Understanding efficiency of human muscular movement exemplifies integrative and translational physiology.
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Adenosine Triphosphate↗
Biomedical subjects
Edward F Coyle
Publications and source records attributed to Edward F Coyle.
Maximal mechanical power during a taper in elite swimmers.
INTRODUCTION: Insight regarding the fluctuations in neuromuscular function among athletes during a taper is lacking. PURPOSE: This study examined the time course of changes in maximal mechanical power (Pmax), torque at power maximum (T), velocity at power maximum (V), and swim performance (m x s(-1)) that occur during the taper. METHODS: Using an arm ergometer with inertial loading, measurements were made during the week prior to the initiation of the taper (high volume, HV), during the 2- to 3-wk period of the taper (taper), and during the week of peak competition (peak) in 24 male competitive collegiate swimmers. Subjects were divided into groups that tapered to peak performance at either the conference (CONF, N = 13) or national (NAT, N = 11) championship competitions. RESULTS: CONF increased Pmax 10.2% (P < 0.01) and swim performance 4.4% (P < 0.001). NAT increased Pmax by 11.6% (P < 0.01), T by 7.4% (P < 0.02), and swim performance by 4.7% (P < 0.001). Pmax displayed a biphasic increase with approximately 50, 5, and 45% of the total increase occurring during the first, second, and third weeks of the taper, respectively. The biphasic response was the most common response among individual swimmers. Swimming performance was significantly correlated to both power and torque (P < 0.05). CONCLUSION: In summary, maximal arm power measured using inertial load ergometry increased largely during the first and third weeks after training volume was tapered for peak performance in elite collegiate swimmers.
Adult↗
Improved muscular efficiency displayed as Tour de France champion matures.
This case describes the physiological maturation from ages 21 to 28 yr of the bicyclist who has now become the six-time consecutive Grand Champion of the Tour de France, at ages 27-32 yr. Maximal oxygen uptake (Vo(2 max)) in the trained state remained at approximately 6 l/min, lean body weight remained at approximately 70 kg, and maximal heart rate declined from 207 to 200 beats/min. Blood lactate threshold was typical of competitive cyclists in that it occurred at 76-85% Vo(2 max), yet maximal blood lactate concentration was remarkably low in the trained state. It appears that an 8% improvement in muscular efficiency and thus power production when cycling at a given oxygen uptake (Vo(2)) is the characteristic that improved most as this athlete matured from ages 21 to 28 yr. It is noteworthy that at age 25 yr, this champion developed advanced cancer, requiring surgeries and chemotherapy. During the months leading up to each of his Tour de France victories, he reduced body weight and body fat by 4-7 kg (i.e., approximately 7%). Therefore, over the 7-yr period, an improvement in muscular efficiency and reduced body fat contributed equally to a remarkable 18% improvement in his steady-state power per kilogram body weight when cycling at a given Vo(2) (e.g., 5 l/min). It is hypothesized that the improved muscular efficiency probably reflects changes in muscle myosin type stimulated from years of training intensely for 3-6 h on most days.
Adaptation, Physiological↗
Very intense exercise-training is extremely potent and time efficient: a reminder.
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Adaptation, Physiological↗
Has Armstrong's cycle efficiency improved?
This case describes the physiological maturation from ages 21 to 28 yr of the bicyclist who has now become the six-time consecutive Grand Champion of the Tour de France, at ages 27-32 yr. Maximal oxygen uptake (Vo(2max)) in the trained state remained at approximately 6 l/min, lean body weight remained at approximately 70 kg, and maximal heart rate declined from 207 to 200 beats/min. Blood lactate threshold was typical of competitive cyclists in that it occurred at 76-85% Vo(2max), yet maximal blood lactate concentration was remarkably low in the trained state. It appears that an 8% improvement in muscular efficiency and thus power production when cycling at a given oxygen uptake (Vo(2)) is the characteristic that improved most as this athlete matured from ages 21 to 28 yr. It is noteworthy that at age 25 yr, this champion developed advanced cancer, requiring surgeries and chemotherapy. During the months leading up to each of his Tour de France victories, he reduced body weight and body fat by 4-7 kg (i.e., approximately 7%). Therefore, over the 7-yr period, an improvement in muscular efficiency and reduced body fat contributed equally to a remarkable 18% improvement in his steady-state power per kilogram body weight when cycling at a given Vo(2) (e.g., 5 l/min). It is hypothesized that the improved muscular efficiency probably reflects changes in muscle myosin type stimulated from years of training intensely for 3-6 h on most days.
Adult↗
Scientific considerations for physiological evaluations of elite athletes.
This case describes the physiological maturation from ages 21 to 28 yr of the bicyclist who has now become the six-time consecutive Grand Champion of the Tour de France, at ages 27-32 yr. Maximal oxygen uptake (Vo(2max)) in the trained state remained at approximately 6 l/min, lean body weight remained at approximately 70 kg, and maximal heart rate declined from 207 to 200 beats/min. Blood lactate threshold was typical of competitive cyclists in that it occurred at 76-85% Vo(2max), yet maximal blood lactate concentration was remarkably low in the trained state. It appears that an 8% improvement in muscular efficiency and thus power production when cycling at a given oxygen uptake (Vo(2)) is the characteristic that improved most as this athlete matured from ages 21 to 28 yr. It is noteworthy that at age 25 yr, this champion developed advanced cancer, requiring surgeries and chemotherapy. During the months leading up to each of his Tour de France victories, he reduced body weight and body fat by 4-7 kg (i.e., approximately 7%). Therefore, over the 7-yr period, an improvement in muscular efficiency and reduced body fat contributed equally to a remarkable 18% improvement in his steady-state power per kilogram body weight when cycling at a given Vo(2) (e.g., 5 l/min). It is hypothesized that the improved muscular efficiency probably reflects changes in muscle myosin type stimulated from years of training intensely for 3-6 h on most days.
