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Fundamentals of Anatomy and Physiology: 10.6 Exercise, Nutrition, Hormones and Bone Tissue

Fundamentals of Anatomy and Physiology
10.6 Exercise, Nutrition, Hormones and Bone Tissue
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table of contents
  1. Cover
  2. Title Page
  3. Copyright
  4. Table Of Contents
  5. About the Authors
  6. Acknowledgments
  7. Preface
  8. Levels of Organisation, Homeostasis and Nomenclature
    1. 1.1 Overview of Anatomy and Physiology
    2. 1.2 Structural Organisation of the Human Body
    3. 1.3 Homeostasis
    4. 1.4 Anatomical Terminology
  9. Cells and Reproduction
    1. 2.1 Synthesis of Biological Macromolecules
    2. 2.2 Carbohydrates
    3. 2.3 Lipids
    4. 2.4 Protein
    5. 2.5 Nucleic Acid
    6. 2.6 The Cell Membrane
    7. 2.7 The Cytoplasm and Cellular Organelles
    8. 2.8 The Nucleus and DNA Replication
    9. 2.9 Protein Synthesis
    10. 2.10 Cell Growth and Division
    11. 2.11 Cellular Differentiation
  10. Tissues, Organs, Systems
    1. 3.1 Types of Tissues
    2. 3.2 Epithelial Tissue
    3. 3.3 Connective Tissue Supports and Protects
    4. 3.4 Muscle Tissue and Motion
    5. 3.5 Nervous Tissue Mediates Perception and Response
    6. 3.6 Tissue Injury and Ageing
  11. Integumentary System
    1. 4.1 Layers of the Skin
    2. 4.2 Accessory Structures of the Skin
    3. 4.3 Functions of the Integumentary System
    4. 4.4 Diseases, Disorders and Injuries of the Integumentary System
  12. Blood
    1. 5.1 An Overview of Blood
    2. 5.2 Production of the Formed Elements
    3. 5.3 Erythrocytes
    4. 5.4 Leukocytes and Platelets
    5. 5.5 Haemostasis
    6. 5.6 Blood Typing
  13. Cardiovascular System
    1. 6.1 Heart Anatomy
    2. 6.2 Cardiac Muscle and Electrical Activity
    3. 6.3 Cardiac Cycle
    4. 6.4 Cardiac Physiology
    5. 6.5 Development of the Heart
    6. 6.6 Structure and Function of Blood Vessels
    7. 6.7 Blood Flow, Blood Pressure and Resistance
    8. 6.8 Capillary Exchange
    9. 6.9 Homeostatic Regulation of the Vascular System
    10. 6.10 Circulatory Pathways
    11. 6.11 Development of Blood Vessels and Foetal Circulation
  14. Lymphatic System and Immunity
    1. 7.1 Anatomy of the Lymphatic and Immune Systems
    2. 7.2 Barrier Defences and the Innate Immune Response
    3. 7.3 The Adaptive Immune Response: T Lymphocytes and their Functional Types
    4. 7.4 The Adaptive Immune Response: B-Lymhocytes and Antibodies
    5. 7.5 The Immune Response Against Pathogens
    6. 7.6 Diseases Associated with Depressed or Overactive Immune Responses
    7. 7.7 Transplantation and Cancer Immunology
  15. Respiratory System
    1. 8.1 Organs and Structures of the Respiratory System
    2. 8.2 The Lungs
    3. 8.3 The Process of Breathing
    4. 8.4 Gas Exchange
    5. 8.5 Transport of Gases
    6. 8.6 Modifications in Respiratory Functions
    7. 8.7 Embryonic Development of the Respiratory System
  16. Muscle System
    1. 9.1 Overview of Muscle Tissues
    2. 9.2 Skeletal Muscle
    3. 9.3 Muscle Fibre Contraction and Relaxation
    4. 9.4 Nervous System Control of Muscle Tension
    5. 9.5 Types of Muscle Fibres
    6. 9.6 Exercise and Muscle Performance
    7. 9.7 Cardiac Muscle Tissue
    8. 9.8 Smooth Muscle
    9. 9.9 Development and Regeneration of Muscle Tissue
  17. Skeletal System
    1. 10.1 The Functions of the Skeletal System
