# Exercise Physiology, Bioenergetics (ATP-PC, Glycolysis, Oxidative) & Muscle Fiber Types

> NASM CPT, ACE, and NSCA CSCS exercise physiology mastery covering the three metabolic energy systems (ATP-PCr, anaerobic glycolysis, oxidative phosphorylation), work-to-rest ratios, sliding filament theory, muscle spindles vs Golgi tendon organs, muscle fiber types (I, IIa, IIx), Fick equation, EPOC, RER, and ventilatory thresholds.

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- **Level:** basic
- **Languages:** en → en
- **Total Cards:** 32

## Flashcards (32 Cards)

| # | Front (Term / Prompt) | Back (Definition / Answer) | Example | Multiple-Choice Options |
| :--- | :--- | :--- | :--- | :--- |
| 1 | State Wolff's Law of Bone Remodeling and list the NSCA CSCS requirements for an Osteogenic Exercise Prescription (Minimal Essential Strain). | • Wolff's Law: Bone tissue adapts its internal trabecular architecture and external cortical density in direct response to the mechanical loads and lines of stress placed upon it (osteoblasts deposit bone where stress exceeds the Minimal Essential Strain [MES, ~1/10th of fracture force]). • Osteogenic Exercise Prescription: Must be 1. Axial and weight-bearing (loading the spine and hips directly); 2. High-magnitude and high-rate impact/resistance (>=80% 1RM, structural multi-joint lifts like back squats, deadlifts, overhead press, plus plyometric jumping); 3. Multi-directional and progressive. |  |  |
| 2 | Explain Cardiovascular Drift during prolonged submaximal endurance exercise (>30–60 minutes) in warm environments. | During prolonged steady-state submaximal exercise (especially in heat), cutaneous vasodilation (shifting blood to the skin for cooling) and sweat-induced plasma volume loss reduce venous return and preload (EDV), causing a progressive decline in Stroke Volume (SV). To maintain a constant Cardiac Output (`Q = HR x SV`), Heart Rate gradually drifts UPWARD over time even though running/cycling pace remains unchanged. |  |  |
| 3 | Contrast the location, sensory stimulus, and reflex action of Muscle Spindles vs. Golgi Tendon Organs (GTOs). | • Muscle Spindles (intrafusal fibers parallel to extrafusal muscle fibers): Detect the MAGNITUDE and RATE OF LENGTH CHANGE (stretch). When a muscle is rapidly stretched, the spindle fires via Ia afferents to trigger the Monosynaptic Stretch Reflex—contracting the stretched agonist muscle to prevent overstretching injury. • Golgi Tendon Organs (located in the musculotendinous junction in series with muscle fibers): Detect MUSCLE TENSION (force). When tension is sustained (e.g., holding a static stretch for >=6 to 30 seconds), the GTO fires via Ib afferents to inhibit its own muscle (Autogenic Inhibition), allowing it to relax and lengthen. |  |  |
| 4 | Compare Type I, Type IIa, and Type IIx skeletal muscle fibers across contraction speed, force output, fatigue resistance, capillary/mitochondrial density, and predominant energy system. | • Type I (Slow-Twitch Oxidative): Slow contraction speed, low force/power, highest fatigue resistance, high capillary/mitochondrial/myoglobin density ('red fibers'), small motor neuron, aerobic oxidative system. • Type IIa (Fast-Twitch Oxidative-Glycolytic / FOG): Fast contraction speed, high force/power, intermediate fatigue resistance, moderate mitochondrial/capillary density, uses both aerobic and anaerobic metabolism. • Type IIx (Fast-Twitch Glycolytic): Fastest contraction speed, highest force/power output, lowest fatigue resistance (fatigues rapidly), low capillary/mitochondrial density ('white fibers'), large motor neuron, anaerobic ATP-PCr/glycolytic. |  |  |
