Exercise Physiology Final Exam Review

Usual aging

a gradual, continuous process of natural change that begins in early adulthood.

extrinsic factors such as passive lifestyle heighten the effects of normal aging

Successful aging

extrinsic factors positively influence the aging process– lifestyle factors such as physical activity, sleep and diet.

Chronological aging

refers only to the passage of time

Biological aging

relates to the decline of function and increase in disease over time (lifestyle factors can influence biological aging, while chronological aging continues regardless over time).

Trainability with age

No upper limit

Exercise improves physiologic responses at any age

Some factors that affect magnitude of trainability

 Initial fitness, genetics, hormones, nutrition, sleep, and type of training.

Physical activity and longevity’

Some factors that affect magnitude of trainability include:

initial fitness, genetics, hormones, nutrition, sleep, and type of training.

How can society impact these issues?

Healthy people 2030

• 1. Quantifiable goals + objectives 2. Health promotion and disease prevention 3. 10-year plan

• Maintaining high quality, longer lives free of preventable death and disease, Achieve health equity, Create social and physical environments that promote good health, and Promote quality of life, healthy development, and healthy behaviors

Impact of sedentary behaviors on longevity and health

double risk of developing heart disease, strength of association between lack of exercise and heart disease risk equals that for high blood pressure, cigarette smoking, and high cholesterol.

Influence on of disease on longevity and health

low physical fitness is a more powerful risk factor for chronic disease than high blood pressure, high cholesterol, obesity, and family history. Physical activity reduced death rate in ½ trained hypertension individuals, counters effects of cigarettes, excess body weight, and genetic tendencies toward early death.

3 main energy system in the body?

ATP-PCr (phosphocreatine), Anaerobic Glycolysis (Fast glycolysis), Aerobic Glycolysis (slow glycolysis)

ATP-PCr

PCr reaches its maximum energy yield in about 10s. Yield: 1 ATP per PCR molecule (very rapid)

Cells store approximately 4-6x more PCr than ATP

how: energy for ATP resynthesis from anerbic splitting of phosphate from PCr

Anaerobic Glycolysis

how: glycolysis that results in pyruate conversion to lactate, does not require oxygen, fast/rapid glycolysis

2 net ATP produced

takes place in cytosol of cell

Aerobic Glycolysis

how: pyruvate proceeds into the Citric Acid Cycle AKA Krebs Cycle/TCA Cycle,

Moderate rate of ATP productions, requires oxygen

bi products move into electron transport chain (ETC) to generate large amounts of ATP.

Pyruvate → Acetyl-CoA → Krebs Cycle + ETC

takes place in the mitochondria of the cell

What is the Fate of Lactate?

formed in anaerobic glycolysis when pyruvate converts to lactate

can be:

1. Reconverted to pyruvate in muscle

2. Transported to liver for glucose production (Cori Cycle)

3. Used as a fuel source in aerobic tissues

Anaerobic vs. Aerobic Metabolism?

Anaerobic: is fast, doesn’t require oxygen, supports short (≤ 90s), 2 net ATP, takes place in the cytosol, and has end products: lactate, small ATP

Aerobic is slow, requires oxygen, supports long durations, 32 net ATP, takes place in the mitochondria and has end products: CO₂, H₂O, large ATP

What activity type is ATP-PCr predominately at play?

1-10s sprint/lift

What activity type is Anaerobic Glycolysis predominately at play?

30-90s high intensity

What activity type is Aerobic Glycolysis predominately at play?

2+min of steady effort, and long, slow endurance

Blood Lactate Accumulation & Threshold

Lactate threshold: point during exercise when lactate accumulates faster than it can be cleared

occurs when anaerobic metabolism dominates.

Use of lactate as fuel: converted back into glucose in lier (cori cycle), converted back into pyruvate in muscle, used by heart and other aerobic tissues as energy

Oxygen Deficit

• Oxygen delivery doesn't meet energy demand right away.

• Occurs at exercise onset due to delay in oxygen supply; anaerobic systems fill the gap.

EPOC (Excess Post-Exercise Oxygen Consumption)

• Elevated oxygen uptake restores:

  • ATP/PCr stores

  • Oxygen levels in blood/muscle

  • Lactate clearance

  • Thermoregulation and hormone balance

• Reflects body's return to homeostasis

• Occurs after exercise ends.

How are the 3 main energy system regenerated?

ATP-PCr (Phosphocreatine System): PCr donates phosphate to ADP → ATP (via enzyme control)

Anaerobic Glycolysis (Fast Glycolysis): Substrate-level phosphorylation

Aerobic Glycolysis + Oxidative Phosphorylation: via oxidative phosphorylation in mitochondria

What are the components of the sarcomere?

