A.2.3 Energy systems – Comprehensive study notes
A.2.3 Energy systems
Syllabus understandings
A.2.3.1 The body relies on the phosphagen, glycolytic and oxidative systems for energy production to sustain life and physical activity.
A.2.3.2 Maximal oxygen consumption (VO2max) is influenced by an individual's age, sex differences, body composition, lifestyle factors and level of fitness.
A.2.3.3 The lactate inflection point is the maximum intensity at which the body can metabolize lactate at the same rate as its production.
A.2.3.4 Excess post-exercise oxygen consumption (EPOC) is required for the body to return to homeostasis and is dependent on the oxygen deficit incurred during exercise. EPOC is typically divided into two subsections: fast and slow.
Introduction to energy and macronutrients
The amount and composition of carbohydrates, fats and proteins in the diet determine energy availability.
Macronutrients that can be stored easily (e.g., fat in adipose tissue) are metabolized more slowly than proteins, which the body cannot store in large amounts.
After a mixed meal, the body metabolizes proteins first, then carbohydrates, then fat.
Not all energy in food is metabolizable. Fibre cannot be digested/absorbed (energy lost in faeces). Even digestible nutrients have end products with energy; e.g., urea and ammonia in protein metabolism. Only metabolizable energy of food is relevant for human energy metabolism.
Metabolism
Metabolism = all chemical processes in living organisms required for maintenance of life.
Two phases:
Anabolism: constructive phase; smaller molecules → larger molecules (e.g., glucose → glycogen).
Catabolism: destructive phase; larger molecules → smaller molecules (e.g., triglycerides → glycerol + fatty acids).
The role of mitochondria
All cells require energy for biological work; mitochondria are the sites of aerobic metabolism and the only site where oxygen is used (except red blood cells, which lack mitochondria).
Mitochondria host the Krebs cycle and the electron transport chain (ETC).
The Krebs cycle produces a large amount of ATP.
Carbohydrates and fats are the principal energy substrates; proteins contribute ~15% of resting energy metabolism.
Mitochondrion ultrastructure: cristae, matrix, inner membrane, outer membrane (Figure 1).
The ATP energy currency
In cells, catabolic reactions release energy that is captured in ATP.
ATP is the universal energy currency of the cell (Figure 4).
ATP hydrolysis releases energy when a phosphate group is split from ATP:
\mathrm{ATP} + \mathrm{H2O} \rightarrow \mathrm{ADP} + \mathrm{Pi} + \text{energy}
In phosphorylation, ATP is regenerated from ADP by adding a phosphate group.
The ATP-ADP-Pi cycle connects energy release to cellular work.
Energy provision in muscle and the energy systems
Muscle contraction requires ATP; actin–myosin interactions use ATP for chemical energy to drive contraction.
A resting muscle contains enough ATP for about 2 seconds of activity; longer efforts require ATP from other sources.
The energy systems operate within muscle fibers to continuously supply ATP during movement.
Carbohydrate metabolism
Carbohydrates are digested to monosaccharides (glucose, fructose, galactose).
In the liver, fructose and galactose are converted to glucose; glucose is then delivered to tissues.
Glycolysis (in the cytosol) breaks glucose down to pyruvate, yielding ATP and NADH.
Under aerobic conditions, pyruvate enters mitochondria and is oxidized to CO2 and H2O via the Krebs cycle and ETC.
Under anaerobic conditions (e.g., high-intensity exercise), pyruvate is reduced to lactate; lactate can be transported to the liver for gluconeogenesis (Cori cycle) or oxidized to pyruvate in muscle.
Glucose storage and mobilization
Glucose stored as glycogen in liver and muscle via glycogenesis.
When energy is needed, glycogen is broken down to glucose-6-phosphate in muscles, and glycogenolysis releases glucose for energy.
This glycogen-derived glucose supports immediate energy for muscle in work.
Key point (glycolysis and glycogen):
Glucose is broken down to provide energy via glycolysis (the breakdown of glucose to pyruvate).
Glucose not used immediately is stored as glycogen (glycogenesis).
When glycogen energy is needed, it is turned back into glucose (glycogenolysis).
