By Edward F. Coyle, Ph.D.- University of Texas at Austin
Running a marathon at the fastest speed possible seems limited by the aerobic metabolism of a limited amount of carbohydrate energy and the economical conversion of this energy to velocity. Aspects of this concept have been long recognized. Approximately 35 years ago D.L. Costill wrote a monograph entitled 'What Research Tells the Coach About Distance Running' in which he distilled the physiological literature into an intuitive paradigm that focused upon maximal oxygen uptake and its fractional utilization as well as running economy (1). The validity of these concepts for predicting marathon performance was validated by Farrell et al in 1979 (2) and the utility of blood lactate measures for identifying competitive marathon running pace was further solidified. By this time, the phenomenon of 'hitting the wall' during a marathon due to inadequate carbohydrate oxidation was linked largely to muscle glycogen depletion. Therefore, the frame work under which to view the physiological limits to marathon performance is similar today as that discussed thirty years ago during the meeting sponsored by the NY Academy of Sciences (1976).
Oxidative ATP Resynthesis. The key concepts of this framework are displayed in Figure 1. Marathon runners perform at the highest velocity and rate of oxygen consumption (i.e.; VO2 of marathon) that their exercising muscles are able to tolerate without experiencing fatigue that progresses and causes them to slow during the first 20 km. The VO2 during a properly paced competitive marathon is the highest steady-state rate of oxidative ATP resynthesis possible.
Figure 1. Concept of the physiological factors limiting marathon performance.
One cause of muscle fatigue might be progressive acidosis and or ionic disturbance. Marathon velocity approximates the intensity at which lactate begins to accumulate in the blood (i.e.; the blood lactate threshold) as well as the muscle fibers (2). The measurement of blood lactate to estimate competitive marathon pace has become popular because it is practical and theoretically sound. The concept is not that the lactate molecule per se causes fatigue, but rather that it's accumulation in blood reflects a disturbance of muscle cell homeostasis.
Marathons are run at intensities well below maximal oxygen consumption (e.g.: 65-85 % VO2max) and because fatigue is associated with accelerated glycogenolysis and not muscle hypoxia, it could be hypothesized that increases in oxygen delivery to exercising muscle (e.g.; blood flow and hemoglobin concentration) would do little to increase marathon velocity. However, it is possible that increased oxygen delivery that raises muscle oxygen pressure could elicit an improved redox state (e.g.; NAD/NADH; ADP/ATP ratio) that slows glycogenolysis for a given rate of oxidative ATP regeneration or a given running velocity.
Marathon Duration and Thus Intensity. Top marathon runners finish in approximately 2.5 h or faster whereas the majority of runners in charity races finish in 4-5 h. Given the inverse relationship between exercise duration and intensity, coupled with the fact that better endurance athletes can exercise at a higher VO2 before fatigue, there exists a wide range regarding % VO2max during competition in various individuals. On one end, slow runner may average 50-60% VO2max, whereas top runner can average over 80% VO2max. If running economy is not different when comparing given slow and fast runners, the total caloric expenditure by definition would be the same yet the respiratory exchange ratio and total amount of carbohydrate oxidized should be higher in the faster runner. The author is not aware of data addressing the possibility that slow and fast marathon runners differ in the extent to which carbohydrate depletion causes fatigue.
Carbohydrate and Fat Metabolism. Top marathon runners derive more than two-thirds of their energy from carbohydrate stemming from muscle glycogen and to a lesser extent blood glucose oxidation. Exercise at 70-85% VO2max can not be maintained without sufficient carbohydrate oxidation and thus the severe lowering of muscle glycogen, often coupled with hypoglycemia, results in the need to reduce intensity to approximately 40-60% VO2max. This phenomenon has been termed 'hitting the wall' and the subsequent velocity appears to be that which can be maintained largely by oxidation of fat, blood glucose and lactate. The latter seems to be generated from glycogen in inactive muscle fibers.
Well-trained endurance athletes possess more muscle mitochondria, and thus enhanced ability to oxidize both glycogen and triglyceride (i.e.; intramuscular or specifically intramyocellular triglyceride; IMTG). Compared to untrained, trained individuals are typically compared while running at a given absolute VO2 (ml/kg/min) at which time the difference in substrate oxidation is elevated fat oxidation, derived from IMTG, and reduced muscle glycogen oxidation. Thus endurance training increases the ability to oxidize fat yet this is most obvious at intensities below that of a competitive marathon. The higher VO2 that top marathon runners can maintain during a race is fueled by increased oxidation of both muscle glycogen and IMTG, the substrates located within the muscle.