| 5 | Compare Myofibrillar Hypertrophy, Sarcoplasmic Hypertrophy, and Muscle Hyperplasia. | • Myofibrillar Hypertrophy: Increase in the size and number of contractile actin and myosin myofibrils within existing muscle fibers, directly increasing maximal force production and tissue density. • Sarcoplasmic Hypertrophy: Increase in the volume of non-contractile sarcoplasmic fluid, glycogen, water (3g H2O per 1g glycogen), and mitochondrial proteins without a proportional increase in peak force. • Hyperplasia: Splitting/proliferation to increase the total number of muscle fibers (negligible or minimal in humans compared to hypertrophy). |  |  |
| 6 | Compare the physiological effects of Detraining (reversibility) on Cardiorespiratory Endurance (VO2max) vs. Muscular Strength when training ceases. | • Cardiorespiratory Endurance (VO2max) declines RAPIDLY within 2 to 4 weeks of detraining: the immediate drop during the first 12–21 days is driven by a rapid 5–12% loss of blood plasma volume (decreasing Stroke Volume and maximal cardiac output), followed by a rapid decline in oxidative mitochondrial enzymes (citrate synthase, SDH, revert within 4 weeks). • Muscular Strength and Power decline much MORE SLOWLY: neural adaptations and myofibrillar cross-sectional area are largely retained for 2–4 weeks and can be maintained with just 1 high-intensity session per week. |  |  |
| 7 | State the Fick Equation for Maximal Oxygen Uptake (VO2max) and the Cardiac Output equation, including normal resting and maximal values. | • Cardiac Output (`Q`): `Q = Heart Rate (HR) x Stroke Volume (SV)`. At rest, `Q ≈ 70 bpm x 70 mL/beat = ~5.0 L/min`; at maximal exercise, `Q` increases to `20–25 L/min` in untrained adults and `35–40 L/min` in elite endurance athletes. • Fick Equation: `VO2 = Q x (a-vO2 difference) = HR x SV x (CaO2 - CvO2)`, where `a-vO2 difference` is the arteriovenous oxygen difference (mL O2 extracted by tissues per 100 mL blood, rising from ~5 mL/dL at rest to ~15–16 mL/dL at max exercise). Relative VO2max is expressed in `mL/kg/min` (`1 MET = 3.5 mL/kg/min`). |  |  |
| 8 | What is Excess Post-Exercise Oxygen Consumption (EPOC), and what physiological processes occur during its rapid and slow components? | EPOC ('oxygen debt') is the elevated oxygen uptake above resting baseline following cessation of exercise to restore homeostasis. 1. Rapid Component (2–3 minutes): Resynthesis of muscular ATP and Phosphocreatine (PCr) stores (~70% restored in 30s, 100% in 3–5m) and reloading of oxygen onto blood hemoglobin and muscle myoglobin. 2. Slow Component (minutes to hours): Elevated core temperature, elevated catecholamines (epinephrine/norepinephrine), conversion of lactate to glucose (Cori cycle), and increased cardiopulmonary work. High-intensity interval training (HIIT) and heavy resistance training generate the largest EPOC. |  |  |
| 9 | Explain the Bohr Effect on the Oxyhemoglobin Dissociation Curve during intense exercise. | The Bohr Effect is a RIGHTWARD shift of the oxyhemoglobin dissociation curve in active skeletal muscle capillaries caused by four exercise-induced factors ('CADET, face Right!'): 1. Increased Carbon Dioxide (`PaCO2`); 2. Increased Acidity / H+ ions (decreased pH from lactic/carbonic acid); 3. Increased 2,3-DPG (2,3-bisphosphoglycerate); 4. Elevated Temperature. A rightward shift decreases hemoglobin's affinity for oxygen, facilitating greater unloading of O2 directly into working muscle mitochondria. |  |  |
| 10 | Outline the step-by-step molecular physiology of the Sliding Filament Theory and Excitation-Contraction Coupling. | 1. Action potential travels down alpha motor neuron and releases Acetylcholine (ACh) across neuromuscular junction; 2. Depolarization travels down T-tubules, triggering the Sarcoplasmic Reticulum (SR) to release Calcium ions (Ca2+); 3. Ca2+ binds to Troponin C, causing Tropomyosin to shift off the active binding sites on Actin; 4. energized Myosin heads bind Actin (forming cross-bridges) and execute the Power Stroke (releasing ADP + Pi); 5. A new ATP molecule binds Myosin to detach the cross-bridge (rigor without ATP); 6. SERCA pump actively transports Ca2+ back into SR for relaxation. |  |  |
