Skeletal Muscle Structure and Function

• The human body has over 600 skeletal muscles.
• Skeletal muscles constitute 40% to 50% of total body weight.

Functions of Skeletal Muscle

• Skeletal muscles produce force for locomotion and breathing.
• Skeletal muscles are responsible for force production for postural support.
• Skeletal muscles generate heat during cold stress.

Structure of Skeletal Muscles

• The epimysium surrounds the entire muscle and is made of connective tissue.
• The perimysium surrounds bundles of muscle fibers.
• Connective tissue and fascicles are a component of the perimysium.
• The endomysium surrounds individual muscle fibers.
• The basement membrane is just below the endomysium.
• The sarcolemma functions as the muscle cell membrane.

Satellite Cells

• Satellite cells serve as precursors to muscle cells.
• Satellite cells play a key role in muscle growth and repair.
• During muscle growth, satellite cells increase the number of nuclei in mature muscle fibers.
• Mature muscle fibers contain more than one nucleus.
• The myonuclear domain is the volume of cytoplasm surrounding each nucleus.
• Each nucleus supports a limited myonuclear domain.
• More nuclei allow for greater protein synthesis.
• Satellite cells are important for muscle growth in response to strength training.

Microstructure of Skeletal Muscle

• Myofibrils contain contractile proteins.
  • These proteins include actin (thin filament) and myosin (thick filament)
• The sarcomere includes the Z line, M line, H zone, A band, and I band.
• The sarcoplasmic reticulum stores calcium.
  • Calcium release from the sarcoplasmic reticulum is necessary for muscle contraction.
• Transverse tubules extend from the sarcolemma to the sarcoplasmic reticulum.

Neuromuscular Junction

• The neuromuscular junction is the junction between a motor neuron and a muscle fiber.
• A motor unit includes the motor end plate.
• The motor end plate forms a pocket around the motor neuron by the sarcolemma.
• The neuromuscular cleft is a short gap between the neuron and muscle fiber.
• Acetylcholine is released from the motor neuron.
• Acetylcholine causes an end-plate potential (EPP).
  • EPP leads to depolarization of the muscle fiber.
  • The threshold initiates muscle contraction.

NMJ Adaptations to Training

• Endurance and resistance training causes:
  • An increase in the size of the NMJ.
  • An expanding number of synaptic vesicles containing acetylcholine.
  • An increase in the number of acetylcholine receptors.

Sliding Filament Model

• Muscle shortening is due to the movement of actin filaments over myosin filaments.
• Cross-bridges form between actin and myosin filaments.
• The power stroke involves a single contraction cycle.
• The distance between Z discs of the sarcomere is reduced.

Troponin and Tropomyosin

• Calcium ions bind to troponin, which removes tropomyosin from actin, allowing cross-bridges to form.
• Tropomyosin normally covers a binding site on the muscle fiber.

Energy for Muscle Contraction

• ATP is broken down by the enzyme myosin ATPase.
• The breakdown of ATP to ADP and inorganic phosphate releases energy that energizes myosin cross-bridges.
  • The release of energy can be used by the body.
• Myosin cross-bridges pull actin molecules over myosin shortening the muscle.
• Three pathways for ATP:
  • Phosphocreatine.
  • Glycolysis.
  • Oxidative phosphorylation.

Excitation-Contraction Coupling

• Depolarization of the motor neuron within the spinal cord.
• Nerve impulse arrives at the NMJ, releasing acetylcholine.
• Acetylcholine binds to receptors on the motor end plate:
  • This binding allows sodium ions to move into the muscle fiber, causing depolarization.
• Depolarization of the muscle cell travels down T-tubules.
  • Calcium ions are released.
  • Calcium ions bind to troponin.
  • Troponin removes tropomyosin from actin.
  • Myosin-actin cross-bridge occurs.

Relaxation

• The motor neuron stops firing:
  • No acetylcholine is released, initiating repolarization.
• Calcium ions are pumped into the sarcoplasmic reticulum for storage.
  • No calcium means troponin moves tropomyosin back into position, covering the myosin sites on actin.
  • This prevents cross-bridge formation and leads to muscle contraction.

