Sports

πŸ”Ή Energy Metabolism & Skeletal Muscle (Carbohydrate Lecture)

1. Role of Carbohydrates

  • Primary fuel for contracting skeletal muscle, especially at higher intensities.

  • Stored as muscle glycogen (~300–400 g) and liver glycogen (~80–110 g).

  • Glycogen depletion is a major cause of fatigue in endurance exercise.

πŸ“– Reference: Bergstrom et al. (1960s) β†’ discovery of glycogen’s role; led to CHO-loading recommendations.

2. Energy metabolism at different exercise intensities

  • Low–moderate intensity: fat provides more energy, CHO contribution lower.

  • High intensity (>80% VOβ‚‚max): muscle depends heavily on CHO, glycogen use ↑.

  • During prolonged exercise β†’ liver glycogen + gluconeogenesis help maintain blood glucose.

  • Hypoglycemia (<3 mmol/L blood glucose) causes dizziness, poor motor skill, ↓ concentration.

πŸ“– Reference: Krogh & Lindhart (1920s) β†’ exercise easier on high-CHO vs high-fat diet.
πŸ“– Christensen (1960s) β†’ high-intensity exercise uses more CHO.
πŸ“– Dill et al. (1960s) β†’ CHO feeding during exercise prolongs performance.

3. Regulation of Blood Glucose

  • Resting BG ~4–4.5 mmol/L.

  • Insulin ↓ during exercise (catecholamine effect).

  • Glucagon + epinephrine ↑ liver glycogenolysis & gluconeogenesis.

  • Muscle glucose uptake enhanced by contraction-stimulated GLUT4 (insulin-independent).

πŸ“– Levine et al. (1930s) β†’ CHO before/during marathon prevented hypoglycemia.

4. Carbohydrate Loading

  • Aim: maximize/supercompensate glycogen stores before endurance event (>90 min).

  • Classical model (1960s):

    • 3–4 d glycogen depletion (low CHO + hard training) β†’ then 3–4 d high CHO.

    • Issues: hypoglycemia, GI problems, mood, injury risk.

  • Modified model (Sherman 1981):

    • Just 3 d of high CHO (8–12 g/kg BM/d) + tapering exercise.

    • More practical, widely used.

Effects:

  • ↑ glycogen to ~150–250 mmol/kg ww (vs ~100–120 mmol/kg baseline).

  • Delays fatigue, extends steady-state exercise by ~20%, improves performance by ~2–3%.

πŸ“– Reference: Sherman et al. (1981) β†’ modified CHO loading effective.
πŸ“– Reference: Hawley (1997) β†’ ~20% delay in fatigue, 2–3% performance improvement.

5. Factors influencing carbohydrate use

  • Intensity: higher intensity = ↑ glycogen reliance.

  • Duration: prolonged β†’ greater risk of glycogen depletion/hypoglycemia.

  • Training status: trained athletes store more glycogen, oxidize fat better.

  • Pre-exercise CHO intake: ↑ glycogen stores.

πŸ“– Burke (2015) β†’ CHO loading guidelines.
πŸ“– Thomas et al. (2016) β†’ daily CHO recommendations (3–12 g/kg depending on training load).

✍ Revision Summary (for exam)

  • Carbohydrates = main fuel for skeletal muscle at high intensities.

  • Glycogen depletion = fatigue, hypoglycemia impairs CNS + motor function.

  • Liver glycogen + gluconeogenesis maintain blood glucose.

  • CHO loading boosts glycogen, delays fatigue, improves endurance performance (esp >90 min events).

  • Modified loading model (high CHO for 3 days + taper) is more practical than the classical depletion model.

  • Key refs: Krogh & Lindhart, Bergstrom, Sherman 1981, Hawley 1997, Burke 2015, Thomas 2016.

πŸ”Ή Fat as a Fuel During Exercise

1. Role of Fat in Skeletal Muscle Metabolism

  • Fat is the largest energy reserve in the body (~80,000–100,000 kcal in adipose tissue vs ~2,000 kcal glycogen).

  • Provides sustained energy at low–moderate exercise intensities.

  • Major sources:

    • Plasma free fatty acids (FFA) (adipose tissue lipolysis).

    • Intramuscular triglycerides (IMTG) (stored near mitochondria).

πŸ“– Key ref: Romijn et al. (1993) β†’ contribution of fat and CHO changes with exercise intensity.

2. Fuel Selection & Exercise Intensity

  • Low intensity (~25% VOβ‚‚max): mostly plasma FFA oxidation.