| 11 | Differentiate Onset of Blood Lactate Accumulation (OBLA) from the Lactate Threshold (LT), including their typical blood lactate concentrations. | • Lactate Threshold (LT / VT1): The exercise intensity at which blood lactate begins to accumulate above resting baseline levels (~1–2 mmol/L), occurring at 50–60% VO2max in untrained individuals and 70–80% VO2max in endurance athletes. • Onset of Blood Lactate Accumulation (OBLA / VT2): A second inflection point at a fixed blood lactate concentration of 4.0 mmol/L where lactate production rapidly exceeds clearance. |  |  |
| 12 | Distinguish between Autogenic Inhibition and Reciprocal Inhibition in neuromuscular stretching (SMR, Static Stretching, and PNF). | • Autogenic Inhibition: Activation of the Golgi Tendon Organ within the SAME muscle being stretched or foam-rolled (sustained tension for >=30 seconds inhibits alpha motor neuron activity in that same tight muscle, allowing relaxation). • Reciprocal Inhibition: Concentric contraction of the functional ANTAGONIST muscle sends inhibitory signals via spinal interneurons to relax the opposing target muscle being stretched (e.g., actively contracting the gluteus maximus to reciprocally inhibit and stretch a tight hip flexor/psoas during Active-Isolated Stretching). |  |  |
| 13 | What is Delayed Onset Muscle Soreness (DOMS), when does it peak, what type of muscle action causes it, and what is the 'Repeated Bout Effect'? | DOMS is muscle pain, stiffness, and temporary loss of force peaking 24 to 72 hours after unaccustomed exercise—caused NOT by lactic acid (which clears within 60 minutes post-exercise!), but by structural microtrauma to Z-discs and sarcolemma primarily during ECCENTRIC (lengthening) muscle actions, followed by calcium homeostasis disruption and inflammatory edema/prostaglandin sensitization of Group III/IV nociceptors. The Repeated Bout Effect is the rapid protective adaptation whereby a single eccentric session protects against severe DOMS in subsequent workouts for weeks. |  |  |
| 14 | What is a Motor Unit, what is the All-or-None Principle, and how does Henneman's Size Principle govern motor unit recruitment? | • Motor Unit: A single alpha motor neuron and all of the individual muscle fibers it innervates. • All-or-None Principle: When a motor neuron fires an action potential, ALL muscle fibers within that specific motor unit contract maximally and simultaneously, or none do. • Henneman's Size Principle: Motor units are recruited in order from smallest to largest soma/axon diameter as force requirements increase: low-threshold Type I (slow-twitch) units are recruited first, followed by Type IIa, and finally high-threshold Type IIx (fast-twitch) units for maximal force/power. |  |  |
| 15 | What are the three primary mechanisms of exercise-induced Skeletal Muscle Hypertrophy (Brad Schoenfeld model), and what role do Satellite Cells play? | 1. Mechanical Tension (most important driver): Heavy external loading across a full range of motion activates mechanosensors (integrins) and the mTORC1 intracellular signaling pathway. 2. Metabolic Stress: Accumulation of anaerobic metabolites (lactate, H+, inorganic phosphate, cell swelling) during moderate-rep/short-rest training. 3. Muscle Damage: Micro-tears in Z-discs from eccentric loading trigger inflammatory repair. Satellite Cells (quiescent myogenic stem cells between sarcolemma and basal lamina) proliferate and donate their nuclei to damaged fibers to preserve the myonuclear domain and support protein synthesis. |  |  |
| 16 | What is the rate-limiting enzyme of each metabolic pathway: ATP-PCr, Glycolysis, Krebs (Citric Acid) Cycle, and the Electron Transport Chain? | • ATP-PCr system: Creatine Kinase (stimulated by elevated ADP, inhibited by elevated ATP). • Glycolysis: Phosphofructokinase (PFK). • Krebs Cycle: Isocitrate Dehydrogenase. • Electron Transport Chain: Cytochrome Oxidase. All are allosterically stimulated by high ADP/AMP and inorganic phosphate (Pi), and inhibited by high ATP, NADH, or citrate. |  |  |
