Humble Beginnings
Matter is something that occupies space, some sort of physical object. Matter forms into atoms, and an electromagnetic force and chemical bonds of atoms forms in a molecule. A Molecule is simply a faction of two or more atoms. Molecules form into tissues, which job is to carry out a specific function. Tissues form a group into organs, which are a collection of tissues that joined in a unit to serve a common function. Organs cooperate to form organ systems, which becomes an organism of life.
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Macroscopic Anatomy of Bone
Bone is also known as osteo. There are two parts of skeleton; Axial and appendicular. Axial which is the central axis of skeleton, consists of the skull, vertebrae, pelvis, ribs, and sternum. The appendicular make up appendages, like the arms, legs, pelvic and shoulder girdles, as well as the hand and foot bones (Lecture, 2013).
There is a total of 206 different bones in the human body that are categorized. The four categories of bone are: long, short, flat, and irregular (Book).
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Function of Bone
Both functions metabolically and structurally. Structurally bone provides support, protection, and muscle attachment. Bone is both an organ and tissue, and structurally it is strong and light. Metabolically bone is a storage site. Fat storage is in the interior of bone, as well as minerals like calcium and phosphorous. Within the bone marrow blood cells are formed. Hematopoiesis is the production of blood cells that transpires in bone marrow. (Lecture, 2013).
Bone Matrix
In bone there is an organic and inorganic matrix, which are metabolic functions. Organic makes up 20-25% and is type 1 collagen, and bone cells. Collagen is a protein and it is a fundamental structural element of bone. Inorganic makes up 70% and is calcium hyroxyapatitie, and phosphate. 5% by body weight is made up of water (Lecture, 2013).
Bone Cells
There are four major types of bone cells.1) osteoblast: cells found along the surface of bone that build up bone and make it strong.
2) osteoclasts: cells that are responsible for the break down of old bone.
3) osteocytes: regulate bone turnover, and assist in sensing bone deformation. Think of them as more developed osteoblasts.
4) bone lining cells: detects load (stress) or the force being applied on bone.
(Lecture, 2013)
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Osteon: Major structure unit of the cortical bone, and it surrounds blood vessels.
Cortical Bone: Also known as Compact Bone; forms external portion of bone and makes up 80% of our bone tissue. Its mainly for structure and protection, and is dense tissue.
Trabecular Bone: Also known as Cancellous or Spongy Bone; less dense, soft and weaker. Allows for connective tissues, blood vessels, and bone marrow to interact with bone chemically.
Woven Bone: An immature bone that has disorganized collagen cells, which makes it weak.
Lamellar Bone: Replaces woven bone, usually after 4 years of age, and its organized cells allow it to uphold loads or forces.
(Lecture, 2013)
Bone Remodeling
Remodeling: is the process of building up and breaking down bone. Remodeling occurs since the day of birth. Simply its process is to constantly renew bone so it may preserve mineral balance and optimal durability (Lecture, 2013).
Epiphysis: end portions of bone, and provides joint surfaces that take in impact.
Diaphysis: main shaft of bone, and provides structure because of its length and surface area for tendon or muscle attachment.
Metaphysis: where growth occurs from childhood, and the site where bone remodeling transpires. Metaphysis is located between the epiphysis and the diaphysis.
(Lecture, 2013)
Mechanotransduction
Mechanotransduction is a 4 step process that allows bone adaptation to transpire . The first step; mechanocoupling: is when stress and force is detected by the sensor cells osteocytes and bone lining cells. The second step; biochemical coupling: is when cells convey the load (stress) to the nucleus. Nucleus contains most of the genetic makeup of a cell, simply put it is a cells control center. The third step; signal transmission: which involves the signaling from sensor cells that are detected by the load and delivered to the osteoblasts. The fourth step; bone cells respond: is when osteoblasts respond by making new bone, and this step is also known as the effector response. Simply put, when you participate in physical activity, you put stress on bones, which causes bone formation. The cells within detect bone formation, then signal when to stop formation (Lecture, 2013).
Hormonal Influences
Important Hormones Involved in Regulating Bone Turnover & Their Actions
Controlling Hormones (aka Calciotropic Hormones) that regulate bone turnover by controlling calcium levels in the bone and blood. They include: Calcitonin, Vitamin D, and Parathyroid.
Calcitonin: is released from the thyroid gland, and is released when blood calcium levels are high. This is done by bone, kidneys, the small intestines. Its actions: limit bone resorption (removal of old bone), increase calcium excretion (reabsorbs bone and releases calcium into blood stream) through urine, and delays calcium absorption in the intestines. Its end result is to bring blood high calcium levels back to normal.