  • Moderate intensity (~65% VOβ‚‚max): fat oxidation peaks (mix of plasma FFA + IMTG).

  • High intensity (~85% VOβ‚‚max): fat oxidation suppressed, CHO dominates.

  • Suppression at high intensity due to:

    • Reduced adipose tissue blood flow (↓ FFA delivery).

    • ↑ lactate β†’ inhibits FFA mobilization.

    • Limited time for fat oxidation due to higher ATP turnover needs.

πŸ“– Key ref: Brooks & Mercier (1994) β€œcrossover concept” β†’ as exercise intensity ↑, fuel use crosses over from fat β†’ CHO.

3. Fat Oxidation & Endurance Training

  • Endurance training adaptations:

    • ↑ mitochondrial density.

    • ↑ IMTG storage in trained muscle.

    • ↑ capacity to mobilize & oxidize fat at given workload.

    • β€œGlycogen sparing effect” β†’ trained athletes use relatively more fat, preserving glycogen.

  • Benefit: delays glycogen depletion, enhances endurance capacity.

πŸ“– Key ref: Holloszy & Coyle (1984) β†’ endurance training increases fat oxidation.

4. High-Fat Diets & Performance

  • Short-term high-fat diets: increase fat oxidation but may impair high-intensity performance (due to ↓ muscle glycogen availability, ↓ glycolytic enzyme activity).

  • β€œFat-adaptation + CHO restoration” strategy: 5–7 d high-fat diet, then CHO load before event β†’ mixed evidence; may ↑ fat oxidation but performance benefits not consistent.

  • Ketogenic diets (very low CHO):

    • ↑ fat oxidation, ↓ reliance on CHO.

    • But ↓ ability to perform at high intensities (e.g. sprints, surges).

πŸ“– Key refs:

  • Burke et al. (2002) β†’ fat adaptation can ↑ fat oxidation, but no consistent performance gain.

  • Burke et al. (2017) β†’ ketogenic diet impaired performance in elite race walkers despite ↑ fat oxidation.

5. Practical Implications

  • Fat is important for long-duration, lower-intensity exercise.

  • For high-intensity or competitive endurance events, CHO remains critical.

  • High-fat or ketogenic diets are not generally recommended for athletes aiming for peak high-intensity performance.

✍ Revision Summary (for exam)

  • Fat = major energy store, fuels low–moderate intensity exercise.

  • At moderate intensity (~65% VOβ‚‚max), fat oxidation peaks (plasma FFA + IMTG).

  • At high intensity, CHO dominates (due to faster ATP needs + inhibited fat metabolism).

  • Endurance training ↑ fat oxidation (glycogen sparing).

  • High-fat or ketogenic diets ↑ fat oxidation but can impair high-intensity performance.

  • Key refs: Romijn 1993, Brooks & Mercier 1994 (crossover), Holloszy & Coyle 1984, Burke 2002, Burke 2017.

πŸ”Ή Protein & Exercise (Exercise and Protein Requirements_Feb2025_student version.pdf)

1. Protein & Muscle Protein Synthesis (MPS)

  • Resistance exercise stimulates MPS, but net muscle protein balance only becomes positive when dietary protein is ingested.

  • Amino acids (especially leucine) are key regulators of MPS.

  • Leucine threshold: ~2–3 g leucine (β‰ˆ20–25 g high-quality protein) required per meal to maximally stimulate MPS.

πŸ“– Refs: Tipton et al. (2001) β†’ protein + resistance exercise synergistically ↑ MPS.
Moore et al. (2009) β†’ 20 g high-quality protein (~3 g leucine) sufficient for maximal MPS in young adults.

2. Daily Protein Requirements

  • General population: 0.8 g/kg/d.

  • Athletes (IOC 2010, Thomas et al. 2016):

    • Endurance: 1.2–1.6 g/kg/d.

    • Strength/power: 1.6–2.2 g/kg/d.

  • Protein needs ↑ with energy deficit, injury, or intense training.

πŸ“– Refs: Phillips & Van Loon (2011); IOC Consensus Statement (2010).

3. Protein Timing

  • Post-exercise β€œwindow”: protein within 0–2 h enhances recovery and MPS.

  • Distribution over the day: 3–5 meals with 20–40 g protein (0.25–0.4 g/kg) each optimizes MPS.

  • Before sleep: casein protein (~40 g) ↑ overnight MPS.

πŸ“– Refs: Witard et al. (2014); Res et al. (2012, pre-sleep protein).

4. Protein Type & Quality

  • Whey protein: fast-digesting, high leucine β†’ potent stimulator of MPS.

