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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