Vitamin D: is made by the skin from ultra violet radiation, and its main function is blood calcium regulation, by increasing or decreasing blood calcium.
Parathyroid: is released when blood calcium levels are low, done by bone and kidneys. It stimulates osteoclasts for bone resorption, increases re-absorption of calcium from the kidneys, and stimulates kidneys to activate Vitamin D. Its end result is to bring low blood calcium levels back to normal.
Influencing Hormones are more complex and control a much wider range on bone. They include: Sex Hormones, Growth Hormones, Glucocorticoid Steroids, and Thyroid Stimulating Hormone.
Estrogen & Progesterone (sex hormones): increase bone formation, and decrease resorption
Testosterone (also sex hormone): increases peak bone mass in men, cortical thickness, and the width of the surface which all contribute to bones strength.
GH (growth hormone): stimulates insulin Like Growth Factor (IGF), and increases bone mineral density.
IGF-1 (Insulin Like Growth Factor)(also growth hormone): stimulates bone growth as well as an increase in bone mineral density.
Bone Maturation: thyroid hormone stimulates bone maturation which results in bone development
Osteoclasts: thyroid hormone stimulates osteoclasts which results in bone resorption.
Cortisol (glucocorticoid steroid hormone): increases bone resorption and calcium excretion through urine, decreases calcium absorption, inhibits bone formation, and decreases sex steroid production.
Factors that Impact these Hormones
Important factors that impact these hormones include age, gender, dietary intake, and genetics. Genetics influences peak bone mass by as much as 50 to 85%. Dietary intake stimulates our body depending on what nutrients we absorb and store for later usage. Men have a bio mechanical advantage because of their structural characteristics of bone, like size, shape, bone design, and bone thickness. Before puberty men and women acquire bone mass at similar rates, but after puberty men grow bone longer, faster, and obtain more skeletal and bone mass than women..
Information on Peak Bone Mass
Peak bone mass is acquired from ages 18 to 30 years of age. You have about a decade after age 30, before peak bone mass begins to decline. In men most bone mass is produced by age 20, in contrast to women who acquire most of their bone mass by 18 years of age. Declination in peak bone mass is caused by menopause in women.
Exercise
The Female Athlete Triad
The female athlete triad is an additional factor in the loss of bone mass, and includes a mixture of:
Risk Factors
According to Medicine & Science in Sports & Exercise (2005) a diet that is low in calcium and vitamin D, and a lack of weight bearing exercise are three factors that can cause osteoporosis and can be changed by you. Other factors include:
In Men
Men can develop osteoporosis as well, at least partially, to a decline in circulating testosterone levels as men age (Medicine & Science in Sports & Exercise, 2005).
Osteoporosis is diagnosed when a person’s BMD is equal to or more than 2.5 standard deviations below this reference measurement below. Osteopenia is diagnosed when the measurement is between 1 and 2.5 standard deviations below the young adult reference measurement below (iboneofhealth.org):
iofbonehealth.org offers a pretty cool risk awareness test for osteoporosis at
How to Prevent Osteoporosis
Pathophysiology of Osteoporosis
Bone maintenance is a very delicate process. In adults, daily removal of the small amounts of bone mineral, a process called resorption, and must be balanced by an equal deposition of new mineral if the strength of bone is to be maintained (Medicine & Science in Sports & Exercise, 2005). A metabolic bone disease called osteoporosis, is characterized by low bone mass, and the deterioration of bone tissue that causes bone to be more prone to injury and fracture (Dobrowolski, 2013).
Preventing Osteoporosis
Building and maintaining bone mass requires a combination of exercise and proper nutrients. Constructing bone density early on in life is the best way to combat osteoporosis later in life. The best way to uphold bone mass is the same way you build it, by adequate daily consumption adequate calcium in your diet and weight bearing exercise (Dobrowolski, 2013).Exercise
Evidence shows that exercise aids in the formation of building and sustaining bone density at pretty much any age. Studies have exhibited an increase in bone density by performing regular resistance exercises, such as lifting weights, 2 or 3 times a week for at least 30 minutes. Weight bearing exercise stimulates bone formation, as well as the retention of calcium in the bones that are bearing the load (stress). Therefore any exercise that places a force on bone will strengthen it (Medicine & Science in Sports & Exercise, 2005).
