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Fundamentals of Anatomy and Physiology: 9.6 Exercise and Muscle Performance

Fundamentals of Anatomy and Physiology
9.6 Exercise and Muscle Performance
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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

9.6 Exercise and Muscle Performance

Learning Objectives

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

  • Describe hypertrophy and atrophy
  • Explain how resistance exercise builds skeletal muscle
  • Explain how performance-enhancing substances affect muscle

Physical training alters the appearance of skeletal muscles and can produce changes in muscle performance. Conversely, a lack of use can result in decreased performance and muscle appearance. Although muscle cells can change in size, new cells are not formed when muscles grow. Instead, structural proteins are added to muscle fibres in a process called hypertrophy, so cell diameter increases. The reverse, when structural proteins are lost and muscle mass decreases, is called atrophy. Age-related muscle atrophy is called sarcopenia. Cellular components of muscles can also undergo changes in response to changes in muscle use.

Endurance Exercise

Slow fibres are predominantly used in endurance exercises that require little force but involve numerous repetitions. The aerobic metabolism used by slow-twitch fibres allows them to maintain contractions over long periods. Endurance training modifies these slow fibres to make them even more efficient by producing more mitochondria to enable more aerobic metabolism and more ATP production. Endurance exercise can also increase the amount of myoglobin in a cell, as increased aerobic respiration increases the need for oxygen. Myoglobin is found in the sarcoplasm and acts as an oxygen storage supply for the mitochondria.

The training can trigger the formation of more extensive capillary networks around the fibre, a process called angiogenesis, to supply oxygen and remove metabolic waste. To allow these capillary networks to supply the deep portions of the muscle, muscle mass does not greatly increase in order to maintain a smaller area for the diffusion of nutrients and gases. All these cellular changes result in the ability to sustain low levels of muscle contractions for greater periods without fatiguing.

The proportion of SO muscle fibres in muscle determines the suitability of that muscle for endurance and may benefit those participating in endurance activities. Postural muscles have a large number of SO fibres and relatively few FO and FG fibres, to keep the back straight (Figure 9.6.1). Endurance athletes, like marathon-runners also would benefit from a larger proportion of SO fibres, but it is unclear if the most-successful marathoners are those with naturally high numbers of SO fibres, or whether the most successful marathon runners develop high numbers of SO fibres with repetitive training. Endurance training can result in overuse injuries such as stress fractures and joint and tendon inflammation.

Photo of mararthon runners
Figure 9.6.1. Marathoners. Long-distance runners have many SO fibres and relatively few FO and FG fibres. (credit: “Tseo2”/Wikimedia Commons).

Resistance Exercise

Resistance exercises, as opposed to endurance exercise, require large amounts of FG fibres to produce short, powerful movements that are not repeated over long periods. The high rates of ATP hydrolysis and cross-bridge formation in FG fibres result in powerful muscle contractions. Muscles used for power have a higher ratio of FG to SO/FO fibres, and trained athletes possess even higher levels of FG fibres in their muscles. Resistance exercise affects muscles by increasing the formation of myofibrils, thereby increasing the thickness of muscle fibres. This added structure causes hypertrophy, or the enlargement of muscles, exemplified by the fibres skeletal muscles seen in body builders and other athletes (Figure 9.6.2). Because this muscular enlargement is achieved by the addition of structural proteins, athletes trying to build muscle mass often ingest large amounts of protein.

Muscle man
Figure 9.6.2. Hypertrophy. Body builders have many FG fibres and relatively few FO and SO fibres. (credit: Lin Mei/flickr).

Except for the hypertrophy that follows an increase in the number of sarcomeres and myofibrils in a skeletal muscle, the cellular changes observed during endurance training do not usually occur with resistance training. There is usually no significant increase in mitochondria or capillary density. However, resistance training does increase the development of connective tissue, which adds to the overall mass of the muscle and helps to contain muscles as they produce increasingly powerful contractions. Tendons also become stronger to prevent tendon damage, as the force produced by muscles is transferred to tendons that attach the muscle to bone.

For effective strength training, the intensity of the exercise must continually be increased. For instance, continued weightlifting without increasing the weight of the load does not increase muscle size. To produce ever-greater results, the weights lifted must become increasingly heavier, making it more difficult for muscles to move the load. The muscle then adapts to this heavier load, and an even heavier load must be used if even greater muscle mass is desired.