| 17 | Compare the physiological definitions and Talk Test markers of Ventilatory Threshold 1 (VT1) and Ventilatory Threshold 2 (VT2) in the ACE/NASM Cardiorespiratory Model. | • Ventilatory Threshold 1 (VT1 — First Aerobic Threshold): The intensity where ventilation (`VE`) begins to increase non-linearly relative to oxygen uptake (`VO2`) as blood lactate rises slightly above baseline and bicarbonate buffering produces extra CO2. Talk Test: The point where continuous speaking becomes slightly uncomfortable ('can talk in complete sentences, but cannot sing'). • Ventilatory Threshold 2 (VT2 — Anaerobic Threshold / Respiratory Compensation Point / OBLA): Ventilation spikes dramatically due to unbuffered metabolic acidosis. Talk Test: Speech is limited to single words or short gasps ('cannot speak comfortably at all'). |  |  |
| 18 | What is the Valsalva Maneuver, how does it affect blood pressure and venous return, and in which populations is it strictly contraindicated? | The Valsalva Maneuver is a forced expiratory effort against a closed glottis (holding one's breath while straining during a heavy lift). It dramatically spikes intrathoracic and intra-abdominal pressure (enhancing spinal stability for competitive powerlifters), which initially causes an extreme spike in arterial blood pressure (>300/150 mmHg), then compresses the vena cava—collapsing venous return, stroke volume, and cardiac output (causing dizziness/syncope), followed by a rebound BP surge. Strictly contraindicated in clients with hypertension, cardiovascular disease, pregnancy, or glaucoma; instruct clients to exhale through the sticking point (concentric phase). |  |  |
| 19 | What are the acute and chronic responses of Anabolic Hormones (Testosterone, Growth Hormone, IGF-1, Insulin) vs. Catabolic Hormones (Cortisol, Catecholamines) to resistance exercise? | • Anabolic Hormones: Testosterone, Growth Hormone (GH), and Insulin-Like Growth Factor-1 (IGF-1) acutely spike most dramatically following workouts involving large-muscle-mass multi-joint exercises (squats, deadlifts), moderate-to-high volume (3–4 sets of 8–12 reps at 75–85% 1RM), and short rest intervals (60–90 seconds). Insulin promotes glucose/amino acid uptake and inhibits proteolysis. • Catabolic Hormones: Cortisol (adrenal cortex glucocorticoid) breaks down muscle protein for gluconeogenesis during prolonged energy depletion or chronic overtraining; Epinephrine/Norepinephrine (adrenal medulla) acutely mobilize glycogen/FFA and increase contractility. |  |  |
| 20 | Compare the chronic cardiovascular adaptations to Aerobic Endurance Training vs. Heavy Resistance Training (eccentric vs. concentric ventricular hypertrophy). | • Aerobic Endurance Training ('Athlete's Heart' — Volume Overload): Causes Eccentric Left Ventricular Hypertrophy (increase in left ventricular internal chamber cavity dimension + mild wall thickening), expanded plasma/blood volume, increased maximal Stroke Volume (EDV), and resting bradycardia (<60 bpm due to high vagal parasympathetic tone). • Heavy Resistance Training (Pressure Overload from high afterload/Valsalva): Causes Concentric Left Ventricular Hypertrophy (thickening of the interventricular septum and LV myocardial wall with minimal change in internal cavity volume). |  |  |
| 21 | What are the NSCA CSCS recommended Work-to-Rest Ratios for training the Phosphagen (ATP-PCr), Fast Glycolytic, and Oxidative energy systems? | • Phosphagen (ATP-PCr) System (90–100% max power, 5–10s work): Work-to-rest ratio of 1:12 to 1:20 (full phosphocreatine resynthesis requires 3–5 minutes; 50% replenished in ~30 seconds, 85–90% in 3 minutes). • Fast Glycolytic System (75–90% max power, 15–30s work): 1:3 to 1:5. • Fast Glycolytic + Oxidative (60–75% max power, 1–3m work): 1:3 to 1:4. • Oxidative System (<60% max power, >3m work): 1:1 to 1:3. |  |  |