  • Casein protein: slow-digesting β†’ supports overnight MPS.

  • Soy protein: plant-based, lower leucine content, but still effective (need larger amounts).

  • Mixed plant proteins can provide adequate EAAs if combined well.

πŸ“– Refs: Tang et al. (2009) whey > soy > casein for acute MPS.
van Vliet et al. (2015) β†’ plant proteins can support adaptations if sufficient dose.

5. Protein & Endurance Exercise

  • Endurance exercise increases amino acid oxidation (esp. BCAAs).

  • Protein important for repair, mitochondrial biogenesis, and immune function.

  • CHO + protein post-exercise enhances glycogen resynthesis compared with CHO alone if CHO intake is suboptimal.

πŸ“– Refs: Howarth et al. (2009); Betts & Williams (2010).

✍ Revision Summary (Protein)

  • Athletes need more protein than general population (1.2–2.2 g/kg/d).

  • Leucine threshold critical (~20–25 g protein/meal).

  • Spread intake evenly (3–5 meals + pre-sleep casein).

  • Whey > casein > soy for acute MPS.

  • Endurance athletes: protein aids recovery & glycogen resynthesis.

  • Key refs: Tipton 2001, Moore 2009, Phillips & Van Loon 2011, Witard 2014, Res 2012, Tang 2009.

πŸ”Ή Fluids & Hydration (Fluid Requirements of Athletes.pdf + Hydration and Health.pdf)

1. Body Water & Fluid Balance

  • ~60% body mass = water.

  • Exercise β†’ fluid losses via sweat (can be 1–2 L/h in hot/humid conditions).

  • Even 2% BM loss (dehydration) impairs performance (endurance, cognition, thermoregulation).

πŸ“– Sawka et al. (2007); EFSA (2010) hydration guidelines.

2. Fluid Requirements in Athletes

  • Before exercise: 5–7 mL/kg BW 4 h before exercise.

  • During exercise: aim to prevent >2% BM loss.

    • Typical: 0.4–0.8 L/h, depending on sweat rate.

    • For events >2 h: fluids with electrolytes + carbs (4–8%).

  • After exercise: replace 150% of fluid lost (to account for ongoing losses).

πŸ“– ACSM Position Stand (Sawka 2007); EFSA 2010.

3. Electrolytes & Sodium

  • Sweat contains Na⁺, Cl⁻, K⁺.

  • Sodium replacement important for events >2 h or heavy sweaters.

  • Hyponatremia risk if overdrinking water without sodium (esp. endurance events).

πŸ“– Hew-Butler et al. (2015) β†’ exercise-associated hyponatremia.

4. Hydration & Health

  • Inadequate hydration linked to ↑ risk of kidney stones, urinary tract infections, constipation.

  • Sugar-sweetened beverages (SSBs) associated with obesity, T2D, CVD risk.

πŸ“– EFSA 2010; IOM 2005; WHO guidelines on SSBs.

✍ Revision Summary (Fluids)

  • 2% dehydration impairs performance; sweat loss can exceed 1 L/h.

  • Pre-exercise: 5–7 mL/kg BW ~4 h before.

  • During: 0.4–0.8 L/h, CHO+Na for >2 h.

  • Post: 150% of fluid lost.

  • Risks: dehydration, overhydration (hyponatremia).

  • Key refs: Sawka 2007, EFSA 2010, Hew-Butler 2015.

πŸ”Ή Nutrition & Exercise in Disease Prevention

(Lecture slides (2025) HANDOUT nutrition and exercise in disease prevention.pdf + Past exam questions.pdf)

1. Obesity & T2D

  • Exercise ↑ insulin sensitivity, GLUT4 translocation.

  • Regular PA ↓ risk of T2D by ~30–40%.

  • Exercise + diet more effective than diet alone for weight management.

πŸ“– Refs: Knowler et al. (2002) Diabetes Prevention Program; Colberg et al. (2016) ACSM Diabetes guidelines.

2. Cardiovascular Disease (CVD)

  • Exercise improves endothelial function, ↓ BP, ↑ HDL, ↓ TGs.

  • High fruit/veg, fibre, Mediterranean diet patterns protective.

  • PA ↓ CHD risk by ~20–30%.

πŸ“– Refs: Blair et al. (1989) physical fitness & CVD mortality; Estruch et al. (2013) PREDIMED trial (Mediterranean diet).

3. Cancer

  • PA reduces risk of colon, breast, endometrial cancers.

  • Mechanisms: ↓ adiposity, ↓ sex hormones, ↑ immune surveillance.