Carbohydrate pathways (summary):
Glycogenolysis → Glycolysis → Pyruvate → (aerobic) Acetyl-CoA → Krebs cycle → ETC → ATP
Pyruvate fate: under aerobic conditions, pyruvate becomes acetyl-CoA; under anaerobic conditions, lactate is produced.
Beta-oxidation and fat oxidation (intro to fat metabolism)
Fat oxidation occurs via β-oxidation in mitochondria, with transport of fatty acids by the carnitine shuttle into the mitochondrial matrix.
The β-oxidation cycle shortens the fatty acid by two carbons per cycle, generating acetyl-CoA units that enter the Krebs cycle.
Fatty acids (especially mono-/polyunsaturated) may be oxidized more slowly than saturated fats, and overall energy yield depends on chain length and degree of saturation.
Higher oxidation of fats occurs in aerobic conditions; fats are not used during high-intensity, anaerobic activity.
Lipolysis and fat stores
Excess energy from fat is stored as triglycerides in adipose tissue and muscles.
Lipolysis releases triglycerides from stores, yielding glycerol and fatty acids for β-oxidation.
Anaerobic energy systems
Phosphagen (creatine phosphate) system
PCr provides rapid ATP resynthesis in the early phase of exercise, supplementing the small amount of ATP already present in muscle.
The creatine kinase reaction can proceed quickly and is important during high-intensity efforts (e.g., sprinting).
PCr contribution dominates for up to the first ~20 seconds of all-out exercise; stores can be replenished during rest.
The reaction is reversible: during recovery, ATP can be used to resynthesize PCr in muscle.
Key reaction (conceptual): \mathrm{PCr} + \mathrm{ADP} \rightleftharpoons \mathrm{ATP} + \mathrm{Cr} (catalysed by creatine kinase)
Glycolytic system (anaerobic glycolysis)
When aerobic capacity is limited (oxygen or mitochondria), pyruvate is converted to lactate (glycolysis).
This yields a small amount of ATP (net 2 ATP per glucose) but can occur very quickly, supporting high-energy demands of hard exercise.
As PCr stores fade, glycolysis increasingly dominates energy provision, but this energy supply is short-lived.
Hormonal regulation of energy metabolism
Hormones coordinate energy availability and substrate utilization:
Insulin
Released after a meal when blood glucose rises; promotes glucose uptake via GLUT4 (especially in skeletal muscle) and glycogen synthesis (glycogenesis).
Stimulates glycolysis, inhibits gluconeogenesis, and suppresses lipolysis and protein breakdown.
Glucagon
Secreted during fasting or exercise when blood glucose falls; stimulates glycogenolysis and gluconeogenesis to raise blood glucose; activates lipolysis to provide fatty acids for energy.
Epinephrine (adrenaline)
Acts similarly to glucagon, promoting glycogenolysis and lipolysis in response to stress/exercise;
Can act in concert with glucagon to mobilize energy substrates.
Other hormones: cortisol and growth hormone also influence metabolism during prolonged exercise and fasting.
Glucose uptake and transport into muscle
Blood glucose enters cells via GLUT transporters; insulin stimulates GLUT4 translocation to the cell membrane to increase uptake.
Muscle contractions can also stimulate GLUT4 translocation independent of insulin, aiding glucose uptake during exercise.
Insulin promotes glycolysis and glycogenesis; suppresses gluconeogenesis and lipolysis.
Linking concepts: energy systems during exercise and regulation
At exercise onset, anaerobic systems dominate due to immediate ATP demand.
Pre-existing ATP in muscle provides energy for the first ~2 seconds.
PCr contribution fades after ~20 seconds; glycolysis becomes more active to supply ATP quickly.
As exercise continues, the oxidative (aerobic) system rapidly increases and eventually dominates energy provision.
Fat oxidation occurs primarily during aerobic, lower-intensity activity; fats are not used during high-intensity, anaerobic activity.
Glucose is important across the full range of intensities; fatty acids are more prominent at lower intensities.
PCr contributes only to brief, high-intensity work; its contribution ends after ~20 seconds of all-out effort.