The Female Athlete Triad
The female athlete triad is an additional factor in the loss of bone mass, and includes a mixture of:
- Low energy availability from eating disorder
- Missed periods
- Weak bones
Risk Factors
According to Medicine & Science in Sports & Exercise (2005) a diet that is low in calcium and vitamin D, and a lack of weight bearing exercise are three factors that can cause osteoporosis and can be changed by you. Other factors include:
- lower body weight
- rheumatoid arthritis
- anorexia nervosa
- advanced age
- female gender
- family history of osteoporosis
- thin or small frame
- early menopause or amenorrhea
- use of corticosteroid medications
- use of anticonvulsant drugs
- diet low in calcium
- lack of exercise
- cigarette smoking
- excessive use of alcohol of caffeine
In Men
Men can develop osteoporosis as well, at least partially, to a decline in circulating testosterone levels as men age (Medicine & Science in Sports & Exercise, 2005).
Diagnostic Test
The most commonly used technique for assessing osteoporosis is a DXA (dual-energy X-ray absorptiometry) scan. As mentioned earlier, DXA is a low radiation x-ray that detects small percentages of bone loss. It is used to measure spine and hip bone density, and can also measure bone density of the whole skeleton (Dobrowolski, 2013).Osteoporosis is diagnosed when a person’s BMD is equal to or more than 2.5 standard deviations below this reference measurement below. Osteopenia is diagnosed when the measurement is between 1 and 2.5 standard deviations below the young adult reference measurement below (iboneofhealth.org):
| Status | Hip BMD |
| Normal | T-score of -1 or above |
| Osteopenia | T-score lower than -1 and greater than -2.5 |
| Osteoporosis | T-score of -2.5 or lower |
| Severe osteoporosis | T-score of -2.5 or lower, and presence of at least one fragility fracture |
http://www.iofbonehealth.org/iof-one-minute-osteoporosis-risk-test.
Muscle Development
Basic Muscle Anatomy
Mesoderm: is one of three germ layers, and is the primary germ layer in the early embryo.
Somite: block of mesoderm.
Myogenesis: embryonic muscle cell setup.
Myoblasts: premature muscle cells in the mesoderm.
Myocyte (aka Muscle Cell or Muscle Fiber): mulit-nucleated cell composed of myofibrils.
Fascicle: contain muscle cells, and are simply a bundle of muscle cells or muscle fibers.
Myofilament: filaments of myofibrils; thick (myosin) and thin (actin) filaments. Mysoin and actin are the two main protein filaments in the muscle.
Myofibril: rod-like shape in the muscle, and contains long chains of sarcomeres.
Sarcomere: is the basic unit of a muscle, it consist of long proteins actin and myosin that overlap when the muscle contracts.
Actin: the thin protein filament in muscle.
Myosin: the thick protein filament in muscle.
Myofibrillogenesis: the formation of myofibrils, that is one of the early and important steps of muscle formation.
Hyperplasia: occurs mainly during fetal development, and is the increase in muscle cell (fiber) number.
Hypertrophy: increase in the size of the cells.
Types of Muscle Contractions
Concentric: shortening of muscle, like the pulling yourself up on a pull up bar.
Eccentric: lengthening of muscle, like when you lower your arm from a bicep curl.
Isometric: muscle length and joint of angle do not change during the contraction of the muscle. This is like going down half way on a push up and holding it.
In all 3 types, the muscle is actively working
(Dobrowolski, 2013)
Description of Muscle Development
Myogenesis is the embryonic development of muscle that consists of a 4 step process:
1. Formation: when the primary germ layer (mesoderm) is formed. The formation of the 3 muscle tissues cardiac, skeletal, and smooth are made.
2. Separation: the mesoderm separates into somites (blocks). The cells of the mesoderm begin to develop vertebral column like the ribs, and skin, blood vessels, and connective tissues.
3. Proliferation: the myoblasts begin to increase in number, which ultimately join together to form one muscle.
4. Differentiation: the myoblasts differentiate into muscle tubes that fuse together, and become muscle cells or fibers.
There are 3 Different Types of Muscle:
1. Skeletal- striated muscle tissue, and are mostly attached to bones, collagen, and tendons.
2. Cardiac- striated muscle found in the walls of the heart, called myocardium.
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3. Smooth- non-striated muscle tissue, found in the walls of blood vessels, arteries, veins, eye, stomach, kidneys, respiratory tract, and aorta.
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How Muscles Grow Larger in Size
Hormones involved in Muscle growth include:
Growth Hormone (GH) & Insulin Growth Like Factor (IGF): work together as building factors.
Testosterone: promotes a training response from exercise, by stimulating myofibril hypertrophy, and the release of GH.
Insulin & Thyroid Hormone (TH): are necessary for muscle to grow in length, size, and reaching maturity.
