional large proteins—tropomyosin and troponin. Tropomyosin normally shields the myosin-binding sites on actin in the muscle's noncontractile state. However, the release of Ca2+ from the sarcoplasmic reticulum triggers troponin to bind with it, causing a structural shift in tropomyosin. This alteration exposes the myosin binding site on actin, essentially enabling the formation of the actin-myosin crossbridge.
FIGURE 3: CA2+ IONS HELP IN INITIATING THE ACTIN-MYOSIN CROSSBRIDGE CYCLE
FIGURE 4: ACTION POTENTIAL PROPAGATION AT THE NEUROMUSCULAR JUNCTION. (1) ACTION POTENTIAL TRAVELS DOWN AXON AND ACETYLCHOLINE IS RELEASED INTO SYNAPTIC CLEFT. (2) ACETYLCHOLINE BINDS TO SARCOLEMMA, OPENING ION CHANNELS AND PROPAGATING ACTION POTENTIAL THROUGH T-TUBULES.
Once exposed, the myosin head undergoes a power stroke. The power stroke is propelled by the release of ADP and inorganic phosphate from ATP, enabling the myosin to pull along the actin filament. Repeated power strokes of multiple myosin heads lead to sarcomere shortening.
Post-power stroke, ATP binds to the myosin head, detaching it from actin. Tropomyosin promptly recovers the binding site. ATP hydrolysis enables the myosin head to return to its initial high-energy position, beginning the cycle anew.
FIGURE 5: ACTIN-MYOSIN CROSSBRIDGE CYCLE. (1) RESTING STATE; MYOSIN HEAD ALREADY COCKED BACK IN HIGH-ENERGY POSITION. (2) CA2+ BINDS TO TROPONIN TO EXPOSE THE BINDING SITE. (3) POWER STROKE; CONTRACTION. ADP + PI DISSOCIATE. (4) NEW ATP BINDS TO MYOSIN. MYOSIN DETACHES FROM ACTIN, CA2+ DETACHES FROM TROPONIN. (5) HYDROLYSIS OF ATP; RESETTING OF MYOSIN HEAD
Muscle function is governed by the nervous system, with voluntary movements managed by the somatic nervous system and involuntary movements, such as shivering that assists in thermoregulation, controlled by the autonomic nervous system. The autonomic nervous system orchestrates sympathetic (e.g., dilation of blood vessel smooth muscle and slowed digestive tract) and parasympathetic responses (e.g., opposing effects), regulating innervated muscle behaviors.
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