Exercise is dynamic: bouts of high intensity with rest/recovery periods rely on phosphagen and glycolytic systems, interspersed with aerobic metabolism.
Patterns of energy systems by exercise type (Figure 14 and 15 summary)
Relationship between exercise intensity and rate of ATP demand:
Fatty acids (aerobic) and carbohydrates (aerobic and anaerobic) supply energy as intensity increases.
PCr (anaerobic) contributes at the onset of high-intensity effort.
Relative contributions to ATP synthesis across exercise types:
Low-intensity, long-duration (e.g., marathon): predominantly oxidative metabolism with substantial fat oxidation.
Moderate to high-intensity: increasing carbohydrate oxidation and glycolytic contribution.
Maximal intensity (short duration, e.g., sprint): dominated by PCr and glycolysis (anaerobic) with limited contribution from fats.
CHO = carbohydrates (glucose);
FFA = free fatty acids; PCr = phosphocreatine; Cr = creatine.
Activity 1 (conceptual diagram task)
Draw relationships among:
liver, muscle, bloodstream, food, glucose, glycogen, lactate, carbon dioxide, water, glycolysis (aerobic & anaerobic), glycogenolysis, glycogenesis.
Aerobic (oxidative) energy system: glucose oxidation and fat oxidation
Final fate of glycolysis-derived pyruvate depends on oxygen availability:
In presence of oxygen: pyruvate → acetyl-CoA → Krebs cycle → ETC → CO2 + H2O; hydrogen ions are carried by NADH/FADH2 to the ETC to drive ATP synthesis.
In absence of oxygen: pyruvate is reduced to lactate; lactate can be transported to liver for gluconeogenesis or oxidized back to pyruvate in muscle.
Fat oxidation details (β-oxidation):
Fatty acids enter mitochondria via carnitine shuttle; in the matrix, β-oxidation shortens the fatty acid by two carbons per cycle to form acetyl-CoA.
Each cycle yields reducing equivalents (NADH, FADH2) that inform ATP production via the ETC; acetyl-CoA enters the Krebs cycle.
The energy yield is influenced by chain length and level of saturation; unsaturated fats are generally oxidized more readily than saturated fats.
Important health and dietary implications:
The rate of fat oxidation and its involvement in energy production are influenced by the type of fat consumed; slower oxidation can lead to longer presence of fatty acids in the bloodstream and influence cholesterol metabolism and cardiovascular risk.
Energy systems and endurance nutrition (brief discussion prompts)
A high-carbohydrate diet improves endurance performance and carbohydrate intake during exercise can delay fatigue.
Consider research directions: the role of sports drinks and energy bars during endurance performance and the impact of the sports nutrition industry on future research.
Oxidative (aerobic) energy system and VO2max
VO2max = maximal oxygen uptake; the maximum rate at which an individual can take in and use oxygen; gold standard for evaluating cardiovascular–respiratory function.
Central factors (circulatory): maximal cardiac output is a primary determinant of VO2max in most healthy individuals.
Peripheral factors (muscular): muscle oxidative capacity, mitochondrial density, capillary density, and myocyte oxygen extraction also influence VO2max.
Absolute vs relative VO2max and population ranges
Absolute VO2max: measured in L min^-1 (L/min).
Relative VO2max: normalized to body mass, measured in ml kg^-1 min^-1 (ml kg^-1 min^-1).
Relative VO2max is preferred for weight-bearing activities to account for body size differences.
Example: A 70 kg person with VO2maxabs = 3.01 L/min → VO2maxrel ≈ 42.9 ml kg^-1 min^-1; a 58 kg player with the same VO2maxabs would have VO2maxrel ≈ 51.7 ml kg^-1 min^-1.
Humans exhibit wide variability; some elite endurance athletes exceed 90 ml kg^-1 min^-1; very ill individuals may fall below 20 ml kg^-1 min^-1.
Population ranges (typical relative VO2max, 20-year-olds):
Untrained males: 40–45 ml kg^-1 min^-1; females: 35–40 ml kg^-1 min^-1
Moderately trained males: 45–55; females: 40–50
Professional team sport athletes: males 50–60; females 45–55
Top endurance athletes: males > 65; females > 55
Table 1 notes: These are population averages with substantial individual variation.