| 22 | How does acute exposure to High Altitude (>1,200–1,500 meters / 4,000–5,000 feet) affect barometric pressure, PaO2, VO2max, and chronic acclimatization? | At high altitude, the percentage of oxygen in air remains constant at 20.93%, but lower Barometric Pressure decreases the Partial Pressure of Oxygen (`PO2`), reducing alveolar-capillary oxygen diffusion and arterial hemoglobin saturation (`SaO2`). Acute response: Immediate hyperventilation (causing respiratory alkalosis), increased submaximal heart rate and cardiac output, and decreased VO2max (~10% drop per 1,000m above 1,500m). Chronic acclimatization: Kidneys secrete Erythropoietin (EPO) within hours, increasing RBC mass and hematocrit over 2–4 weeks, accompanied by increased capillary density and 2,3-DPG. |  |  |
| 23 | Compare the anatomical structure, blood supply, and adaptation timeline of Tendons, Ligaments, and Hyaline Articular Cartilage. | • Tendons (connect muscle to bone; parallel Type I collagen bundles) and Ligaments (connect bone to bone; Type I collagen + elastin in multidirectional weave): Have poor vascularity compared to skeletal muscle and adapt much more slowly (require months of progressive loading across full ROM to increase collagen fibril diameter and covalent cross-linking). • Hyaline Articular Cartilage (Type II collagen + proteoglycans): Completely AVASCULAR and ANEURONAL; receives all nutrients and waste removal via synovial fluid diffusion driven by cyclic joint compression and decompression ('joint pump') during dynamic movement. |  |  |
| 24 | Describe the microscopic structure of the skeletal muscle Sarcomere (Z-disc, M-line, I-band, A-band, H-zone) and how each band changes during concentric contraction. | A sarcomere extends from Z-disc to Z-disc. • A-band (Anisotropic, dark): Entire length of thick Myosin filaments (with overlapping actin); DOES NOT CHANGE LENGTH during contraction. • I-band (Isotropic, light): Thin Actin filaments only (straddling the Z-disc) + titin; SHORTENS during contraction. • H-zone: Central region of the A-band containing thick myosin filaments only (no actin overlap); SHORTENS/DISAPPEARS during contraction as Z-discs are pulled toward the central M-line. |  |  |
| 25 | Compare the three metabolic energy systems (Phosphagen / ATP-PCr, Anaerobic Glycolysis, and Oxidative System) across fuel substrate, rate/capacity of ATP production, and primary activity duration. | 1. Phosphagen (ATP-PCr): Uses stored ATP and Phosphocreatine (creatine kinase); fastest rate of ATP production, lowest capacity; dominates 0–10 seconds of maximal power (1RM lift, 100m sprint). 2. Anaerobic Glycolysis: Breaks down blood glucose or muscle glycogen in sarcoplasm without oxygen; rapid ATP rate, intermediate capacity; dominates 15 seconds to 2 minutes of high-intensity effort (400m sprint). 3. Oxidative (Aerobic): Uses carbohydrates, fats (beta-oxidation), and protein in mitochondria (Krebs cycle + ETC); slowest rate, virtually unlimited capacity; dominates >2 minutes. |  |  |
| 26 | How is the Respiratory Exchange Ratio (RER) calculated, and what do RER values of 0.70, 0.85, 1.00, and >=1.10 indicate? | `RER = VCO2 / VO2` (volume of carbon dioxide expired divided by volume of oxygen consumed at the mouth). • `RER = 0.70`: 100% Fat oxidation (palmitic acid C16H32O2 requires 23 O2 to produce 16 CO2: `16/23 = 0.70`). • `RER = 0.85`: ~50% Carbohydrate and ~50% Fat oxidation (typical quiet rest is ~0.78–0.82). • `RER = 1.00`: 100% Carbohydrate oxidation (glucose C6H12O6 requires 6 O2 to produce 6 CO2: `6/6 = 1.00`). • `RER >= 1.10`: Criterion for achieving true VO2max during a graded exercise test (hyperventilation and bicarbonate buffering of lactic acid H+ ions expel non-metabolic CO2). |  |  |