  • WHO: β‰₯150 min moderate PA /wk recommended for prevention.

πŸ“– Refs: World Cancer Research Fund (2018).

4. General health

  • Adequate nutrition + regular exercise improves immune function, reduces inflammation, maintains musculoskeletal health (sarcopenia prevention).

πŸ“– Refs: ACSM 2010 Position Stand on PA & health.

✍ Revision Summary (Disease Prevention)

  • T2D: PA ↑ insulin sensitivity, ↓ risk ~30–40% (Knowler 2002).

  • CVD: exercise + Mediterranean diet ↓ risk, improves lipid profile (Blair 1989; PREDIMED 2013).

  • Cancer: PA protective for colon, breast, endometrial cancers (WCRF 2018).

  • General: PA + diet essential for chronic disease prevention.

πŸ”Ή Nutritional Ergogenic Aids

(Nutritional Ergogenic Aids.pdf)

1. Caffeine

  • Dose: 3–6 mg/kg ~60 min before exercise.

  • Benefits: ↑ endurance, alertness, reduced perceived exertion, performance in stop-and-go sports.

  • Risks: GI upset, insomnia, anxiety.

πŸ“– Refs: Graham (2001); Spriet (2014).

2. Creatine

  • Dose: 20 g/d (5–7 d) then 3–5 g/d maintenance.

  • Benefits: ↑ phosphocreatine stores, ↑ high-intensity, short duration exercise (e.g., sprint, strength).

  • Evidence strongest among ergogenic aids.

  • Safe for long-term use.

πŸ“– Refs: Kreider et al. (2017, ISSN Position Stand).

3. Sodium Bicarbonate

  • Dose: 0.3 g/kg 1–2 h before exercise.

  • Buffering agent β†’ delays acidosis, improves performance in 1–10 min high-intensity events.

  • Risks: GI distress.

πŸ“– Refs: Carr et al. (2011).

4. Ξ²-Alanine

  • Dose: 4–6 g/d for 4–6 wk.

  • ↑ muscle carnosine β†’ buffer H+ in muscle.

  • Benefits: repeated high-intensity efforts, events 1–4 min.

  • Risks: paraesthesia.

πŸ“– Refs: Hobson et al. (2012).

5. Beetroot juice (Nitrate)

  • Dose: 5–8 mmol nitrate ~2–3 h pre-exercise.

  • Benefits: ↓ Oβ‚‚ cost of exercise, ↑ time-to-exhaustion, improved performance in moderate-intensity endurance.

  • Less benefit in elite athletes.

πŸ“– Refs: Bailey et al. (2009); Jones (2014).

6. Others

  • Glycerol: once used for hyperhydration; banned by WADA (2010s).

  • Risks: contamination, banned substances (DSHEA regulation issues).

✍ Revision Summary (Ergogenic Aids)

  • Caffeine (3–6 mg/kg), creatine (high-intensity), sodium bicarb (buffering), Ξ²-alanine (carnosine), beetroot (Oβ‚‚ cost).

  • Creatine + caffeine = strongest evidence.

  • Consider side effects, legality, and individual response.

  • Key refs: Graham 2001, Kreider 2017, Hobson 2012, Bailey 2009.

πŸ”Ή Micronutrients – Vitamin D

(VitD_April2025.pdf + Micronutrients For Athletes.pdf)

1. Vitamin D & Health

  • Regulates calcium, bone health, muscle function, immunity.

  • Deficiency β†’ ↑ risk of stress fractures, impaired muscle recovery, illness.

πŸ“– Refs: Holick (2007); Larson-Meyer & Willis (2010).

2. Sources & Status

  • Synthesized in skin (UVB exposure) + dietary sources (oily fish, fortified foods).

  • Serum 25(OH)D is status marker.

  • Deficiency common in indoor athletes, winter, higher latitudes.

πŸ“– Refs: Holick 2007; Owens et al. (2018).

3. Supplementation

  • 1000–2000 IU/d recommended for at-risk athletes.

  • May improve muscle strength, sprint performance in deficient athletes.

  • No clear benefit if already sufficient (>75 nmol/L).

πŸ“– Refs: Close et al. (2013) β†’ supplementation improved sprint capacity in deficient athletes.

✍ Revision Summary (Vit D)

  • Vit D essential for bone, muscle, immunity.

  • Deficiency common in athletes (indoor, winter).

  • Supplementation beneficial if deficient (<50 nmol/L).

  • Key refs: Holick 2007, Larson-Meyer 2010, Close 2013.