• Z disc: Separates sarcomeres; provides structural stability.

• I band: Light area; contains only thin (actin) filaments.

• A band: Dark area; contains both thick (myosin) and thin (actin) filaments.

• H zone: Central part of A band; contains only myosin.

• M line: Bisects the H zone; stabilizes myosin filaments.

What moves during muscle contraction?

• Actin filaments slide over myosin, shortening the sarcomere.

• I band and H zone shorten.

• A band remains the same

What are the contractile units of the muscle and characteristics?

• Actin (thin filament): Contains active sites for myosin binding.

• Myosin (thick filament): Has heads that form crossbridges with actin.

• Titin: Anchors myosin to the Z disc; provides elasticity and stability.

  Character

• Muscle = 75% water, 20% protein (mostly actin, myosin, tropomyosin), 5% salts/other.

• Sarcomeres are the smallest functional unit.

• Myofibrils are made of sarcomeres end-to-end.

Sliding filament theory

• Actin and myosin filaments slide past each other to shorten the muscle.

• Myosin heads attach to actin → pull → detach → reset (requires ATP).

Excitation-Contraction Coupling (ECC) Steps?

Basic Steps

1. Action potential arrives at muscle fiber.

2. Ca²⁺ released from sarcoplasmic reticulum.

3. Ca²⁺ binds troponin, exposing actin binding sites.

4. Myosin heads bind to actin forming crossbridges.

5. Power stroke: Myosin pulls actin (requires ATP hydrolysis).

6. New ATP binds to release myosin.

7. Ca²⁺ is pumped back into sarcoplasmic reticulum (relaxation).

What is the role of ATP in Excitation-Contraction Coupling (ECC)?

Role of ATP:

• Breaks rigor bond.

• Powers the myosin head cocking.

• Drives Ca²⁺ reuptake during relaxation.

Role of Calcium

Triggers troponin to shift tropomyosin, exposing actin’s binding sites.

What happens during the relaxation go muscle fiber?

• Ca²⁺ is actively pumped back into sarcoplasmic reticulum.

• Troponin inhibits actin-myosin binding.

• Muscle returns to resting state.

The 7 factors that affect force production

7 FACTORS THAT AFFECT FORCE PRODUCTION (WITH EXAMPLES)

1. Muscle Architecture

2. Muscle Cross-Sectional Area (CSA)

3. Fiber Type Proportion

4. Length-Tension Relationship

5. Force-Velocity Relationship

6. Lever Systems

7. Stretch-Shortening Cycle (SSC)

How does Muscle Architecture affect force production?

• Pennate muscles (e.g., soleus) generate more force due to more fibers packed in parallel.

• Fusiform muscles (e.g., biceps) are built for speed, not force.

How does Muscle Cross-Sectional Area (CSA) affect force production?

• Larger CSA = more force.

  • Example: A bodybuilder's large quadriceps generate more force than a slimmer person's.

How does Fiber Type Proportion affect force production:

• Type II (Fast-twitch): High force, quick fatigue (e.g., sprinters).

• Type I (Slow-twitch): Low force, high endurance (e.g., marathon runners).

How does Length-Tension Relationship affect force production:

• Optimal overlap of actin and myosin = max force.

  • Example: A mid-range biceps curl (~90° elbow flexion) allows more force than at 25°.

How does Force-Velocity Relationship affect force production?

• High force = low velocity (heavy lifts).

• High speed = low force (sprinting, fast throws).

How do Lever Systems affect force production:

• 2nd class (e.g., ankle) = high force.

• 3rd class (e.g., biceps curl) = high speed, lower force.

How does th Stretch-Shortening Cycle (SSC) affect force production?

• Pre-stretching muscle (eccentric → concentric) boosts force.

  • Example: Jumping after a quick dip squat.

Muscle contraction types:

• Isometric: No length change; force = resistance (e.g., plank).

• Concentric: Muscle shortens; force > resistance (e.g., lifting).

• Eccentric: Muscle lengthens; force < resistance (e.g., lowering a dumbbell).

What initiates movement?

Movement is initiated in the brain, starting in the premotor cortex (where complex movements are planned and coordinated). The final signal to contract muscles is sent from the primary motor cortex (transmits action potentials down the spinal cord to motor neurons).

Brain structures involved in movement

• Frontal Lobe: Key for movement, decision-making, and personality.

  • Premotor Cortex: Plans and coordinates movement.

  • Primary Motor Cortex: Sends neural output to muscles to cause contraction.

• Cerebrum: Includes all lobes and is the largest part of the brain involved in voluntary movement.

