Exercise Physiology: ATP Systems, Metabolic & Cardiovascular Responses

ATP Production Pathways in Skeletal Muscle

  • Three concurrent, layered systems supply ATP\text{ATP} to working muscle fibres

  • Aerobic (cellular) respiration – mitochondria use oxygen, glucose & triglycerides. • Dominant while oxygen delivery is sufficient.

  • Anaerobic respiration (lactic-acid fermentation) – cytosolic glycolysis continues when aerobic flux is inadequate

    • Substrates = glucose, glycerol component of triglycerides.

    • Produces lactate, ↓pH

  • Phosphocreatine (PCr) shuttle – single-step, enzyme-catalysed phosphate transfer.

    • Creatine + ATP $\xrightarrow{\text{creatine kinase}} $ PCr + ADP (occurs at rest).

    • When [ATP] drops: PCr + ADP → ATP + creatine (one fast reaction).

    • Acts as an “external battery” that re-charges during rest (minutes).

    • Limited by total creatine & ATP pools.

Creatine Supplementation

• Oral creatine monohydrate ↑ intramuscular creatine → ↑ PCr “battery” size.
• Functional outcomes (typical):
• Greater ability to resynthesise ATP during brief, high-power efforts.
• ≈ 5 % improvement in force/volume; small but meaningful in competitive sport.

Hemoglobin O2 Dissociation During Exercise

  • Hemoglobin curve at rest

    • Aveolar O2 pressure ~ 100 mmHg → Hemoglobin saturation = 100%

    • Resting tissue O2 pressure = 40 mmHg

  • Hemoglobin curve during exercise:

    • Saturation is around 75 mmHg

    • Resting tissue saturation drops to 23%

    • contracting skeletal muscle O2 pressure can fall to 23 mmHg

    • Hb saturation ≈ 40%40\% ⇒ additional 35 % unloaded DURING EXCERCISE
      • Net O2 release ≈ 60 % of Hb content during intense exercise.

Metabolic Consequences of Increasing Intensity

  • ↑ motor-unit recruitment → ↑ cross-bridge cycling → ↑ ATP demand.

  • Aerobic output ramps until limited (often by O2 delivery).

  • Beyond limit: anaerobic ATP production ↑; lactic acid increases, increases H+ ↓ pH.

  • By-products: ↑ CO2, heat, catecholamines.

Feed-Forward vs Feedback Control at Exercise Onset

• Observed: ventilation & cardiac output jump within seconds – before acidosis, ↑PCO2 or ↓BP develop.
• Mechanism: “Central Command” feed-forward signal from higher brain centres (limbic, motor cortex).
• Resets set-points in medullary respiratory & cardiovascular centres.
• Feedback (chemo- & baro-receptors) then maintains new set-points.
• Anticipatory rise: HR often elevates on start line via same pathway.

Substrate Utilisation Across Intensities

  • At rest: ≈ 70 % ATP from fats, 30 % from carbohydrates.

  • With rising VO2 , there’s a decrease in fat usage, and in increase from carbohydrate usage

    • Fast twich fibers and epinephrine favor glycolysis

    • Total energy demand also increases, so absolute fat oxidation (blue fat % x total ATP rate) peaks near 60% VO2

VO(_2$$ Kinetics, Oxygen Deficit & EPOC

  • Exercise energy demand rises instantly, but measured VO2 lags 2-3 minutes which creates an oxygen deficit

    • Oyxgen deficit is govered by PCr breakdown, anaeorobic glycolysis, and myoglobin O2 storage

    • Post-exercise VO2 remains elevated (Excess Post-exercise O2 consumption- EPOC on the graph)

    • Rapid phase (≤3 min) – replenishes PCr, myoglobin O2 restores ion gradients.
      • Slow phase (≤30 + min) – lactate → glucose (Cori cycle), thermogenic & catecholamine effects maintain high metabolic rate.
      • Hyperventilating before work only modestly reduces deficit; cardiac output ramp remains limiting.

Cardiopulmonary Variables: Low vs High Intensity

  • Main comparisons (rest → low → high intensity):

  • Predominant fuel: fat → mixed → carbohydrate.

  • Main ATP pathway: aerobic → aerobic + anaerobic → anaerobic-dominant.

  • Motor units: small (Type I) → recruit larger (Type IIa) → all types

  • Ventilation: low → increases proportionally

  • Arterial Partial O2 pressure stays around 100 mmHg at ALL intensities

    • regulated by increased ventilation

    • Cardiac output & systolic BP progressively increase

  • Diastolic BP stays stable due to muscle vasodialation

    • Stroke volume increases and plateaus around 40% VO2 because reduced diastolic filling time offsets rising contractility

Left-Ventricular Pressure–Volume (PV) Loops in Exercise

• Intensities labelled Rest (C) → Light (A) → Heavy (B):
• End-systolic volume (ESV) ↓ as contractility ↑.
• Systolic pressure ↑ with intensity (reflects contractility).
• End-diastolic volume (EDV) ↑ from rest to moderate (more venous return) then ↓ at very high intensity (short diastole).
• Net result: loop becomes taller (higher pressure) & narrower (lower ESV); area (stroke work) ↑ until SV plateau.

Musculoskeletal Considerations

• Knee pain during leg extensions/squats usually due to:
• Overloading too quickly.
• Unresolved prior injury.
• Solutions: regress load, progress gradually, address pre-existing pathology, choose alternate movements.

Practical / Ethical / Application Notes

• Creatine is legal, inexpensive, generally safe
• Understanding feed-forward control aids clinical interpretation (e.g.
hyperventilation ≠ pathology if patient just climbed stairs).
• EPOC’s modest extra fat oxidation is not a major weight-loss tool by itself; intensity & duration still matter.