Edward F. Coyle

Plasma lactate accumulation and distance running performance

Laboratory and field assessments were made on eighteen male distance runners. Performance data were obtained for distances of 3.2, 9.7, 15, 19.3 km (n = 18) and the marathon (n = 13). Muscle fiber composition expressed as percent of slow twitch fibers (%ST), maximal oxygen consumption (Vo2max), running economy (Vo2 for a treadmill velocity of 268 m/min), and the Vo2 and treadmill velocity corresponding to the onset of plasma lactate accumulation (OPLA) were determined for each subject. %ST (R greater than or equal to .47), Vo2max (r greater than or equal to .83), running economy (r greater than or equal to .49), Vo2 in ml/kg min corresponding to the OPLA (r greater than or equal to .91) and the treadmill velocity corresponding to the OPLA (r greater than or equal to .91) were significantly (p less than .05) related to performance at all distances. Multiple regression analysis howed that the treadmill velocity corresponding to the OPLA was most closely related to performance and the addition of other factors did not significantly raise the multiple R values suggesting that these other variables may interact with the purpose of keeping plasma lactates low during distance races. The slowest and fastest marathoners ran their marathons 7 and 3 m/min faster than their treadmill velocities corresponding to their OPLA which indicates that this relationship is independent of the competitive level of the runner. Runners appear to set a race pace which allows the utilization of the largest possible Vo2 which just avoids the exponential rise in plasma lactate.

Cycling efficiency is related to the percentage of type I muscle fibers.

We determined that the variability in the oxygen cost and thus the caloric expenditure of cycling at a given work rate (i.e., cycling economy) observed among highly endurance-trained cyclists (N = 19; mean +/- SE; VO2max, 4.9 +/- 0.1 l.min-1; body weight, 71 +/- 1 kg) is related to differences in their % Type I muscle fibers. The percentage of Type I and II muscle fibers was determined from biopsies of the vastus lateralis muscle that were histochemically stained for ATPase activity. When cycling a Monark ergometer at 80 RPM at work rates eliciting 52 +/- 1, 61 +/- 1, and 71 +/- 1% VO2max, efficiency was determined from the caloric expenditure responses (VO2 and RER using open circuit spirometry) to steady-state exercise. Gross efficiency (GE) was calculated as the ratio of work accomplished.min-1 to caloric expenditure.min-1, whereas delta efficiency (DE) was calculated as the slope of this relationship between approximately 50 and 70% VO2max. The % Type I fibers ranged from 32 to 76%, and DE when cycling ranged from 18.3 to 25.6% in these subjects. The % Type I fibers was positively correlated with both DE (r = 0.85; P less than 0.001; N = 19) and GE (r = 0.75; P less than 0.001; N = 19) during cycling. Additionally, % Type I fibers was positively correlated with GE (r = 0.74; P less than 0.001; N = 13) measured during the novel task of two-legged knee extension; performed at a velocity of 177 +/- 6 degrees.s-1 and intensity of 50 and 70% of peak VO2 for that activity.(ABSTRACT TRUNCATED AT 250 WORDS)

Endurance exercise performance: the physiology of champions

Efforts to understand human physiology through the study of champion athletes and record performances have been ongoing for about a century. For endurance sports three main factors – maximal oxygen consumption , the so‐called ‘lactate threshold’ and efficiency (i.e. the oxygen cost to generate a give running speed or cycling power output) – appear to play key roles in endurance performance. and lactate threshold interact to determine the ‘performance ‘ which is the oxygen consumption that can be sustained for a given period of time. Efficiency interacts with the performance to establish the speed or power that can be generated at this oxygen consumption. This review focuses on what is currently known about how these factors interact, their utility as predictors of elite performance, and areas where there is relatively less information to guide current thinking. In this context, definitive ideas about the physiological determinants of running and cycling efficiency is relatively lacking in comparison with and the lactate threshold, and there is surprisingly limited and clear information about the genetic factors that might pre‐dispose for elite performance. It should also be cautioned that complex motivational and sociological factors also play important roles in who does or does not become a champion and these factors go far beyond simple physiological explanations. Therefore, the performance of elite athletes is likely to defy the types of easy explanations sought by scientific reductionism and remain an important puzzle for those interested in physiological integration well into the future.

Fluid and fuel intake during exercise.

