Exercise and Training Summary Questions

Exercise and Muscle Performance

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

• Describe hypertrophy and atrophy
• Explain how resistance exercise builds 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 fibers 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 fibers are predominantly used in endurance exercises that require little force but involve numerous repetitions.

• The aerobic metabolism used by slow-twitch fibers allows them to maintain contractions over long periods.
  • Endurance training modifies these slow fibers 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 fiber, 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 of these cellular changes result in the ability to sustain low levels of muscle contractions for greater periods without fatiguing.
  • The proportion of SO muscle fibers 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 fibers and relatively few FO and FG fibers, to keep the back straight.
    • Endurance athletes, like marathon-runners also would benefit from a larger proportion of SO fibers, but it is unclear if the most-successful marathoners are those with naturally high numbers of SO fibers, or whether the most successful marathon runners develop high numbers of SO fibers with repetitive training.
    • Endurance training can result in overuse injuries such as stress fractures and joint and tendon inflammation.

      

Marathoners Long-distance runners have a large number of SO fibers and relatively few FO and FG fibers.

 

Resistance Exercise

Resistance exercises, as opposed to endurance exercise, require large amounts of FG fibers to produce short, powerful movements that are not repeated over long periods.

• The high rates of ATP hydrolysis and cross-bridge formation in FG fibers result in powerful muscle contractions.
  • Muscles used for power have a higher ratio of FG to SO/FO fibers, and trained athletes possess even higher levels of FG fibers in their muscles.
• Resistance exercise affects muscles by increasing the formation of myofibrils, thereby increasing the thickness of muscle fibers.
  • This added structure causes hypertrophy, or the enlargement of muscles, exemplified by the large skeletal muscles seen in body builders and other athletes.
  • Because this muscular enlargement is achieved by the addition of structural proteins, athletes trying to build muscle mass often ingest large amounts of protein.

    

Hypertrophy Body builders have a large number of FG fibers and relatively few FO and SO fibers.

 

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 weight lifting 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 fibers 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, nonreversible, 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 behavior, 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.

 

Aging 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 fibers die, and they are replaced by connective tissue and adipose tissue.
  • 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 fibers that hydrolyze ATP quickly to produce short, powerful contractions. Muscles in older people sometimes possess greater numbers of SO fibers, 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 fibers being stimulated and less muscle tension being produced.

    

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 stabilize bones and joints are weakened.
  • Problems with locomotion and balance can also cause various injuries due to falls.

 

Cardiac Muscle Tissue

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

• Describe intercalated discs and gap junctions
• Describe a desmosome

 

Cardiac muscle tissue is only found in the heart.

• Highly coordinated contractions of cardiac muscle pump blood into the vessels of the circulatory system.
• Similar to skeletal muscle, cardiac muscle is striated and organized into sarcomeres, possessing the same banding organization as skeletal muscle.
  • However, cardiac muscle fibers are shorter than skeletal muscle fibers and usually contain only one nucleus, which is located in the central region of the cell.
  • Cardiac muscle fibers also possess many mitochondria and myoglobin, as ATP is produced primarily through aerobic metabolism.

 

Cardiac muscle fibers cells also are extensively branched and are connected to one another at their ends by intercalated discs.

• An intercalated disc allows the cardiac muscle cells to contract in a wave-like pattern so that the heart can work as a pump.

   

Cardiac Muscle Tissue Cardiac muscle tissue is only found in the heart. LM × 1600. (Micrograph provided by the Regents of University of Michigan Medical School c 2012)

 

Intercalated discs are part of the sarcolemma and contain two structures important in cardiac muscle contraction: gap junctions and desmosomes.

• A gap junction forms channels between adjacent cardiac muscle fibers that allow the depolarizing current produced by cations to flow from one cardiac muscle cell to the next.
  • This joining is called electric coupling, and in cardiac muscle it allows the quick transmission of action potentials and the coordinated contraction of the entire heart.
  • This network of electrically connected cardiac muscle cells creates a functional unit of contraction called a syncytium.
• The remainder of the intercalated disc is composed of desmosomes.
  • A desmosome is a cell structure that anchors the ends of cardiac muscle fibers together so the cells do not pull apart during the stress of individual fibers contracting.

 

  

Cardiac Muscle Intercalated discs are part of the cardiac muscle sarcolemma and they contain gap junctions and desmosomes.

 

Contractions of the heart (heartbeats) are controlled by specialized cardiac muscle cells called pacemaker cells that directly control heart rate.

• Although cardiac muscle cannot be consciously controlled, the pacemaker cells respond to signals from the autonomic nervous system (ANS) to speed up or slow down the heart rate.
• The pacemaker cells can also respond to various hormones that modulate heart rate to control blood pressure.

 

The wave of contraction that allows the heart to work as a unit, called a functional syncytium, begins with the pacemaker cells.