    2. 10.2 Bone Classification
    3. 10.3 Bone Structure
    4. 10.4 Bone Formation and Development
    5. 10.5 Fractures: Bone Repair
    6. 10.6 Exercise, Nutrition, Hormones and Bone Tissue
    7. 10.7 Calcium Homeostasis: Interactions of the Skeletal System and Other Organ Systems
    8. 10.8 Divisions of the Skeletal System
    9. 10.9 The Skull
    10. 10.10 The Vertebral Column
    11. 10.11 The Thoracic Cage
    12. 10.12 Embryonic Development of the Axial Skeleton
  18. Musculoskeletal System
    1. 11.1 The Pectoral Girdle
    2. 11.2 Bones of the Upper Limb
    3. 11.3 The Pelvic Girdle and Pelvis
    4. 11.4 Bones of the Lower Limb
    5. 11.5 Development of the Appendicular Skeleton
    6. 11.6 Classification of Joints
    7. 11.7 Fibrous Joints
    8. 11.8 Cartilaginous Joints
    9. 11.9 Synovial Joints
    10. 11.10 Types of Body Movements
    11. 11.11 Anatomy of Selected Synovial Joints
    12. 11.12 Development of Joints
  19. Digestive System
    1. 12.1 Overview of the Digestive System
    2. 12.2 Digestive System Processes and Regulation
    3. 12.3 The Mouth, Pharynx and Oesophagus
    4. 12.4 The Stomach
    5. 12.5 The Small and Large Intestines
    6. 12.6 Accessory Organs in Digestion: the Liver, Pancreas and Gallbladder
    7. 12.7 Chemical Digestion and Absorption
  20. Nervous System
    1. 13.1 Basic Structure and Function of the Nervous System
    2. 13.2 Nervous Tissue
    3. 13.3 The Function of Nervous Tissue
    4. 13.4 The Action Potential
    5. 13.5 Communication between Neurons
    6. 13.6 The Embyrologic Perspective
    7. 13.7 The Central Nervous System
    8. 13.8 Circulation and the Central Nervous System
    9. 13.9 The Peripheral Nervous System
    10. 13.10 Sensory Perception
    11. 13.11 Central Processing
    12. 13.12 Motor Responses
  21. Endocrine System
    1. 14.1 An Overview of the Endocrine System
    2. 14.2 Hormones
    3. 14.3 The Pituitary Gland and Hypothalamus
    4. 14.4 The Thyroid Gland
    5. 14.5 The Parathyroid Glands
    6. 14.6 The Adrenal Glands
    7. 14.7 The Pineal Gland
    8. 14.8 Gonadal and Placental Hormones
    9. 14.9 The Endocrine Pancreas
    10. 14.10 Organs with Secondary Endocrine Functions
    11. 14.11 Development and Ageing of the Endocrine System
  22. Reproductive System
    1. 15.1 Anatomy and Physiology of the Male Reproductive System
    2. 15.2 Anatomy and Physiology of the Female Reproductive System
    3. 15.3 Development of the Male and Female Reproductive Systems
  23. Pregnancy and Human Development
    1. 16.1 Fertilisation
    2. 16.2 Embryonic Development
    3. 16.3 Foetal Development
  24. Urinary System
    1. 17.1 Physical Characteristics of Urine
    2. 17.2 Gross Anatomy of Urine Transport
    3. 17.3 Gross Anatomy of the Kidney
    4. 17.4 Microscopic Anatomy of the Kidney
    5. 17.5 Physiology of Urine Formation
    6. 17.6 Tubular Reabsorption
    7. 17.7 Regulation of Renal Blood Flow
    8. 17.8 Endocrine Regulation of Kidney Function
    9. 17.9 Regulation of Fluid Volume and Composition
    10. 17.10 The Urinary System and Homeostasis
    11. 17.11 Body Fluids and Fluid Compartments
    12. 17.12 Water Balance
    13. 17.13 Electrolyte Balance
    14. 17.14 Acid-Base Balance
    15. 17.15 Disorders of Acid-Base Balance
  25. Appendix A: Unit Measurements and Calculations
  26. Appendix B: Chemical Abbreviations
  27. Glossary
  28. Bibliography