If done improperly, resistance training can lead to overuse injuries of the muscle, tendon, or bone. These injuries can occur if the load is too heavy or if the muscles are not given sufficient time between workouts to recover or if joints are not aligned properly during the exercises. Cellular damage to muscle fibres that occurs after intense exercise includes damage to the sarcolemma and myofibrils. This muscle damage contributes to the feeling of soreness after strenuous exercise, but muscles gain mass as this damage is repaired, and additional structural proteins are added to replace the damaged ones. Overworking skeletal muscles can also lead to tendon damage and even skeletal damage if the load is too great for the muscles to bear.

Performance-Enhancing Substances

Some athletes attempt to boost their performance by using various agents that may enhance muscle performance. Anabolic steroids are one of the more widely known agents used to boost muscle mass and increase power output. Anabolic steroids are a form of testosterone, a male sex hormone that stimulates muscle formation, leading to increased muscle mass.

Endurance athletes may also try to boost the availability of oxygen to muscles to increase aerobic respiration by using substances such as erythropoietin (EPO), a hormone normally produced in the kidneys, which triggers the production of red blood cells. The extra oxygen carried by these blood cells can then be used by muscles for aerobic respiration. Human growth hormone (hGH) is another supplement, and although it can facilitate building muscle mass, its main role is to promote the healing of muscle and other tissues after strenuous exercise. Increased hGH may allow for faster recovery after muscle damage, reducing the rest required after exercise, and allowing for more sustained high-level performance.

Although performance-enhancing substances often do improve performance, most are banned by governing bodies in sports and are illegal for nonmedical purposes. Their use to enhance performance raises ethical issues of cheating because they give users an unfair advantage over nonusers. A greater concern, however, is that their use carries serious health risks. The side effects of these substances are often significant, non-reversible, and in some cases fatal. The physiological strain caused by these substances is often greater than what the body can handle, leading to effects that are unpredictable and dangerous. Anabolic steroid use has been linked to infertility, aggressive behaviour, cardiovascular disease, and brain cancer.

Similarly, some athletes have used creatine to increase power output. Creatine phosphate provides quick bursts of ATP to muscles in the initial stages of contraction. Increasing the amount of creatine available to cells is thought to produce more ATP and therefore increase explosive power output, although its effectiveness as a supplement has been questioned.

Everyday Connection

Ageing and Muscle Tissue

Although atrophy due to disuse can often be reversed with exercise, muscle atrophy with age, referred to as sarcopenia, is irreversible. This is a primary reason why even highly trained athletes succumb to declining performance with age. This decline is noticeable in athletes whose sports require strength and powerful movements, such as sprinting, whereas the effects of age are less noticeable in endurance athletes such as marathon runners or long-distance cyclists. As muscles age, muscle fibres die, and they are replaced by connective tissue and adipose tissue (Figure 9.6.3). Because those tissues cannot contract and generate force as muscle can, muscles lose the ability to produce powerful contractions. The decline in muscle mass causes a loss of strength, including the strength required for posture and mobility. This may be caused by a reduction in FG fibres that hydrolyse ATP quickly to produce short, powerful contractions. Muscles in older people sometimes possess greater numbers of SO fibres, which are responsible for longer contractions and do not produce powerful movements. There may also be a reduction in the size of motor units, resulting in fewer fibres being stimulated and less muscle tension being produced.

Diagram of normal muscle and atrophied muscle
Figure 9.6.3. Atrophy. Muscle mass is reduced as muscles atrophy with disuse.

Sarcopenia can be delayed to some extent by exercise, as training adds structural proteins and causes cellular changes that can offset the effects of atrophy. Increased exercise can produce greater numbers of cellular mitochondria, increase capillary density, and increase the mass and strength of connective tissue. The effects of age-related atrophy are especially pronounced in people who are sedentary, as the loss of muscle cells is displayed as functional impairments such as trouble with locomotion, balance, and posture. This can lead to a decrease in quality of life and medical problems, such as joint problems because the muscles that stabilise bones and joints are weakened. Problems with locomotion and balance can also cause various injuries due to falls.

Section Review

Hypertrophy is an increase in muscle mass due to the addition of structural proteins. The opposite of hypertrophy is atrophy, the loss of muscle mass due to the breakdown of structural proteins. Endurance exercise causes an increase in cellular mitochondria, myoglobin, and capillary networks in SO fibres. Endurance athletes have a high level of SO fibres relative to the other fibre types. Resistance exercise causes hypertrophy. Power-producing muscles have a higher number of FG fibres than of slow fibres. Strenuous exercise causes muscle cell damage that requires time to heal. Some athletes use performance-enhancing substances to enhance muscle performance. Muscle atrophy due to age is called sarcopenia and occurs as muscle fibres die and are replaced by connective and adipose tissue.

Review Questions

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9.7 Cardiac Muscle Tissue
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