• This group of cells is self-excitable and able to depolarize to threshold and fire action potentials on their own, a feature called autorhythmicity; they do this at set intervals which determine heart rate.
• Because they are connected with gap junctions to surrounding muscle fibers and the specialized fibers of the heart’s conduction system, the pacemaker cells are able to transfer the depolarization to the other cardiac muscle fibers in a manner that allows the heart to contract in a coordinated manner.

 

Another feature of cardiac muscle is its relatively long action potentials in its fibers, having a sustained depolarization “plateau.”

• The plateau is produced by Ca++ entry though voltage-gated calcium channels in the sarcolemma of cardiac muscle fibers.
• This sustained depolarization (and Ca++ entry) provides for a longer contraction than is produced by an action potential in skeletal muscle.
  • Unlike skeletal muscle, a large percentage of the Ca++ that initiates contraction in cardiac muscles comes from outside the cell rather than from the SR.

 

Smooth Muscle

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

• Describe a dense body
• Explain how smooth muscle works with internal organs and passageways through the body
• Explain how smooth muscles differ from skeletal and cardiac muscles
• Explain the difference between single-unit and multi-unit smooth muscle

 

Smooth muscle (so-named because the cells do not have striations) is present in the walls of hollow organs like the urinary bladder, uterus, stomach, intestines, and in the walls of passageways, such as the arteries and veins of the circulatory system, and the tracts of the respiratory, urinary, and reproductive systems.

• Smooth muscle is also present in the eyes, where it functions to change the size of the iris and alter the shape of the lens; and in the skin where it causes hair to stand erect in response to cold temperature or fear.

 

   

Smooth Muscle Tissue Smooth muscle tissue is found around organs in the digestive, respiratory, reproductive tracts and the iris of the eye. LM × 1600. (Micrograph provided by the Regents of University of Michigan Medical School c 2012)

 

Smooth muscle fibers are spindle-shaped (wide in the middle and tapered at both ends, somewhat like a football) and have a single nucleus; they range from about 30 to 200 μm (thousands of times shorter than skeletal muscle fibers), and they produce their own connective tissue, endomysium.

• Although they do not have striations and sarcomeres, smooth muscle fibers do have actin and myosin contractile proteins, and thick and thin filaments.
• These thin filaments are anchored by dense bodies.
  • A dense body is analogous to the Z-discs of skeletal and cardiac muscle fibers and is fastened to the sarcolemma.
  • Calcium ions are supplied by the SR in the fibers and by sequestration from the extracellular fluid through membrane indentations called calveoli.

 

Because smooth muscle cells do not contain troponin, cross-bridge formation is not regulated by the troponin-tropomyosin complex but instead by the regulatory protein calmodulin.

• In a smooth muscle fiber, external Ca++ ions passing through opened calcium channels in the sarcolemma, and additional Ca++ released from SR, bind to calmodulin.
  • The Ca++- calmodulin complex then activates an enzyme called myosin (light chain) kinase, which, in turn, activates the myosin heads by phosphorylating them (converting ATP to ADP and Pi, with the Pi attaching to the head).
  • The heads can then attach to actin-binding sites and pull on the thin filaments.
• The thin filaments also are anchored to the dense bodies; the structures invested in the inner membrane of the sarcolemma (at adherens junctions) that also have cord-like intermediate filaments attached to them.
  • When the thin filaments slide past the thick filaments, they pull on the dense bodies, structures tethered to the sarcolemma, which then pull on the intermediate filaments networks throughout the sarcoplasm. This arrangement causes the entire muscle fiber to contract in a manner whereby the ends are pulled toward the center, causing the midsection to bulge in a corkscrew motion.

 

   

Muscle Contraction The dense bodies and intermediate filaments are networked through the sarcoplasm, which cause the muscle fiber to contract.

 

Although smooth muscle contraction relies on the presence of Ca++ ions, smooth muscle fibers have a much smaller diameter than skeletal muscle cells.

• T-tubules are not required to reach the interior of the cell and therefore not necessary to transmit an action potential deep into the fiber.
• Smooth muscle fibers have a limited calcium-storing SR but have calcium channels in the sarcolemma (similar to cardiac muscle fibers) that open during the action potential along the sarcolemma.
  • The influx of extracellular Ca++ ions, which diffuse into the sarcoplasm to reach the calmodulin, accounts for most of the Ca++ that triggers contraction of a smooth muscle cell.

 

Muscle contraction continues until ATP-dependent calcium pumps actively transport Ca++ ions back into the SR and out of the cell.

• However, a low concentration of calcium remains in the sarcoplasm to maintain muscle tone.
• This remaining calcium keeps the muscle slightly contracted, which is important in certain tracts and around blood vessels.

 

Because most smooth muscles must function for long periods without rest, their power output is relatively low, but contractions can continue without using large amounts of energy.

• Some smooth muscle can also maintain contractions even as Ca++ is removed and myosin kinase is inactivated/dephosphorylated.
  • This can happen as a subset of cross-bridges between myosin heads and actin, called latch-bridges, keep the thick and thin filaments linked together for a prolonged period, and without the need for ATP.
  • This allows for the maintaining of muscle “tone” in smooth muscle that lines arterioles and other visceral organs with very little energy expenditure.