10.6 Exercise, Nutrition, Hormones and Bone Tissue

Learning Objectives

By the end of this section, you will be able to:

  • Describe the effect exercise has on bone tissue
  • List the nutrients that affect bone health
  • Discuss the role those nutrients play in bone health
  • Describe the effects of hormones on bone tissue

All the organ systems of your body are interdependent, and the skeletal system is no exception. The food you take in via your digestive system and the hormones secreted by your endocrine system affect your bones. Even using your muscles to engage in exercise has an impact on your bones.

Exercise and Bone Tissue

During long space missions, astronauts can lose approximately 1 to 2 percent of their bone mass per month. This loss of bone mass is thought to be caused by the lack of mechanical stress on astronauts’ bones due to the low gravitational forces in space. Lack of mechanical stress causes bones to lose mineral salts and collagen fibres, and thus strength. Similarly, mechanical stress stimulates the deposition of mineral salts and collagen fibres. The internal and external structure of a bone will change as stress increases or decreases so that the bone is an ideal size and weight for the amount of activity it endures. That is why people who exercise regularly have thicker bones than people who are more sedentary. It is also why a broken bone in a cast atrophies while its contralateral mate maintains its concentration of mineral salts and collagen fibres. The bones undergo remodelling because of forces (or lack of forces) placed on them.

Numerous, controlled studies have demonstrated that people who exercise regularly have greater bone density than those who are more sedentary. Any type of exercise will stimulate the deposition of more bone tissue, but resistance training has a greater effect than cardiovascular activities. Resistance training is especially important to slow down the eventual bone loss due to ageing and for preventing osteoporosis.

Nutrition and Bone Tissue

The vitamins and minerals contained in all the food we consume are important for all our organ systems. However, there are certain nutrients that affect bone health.

Calcium and Vitamin D

You already know that calcium is a critical component of bone, especially in the form of calcium phosphate and calcium carbonate. Since the body cannot make calcium, it must be obtained from the diet. However, calcium cannot be absorbed from the small intestine without vitamin D. Therefore, intake of vitamin D is also critical to bone health. In addition to vitamin D’s role in calcium absorption, it also plays a role, though not as clearly understood, in bone remodelling.

Milk and other dairy foods are not the only sources of calcium. This important nutrient is also found in green leafy vegetables, broccoli, and intact salmon and canned sardines with their soft bones. Nuts, beans, seeds, and shellfish provide calcium in smaller quantities.

Except for fatty fish like salmon and tuna, or fortified milk or cereal, vitamin D is not found naturally in many foods. The action of sunlight on the skin triggers the body to produce its own vitamin D (Figure 10.6.1), but many people, especially those of darker complexion and those living in northern latitudes where the sun’s rays are not as strong, are deficient in vitamin D. In cases of deficiency, a doctor can prescribe a vitamin D supplement.

Diagram of vitamin D synthesis
Figure 10.6.1. Synthesis of vitamin D. Sunlight is one source of vitamin D.

Other Nutrients

Vitamin K also supports bone mineralisation and may have a synergistic role with vitamin D in the regulation of bone growth. Green leafy vegetables are a reliable source of vitamin K.

The minerals magnesium and fluoride may also play a role in supporting bone health. While magnesium is only found in trace amounts in the human body, more than 60 percent of it is in the skeleton, suggesting it plays a role in the structure of bone. Fluoride can displace the hydroxyl group in bone’s hydroxyapatite crystals and form fluorapatite. Like its effect on dental enamel, fluorapatite helps stabilise and strengthen bone mineral. Fluoride can also enter spaces within hydroxyapatite crystals, thus increasing their density.

Omega-3 fatty acids have long been known to reduce inflammation in various parts of the body. Inflammation can interfere with the function of osteoblasts, so consuming omega-3 fatty acids, in the diet or in supplements, may also help enhance production of new osseous tissue. Table 10.6.1summarises the role of nutrients in bone health.