The amounts of water, carbohydrate and salt that athletes are advised to ingest during exercise are based upon their effectiveness in attenuating both fatigue as well as illness due to hyperthermia, dehydration or hyperhydration. When possible, fluid should be ingested at rates that most closely match sweating rate. When that is not possible or practical or sufficiently ergogenic, some athletes might tolerate body water losses amounting to 2% of body weight without significant risk to physical well-being or performance when the environment is cold (e.g. 5–10°C) or temperate (e.g. 21–22°C). However, when exercising in a hot environment ( >30°C), dehydration by 2% of body weight impairs absolute power production and predisposes individuals to heat injury. Fluid should not be ingested at rates in excess of sweating rate and thus body water and weight should not increase during exercise. Fatigue can be reduced by adding carbohydrate to the fluids consumed so that 30–60 g of rapidly absorbed carbohydrate are ingested throughout each hour of an athletic event. Furthermore, sodium should be included in fluids consumed during exercise lasting longer than 2 h or by individuals during any event that stimulates heavy sodium loss (more than 3–4 g of sodium). Athletes do not benefit by ingesting glycerol, amino acids or alleged precursors of neurotransmitter. Ingestion of other substances during exercise, with the possible exception of caffeine, is discouraged. Athletes will benefit the most by tailoring their individual needs for water, carbohydrate and salt to the specific challenges of their sport, especially considering the environments impact on sweating and heat stress.

Acsm Position Stand: Exercise and Fluid Replacement

SUMMARYIt is the position of the American College of Sports Medicine that adequate fluid replacement helps maintain hydration and, therefore, promotes the health, safety, and optimal physical performance of individuals participating in regular physical activity. This position statement is based on a

Fluid and carbohydrate ingestion independently improve performance during 1 h of intense exercise

This study determined the effects of fluid and carbohydrate ingestion on performance, core temperature, and cardiovascular responses during intense exercise lasting 1 h. On four occasions, eight men cycled at 80 +/- 1% (+/- SEM) of VO2max for 50 min followed by a performance test. During exercise, they consumed either a large volume (1330 +/- 60 ml) of a 6% carbohydrate (79 +/- 4 g) solution or water or a small volume (200 +/- 10 ml) of a 40% maltodextrin (79 +/- 4 g) solution or water. These trials were pooled so the effects of fluid replacement (Large FR vs Small FR) and carbohydrate ingestion (CHO vs NO CHO) could be determined. Performance times were 6.5% faster during Large FR than Small FR and 6.3% faster during CHO than NO CHO (P < 0.05). At 50 min, heart rate was 4 +/- 1 b.min-1 lower and esophageal temperature was 0.33 +/- 0.04 degrees C lower during Large FR than Small FR (P < 0.05) but no differences occurred between CHO and NO CHO. In summary, Large FR slightly attenuates the increase in heart rate and core temperature which occurs during Small FR. Both fluid and carbohydrate ingestion equally improve cycling performance and their effects are additive.

Integration of the physiological factors determining endurance performance ability.

This model is used to understand the interrelationships of the physiological factors determining endurance performance ability during prolonged exercise. Early studies found that marathon runners maintain a velocity in competition that corresponds to the intensity at which lactate begins to accumulate in blood and muscle [7, 8, 19]. From this observation, the concept developed that this blood lactate threshold (LT Vo2) reflects the degree of muscular stress, glycogenolysis and fatigue. However, it was not clear whether the lactate accumulation was a result of cardiovascular limitations linked to oxygen delivery, as reflected by Vo2max [54], as opposed to metabolic factors in the exercising muscle related to the extent to which mitochondrial respiration is disturbed to maintain a given rate of O2 consumption [29, 30]. Two studies were performed to determine whether LT Vo2 was tightly coupled to Vo2max. In one study, endurance-trained ischemic heart disease patients were observed to possess a Vo2max that was 18% below that of normal master athletes who followed the patients training program and who displayed the same performance ability as the patients. Both the patients and the normal men displayed an identical LT Vo2 (i.e., 37 ml/kg/min) (Fig. 2.5). Therefore, performance was determined primarily by LT Vo2 instead of Vo2max in this situation, albeit with abnormal subjects. In a second study we assembled two groups of competitive cyclists who were identical in Vo2max but differed by having a high or low LT Vo2 (82% vs. 66% Vo2max) [13]. When cycling at 80-88% Vo2max, the low LT group displayed more than a 2-fold higher rate of muscle glycogen use and blood lactate concentration, and as a result were able to exercise only one-half as long as the high LT group. Performance time for a given Vo2 was clearly related to LT Vo2 instead of Vo2max (Fig. 2.6). This is not to say that Vo2max plays no role in determining LT Vo2, because as in heart disease patients, it clearly sets the upper limit. Indeed, we have seen that much of the variance (i.e., 31-72%) in LT Vo2 is related to Vo2max. (Fig. 2.11.) However, improvements in performance after the first 2-3 yr of intense training are associated with improvements in LT Vo2, whereas Vo2max generally increases very little thereafter (Table 2.3). The next question concerns the factors responsible for further increases in LT Vo2 and Performance. Another major factor determining LT Vo2 is the muscles Aerobic Enzyme Activity or mitochondrial respiratory capacity, as discussed in previous reviews [29, 30].(ABSTRACT TRUNCATED AT 400 WORDS)

Carbohydrate ingestion during prolonged exercise: effects on metabolism and performance.