VO2max and sex differences
Absolute VO2max is typically lower in biological females than males due to smaller heart size, lower blood volume, and lower haemoglobin concentration.
Even relative VO2max is typically lower in females, though the gap narrows with higher training status.
Key factors contributing to differences:
Cardiac output (smaller heart in females)
Blood volume and haemoglobin concentration
Lung capacity
Body composition (higher fat percentage impacting mass-normalized VO2max)
Sex differences in body size and muscle mass also influence strength, power, and anaerobic performance.
Running biomechanics differences may contribute to endurance performance differences.
Some studies suggest females may have more slow-twitch fibers and greater fatty acid oxidation during prolonged running, but other factors counterbalance this advantage.
VO2max and age
Age-related changes: absolute VO2max tends to peak in adolescence for females (mid-teens) and in early adulthood for males (early 20s); relative VO2max declines with growth and maturation, influenced by body composition changes.
Expression matters: relative VO2max is influenced by body mass, so weight gain in adolescence can lower relative VO2max even if absolute VO2max is stable or rising.
Across adulthood, VO2max generally declines by about 1% per year on average, largely due to a gradual decline in maximal heart rate; training can slow this decline.
The practical point: an inactive older adult may have a much lower VO2max than a trained younger person, but training can markedly improve VO2max in older adults (masters athletes still show high VO2max and endurance).
Peak training effects can still yield substantial gains in older adults, e.g., Fauja Singh's marathon at age 100.
VO2max and training adaptations
Training can increase VO2max; improvements are due to central adaptations (cardiovascular) and peripheral adaptations (muscle).
Central adaptations: increased stroke volume, leading to higher cardiac output and improved oxygen delivery.
Peripheral adaptations: increased capillarization and mitochondrial density; improved muscle oxygen extraction.
The main mechanism for increased VO2max is increased stroke volume via enlargement of the left ventricle, allowing more blood to fill before each beat.
Training also reduces submaximal heart rate and can improve efficiency; maximum heart rate remains largely unchanged, but achieving it requires greater effort post-training due to higher capacity.
Genetic influences on VO2max
Genetic variation explains some differences in VO2max between individuals.
Twin studies (identical vs. fraternal) show that training improves VO2max in both groups, but identical twins show more similar responses, indicating a genetic component.
Concept of a genetic ceiling: everyone may have a potential VO2max ceiling set by genes; training can push toward that ceiling, but the ceiling itself varies.
This explains why some individuals respond better to training than others, yet everyone benefits from aerobic training to some extent.
VO2max and type of exercise
VO2max values depend on the mode of exercise; running generally yields higher VO2max than cycling for the same individual due to involvement of more muscle mass (including upper body and postural muscles).
Cross-country skiing often yields the highest VO2max values because it engages upper-body muscles in addition to large lower-body muscle groups.
Running economy (RE)
RE is the steady-state oxygen consumption at a given submaximal running speed; lower oxygen cost at the same speed indicates better RE.
RE is a predictor of endurance performance and reflects the integrated function of metabolic, cardiovascular, biomechanical and neuromuscular systems.
RE can be improved with training; athletes with the same VO2max can have different RE, influencing performance at submaximal speeds.
Example (conceptual): two runners with the same VO2max may show different RE profiles at the same velocity, leading to different endurance performances.
Evaluation and synthesis (study prompts)
Activity 2: Evaluate dominating energy systems during different sports (e.g., rugby, Tour de France cycling, high jump) and label a diagram by sport type and energy system contribution (phosphagen, glycolytic, oxidative).
Activity 3: Discuss genetic vs training determinants of VO2max, referencing twin studies and the concept of a genetic ceiling; explain why identical twins show more similar training responses than non-identical twins.
Linking questions and ATL thinking: reflect on how ATP availability constrains muscular contraction and how metabolic pathways adapt to meet energy demands during different activities.