Table 10.6.1. Nutrients and bone health

NutrientRole in bone health
CalciumNeeded to make calcium phosphate and calcium carbonate, which form the hydroxyapatite crystals that give bone its hardness
Vitamin DNeeded for calcium absorption
Vitamin KSupports bone mineralisation; may have synergistic effects with vitamin D
MagnesiumStructural component of bone
FluorideStructural component of bone
Omega-3 fatty acidsReduces inflammation that may interfere with osteoblast function

Hormones and Bone Tissue

The endocrine system produces and secretes hormones, many of which interact with the skeletal system. These hormones are involved in controlling bone growth, maintaining bone once it is formed, and remodelling it.

Hormones that influence Osteoblasts and/or Maintain the Matrix

Several hormones are necessary for controlling bone growth and maintaining the bone matrix. The pituitary gland secretes growth hormone (GH), which, as its name implies, controls bone growth in several ways. It triggers chondrocyte proliferation in epiphyseal plates, resulting in the increasing length of long bones. GH also increases calcium retention, which enhances mineralisation, and stimulates osteoblastic activity, which improves bone density.

GH is not alone in stimulating bone growth and maintaining osseous tissue. Thyroxine, a hormone secreted by the thyroid gland promotes osteoblastic activity and the synthesis of bone matrix. During puberty, the sex hormones (oestrogen in girls, testosterone in boys) also come into play. They too promote osteoblastic activity and production of bone matrix, and in addition, are responsible for the growth spurt that often occurs during adolescence. They also promote the conversion of the epiphyseal plate to the epiphyseal line (i.e., cartilage to its bony remnant), thus bringing an end to the longitudinal growth of bones. Additionally, calcitriol, the active form of vitamin D, is produced by the kidneys and stimulates the absorption of calcium and phosphate from the digestive tract.

Ageing and the Skeletal System

Osteoporosis is a disease characterised by a decrease in bone mass that occurs when the rate of bone resorption exceeds the rate of bone formation, a common occurrence as the body ages. Notice how this is different from Paget’s disease. In Paget’s disease, new bone is formed to keep up with the resorption by the overactive osteoclasts, but that new bone is produced haphazardly. In fact, when a physician is evaluating a patient with thinning bone, they will typically test for osteoporosis and Paget’s disease (as well as other diseases). Osteoporosis does not have the elevated blood levels of alkaline phosphatase found in Paget’s disease.

Graph showing relationship between age and bone mass.
Figure 10.6.2. Graph showing relationship between age and bone mass. Bone density peaks at about 30 years of age. Women lose bone mass more rapidly than men.

While osteoporosis can involve any bone, it most commonly affects the proximal ends of the femur, vertebrae, and wrist. As a result of the loss of bone density, the osseous tissue may not provide adequate support for everyday functions, and something as simple as a sneeze can cause a vertebral fracture. When an elderly person falls and breaks a hip (really, the femur), it is very likely the femur that broke first, which resulted in the fall. Histologically, osteoporosis is characterised by a reduction in the thickness of compact bone and the number and size of trabeculae in cancellous bone.

Figure 10.6.2 shows that women lose bone mass more quickly than men starting at about 50 years of age. This occurs because 50 is the approximate age at which women go through menopause. Not only do their menstrual periods lessen and eventually cease, but their ovaries reduce in size and then cease the production of oestrogen, a hormone that promotes osteoblastic activity and production of bone matrix. Thus, osteoporosis is more common in women than in men, but men can develop it, too. Anyone with a family history of osteoporosis has a greater risk of developing the disease, so the best treatment is prevention, which should start with a childhood diet that includes adequate intake of calcium and vitamin D and a lifestyle that includes weight-bearing exercise. These actions, as discussed above, are important in building bone mass. Promoting proper nutrition and weight-bearing exercise early in life can maximise bone mass before the age of 30, thus reducing the risk of osteoporosis.

