Energy Systems - Fueling the Fire
ATP regeneration for exercise uses three systems, based on intensity and duration:
| Feature | ATP-PCr (Phosphagen) | Anaerobic Glycolysis | Aerobic System (Oxidative) |
|---|---|---|---|
| Onset | Immediate | Rapid | Slower |
| Duration | <10-15s (Maximal effort) | ~1-2 min (High intensity) | >2 min (Sustained) |
| ATP Yield | Very Low (1/PCr) | Low (2/glucose) | High (32+/glucose) |
| Power | Highest | High | Moderate/Low |
| Fuel | PCr | Glucose/Glycogen | Glucose, Fats, Amino Acids |
| Reaction | $PCr + ADP + H^+ \leftrightarrow ATP + Cr## Energy Systems - Fueling the Fire |
ATP regeneration for exercise uses three systems, based on intensity and duration:
| $Glucose \rightarrow 2ATP + 2Lactate## Energy Systems - Fueling the Fire
ATP regeneration for exercise uses three systems, based on intensity and duration:
| Krebs & Oxidative Phos. | | Examples | Sprints, lifts | 200-800m races | Endurance (Marathon) |> β Creatine phosphate (PCr) system provides ATP for the initial ~10-15 seconds of maximal intensity exercise, acting as the most rapid ATP buffer.
- Systems overlap; contribution varies with exercise type.
Hormonal Regulation - Conductors of Change
Key hormones adapt to fuel exercise demands. π CAGE: Hormones β in exercise: Cortisol, Adrenaline (Catecholamines), Glucagon. Growth Hormone also β.
| Hormone | Source | Stimulus (Exercise) | Major Actions (Exercise) | Trend |
|---|---|---|---|---|
| Insulin | Pancreas (Ξ²-cells) | β SNS, β Catecholamines (Ξ±-eff) | β Glucose uptake (inactive), β Anti-lipolysis | β |
| Glucagon | Pancreas (Ξ±-cells) | β Catecholamines, β Glucose | β Hepatic glycogenolysis & gluconeogenesis | β |
| Catecholamines | Adrenal Medulla/SNS | β SNS activity | β Glycogenolysis, β Lipolysis, β Glucagon, β Insulin | β |
| Cortisol | Adrenal Cortex | β ACTH (stress) | β Proteolysis, β Gluconeogenesis, β Lipolysis (permissive) | β |
| Growth Hormone | Anterior Pituitary | β Intensity/duration, β Glucose | β Lipolysis, β Gluconeogenesis, β Glucose uptake | β |
Tissue-Specific Metabolism - Cellular Symphony
- Skeletal Muscle:
- Fuel shift: Initial glucose (glycogen) β FFAs (adipose/IMTG) β Ketones (prolonged, intense).
- GLUT4 translocation: Insulin-independent (contraction via AMPK) & insulin-dependent.
- Lactate: $Pyruvate + NADH \leftrightarrow Lactate + NAD^+$. Cori cycle or oxidized by other tissues.
- BCAA oxidation for energy.
- Liver:
- Maintains blood glucose: Hepatic glycogenolysis & gluconeogenesis (substrates: lactate, alanine, glycerol).
- Urea cycle: Detoxifies ammonia ($NH_3$) from amino acid catabolism.
- Ketogenesis: During prolonged, high-intensity exercise.
- Adipose Tissue:
- Lipolysis β: Catecholamines activate HSL β FFAs + Glycerol released.
- FFAs (albumin-bound) fuel muscles; Glycerol for hepatic gluconeogenesis.
β AMPK (AMP-activated protein kinase): Master metabolic regulator. Activated by β AMP/ATP ratio during exercise. Stimulates glucose uptake (GLUT4 translocation) & fatty acid oxidation in muscle.
Adaptations to Training - Built to Last
- Chronic exercise: specific, lasting metabolic & physiological changes.
- Endurance Training (ET) adaptations:
- β Muscle glycogen & intramuscular triglyceride (IMTG) stores
- β Oxidative enzyme activity (e.g., citrate synthase)
- β Mitochondrial density & biogenesis (PGC-1Ξ± mediated)
- β Capillary density; β $VO_2$ max
- Fiber type: IIx β IIa shift; β Type I characteristics
- Enhanced fat oxidation, glycogen sparing.
- Resistance Training (RT) adaptations:
- β Muscle glycogen stores
- β Glycolytic enzyme activity (e.g., PFK)
- Muscle hypertrophy (β fiber cross-sectional area)
- β Strength & power
- Minimal change: mitochondrial density, $VO_2$ max (vs ET)
- Fiber type: IIx β IIa shift.
β Endurance training significantly increases mitochondrial biogenesis (e.g., via PGC-1Ξ±) and capillary density in muscles, enhancing oxidative capacity and leading to glycogen sparing.
vs. resistance training (fiber hypertrophy))
HighβYield Points - β‘ Biggest Takeaways
- ATP demand ββ; phosphocreatine provides immediate ATP.
- Muscle glycogen for initial burst; liver glycogenolysis & gluconeogenesis sustain blood glucose.
- Hormonal milieu: β glucagon, epinephrine, cortisol; β insulin, favoring catabolism.
- AMPK activation is crucial: β glucose uptake (muscle), β fatty acid oxidation.
- Prolonged exercise: β reliance on fatty acid oxidation from adipose stores.
- Lactate is a key fuel (Cori cycle, direct oxidation), not just waste_._
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