Ex Phys Exam 3 free response

How are central fatigue and peripheral fatigue defined in exercise physiology?

• Peripheral Fatigue: A failure of the motor neuron or muscle fiber to function properly, directly decreasing local force production.

• Central Fatigue: Psychological and central nervous system (CNS) factors that serve to limit force production.

What are the three primary local sites where peripheral fatigue occurs, and what specific failure happens at each?

1. Action Potential Propagation: Disruption of local sarcolemma ion gradients.

2. Neuromuscular Transmission (NMJ): Decreased acetylcholine (ACh) release.

3. Excitation-Contraction (E-C) Coupling: Failure of T-tubule depolarization to properly release Ca2+ from the sarcoplasmic reticulum (SR).

Where does central fatigue originate, and what molecules, neural pathways, and physiological signals drive it?

• Origin: The central nervous system (brain and spinal cord) involving descending motor pathways and decreased neural drive.

• Involved Factors: Neurotransmitter concentrations in the brain (serotonin and dopamine), circulating inflammatory cytokines, low blood glucose, and sensory feedback from working muscles.

What ions, by-products, and substrates accumulate or deplete during peripheral fatigue, and how do H+ ions impair performance?

• Accumulations: H+ ions, inorganic phosphate (Pi), and intracellular calcium (Ca2+).

• Substrate Depletion: Phosphocreatine (PCr) during high-intensity exercise; glycogen during long-duration endurance exercise.

• H+ Impairments: Impairs E-C coupling, inhibits troponin binding, and slows PFK and myosin ATPase activity.

What is the typical prevalence of central vs. peripheral fatigue in everyday life, and what is a classic example of each?

• Peripheral Prevalence & Example: Highly prevalent during intense, short-term muscular exertion (e.g., muscle failure on the final heavy barbell repetition due to H+ accumulation and PCr depletion).

• Central Prevalence & Example: Believed to be the cause of most daily fatigue and prolonged exertion (e.g., severe mental and physical exhaustion after a long workday or marathon, where the brain limits motor unit recruitment to protect tissues).

Using the stroke volume equation (SV = EDV - ESV), explain why stroke volume increases from rest up to 40–60% of maximal work rate.

• Driven by an increase in preload (EDV).

• Rhythmic contractions from the skeletal muscle pump increase venous return, stretching the myocardial fibers during ventricular filling.

• According to the Frank-Starling mechanism, this increased stretch produces a stronger contractile force, ejecting a larger volume of blood per beat.

Why does stroke volume eventually plateau or decrease when exercise intensity exceeds 40–60% of maximal work rate?

• As heart rate climbs dramatically at higher work rates, the duration of diastolic filling time is severely shortened.

• The ventricles have less time to fill with blood, causing End-Diastolic Volume (EDV) to drop or plateau, which limits further increases in stroke volume.

What are the two primary physiological pumps that increase venous return to the heart during exercise?

• The Skeletal Muscle Pump: Active muscles rhythmically compress deep veins, mechanically pushing blood toward the heart. One-way internal valves prevent backflow against gravity.

• The Thoracic (Respiratory) Pump: Increased breathing frequency and depth lower intrathoracic pressure (creating a vacuum) and raise intra-abdominal pressure, forcing blood back into the central circulation.

What are the two primary components of blood (with percentages), what are blood's main functions, and what specific molecule enables oxygen transport?

• Composition: Plasma (~55–60%) and Hematocrit/Formed elements (~45–50% red/white blood cells and platelets).

• Main Functions: Gas transport (O2/CO2), nutrient delivery/waste removal, temperature regulation, and acid-base ($\text{H}^+$ buffer) balance.

• Oxygen Molecule: Hemoglobin (binds 4 O2 molecules per protein unit inside red blood cells).

List the four variables that determine and regulate stroke volume, along with the core factor affecting each.

• Preload: Amount of ventricular stretch at end-diastole; affected by venous return, blood volume, pumps, posture, and venous tone. (Queen Mary’s Boat’s Probably Very Haunted)

• Afterload: Aortic pressure/resistance the ventricle must overcome; affected by arterial BP, hypertension, and the Valsalva maneuver.

• Contractility: Inotropic strength of contraction; increased by sympathetic stimulation and inotropic agents; decreased by hypoxia, acidosis, or tissue death.

• Heart Rate: Contraction frequency; extremely high rates limit filling time (EDV).

How does blood distribution shift from rest to exercise, which vascular structure enables this, and what two control mechanisms signal the shift?

• Shift: Visceral organs (liver ~27%, kidneys ~22%) receive ~50% at rest, while skeletal muscle gets ~15%. During exercise, active muscle receives at least 80% via widespread visceral vasoconstriction.

• Vascular Structure: Arterioles (resistance vessels containing smooth muscle cells that alter vessel diameter).

• Signaling Mechanisms:

  1. Autoregulation (Local): H+, K+, lactate, O2 drop, and shear-stress nitric oxide (NO) release.

  2. Extrinsic Neural Control: Sympathetic nervous system alpha-receptors (vasoconstriction) and beta_2-receptors (vasodilation).

Describe the response curves of HR, SV, and (a-v)\O2 diff during a maximal exercise test, and identify which variable dictates VO2max.

• Heart Rate: Increases linearly to HRmax (220-age) via parasympathetic withdrawal and sympathetic drive.

• Stroke Volume: Increases up to 40–60% intensity, then plateaus due to shortened filling time.

• (a-v) O₂ Diff: Increases progressively as active tissue extracts more oxygen from arterial blood.

• Key VO2max Determinant: Stroke Volume (since max HR is age-fixed and extraction maxes out similarly across trained individuals).

If gravity aids venous return and increases preload when suspended upside down, why is stroke volume measured as unchanged?

• The heart is operating near the flat/plateau portion of the Frank-Starling curve.

• Once the heart reaches its anatomical filling and compliance limit (pericardial constraint), additional venous return cannot stretch the sarcomeres any further to produce a stronger contraction.

Why must absolute VO2max (L/min) be converted to relative units (mL/kg/min)?

• Oxygen consumption scales heavily with total body mass (larger individuals naturally have bigger hearts, blood volumes, and muscle mass).

• Relative units allow fair cardiorespiratory fitness comparisons across individuals of different sizes and account for weight-bearing movement against gravity.

Where do insulin and glucagon come from, how do they change during exercise, and why?

• Insulin (beta-cells of pancreas): Decreases during exercise to prevent severe hypoglycemia; muscle contraction independently translocates GLUT-4 transporters.

• Glucagon (alpha-cells of pancreas): Increases during exercise to maintain blood glucose via glycogenolysis, gluconeogenesis, and FFA mobilization.

Where do T3/T4 and catecholamines come from, how do they change, and what are their exercise roles?

• Thyroid Hormones (T3/T4 from Thyroid Gland): Increase to elevate basal metabolism; exert a permissive effect allowing catecholamines to function fully.

• Catecholamines (Epi/Norepi from Adrenal Medulla): Increase significantly to drive the fight-or-flight response, raising HR, BP, SV, respiratory rate, and stimulating glycogenolysis/lipolysis.

Where do cortisol and growth hormone originate, how do they change, and why do they change during exercise?

• Cortisol (Adrenal Cortex): Increases (especially early in intense exercise) to maintain blood glucose via gluconeogenesis, protein catabolism, and FFA mobilization.

• Growth Hormone (Anterior Pituitary): Increases to promote tissue growth/repair, mobilize FFAs to spare carbohydrates, and blunt insulin action to keep blood glucose elevated.