The long slow run is a staple in endurance training designed to build your endurance by improving your utilization of the aerobic system through a variety of physiological and metabolic changes. Endurance can be defined as: “The capacity to sustain a given velocity or power output for the longest possible time”. An endurance runner wants to develop their aerobic energy system because they have a higher energy requirement that would not be sustained by the anaerobic energy system. If you are running slow enough on the long run, your energy needs will come from almost exclusively your aerobic system at around 96-99%. It is common for a novice runner to run too fast, thus not utilizing the aerobic system as much as it is intended during this type of training run. The long slow run is more about enhancing your aerobic capacity, as opposed to utilizing a higher percentage of it.
The aerobic energy system encompasses many complex steps, and there are steps along every phase of this pathway than can enhance its utilization and efficiency. The adaptations that happen in the body during endurance training ranges from an increase in heart size, increase in plasma volume, to higher volumes of enzymes that are used during the Krebs cycle such as pyruvic acid dehydrogenase. Physiological adaptations in the muscle are strongly correlated with increased aerobic performance. These adaptations are primarily to better utilize oxygen, which is used in the final phase of aerobic energy production via the electron transport chain. Some of these physiological adaptations, as related to endurance training include: 1) increase capillary density – in order to carry oxygen into the muscle tissue 2) myoglobin – which binds and releases the oxygen in the muscle fibers, and 3) increase in quantity and size of mitochondria, which enhances their ability to use oxidative phosphorylation for the breakdown of fat and carbohydrates for energy. Some studies have correlated an increase in mitochondria to increased ability to metabolize fat, which is another staple of energy efficiency, as your body produces 113 ATP through metabolizing fat as opposed to 30 ATP metabolizing carbohydrates through the aerobic system.
To optimally develop these things correlate strongly with running as a percentage range of your V02 max, for a specific duration. There were two breakthrough studies in the 1960’s and 1980’s by John O. Holloszy, and Gary Dudley, respectively. Holloszy first studied rats and mitochondrial growth at various run durations all with the same speed, which was measured roughly at 50-75% of the V02 max. He concluded that mitochondria are optimally developed during a run of 2 hours of duration. Dudley enhanced Holloszy’s study by measuring run intensity, not only duration, which supplemented the original research by determining that a slightly faster pace of 70-75% of V02 max will more optimally develop mitochondria than at 50%, but any faster than that will begin to diminish the rate of mitochondrial development. Endurance training also increases your V02, although this type of run is not the optimal training run to enhance this aspect. Endurance athletes will have a much higher V02 max, which is one of the cornerstone parameters of measuring aerobic fitness, as it allows for more oxygen to move through the body and to aid in the other physiological changes.
Essentially, running the correct pace, which is highly individualized and best measured as a percentage of your V02 max, along with timing your nutrition and hydration correctly, you will be utilizing almost exclusively your aerobic energy system and enhancing it during the long slow run.
 Jones, A., & Carter, H. (2000). The Effect of Endurance Training on Parameters of Aerobic Fitness. Sports Medicine, 29(6), 373–386.
 Gastin, P. B. (2001). Energy system interaction and relative contribution during maximal exercise. Sports Medicine (Auckland, N.Z.), 31(10), 725–741.
 Jones, A., & Carter, H.
 Dunford, M., & Doyle, J. Andrew. (n.d.). Nutrition for Sport and Exercise, 3rd Edition Cengage Learning. Pg. 80-85
 Jones, A., & Carter, H.
Dunford, M., & Doyle, J. Andrew, pg. 86
 Holloszy, J. O. (1967). Biochemical Adaptations in Muscle Effects Of Exercise On Mitochondrial Oxygen Uptake And Respiratory Enzyme Activity In Skelatal Muscle. Journal of Biological Chemistry, 242(9), 2278–2282.
 Dudley, G. A., Tullson, P. C., & Terjung, R. L. (1987). Influence of mitochondrial content on the sensitivity of respiratory control. Journal of Biological Chemistry, 262(19), 9109–9114.