Carbohydrate Depletion. When racing 42 km compared to 10 km, it is noteworthy that despite running more than four times farther, the typical marathon race velocity is reduced only by approximately 10% compared to a 10 km race. Stated another way, if marathon runners were to set a pace that is slightly (e.g.; 5-10%) faster than ideal (e.g.; lactate threshold velocity is close to ideal) for the 42 km distance, they will fatigue prematurely (i.e.; after 5-10 km) due to accelerated glycogenolysis. This fatigue could be manifested by acidosis and eventual depletion of glycogen in the more easily recruited motor units of the running musculature. Even when pacing is ideal and constant during the marathon, the sensation of effort needed for sufficient motor unit recruitment increases especially after running approximately 25-35 km. At this point in the race, muscle glycogen is low in many muscle fibers, particularly in the easily recruited Type I muscle fibers. If oxidation, primarily from carbohydrate, can not be maintained at sufficiently high rates in enough muscle fibers, pace must be slowed (i.e.; fatigue termed 'hitting the wall'). Ingestion of carbohydrate during exercise delays the time of fatigue as exogenous glucose appears in the blood and helps maintain the rate of carbohydrate oxidation (3). The maintenance of blood glucose concentration by carbohydrate ingestion, and thus prevention of hypoglycemia, prevents neuroglucopenia and the central nervous system symptoms of fatigue that are sometimes manifested in a large catecholamine response and subsequent paleness of skin associated with irritability, confusion and lethargy.
Heat. Hyperthermia can limit marathon performance as it stresses the cardiovascular, central nervous and muscular systems (4). The level of bodily hyperthermia experienced during a marathon reflects the balance between heat production and heat dissipation. Heat is produced from the hydrolysis of ATP and the metabolic processes needed for the oxidative ATP resynthesis (Figure 1). When running on level ground, no physical work is accomplished and almost all metabolic energy, calculated using indirect calorimetry (i.e.; VO2 and RER) is transferred to heat and released into the body (5). The important implication of this is that individuals who have superior running economy, that is a low VO2 for a given running velocity, will also generate proportionally less heat. This should be a distinct advantage when competing in hot environments that limit the amount of heat dissipation.
Dehydration. The primary mechanism for heat dissipation during a marathon is cooling through the evaporation of sweat. Sweat loss that is not matched by fluid intake will produce dehydration. The major problem with dehydration is that it impairs heat dissipation due to reduced skin blood flow (6). The amount of dehydration that can be tolerated without deleterious hyperthermia probably depends upon the environment and the individual's rate of heat production. When the environment is cold (e.g. 5–10 degrees C) or temperate and dry (e.g. 21–22 degrees C) it has been hypothesized that water losses of approximately 2% of body weight might be tolerated without risk to well-being and performance (3). However, marathon running in a hot and/or humid environment, dehydration by 2% of body weight is hypothesized to increase the probability of impaired performance, hyperthermia and heat illness.
Running Economy. An important determinant of marathon performance is the running velocity that can be maintained for the level of VO2 (i.e.; ml/kg/min) generated (1,2). This relationship is termed 'running economy'. The term 'efficiency' is not used because no measurable mechanical work is done when running over level ground. A population of runners display a 25-30% range in running economy (1,2). For example, a given VO2 of 50 ml/kg/min, should generate a marathon time of 2 h 40 min on average for the population. However, the most economical runners are predicted to finish in less than 2h 20 min and the least economical in approximately 3 h. The factors that determine running economy and the extent to which it can be improved with training are unclear. Remarkably, Jones (7) recently reported that running economy improved approximately 1% per year period in an elite female marathon runner as over a period of 5 and 14 years.
Summary. Running a marathon at the fastest speed possible appears to be limited by the rate of aerobic metabolism (i.e.; marathon VO2 ) of a limited amount of carbohydrate energy (i.e.; muscle glycogen and blood glucose) and the velocity that can be maintained without developing hyperthermia.
1. Costill, D.L.. What research tells the coach about distance running.
2. Farrell, PA, Wilmore, JH, Coyle, EF et al. Plasma lactate accumulation and distance running performance. Med Sci Sports 11:338-44, 1979.
3. Coyle, E.F., Fluid and fuel intake during exercise. J.Sport Sciences 22: 39-55, 2005.
4. Gonzalez-Alonso, J., Teller, C., Andersen, S. L. et al. nfluence of body temperature on the development of fatigue during prolonged exercise in the heat. J Appl Physiol 86:1032-9, 1999.
5. Webb, P. Annis, J. ,Troutman. SJ. Human calorimetry with a water-cooled garment J Appl Physiol,; 32: 412-9, 1972.
6. Coyle, E.F. Cardiovascular drift during prolonged exercise: new perspectives. Exerc Sport Sci Rev 29:88-92, 2001.
7. Jones, A.M. A five year physiological case study of an Olympic runner. British J Sports Med 32: 39-43
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