Exercise physiology Study Guide

📖 Core Concepts Exercise Physiology – study of acute and chronic effects of physical activity on muscular, cardiovascular, and neuro‑hormonal systems. Acute Responses vs. Chronic Adaptations – immediate changes (HR, ventilation, hormones) vs. long‑term remodeling (mitochondria, capillaries, substrate use). Training Effect – repeated bouts → metabolic rate ↑, O₂ delivery ↑, contractile efficiency ↑. Energy Systems – phosphocreatine (PCr), fast glycolysis, adenylate kinase; each supplies ATP for a limited time span. VO₂ Max & Fick Equation – $VO2 = Q \times (a\!-\!vO2\text{diff})$; maximal O₂ uptake depends on cardiac output, pulmonary exchange, blood O₂‑carrying capacity, and muscle capillary density. Glucose Homeostasis in Exercise – balance of hepatic glucose output (glycogenolysis, gluconeogenesis) and muscle glucose uptake (GLUT4 translocation). Dehydration & Fluid Balance – hypohydration (pre‑exercise loss) vs. exercise‑induced dehydration (sweat > intake). Fatigue Models – peripheral (ion/homeostasis, calcium leak) and central (central governor, serotonin hypothesis). --- 📌 Must Remember PCr System: fuels first 10–30 s of maximal effort; reaction: PCr + ADP → ATP + Cr. Fast Glycolysis: supplies ATP for ≈ 2 min; produces lactate + H⁺ → acidosis. Adenylate Kinase: $2\ ADP \rightarrow ATP + AMP$. VO₂ Max Determinants: cardiac output, pulmonary diffusion, hemoglobin mass, muscle capillary density. Fick Equation: $VO2 = Q \times (a\!-\!vO2\text{diff})$. Glucose Appearance = Disposal → plasma glucose stable. GLUT4 Translocation occurs independently of insulin during contraction. Hormones rising in exercise: glucagon, epinephrine, growth hormone → hepatic glucose output ↑, lipolysis ↑. Dehydration >2 % body‑mass → aerobic performance ↓, HR ↑, perceived exertion ↑. Fluid Replacement Goal: replace 50–80 % of sweat loss during activity. Hyponatremia Risk: excessive fluid intake → plasma Na⁺ dilution → cerebral edema. Central Governor Theory: brain limits muscle power to protect homeostasis. Serotonin Hypothesis: ↑ plasma tryptophan → ↑ brain 5‑HT → fatigue sensation. --- 🔄 Key Processes PCr Energy Burst Creatine kinase catalyzes PCr + ADP → ATP + Cr → power output for 10–30 s. Fast Glycolysis Glycogen → Glucose‑6‑P → Pyruvate → Lactate + ATP (≈2 min). Accumulated H⁺ → intracellular pH ↓ → fatigue. Adenylate Kinase Regeneration $2\ ADP \rightarrow ATP + AMP$ provides rapid ATP during very short bursts. Glucose Regulation During Exercise Liver: glycogenolysis & gluconeogenesis (substrates: lactate, glycerol, pyruvate). Muscle: GLUT4 translocation → glucose uptake ↑ despite falling insulin. Hormonal drive: glucagon/epinephrine ↑ → hepatic output ↑, adipose lipolysis ↑. Cardiovascular Response HR ↑, stroke volume ↑ → cardiac output $Q = HR \times SV$. Redistribution of blood flow to working muscles; capillary recruitment ↑. Fluid Balance During Exercise Sweat loss → plasma volume ↓ → stroke volume ↓ → cardiac output ↓. Replace 50–80 % of sweat to maintain SV and HR. Fatigue Development (peripheral) Na⁺ influx, K⁺ efflux → Na⁺‑K⁺ pump overload → membrane depolarization. Ryanodine receptor leak → Ca²⁺ loss → reduced force. --- 🔍 Key Comparisons Phosphocreatine vs. Fast Glycolysis Duration: 10–30 s vs. ≈2 min. By‑product: Cr vs. lactate + H⁺. Insulin‑Dependent vs. Insulin‑Independent Glucose Uptake Insulin‑dependent: resting muscle, mediated by GLUT4 translocation via insulin signaling. Insulin‑independent: contracting muscle, GLUT4 translocation triggered by AMP‑activated protein