• Spinal Cord: Transmits signals from the motor cortex to the peripheral nerves.

Role of the Primary Motor Cortex:

controls voluntary muscle contractions.

It sends action potentials to muscles via motor neurons.

Each side of the motor cortex controls the opposite side of the body.

Function of Frontal Lobe:

Key for movement, decision-making, and personality.

includes:

• Premotor Cortex: Plans and coordinates movement.

• Primary Motor Cortex: Sends neural output to muscles to cause contraction.

Function of Cerebrum:

• Includes all lobes and is the largest part of the brain involved in voluntary movement.

Function of Spinal Cord:

Transmits signals from the motor cortex to the peripheral nerves.

Motor Homunculus Representation:

Different body parts are mapped onto the motor cortex. Areas requiring fine motor control (like fingers and face) have a larger representation.

Motor Homunculus impact on function:

More cortical area = greater precision (fine movements). Smaller areas = gross motor control (like legs or trunk).

Resting membrane Potential:

The membrane is polarized (inside is more negative than outside) because uneven distribution of Na⁺ and K⁺ ions across the cell membrane.

Value: ~ -70 mV

Action Potential Steps

1. Depolarization: Na⁺ channels open → Na⁺ rushes in → membrane potential becomes positive (~+30 mV).

2. Repolarization: K⁺ channels open → K⁺ exits → membrane returns to negative.

3. Hyperpolarization: Too much K⁺ exits → membrane becomes more negative than -70 mV.

4. Restoration: Na⁺/K⁺ pump restores ion balance (3 Na⁺ out, 2 K⁺ in).

Saltatory Conduction

• Occurs in myelinated axons.

• APs "jump" between nodes of Ranvier, speeding up conduction.

Myelin and how it impacts the action potential:

• Fatty insulation made by Schwann cells.

• Increases speed of AP conduction.

• Loss of myelin (e.g., in multiple sclerosis) slows or blocks signal transmission.

The Motor Unit, Impacts, Laws:

A motor unit consists of one motor neuron and all the muscle fibers it innervates.

• Impacts:

  • Twitch characteristics (slow or fast).

  • Force production (more or fewer fibers = stronger or weaker contractions).

  • Fatigue resistance (type I = more resistant; type IIx = less).

• Governed by:

  • Henneman’s Size Principle (recruit smallest to largest MUs based on force need).

  • Firing frequency and synchronization improve force and coordination.

What is the Neuromuscular junction (NMJ) ? What happens there?

a specialized synapse where a motor neuron communicates with a muscle fiber to initiate contraction. The process includes:

1. Action potential (AP) travels down the motor neuron's axon to the axon terminal.

2. Voltage-gated Ca²⁺ channels open, allowing calcium ions (Ca²⁺) to enter the terminal.

3. Ca²⁺ triggers the release of acetylcholine (ACh) from synaptic vesicles into the synaptic cleft.

4. ACh binds to receptors on Na⁺ channels located on the muscle’s sarcolemma (muscle cell membrane).

5. Na⁺ channels open, causing depolarization of the sarcolemma.

6. This depolarization propagates along the muscle fiber membrane, eventually leading to excitation-contraction coupling and muscle contraction.

Major Cardiovascular Changes during Exercise:

1. Increased cardiac output – The heart pumps more blood per minute due to an increase in both heart rate and stroke volume.

2. Redistribution of blood flow – Blood is redirected away from non-essential organs toward active skeletal muscles. This is regulated by the sympathetic nervous system, which causes vasoconstriction in inactive regions and vasodilation in arterioles of active muscles to enhance oxygen delivery.

Cardiovascular changes during Recovery:

• Heart rate and cardiac output decrease as the need for high oxygen delivery declines.

• Sympathetic nervous system activity is reduced, and parasympathetic (vagal) tone increases, helping restore a normal heart rate.

• Vasodilation subsides, and blood flow is redirected to balance body functions.

• Plasma volume is restored, especially if fluids are consumed, reversing the effects of dehydration and cardiovascular drift.

How does the body maintain cardiovascular homeostasis during and after exercise?

• Neural control: The autonomic nervous system adjusts heart rate and vessel tone (sympathetic increases output during exercise; parasympathetic restores calm during recovery).

• Hormonal control: Hormones like epinephrine help maintain blood pressure and cardiac output.

• Local regulation: Metabolic byproducts in muscles cause local vasodilation, ensuring oxygen delivery matches demand.

• Thermoregulation: Blood is sent to the skin for cooling, especially in hot environments, which also leads to cardiovascular drift—a temporary shift in function to maintain body temperature and pressure.