Muscle Fatigue

• Muscle fatigue is defined as a decline in muscle power output.
• A decline in muscle power output is due to decreased muscle force production at the cross-bridge level and decreased muscle shortening velocity.
• The cause of muscle fatigue is dependent on the exercise intensity that produced fatigue.

High vs. Low Fatigue

• High-intensity fatigue (lasting less than 10 minutes):
  • Decreased calcium release from the sarcoplasmic reticulum.
  • Accumulation of metabolites that inhibit myofilament sensitivity to calcium.
  • Production of more phosphate, hydrogen ions, and free radicals.
• Low-intensity cardio causes fatigue:
  • Free radical accumulation in muscle fibers on myosin and actin reduces the number of cross-bridges.
  • Depletion of muscle glycogen in over 60 minutes.

Muscle Cramps

• Muscle cramps are spasmodic, involuntary muscle contractions.
• Often associated with prolonged, high-intensity exercise.
• Most exercise-associated cramps are not caused by an electrolyte or dehydration balance.
• Exercise-associated cramps are likely due to hyperactive motor neurons in the spinal cord.
  • Also called 4th quarter cramps.

Muscle Cramps Treatment

• Passive stretching can treat muscle cramps.
• Sending inhibitory stimuli to the spinal cord may lessen muscle cramp activity.
  • Consumption of selected spices and ingredients like ginger and capsaicin in red peppers activates ion channels in sensory nerves called transient receptor potential channels (TRP).
  • TRP activates nerves that inhibit the overactive motor neuron, reducing cramping.

Muscle Fiber Types: Classification

• Includes maximal force production, fatigue resistance, speed of contraction, maximal power output (force x shortening velocity), and muscle fiber efficiency (less ATP to generate force).

• Four main types of muscle fibers:

  • Type 2X: Low # of mitochondria, low resistance to fatigue, anaerobic energy system, highest ATPase activity, highest speed of shortening (Vmax), low efficiency, and high specific tension.
  • Type 2A: High/moderate # of mitochondria, high/moderate resistance to fatigue, combination energy system, high ATPase activity, high speed of shortening (Vmax),moderate efficiency, and high specific tension.
  • Type 1: high # of mitochondria, high resistance to fatigue, aerobic energy system, low ATPase activity, low speed of shortening (Vmax), high efficiency, and moderate specific tension.

Spectrum of Fibers

• Muscles contain pure and hybrid fibers.
• Muscle fiber types:
  • Type 1.
  • Type 1/2a.
  • Type 2a.
  • Type 2a/2x.
  • Type 2x.
• Muscle fibers are determined by biopsy with homogenous vs. single-fiber biopsy.
• HG is not specific enough to estimate hybrid fibers.
• Pure Type IIX fibers exist in very small amounts in humans.
  • There is variability in the vastus lateralis.
• One biopsy represents the entire muscle and provides limited insights.
  • Three biopsies with a minimum of 200 counted fibers are required to estimate vastus lateralis fiber type composition within ±10 percentage points.

Individuality in Muscle Fiber Type

• The percentage of fiber types vary.
• Distance runners have 70-80% slow fibers (type 1) and 20-30% fast fibers (type 2x and 2a).
• Track sprinters have 25-30% slow fibers (type 1) and 70-75% fast fibers (type 2x and 2a).
• Non-athletes have 47-53% both slow twitch and fast twitch fibers.

Muscle Fiber Type: FAQ

• Muscles do have the capability to switch Fiber Type.
  • Current evidence using the most appropriate techniques suggests a clear ability of fibers to shift between hybrid and pure fibers as well as between slow and fast fiber types.
• There is not much difference between muscle fibers in Men vs. Women

Types of Muscle Actions

• Concentric: Muscle contracts with force greater than resistance and shortens.
• Eccentric: Muscle contracts with force less than resistance and lengthens.
• Isometric: Muscle contracts but does not change length.

Factors That Determine Force Production

• The number and types of motor units recruited.
  • More motor units result in greater force.
  • Fast motor units result in greater force.
• Muscle length must reach the "ideal" length for force generation.
  • It can be limited by your weak point.
  • Increased cross-bridge formation improves power.
  • Muscles can get to a point where they are ready to go
• Firing rate of motor neurons:
  • The frequency of simulation determines the rate
  • Each type has a different twitch threshold
    • Simple twitch, Summation, Tetanus.