Key terms and concepts (glossary)
Anabolism, Catabolism, Metabolism
Mitochondria, Krebs cycle, Electron Transport Chain (ETC)
ATP, ADP, Pi (inorganic phosphate)
Glycolysis, Pyruvate, Lactate, Gluconeogenesis, Glycogenesis, Glycogenolysis
β-oxidation, Carnitine shuttle, Acetyl-CoA
Lipolysis, Triglycerides, Free fatty acids (FFA)
Phosphagen system, Phosphocreatine (PCr), Creatine kinase
VO2max, Absolute VO2max, Relative VO2max
Running economy (RE)
GLUT4, Insulin, Glucagon, Epinephrine, Cortisol, Growth hormone
EPOC (fast and slow components)
Lactate inflection point
Notable figures referenced (described in notes)
Figure 1: Ultrastructure of a mitochondrion (cristae, matrix, inner/outer membranes)
Figure 2: Chemical structure of ATP
Figure 3: Energy is released from ATP when a phosphate group splits away
Figure 4: Involvement of ATP in cellular energy provision
Figure 6: Pathways in carbohydrate metabolism (glycogenolysis, glycolysis, gluconeogenesis, pyruvate, lactate)
Figure 7: Liver and muscle roles in carbohydrate metabolism
Figure 8: Aerobic glucose oxidation
Figure 9: β-oxidation of palmitic acid
Figure 10–12: Glucose uptake and lactate monitoring mechanisms
Figure 14: Relationship between exercise intensity and rate of ATP demand
Figure 15: Relative contributions of energy systems during three exercise types
Figure 16–17: Activity diagrams for energy systems in different sports
Figure 18: Fauja Singh (100-year-old marathon finisher)
Figure 19: VO2max by age and sex
Figure 20: Running economy profiles for two athletes with identical VO2max
Practical implications and ethical considerations
Historical research on carbohydrate metabolism and sport performance informed dietary practices for endurance athletes.
Ethical considerations: research in animals (mice, rats, hamsters) raises concerns about welfare, necessity, and applicability to humans; questions asked include justification of animal use and relevance to human metabolism.
Real-world relevance: training programs aim to improve VO2max and running economy; choosing fats and carbohydrates thoughtfully can influence endurance performance and cardiovascular risk profiles.
Summary takeaways
Energy for muscle contraction comes from three overlapping systems: phosphagen (fastest, brief), glycolytic (moderate speed, short-lived), oxidative (slowest, sustainable).
The predominance of each system shifts with exercise intensity and duration; fats are primarily used in aerobic, lower-intensity efforts, while carbohydrates provide energy across a broader range of intensities.
VO2max is a central marker of endurance capacity, influenced by age, sex, body composition, training, and genetics, and can be enhanced with aerobic training via central (heart) and peripheral (muscle) adaptations.
Running economy and CV efficiency critically determine endurance performance, sometimes more than VO2max alone.
Equations and key quantitative relationships (LaTeX)
ATP hydrolysis (energy release): \mathrm{ATP} + \mathrm{H2O} \rightarrow \mathrm{ADP} + \mathrm{Pi} + \text{energy}
Glycolysis (net, glucose to pyruvate, anaerobic): \text{Glucose} + 2\mathrm{NAD^+} + 2\mathrm{ADP} + 2\mathrm{Pi} \rightarrow 2\text{Pyruvate} + 2\mathrm{NADH} + 2\mathrm{ATP} + 2\mathrm{H2O} + 2\mathrm{H^+}
Pyruvate → Acetyl-CoA (aerobic entry to Krebs): \text{Pyruvate} + \mathrm{CoA} + \mathrm{NAD^+} \rightarrow \text{Acetyl-CoA} + \mathrm{CO_2} + \mathrm{NADH}
Fatty acid β-oxidation (palmitoyl-CoA example, simplified): \text{Palmitoyl-CoA} + 7\mathrm{FAD} + 7\mathrm{NAD^+} + 7\mathrm{CoA} + 7\mathrm{H2O} \rightarrow 8\text{Acetyl-CoA} + 7\mathrm{FADH2} + 7\mathrm{NADH} + 7\mathrm{H^+}
VO2max (relative, general expression): \text{VO2max}{rel} = \frac{VO2max{abs} \times 1000}{m} {- where }VO2max_{abs}\text{ is in L/min and }m\text{ is body mass in kg.}
End of notes