It is well recognized that energy from CHO oxidation is required to perform prolonged strenuous (greater than 60% VO2 max) exercise. During the past 25 years, the concept has developed that muscle glycogen is the predominant source of CHO energy for strenuous exercise; as a result, the potential energy contribution of blood glucose has been somewhat overlooked. Although during the first hour of exercise at 70-75% VO2max, most of the CHO energy is derived from muscle glycogen, it is clear that the contribution of muscle glycogen decreases over time as muscle glycogen stores become depleted, and that blood glucose uptake and oxidation increase progressively to maintain CHO oxidation (Fig. 1.7). We theorize that over the course of several hours of strenuous exercise (i.e., 3-4 h), blood glucose and muscle glycogen contribute equal amounts of CHO energy, making blood glucose at least as important as muscle glycogen as a CHO source. During the latter stages of exercise, blood glucose can potentially provide all of the CHO energy needed to support exercise at 70-75% VO2max if blood glucose availability is maintained. During prolonged exercise in the fasted state, however, blood glucose concentration often decreases owing to depletion of liver glycogen stores. This relative hypoglycemia, although only occasionally severe enough to result in fatigue from neuroglucopenia, causes fatigue by limiting blood glucose (and therefore total CHO) oxidation. The primary purpose of CHO ingestion during continuous strenuous exercise is to maintain blood glucose concentration and thus CHO oxidation and exercise tolerance during the latter stages of prolonged exercise. CHO feeding throughout continuous exercise does not alter muscle glycogen use. It appears that blood glucose must be supplemented at a rate of approximately 1 g/min late in exercise. Feeding sufficient amounts of CHO 30 minutes before fatigue is as effective as ingesting CHO throughout exercise in maintaining blood glucose availability and CHO oxidation late in exercise. Most persons should not wait, however, until they are fatigued before ingesting CHO, because it appears that glucose entry into the blood does not occur rapidly enough at this time. It also may be advantageous to ingest CHO throughout intermittent or low-intensity exercise rather than toward the end of exercise because of the potential for glycogen synthesis in resting muscle fibers. Finally, CHO ingestion during prolonged strenuous exercise delays by approximately 45 minutes but does not prevent fatigue, suggesting that factors other than CHO availability eventually cause fatigue.

Cardiovascular drift during prolonged exercise: new perspectives.

COYLE, E. F., and J. GONZÁLEZ-ALONSO. Cardiovascular drift during prolonged exercise: New perspectives. Exerc. Sports Sci. Rev. Vol. 29, No. 2, pp. 88–92, 2001. We propose that cardiovascular drift, characterized by a progressive decline in stroke volume after 10–20 min of exercise, is primarily due to increased heart rate rather than a progressive increase in cutaneous blood flow as body temperature rises.

Lipolytic suppression following carbohydrate ingestion limits fat oxidation during exercise

This study determined if the suppression of lipolysis after preexercise carbohydrate ingestion reduces fat oxidation during exercise. Six healthy, active men cycled 60 min at 44 ± 2% peak oxygen consumption, exactly 1 h after ingesting 0.8 g/kg of glucose (Glc) or fructose (Fru) or after an overnight fast (Fast). The mean plasma insulin concentration during the 50 min before exercise was different among Fast, Fru, and Glc (8 ± 1, 17 ± 1, and 38 ± 5 μU/ml, respectively; P< 0.05). After 25 min of exercise, whole body lipolysis was 6.9 ± 0.2, 4.3 ± 0.3, and 3.2 ± 0.5 μmol ⋅ kg-1 ⋅ min-1and fat oxidation was 6.1 ± 0.2, 4.2 ± 0.5, and 3.1 ± 0.3 μmol ⋅ kg-1 ⋅ min-1during Fast, Fru, and Glc, respectively (all P < 0.05). During Fast, fat oxidation was less than lipolysis ( P < 0.05), whereas fat oxidation approximately equaled lipolysis during Fru and Glc. In an additional trial, the same subjects ingested glucose (0.8 g/kg) 1 h before exercise and lipolysis was simultaneously increased by infusing Intralipid and heparin throughout the resting and exercise periods (Glc+Lipid). This elevation of lipolysis during Glc+Lipid increased fat oxidation 30% above Glc (4.0 ± 0.4 vs. 3.1 ± 0.3 μmol ⋅ kg-1 ⋅ min-1; P < 0.05), confirming that lipolysis limited fat oxidation. In summary, small elevations in plasma insulin before exercise suppressed lipolysis during exercise to the point at which it equaled and appeared to limit fat oxidation.