Contractile History of Muscle

• Rested muscle versus muscle exposed to fatigue exercise.
• Warmup exercise results in "post-activation potentiation," muscles are ready to go.

Length-Tension Relationship

• Muscles produce the most strength at an optimal sarcomere length
• Tension declines if a muscle is too long or too short due to less space to contract

Aging Impact on Muscle

• Age related muscle mass loss is called sarcopenia.
  • 10% muscle mass is typically lost between ages 25-50.
  • An additional 40% is lost between ages 50-80.
  • Aging results in a loss of fast fibers and a gain in slow fibers.
  • Resistance training can delay age-related muscle loss.

Force-Velocity Relationship

• At any absolute force exerted by the muscle, the speed of movement is greater in muscles with a higher percentage of fast-twitch fibers.
• Power decreases at higher velocities because force decreases with increasing movement speed.
• Maximum velocity of shortening is greatest at the lowest force, and this is applicable for both slow and fast fibers.

Adaptations (Chapter 14)

• Muscular Strength: Maximal force that a muscle group can generate.
• Muscular Endurance: The submaximal strength and endurance you can maintain.
  • The Ability to make repeated contractions against a submaximal load.
• Muscle Hypertrophy: An increased size of the muscle fiber.
• Muscle Power: Calculated by: Force x Velocity.

Neural Adaptations

• Responsible for early gains in strength.
  • Strength gains during the first 6-8 weeks of training are largely due to nervous system adaptations.
• Evidence that neural adaptations occur:
  • Muscular strength increases in the first two weeks of training without an increase in muscle fiber size.
• Phenomenon of "cross education:" training of one limb results in increases in the strength of the untrained limb.
• Neural drive is the magnitude of the efferent neural output from the CNS to the muscle.
• Specific adaptations:
  • Increased number of motor units recruited.
  • Increased firing rate of motor units.
  • Increased motor unit synchronization.
  • Improved neural transmission across the neuromuscular junction.

Muscle Fiber Shift

• Muscle fibers go through an amount of flexibility by converting hybrid pure fibers
• Plotkin DL, Roberts MD, Haun CT, Schoenfeld BJ completed trails for Muscle Fiber Type Transitions with Exercise Training: Shifting Perspectives. Sports (Basel). 2021 Sep 10;9(9):127. doi: 10.3390/sports9090127. PMID: 34564332; PMCID: PMC8473039.
• Heavy load 70% 1-RM, slow resistance training produces a shift to Type IIA fibers
  • Change from Type IIX and type 2a/2x -- type 2a
  • No change in type 1
• Sprint, power, and pjuometric training transition forward more of a type 2a: Indidviduals will more 2x fibers may not experience much of transition

Exercise Types & Muscle Shifts

• May see transition from type 1 with this.

• Detraining and Weaning lead to type 2x overshoot.

• Taper in marathon runners: no changes in type 1 fibers, and increased single fiber power and peak power in type 2a fibers with 3 week taper.

  • An uphill sprint at the end is the trigger

• Van Hooren B, Aagaard P, Blazevich AJ. Optimizing Resistance Training for Sprint and Endurance Athletes: Balancing Positive and Negative Adaptations. Sports Med. Published online October 7, 2024.

• Heavy RT (regardless of concurrent program): No shift from Type 1 to Type 2a. Endurance athletes?

• Somestudies how low-load, high velocity RT may lead to shifts from Type 1 to Type 2

  • Usually IIA
  • Need Speed to change from Type I to Type II
  • Endurance athletes? Sprint athletes? Repeated Sprint Athletes?

• Endurance Training will give the following results

  • Type I increase by 5-15% in 13-18 weeks
  • Endurance + Heavy RT results in Type IIX and Type IIA/IIX --> Type IIA
  • Moderate association between the decrease in Type IIX fibers and increase in power during 40-minute all-out cycling

• Sprint athletes achieve different modifications

  • Type IIX decreases when training volume is high and close to failure
  • Low-volume power and heavy resistance training conserves Type IIX fibers

• Practical applications

• Endurance Athletes

  • 2-3 sets/exercise at 2-3 exercises per session = low training volume
  • Heavy Load, Multi-joint
  • Low-load heavy volume often prescribed – Heavy RT more effectively improves running economy