Bicycling↗
Manipulation of dietary carbohydrate and muscle glycogen affects glucose uptake during exercise when fat oxidation is impaired by beta-adrenergic blockade.
We have recently reported that, during moderate intensity exercise, low muscle glycogen concentration and utilization caused by a high-fat diet is associated with a marked increase in fat oxidation with no effect on plasma glucose uptake (R(d) glucose). It is our hypothesis that this increase in fat oxidation compensates for low muscle glycogen, thus preventing an increase in R(d) glucose. Therefore, the purpose of this study was to determine whether low muscle glycogen availability increases R(d) glucose under conditions of impaired fat oxidation. Six cyclists exercised at 50% peak O(2) consumption (Vo(2 peak)) for 1 h after 2 days on either a high-fat (HF, 60% fat, 24% carbohydrate) or control (CON, 22% fat, 65% carbohydrate) diet to manipulate muscle glycogen to low and normal levels, respectively. Two hours before the start of exercise, subjects ingested 80 mg of propanolol (betaB), a nonselective beta-adrenergic receptor blocker, to impair fat oxidation during exercise. HF significantly decreased calculated muscle glycogen oxidation (P < 0.05), and this decrease was partly compensated for by an increase in fat oxidation (P < 0.05), accompanied by an increase in whole body lipolysis (P < 0.05), despite the presence of betaB. Although HF increased fat oxidation, plasma glucose appearance rate, R(d) glucose, and glucose clearance rate were also significantly increased by 13, 15, and 26%, respectively (all P < 0.05). In conclusion, when lipolysis and fat oxidation are impaired, in this case by betaB, fat oxidation cannot completely compensate for a reduction in muscle glycogen utilization, and consequently plasma glucose turnover increases. These findings suggest that there is a hierarchy of substrate compensation for reduced muscle glycogen availability after a high-fat, low-carbohydrate diet, with fat being the primary and plasma glucose the secondary compensatory substrate. This apparent hierarchy likely serves to protect against hypoglycemia when endogenous glucose availability is low.
Adrenergic beta-Antagonists↗
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 degrees C) or temperate (e.g. 21-22 degrees C). However, when exercising in a hot environment ( > 30 degrees 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 environment's impact on sweating and heat stress.
Body Temperature Regulation↗
High-fat diet elevates resting intramuscular triglyceride concentration and whole body lipolysis during exercise.
This study determined the role of intramuscular triglyceride (IMTG) and adipose lipolysis in the elevated fat oxidation during exercise caused by a high-fat diet. In four separate trials, six endurance-trained cyclists exercised at 50% peak O2 consumption for 1 h after a two-day control diet (22% fat, CON) or an isocaloric high-fat diet (60% fat, HF) with or without the ingestion of acipimox, an adipose lipolysis inhibitor, before exercise. During exercise, HF elevated fat oxidation by 72% and whole body lipolysis [i.e., the appearance rate of glycerol in plasma (Ra glycerol)] by 79% compared with CON (P < 0.05), and this was associated with a 36% increase (P < 0.05) in preexercise IMTG concentration. Although acipimox lowered plasma free fatty acid (FFA) availability, HF still increased fat oxidation and Ra glycerol to the same magnitude above control as the increase caused by HF without acipimox (i.e., both increased fat oxidation 13-14 micromol.kg(-1).min(-1)). In conclusion, the marked increase in fat oxidation after a HF diet is associated with elevated IMTG concentration and whole body lipolysis and does not require increased adipose tissue lipolysis and plasma FFA concentration during exercise. This suggests that altered substrate storage in skeletal muscle is responsible for increased fat oxidation during exercise after 2 days of an HF diet.
Adult↗
Different glycemic indexes of breakfast cereals are not due to glucose entry into blood but to glucose removal by tissue.
BACKGROUND: The glycemic index (GI) of a food is thought to directly reflect the rate of digestion and entry of glucose into the systemic circulation. The blood glucose concentration, however, represents a balance of both the entry and the removal of glucose into and from the blood, respectively. Such direct quantification of the postprandial glucose curve with respect to interpreting the GI is lacking in the literature. OBJECTIVE: We compared the plasma glucose kinetics of low- and high-GI breakfast cereals. DESIGN: On 2 occasions, plasma insulin concentrations and plasma glucose kinetics (by constant-rate infusion of [6,6-(2)H(2)]glucose) were measured in 6 healthy males for 180 min after they fasted overnight and then consumed an amount of corn flakes (CF) or bran cereal (BC) containing 50 g available carbohydrate. RESULTS: The GI of CF was more than twice that of BC (131.5 +/- 33.0 compared with 54.5 +/- 7.2; P < 0.05), despite no significant differences in the rate of appearance of glucose into the plasma during the 180-min period. Postprandial hyperinsulinemia occurred earlier with BC than with CF, resulting in a 76% higher plasma insulin concentration at 20 min (20.4 +/- 4.5 compared with 11.6 +/- 2.1 micro U/mL; P < 0.05). This was associated with a 31% higher rate of disappearance of glucose with BC than with CF during the 30-60-min period (28.7 +/- 3.1 compared with 21.9 +/- 3.1 micro mol. kg(-)(1). min(-)(1); P < 0.05). CONCLUSION: The lower GI of BC than of CF was not due to a lower rate of appearance of glucose but instead to an earlier postprandial hyperinsulinemia and an earlier increase in the rate of disappearance of glucose, which attenuated the increase in the plasma glucose concentration.
Adult↗