kinase (AMPK). Dehydration vs. Hyponatremia Dehydration: fluid loss >2 % → performance ↓, HR ↑. Hyponatremia: excess fluid intake → plasma Na⁺ ↓ → cerebral edema. Peripheral Fatigue vs. Central Fatigue Peripheral: ion imbalance, Ca²⁺ leak, metabolic accumulation. Central: brain‑driven power regulation, serotonin rise, hyperthermia. --- ⚠️ Common Misunderstandings “Lactate is waste.” – It is a major fuel for heart, muscle, and brain; also a signaling molecule. “More fluid is always better.” – Over‑hydration can cause hyponatremia; aim for 50–80 % replacement. “Insulin is required for muscle glucose uptake during exercise.” – Contraction‑mediated GLUT4 translocation is insulin‑independent. “Fatigue is only due to lactic acid.” – Fatigue involves ion disturbances, calcium leak, CNS regulation, ROS, etc. “Higher VO₂ max always equals better performance.” – Efficiency, lactate clearance, and thermoregulation also crucial. --- 🧠 Mental Models / Intuition “Fuel Tank Model” – PCr = sprint tank (small, full instantly, empties fast). Glycolysis = mid‑range tank (moderate capacity, produces fumes). Oxidative system = cruise tank (large, refills slowly). “Cardiac Pump Equation” – Think of $VO2$ as water flow: flow (Q) × difference (a‑v O₂). Boost either flow (cardiac output) or extraction (capillary density) to raise VO₂. “Central Governor as a Thermostat” – The brain monitors temperature, metabolite levels, and “budget” of effort, throttling output to keep the system safe. --- 🚩 Exceptions & Edge Cases Altitude/Hyperoxia: VO₂ max limited by reduced arterial O₂ content; hyperoxia can raise $a\!-\!vO2$ diff but not cardiac output. Elite Endurance Athletes: May have blood doping (↑ red‑cell volume) → higher O₂ carrying capacity, but also increased viscosity. Type II Diabetes: Exercise‑induced GLUT4 translocation improves glucose disposal even with insulin resistance. Heat Stress: Even modest dehydration (>1 % body mass) can impair cognition and cerebral blood flow despite maintained VO₂. --- 📍 When to Use Which Choose PCr system for activities ≤30 s (e.g., 100‑m sprint, power lifts). Select Fast Glycolysis for efforts 30 s–2 min (e.g., 400‑m run, high‑intensity interval). Rely on Oxidative metabolism for >2 min sustained work (marathon, prolonged cycling). Apply fluid replacement (50–80 % sweat loss) during >60 min exercise or in warm/humid environments. Use insulin‑independent glucose strategies (e.g., pre‑exercise carbohydrate) for diabetic patients to lower post‑exercise glucose spikes. --- 👀 Patterns to Recognize “Drop in performance + rapid HR rise” → likely >2 % dehydration. “Early fatigue + high K⁺ accumulation” → peripheral ion imbalance. “Elevated lactate + stable pH” → efficient lactate clearance (trained athlete). “Sudden rise in cardiac biomarkers after marathon” → transient cardiac stress, not infarction (if normalizes <24 h). --- 🗂️ Exam Traps Trap: “Lactate accumulation is the primary cause of fatigue.” – Wrong; it’s a fuel and signaling molecule, not the sole cause. Trap: “If VO₂ max is high, dehydration has no effect.” – Incorrect; dehydration reduces stroke volume, lowering VO₂ despite high capacity. Trap: “Insulin must rise for muscles to take up glucose during exercise.” – False; contraction‑mediated GLUT4 translocation works without insulin. Trap: “All elevated troponin after a marathon indicates a heart attack.” – Misleading; usually a reversible rise due to cardiac stress. Trap: “Replacing 100 % of sweat loss eliminates performance loss.” – Over‑hydration risk; optimal is 50–80 % replacement.