• Sprint athletes

  • 3-4 sets/exercise at 3-4 exercises per session = low training volume
  • Heavy Load, Multi-joint
  • Addition of ballistic and plyometric movements
  • Slightly larger because they may benefit from some hypertrophy of proximal muscles
    • Hypertrophy is VOLUME based

Weight & Volume of Training

• VOLUME DOES NOT EQUAL WEIGHT
  • Volume = amount of weight x amount of reps x amounts of sets
• Increased in Muscle Mass
  • Training induced increase in muscle mass

Fibers

• Hyperplasia is increased number of fibers:

• More debate, some studies start to demonstrate

  • Hypertrophy-increased cross-sectional area of muscle fibers

• Hypertrophy is likely the dominant factor in resistance training-induced increases in muscle mass

  • Hypertrophy due to increased muscle proteins - actin and myosin detectable at 3 weeks • More prominent in Type II than Type I muscle fibers

• Other Effects of RT on muscular endurance:

  • Muscle antioxidant enzyme activity
    • Increases key antioxidant enzymes by almost 100%

• Protection against exercise-induced production of free radicals

  • Increase tendon and ligament strength
    • Heavy, Slow Resistance Training
    • Eccentric

• Improve BMS

Muscle protein synthesis

• An intense Workout will create shifts - Key factors that contribute to resistance training-induced increases in muscle protein synthesis
• mRNA increases resulting in protein synthesis at the ribosome
• This can be amplified if the individual is untrained

mTOR, Leucine & Genetics

• Ribosomes are increased in the body, which elevate muscle's protein synthesis capacity
• Activation of the protein kinase "mechanistic target of rapamycin" (mTOR) is the key factor accelerating protein synthesis following a bout of resistance training
• Muscle contractions activate a sarcolemmal mechanoreceptor stimulating synthesis of phosphatidic acid PA
• Summary - Resistance training activates mTOR by synthesizing PA and removing the TSC2 inhibition of Rheb

Nutrition

• Supplementation with the branched chain amino leucine
• Resistance training, promotes a small increase in muscle protein synthesis
• long-term supplementation with leucine does not result in muscle hypertrophy in sedentary individuals
• Do you need a training stimulus?
• Both insulin like growth factor-1 (IGF-1) and growth hormone are linked to mTOR aAbout of resistance training results in small increases in circulating levels of IGF-1 and growth hormone
• Although high circulating levels of these hormones can support resistance training induced hypertrophy, increases in these hormones are not required to achieve resistance-training-induced hypertrophy
  • They are there and have a role help in protein synthesis Resistance training activates satellite cells to divide and fuse with adjacent muscle fibers to increase myonuclei
• Resistance training-induced increases in myonuclei result in a constant ratio between the number of myonuclei and size of muscle fiber (myonuclear domain remains constant)

Genetics

• Approximately 80% of the differences in muscle mass between individuals is due to genetic variation

• 47 different genes are major contributors to muscle mass

• These differences are due to variations between people in their ability to activate specific "protein synthesis” genes in skeletal muscle in response to resistance training

• Cessation of resistance training results in muscle atrophy and a loss of strength: -*Compared to endurance training, the rate of detraining (that is, strength loss) is slower -Movement is muscle is hospitalized adult, Geriatric nursing: -2-5% per4cent decline in muscle mass each day a patient does not walk -Immobile older adults lose up to 10% of their muscle mass in 7 days -40% reduction in muscle strength -Increase in bone resorption -Nutrition is not easy for the hospitalized

Retraining

• Mechanism responsible for muscle memory remains controversial -Recent research suggests that muscle memory is due to resistance training-induced increases in myonuclei in the trained fibers that are not lost during detraining
• Concurrent Training -Strength +endurance -Depend on intensity, volume, and frequenct
• Variable research
• Limit interference = Limit volume of cardio training*
• Subject performed endurance training> 2 days a week and > 30 minutes a day had impaired strength and hypertrophy gains compared to RT alone *Whats your goal?

Training Factors

• Why is strength training not always effective?
• Neural factors that can be addressed: -Impared motor unit recruitment -Limited evidence exists to support this concept -Depressed protein synthesis -Endurance training cell signaling can interfere with protein synthesis -Via inhibition of mTOR by activation of AMPK