The objective of this study was to develop an empirical model relating human running performance to some characteristics of metabolic energy-yielding processes using A, the capacity of anaerobic metabolism (J/kg); MAP, the maximal aerobic power (W/kg); and E, the reduction in peak aerobic power with the natural logarithm of race duration T, when T greater than TMAP = 420 s. Accordingly, the model developed describes the average power output PT (W/kg) sustained over any T as PT = [S/T(1 - e-T/k2)] + 1/T integral of T O [BMR + B(1 - e-t/k1)]dt where S = A and B = MAP - BMR (basal metabolic rate) when T less than TMAP; and S = A + [Af ln(T/TMAP)] and B = (MAP - BMR) + [E ln(T/TMAP)] when T greater than TMAP; k1 = 30 s and k2 = 20 s are time constants describing the kinetics of aerobic and anaerobic metabolism, respectively, at the beginning of exercise; f is a constant describing the reduction in the amount of energy provided from anaerobic metabolism with increasing T; and t is the time from the onset of the race. This model accurately estimates actual power outputs sustained over a wide range of events, e.g., average absolute error between actual and estimated T for men's 1987 world records from 60 m to the marathon = 0.73%. In addition, satisfactory estimations of the metabolic characteristics of world-class male runners were made as follows: A = 1,658 J/kg; MAP = 83.5 ml O2.kg-1.min-1; 83.5% MAP sustained over the marathon distance. Application of the model to analysis of the evolution of A, MAP, and E, and of the progression of men's and women's world records over the years, is presented.
The relative roles of circulatory glucose, muscle glycogen, and lipids in shivering thermogenesis are unclear. Using a combination of indirect calorimetry and stable isotope methodology ([U-13C]glucose ingestion), we have quantified the oxidation rates of these substrates in men acutely exposed to cold for 2 h (liquid conditioned suit perfused with 10 degrees C water). Cold exposure stimulated heat production by 2.6-fold and increased the oxidation of plasma glucose from 39.4 +/- 2.4 to 93.9 +/- 5.5 mg/min (+138%), of muscle glycogen from 126.6 +/- 7.8 to 264.2 +/- 36.9 mg glucosyl units/min (+109%), and of lipids from 46.9 +/- 3.2 to 176.5 +/- 17.3 mg/min (+376%). Despite the observed increase in plasma glucose oxidation, this fuel only supplied 10% of the energy for heat generation. The major source of carbohydrate was muscle glycogen (75% of all glucose oxidized), and lipids produced as much heat as all other fuels combined. During prolonged, low-intensity shivering, we conclude that total heat production is unequally shared among lipids (50%), muscle glycogen (30%), plasma glucose (10%), and proteins (10%). Therefore, future research should focus on lipids and muscle glycogen that provide most of the energy for heat production.
Endurance performance and fuel selection while ingesting glucose (15, 30, and 60 g/h) was studied in 12 cyclists during a 2-h constant-load ride [approximately 77% peak O2 uptake] followed by a 20-km time trial. Total fat and carbohydrate (CHO) oxidation and oxidation of exogenous glucose, plasma glucose, glucose released from the liver, and muscle glycogen were computed using indirect respiratory calorimetry and tracer techniques. Relative to placebo (210+/-36 W), glucose ingestion increased the time trial mean power output (%improvement, 90% confidence limits: 7.4, 1.4 to 13.4 for 15 g/h; 8.3, 1.4 to 15.2 for 30 g/h; and 10.7, 1.8 to 19.6 for 60 g/h glucose ingested; effect size=0.46). With 60 g/h glucose, mean power was 2.3, 0.4 to 4.2% higher, and 3.1, 0.5 to 5.7% higher than with 30 and 15 g/h, respectively, suggesting a relationship between the dose of glucose ingested and improvements in endurance performance. Exogenous glucose oxidation increased with ingestion rate (0.17+/-0.04, 0.33+/-0.04, and 0.52+/-0.09 g/min for 15, 30, and 60 g/h glucose), but endogenous CHO oxidation was reduced only with 30 and 60 g/h due to the progressive inhibition of glucose released from the liver (probably related to higher plasma insulin concentration) with increasing ingestion rate without evidence for muscle glycogen sparing. Thus ingestion of glucose at low rates improved cycling time trial performance in a dose-dependent manner. This was associated with a small increase in CHO oxidation without any reduction in muscle glycogen utilization.
We computed the respective amounts of exogenous glucose (G) and fructose (F), which are oxidized during exercise when ingested simultaneously, with the use of 13C labeling. Six subjects exercised for 2 h at 60.7 +/- 2.9% of maximal O2 uptake on a cycle ergometer while ingesting 50 or 100 g of G or F or a mixture of 50 g each of G and F in 500 ml of water. The amount of exogenous G oxidized increased from 37.8 +/- 2.2 to 58.3 +/- 8.1 g when the total amount ingested increased from 50 to 100 g. The amount of F oxidized was significantly lower (32.2 +/- 1.2 and 45.8 +/- 2.6 g for the 50 and 100 g ingested, respectively). When 50 g each of G and F were simultaneously ingested in the same drink, the amounts oxidized (39.5 +/- 4.8 and 34.1 +/- 1.5 g, respectively) were similar to those observed when 50 g of G or F were ingested separately. The cumulative amount of exogenous hexoses oxidized (73.6 +/- 6.6 g) was 21% larger than when 100 g of G were ingested. This finding could be due to the fact that the routes for absorption and metabolism of exogenous G and F are at least partly different, resulting in less competition for oxidation when a mixture of these two hexoses is ingested than when an isocaloric amount of G is ingested. From a practical point of view, these data may provide experimental support for using mixtures of carbohydrates in the energy supplements for endurance athletes.
Aerobic fitness is associated with numerous physiological adaptations which permit physical stress to be coped with more efficiently. The present experiment examined whether aerobic fitness influences emotional response. Heart rate, biochemical measures (catecholamines, cortisol, prolactin, lactic acid), and self-reported arousal and anxiety were monitored in 15 highly trained and 15 untrained subjects at various points before, during and following exposure to a series of psychosocial stressors. Heart rate and subjective arousal level increased markedly during the stressors in both groups. Trained subjects showed higher levels of norepinephrine and prolactin early in the stress period, more rapid heart rate recovery following the stressors, and lower levels of anxiety at the conclusion of the session. This more rapid heart rate and subjective recovery from psychosocial stress, suggests that aerobically trained individuals may be capable of faster recovery in both physiological and subjective dimensions of emotionality. The differences in reactivity profiles between the aerobically trained and untrained were discussed in light of models that have dealt with the adaptiveness of emotional response.
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