For many elderly people, a hip fracture can be life threatening. The fracture itself may not be serious, but the immobility that comes during the healing process can lead to the formation of blood clots that can lodge in the capillaries of the lungs, resulting in respiratory failure; pneumonia due to the lack of poor air exchange that accompanies immobility; pressure sores (bed sores) that allow pathogens to enter the body and cause infections; and urinary tract infections from catheterisation.

Current treatments for managing osteoporosis include bisphosphonates (the same medications often used in Paget’s disease), calcitonin, and oestrogen (for women only). Minimising the risk of falls, for example, by removing tripping hazards, is also an important step in managing the potential outcomes from the disease.

Hormones That Influence Osteoclasts

Bone modelling and remodelling require osteoclasts to resorb unneeded, damaged, or old bone, and osteoblasts to lay down new bone. Two hormones that affect the osteoclasts are parathyroid hormone (PTH) and calcitonin.

PTH stimulates osteoclast proliferation and activity. As a result, calcium is released from the bones into the circulation, thus increasing the calcium ion concentration in the blood. PTH also promotes the reabsorption of calcium by the kidney tubules, which can affect calcium homeostasis (see below).

The small intestine is also affected by PTH, albeit indirectly. Because another function of PTH is to stimulate the synthesis of vitamin D, and because vitamin D promotes intestinal absorption of calcium, PTH indirectly increases calcium uptake by the small intestine. Calcitonin, a hormone secreted by the thyroid gland, has some effects that counteract those of PTH. Calcitonin inhibits osteoclast activity and stimulates calcium uptake by the bones, thus reducing the concentration of calcium ions in the blood. As evidenced by their opposing functions in maintaining calcium homeostasis, PTH and calcitonin are generally not secreted at the same time. Table 10.6.2 summarises the hormones that influence the skeletal system.

Table 10.6.2 Hormones That Affect the Skeletal System

HormoneRole
Growth hormoneIncreases length of long bones, enhances mineralisation, and improves bone density
ThyroxineStimulates bone growth and promotes synthesis of bone matrix
Sex hormonesPromote osteoblastic activity and production of bone matrix; responsible for adolescent growth spurt; promote conversion of epiphyseal plate to epiphyseal line
CalcitriolStimulates absorption of calcium and phosphate from digestive tract
Parathyroid hormoneStimulates osteoclast proliferation and resorption of bone by osteoclasts; promotes reabsorption of calcium by kidney tubules; indirectly increases calcium absorption by small intestine
CalcitoninInhibits osteoclast activity and stimulates calcium uptake by bones

Section Review

Mechanical stress stimulates the deposition of mineral salts and collagen fibres within bones. Calcium, the predominant mineral in bone, cannot be absorbed from the small intestine if vitamin D is lacking. Vitamin K supports bone mineralisation and may have a synergistic role with vitamin D. Magnesium and fluoride, as structural elements, play a supporting role in bone health. Omega-3 fatty acids reduce inflammation and may promote production of new osseous tissue. Growth hormone increases the length of long bones, enhances mineralisation, and improves bone density. Thyroxine stimulates bone growth and promotes the synthesis of bone matrix. The sex hormones (oestrogen in women; testosterone in men) promote osteoblastic activity and the production of bone matrix, are responsible for the adolescent growth spurt, and promote closure of the epiphyseal plates. Osteoporosis is a disease characterised by decreased bone mass that is common in ageing adults. Calcitriol stimulates the digestive tract to absorb calcium and phosphate. Parathyroid hormone (PTH) stimulates osteoclast proliferation and resorption of bone by osteoclasts. Vitamin D plays a synergistic role with PTH in stimulating the osteoclasts. Additional functions of PTH include promoting reabsorption of calcium by kidney tubules and indirectly increasing calcium absorption from the small intestine. Calcitonin inhibits osteoclast activity and stimulates calcium uptake by bones.

Review Questions

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Critical Thinking Questions

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10.7 Calcium Homeostasis: Interactions of the Skeletal System and Other Organ Systems
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Copyright © 2021 by University of Southern Queensland Fundamentals of Anatomy and Physiology by University of Southern Queensland is licensed under a Creative Commons Attribution-ShareAlike 4.0 International License, except where otherwise noted.
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