| 27 | What are the primary muscles of Inspiration (at rest vs. forced exercise) and Expiration (at rest vs. forced exercise)? | • Quiet Resting Inspiration: Diaphragm (accounts for ~70% of tidal volume; flattens downward) and External Intercostals (elevate ribs outward). • Forced / Heavy Exercise Inspiration: Assisted by secondary inspiratory muscles—Sternocleidomastoid, Scalenes, Pectoralis Minor, and Serratus Anterior. • Quiet Resting Expiration: Completely PASSIVE (driven by elastic recoil of the lungs and thoracic cage). • Forced / Heavy Exercise Expiration: Active contraction of the Abdominal wall muscles (Rectus Abdominis, External/Internal Obliques, Transverse Abdominis) and Internal Intercostals. |  |  |
| 28 | How many net ATP molecules are yielded from 1 molecule of blood Glucose vs. 1 glycosyl unit of Muscle Glycogen during Anaerobic Glycolysis and Complete Aerobic Oxidation? | • Anaerobic Glycolysis (cytoplasm): Yields 2 net ATP from 1 blood glucose molecule (requires 2 ATP investment at hexokinase and PFK) vs. 3 net ATP from muscle glycogen (glycogen phosphorylase bypasses hexokinase). • Complete Aerobic Oxidation (Glycolysis + Krebs Cycle + Electron Transport Chain): Yields ~32 ATP from 1 blood glucose vs. ~33 ATP from muscle glycogen. |  |  |
| 29 | Define Stroke Volume (SV), End-Diastolic Volume (EDV), End-Systolic Volume (ESV), Ejection Fraction (EF), and the Frank-Starling Law of the Heart. | • Stroke Volume: `SV = EDV - ESV` (volume of blood pumped from the left ventricle per beat). • Ejection Fraction: `EF = (SV / EDV) x 100` (normal resting EF is 55–70%, increasing to >75–80% during intense exercise). • Frank-Starling Law: Within physiological limits, the force of ventricular contraction is directly proportional to the initial length (preload stretch) of cardiac muscle fibers at the end of diastole (increased venous return -> higher EDV -> stronger contraction -> higher SV). Stroke volume plateaus at ~40–60% of VO2max in untrained individuals. |  |  |
| 30 | Trace the time course of Neural Adaptations vs. Muscular Hypertrophy during the first 8–12 weeks of a new resistance training program. | • Weeks 1–6 (Neural Adaptations predominate): Rapid strength gains occur with minimal visible muscle cross-sectional growth due to improved motor unit recruitment, increased rate coding (firing frequency), motor unit synchronization, increased central neural drive, and decreased co-activation (autogenic/antagonist inhibition) of Golgi tendon organs and antagonist muscles. • Weeks 6–12+ (Hypertrophic Adaptations predominate): Structural skeletal muscle cross-sectional area increases via myofibrillar protein synthesis (actin and myosin filaments added in parallel). |  |  |
| 31 | Explain the fate of Pyruvate in Fast (Anaerobic) vs. Slow (Aerobic) Glycolysis, and describe the Cori Cycle. | When oxygen supply and mitochondrial capacity meet energy demand (Slow Glycolysis), pyruvate is transported into the mitochondria and converted by pyruvate dehydrogenase into Acetyl-CoA to enter the Krebs cycle. When glycolytic flux exceeds mitochondrial capacity (Fast Glycolysis), Lactate Dehydrogenase (LDH) reduces pyruvate into Lactate (oxidizing NADH back to NAD+ so glycolysis can continue). In the Cori Cycle, blood lactate is transported to the liver and converted back into glucose via gluconeogenesis. |  |  |
| 32 | Compare the Peripheral Vascular Responses (Total Peripheral Resistance and Diastolic Blood Pressure) to Dynamic Aerobic Exercise vs. Heavy Isometric/Resistance Exercise. | • Dynamic Aerobic Exercise (running, cycling): Systolic BP rises linearly with intensity (`~10 mmHg per 1 MET`), while Diastolic BP remains unchanged or decreases slightly (`+/- 10 mmHg`) because local metabolic vasodilation (NO, adenosine, K+) in large working muscle beds lowers Total Peripheral Resistance (TPR). • Heavy Isometric or Resistance Exercise: Both Systolic BP AND Diastolic BP increase substantially because sustained intramuscular mechanical compression (>40–60% MVC) occludes arterial blood flow through the contracting muscles, increasing TPR and cardiac afterload. |  |  |

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