Mechanisms of muscle hypertrophy include:
1. Mechanical Tension: exercise intensity stimulates muscle growth.
2. Muscle Damage: inflammation activates satellite cells, which are cells that can form into muscle cells and facilitate hypertrophy.
3. Metabolic Stress: elements like hydrogen and phosphate, and lactate stimulates hormonal changes.
(Dobrowolski, 2013)
Muscle Life-cycle Changes
As we age changes occur in our muscles, especially a declination in speed is exhibited by athletes. Muscle aging begins between our mid 20's to early 30's. Changes are within our muscle strength, structure, size, fiber type, contractile characteristics, and hormones. Interestingly, from the age of 20 to 80 years of age, there is a 30% reduction in the body's muscle mass (American Journal of Clinical Nutrition, 2010). The peak of muscle lost is age 30, and when muscle mass is reduced, muscle strength is reduced as well (Dobrowolski, 2013).
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Free Radical Theory of Aging
The Free Radical Theory of Aging proposes that free radical damage to our cells structure is the reason why we age. Free radicals emerge from the various chemical reactions in the body and are found in our habitat. Mitochondria produce a large amount of free radicals. Mitochondria construct the ATP (energy currency) in the body and is simply the cells energy workshop. Damage of cellular structures caused by free radicals include lipids, proteins, cell membranes, and DNA. Damage to these structures results in cell death or erroneous functions of the cells (Dobrowolski, 2013).
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Diet
Quality protein provides essential amino acids necessary for muscle protein synthesis. Essential amino acids are the building blocks for protein and is vital in muscle protein synthesis. New protein cannot be manufactured if there are no essential amino acids available. Protein not only are the building blocks to gaining muscle but also is essential for the maintenance of muscle. Quality protein sources include eggs, low-fat milk, yogurt, cheese, cottage cheese, soy based products, and legumes. Also lean meats are excellent sources of protein and essential amino acids. An intake of 1.2-1.7 grams of protein per kg of body weight per day for endurance athletes. For strength athletes, an intake of 1.5-2.0 grams per kg of body weight per day is recommended. Daily amounts depend on sport, type of training, as well as the desire to maintain or increase muscle mass (Dunford & Doyle, 2013).
Vitamin D functions to stimulate muscle cell proliferation and growth. Vitamin D also prevents bone loss, and regulates blood calcium, and increases calcium absorption. Vitamin is known for regulating skeletal, cardiac, and smooth muscle tissue, and aids in the prevention of many diseases like osteoporosis. Food sources high in Vitamin D include milk, yogurt, direct sunlight, beef, fatty fish, green vegetables, and mushrooms exposed to UV light. For adults, recommended intake a day is 600-800 IU. Some studies suggest a much higher dose of 2,000 IU is for adults. Athletes should consume 800-2000 International Units (IU) daily, and 5-30 minutes of ultra violet (sunlight) exposure usually between 10am-3pm twice a week. Exposure to sunlight is important because Vitamin D is synthesized in the body from sunlight exposure (Dunford & Doyle, 2013).
Antioxidants are believed to slow the process of aging by inhibiting the chemical reactions that transfers electrons from a process or a reaction called oxidation. This is important because these reactions create free radicals that can start a chain of reactions, causing death to cells. Foods sources high in antioxidants include cranberries, blueberries, strawberries, blackberries, red, kidney and pinto beans, artichoke, sweet potatoes and russet potatoes, walnuts, pistachios and pecans (Dobrowolski, 2013).
Lifestyle Steps
Strength training for athletes is extremely beneficial because it causes adaptations in the muscle that help with growth, maintenance, and decreasing prevention rate of injury. An adaption commonly seen is neural, which are just in the first few weeks of exercising and is responsible for the various stimulus that travel throughout the muscle like allowing the body to carry a heavier load during exercise. Another is the growth of individual muscle cells, which is called hypertrophy. An increase in anaerobic enzymes, which speed up the rate of reactions in the body, specifically the energy system that does not need oxygen to produce energy. The last adaptation due to resistance training is the conversion of type I fiber to type II fibers, which is important for strength athletes because this cells work in both the aerobic and anaerobic energy systems. As we age there is a substantial loss in type II fibers in comparison to type I, and strength training counters this decline, by increasing the type II muscle fibers. Type I fibers aka slow twitch, metabolize energy using oxygen. type IIa fibers aka intermediate, metabolize energy both with and without oxygen. Lastly type IIb fibers, mostly metabolize energy without oxygen and has the fastest contraction speed among the three muscle fibers (Dobrowolski, 2013).
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