 

Smooth muscle is not under voluntary control; thus, it is called involuntary muscle.

• The triggers for smooth muscle contraction include hormones, neural stimulation by the ANS, and local factors.
• In certain locations, such as the walls of visceral organs, stretching the muscle can trigger its contraction (the stretch-relaxation response).

 

Axons of neurons in the ANS do not form the highly organized NMJs with smooth muscle, as seen between motor neurons and skeletal muscle fibers.

• Instead, there is a series of neurotransmitter-filled bulges called varicosities as an axon courses through smooth muscle, loosely forming motor units.
  • A varicosity releases neurotransmitters into the synaptic cleft.
• Also, visceral muscle in the walls of the hollow organs (except the heart) contains pacesetter cells.
  • A pacesetter cell can spontaneously trigger action potentials and contractions in the muscle.

 

  

Motor Units A series of axon-like swelling, called varicosities or “boutons,” from autonomic neurons form motor units through the smooth muscle.

 

Smooth muscle is organized in two ways: as single-unit smooth muscle, which is much more common; and as multiunit smooth muscle.

• The two types have different locations in the body and have different characteristics.

• Single-unit muscle has its muscle fibers joined by gap junctions so that the muscle contracts as a single unit.
  • This type of smooth muscle is found in the walls of all visceral organs except the heart (which has cardiac muscle in its walls), and so it is commonly called visceral muscle.
• Because the muscle fibers are not constrained by the organization and stretchability limits of sarcomeres, visceral smooth muscle has a stress-relaxation response.
  • This means that as the muscle of a hollow organ is stretched when it fills, the mechanical stress of the stretching will trigger contraction, but this is immediately followed by relaxation so that the organ does not empty its contents prematurely.
  • This is important for hollow organs, such as the stomach or urinary bladder, which continuously expand as they fill.
  • The smooth muscle around these organs also can maintain a muscle tone when the organ empties and shrinks, a feature that prevents “flabbiness” in the empty organ.
• In general, visceral smooth muscle produces slow, steady contractions that allow substances, such as food in the digestive tract, to move through the body.

 

Multiunit smooth muscle cells rarely possess gap junctions, and thus are not electrically coupled.

• As a result, contraction does not spread from one cell to the next, but is instead confined to the cell that was originally stimulated.
  • Stimuli for multiunit smooth muscles come from autonomic nerves or hormones but not from stretching.
  • This type of tissue is found around large blood vessels, in the respiratory airways, and in the eyes.

 

Hyperplasia in Smooth Muscle

Similar to skeletal and cardiac muscle cells, smooth muscle can undergo hypertrophy to increase in size.

• Unlike other muscle, smooth muscle can also divide to produce more cells, a process called hyperplasia.
  • This can most evidently be observed in the uterus at puberty, which responds to increased estrogen levels by producing more uterine smooth muscle fibers, and greatly increases the size of the myometrium.

 

Physical Therapist

As muscle cells die, they are not regenerated but instead are replaced by connective tissue and adipose tissue, which do not possess the contractile abilities of muscle tissue.

• Muscles atrophy when they are not used, and over time if atrophy is prolonged, muscle cells die.
• It is therefore important that those who are susceptible to muscle atrophy exercise to maintain muscle function and prevent the complete loss of muscle tissue.
  • In extreme cases, when movement is not possible, electrical stimulation can be introduced to a muscle from an external source.
  • This acts as a substitute for endogenous neural stimulation, stimulating the muscle to contract and preventing the loss of proteins that occurs with a lack of use.

 

Physiotherapists work with patients to maintain muscles.

• They are trained to target muscles susceptible to atrophy, and to prescribe and monitor exercises designed to stimulate those muscles.
  • There are various causes of atrophy, including mechanical injury, disease, and age.
  • After breaking a limb or undergoing surgery, muscle use is impaired and can lead to disuse atrophy.
    • If the muscles are not exercised, this atrophy can lead to long-term muscle weakness.
  • A stroke can also cause muscle impairment by interrupting neural stimulation to certain muscles.
    • Without neural inputs, these muscles do not contract and thus begin to lose structural proteins.
    • Exercising these muscles can help to restore muscle function and minimize functional impairments.
  • Age-related muscle loss is also a target of physical therapy, as exercise can reduce the effects of age-related atrophy and improve muscle function.

 

The goal of a physiotherapist is to improve physical functioning and reduce functional impairments; this is achieved by understanding the cause of muscle impairment and assessing the capabilities of a patient, after which a program to

enhance these capabilities is designed.

• Some factors that are assessed include strength, balance, and endurance, which are continually monitored as exercises are introduced to track improvements in muscle function.
• Physiotherapists can also instruct patients on the proper use of equipment, such as crutches, and assess whether someone has sufficient strength to use the equipment and when they can function without it.