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Biomedical subjects

E F Coyle

Publications and source records attributed to E F Coyle.

At least 91 records · Page 5Linked to original sources

Adaptations of skeletal muscle to endurance exercise and their metabolic consequences.

Regularly performed endurance exercise induces major adaptations in skeletal muscle. These include increases in the mitochondrial content and respiratory capacity of the muscle fibers. As a consequence of the increase in mitochondria, exercise of the same intensity results in a disturbance in homeostasis that is smaller in trained than in untrained muscles. The major metabolic consequences of the adaptations of muscle to endurance exercise are a slower utilization of muscle glycogen and blood glucose, a greater reliance on fat oxidation, and less lactate production during exercise of a given intensity. These adaptations play an important role in the large increase in the ability to perform prolonged strenuous exercise that occurs in response to endurance exercise training.

Adaptation, Physiological↗

Effects of stopping exercise training on epinephrine-induced lipolysis in humans.

It has been reported that in rats endurance exercise training enhances the sensitivity of adipose tissue to the lipolytic action of catecholamines. The purpose of this study was to determine whether endurance training has a similar effect on the lipolytic response to epinephrine in humans. Four days after cessation of training, a constant infusion of epinephrine resulted in a significantly smaller increase in serum free fatty acids (0.57 +/- 0.40 vs. 1.06 +/- 0.30 mM; P less than 0.01) and blood glycerol (0.07 +/- 0.01 vs. 0.12 +/- 0.03 mM; P less than 0.01) and a greater rise in blood lactate (1.24 +/- 0.51 vs. 0.69 +/- 0.44 mM; P less than 0.01) above preinfusion levels than when the subjects were training. No further change in these responses occurred after 2 mo of inactivity. Plasma glucose and glucagon responses to epinephrine remained constant throughout the study. Plasma insulin concentrations before and during epinephrine infusion were higher than in the trained state only after 2 mo of inactivity. These findings suggest that epinephrine-induced lipolysis is enhanced in endurance-exercise-trained individuals but that this adaptation is lost very rapidly after cessation of exercise.

Adipose Tissue↗

Time course of loss of adaptations after stopping prolonged intense endurance training.

Seven endurance exercise-trained subjects were studied 12, 21, 56, and 84 days after cessation of training. Maximal O2 uptake (VO2 max) declined 7% (P less than 0.05) during the first 21 days of inactivity and stabilized after 56 days at a level 16% (P less than 0.05) below the initial trained value. After 84 days of detraining the experimental subjects still had a higher VO2 max than did eight sedentary control subjects who had never trained (50.8 vs. 43.3 ml X kg-1 X min-1), due primarily to a larger arterial-mixed venous O2 (a-vO2) difference. Stroke volume (SV) during exercise was high initially and declined during the early detraining period to a level not different from control. Skeletal muscle capillarization did not decline with inactivity and remained 50% above (P less than 0.05) sedentary control. Citrate synthase and succinate dehydrogenase activities in muscle declined with a half-time of 12 days and stabilized at levels 50% above sedentary control (P less than 0.05). The initial decline in VO2 max was related to a reduced SV and the later decline to a reduced a-vO2 difference. Muscle capillarization and oxidative enzyme activity remained above sedentary levels and this may help explain why a-vO2 difference and VO2 max after 84 days of detraining were still higher than in untrained subjects.

Adaptation, Physiological↗

Comparison of muscle fiber typing by quantitative enzyme assays and by myosin ATPase staining.

Fibers in cross sections of human and rat muscle were typed by using histochemical ATPase stains, and the results were compared with those of quantitative enzyme assays of fragments of the same fibers dissected from serial freeze-dried sections. Two enzymes previously used to assess the metabolic type were measured in each case: lactate dehydrogenase and either adenylokinase (human fibers) or malate dehydrogenase (rat fibers). With human fibers there was essentially complete agreement between ATPase staining and the metabolic enzyme assays in distinguishing types I and II fibers. The agreement was less consistent with regard to type IIA and IIB fibers. A number of ATPase type IIC fibers were identified in one human muscle, and were found to fall between ATPase types I and IIA on the basis of metabolic enzyme assay results. Rat-fiber ATPase types I, IIA, and IIB from the plantaris muscle were rather well segregated on a two-dimensional lactate dehydrogenase-malate dehydrogenase grid. In the rat soleus muscle, ATPase types I and IIA fibers were shifted to lower lactate dehydrogenase levels, with IIC fibers interposed between them.

3-Hydroxyacyl CoA Dehydrogenases↗

Ergogenic aids.

The catabolism of bodily fuels provides the energy for muscular work. Work output can be limited by the size of fuel reserves, the rate of their catabolism, the build-up of by-products, or the neurologic activation of muscle. A substance that favorably affects a step that is normally limiting, and thus increases work output, can be considered an ergogenic aid. The maximal amount of muscular force generated during brief contractions can be acutely increased during hypnosis and with the ingestion of a placebo or psychomotor stimulant. This effect is most obvious in subjects under laboratory conditions and is less evident in athletes who are highly motivated prior to competition. Fatigue is associated with acidosis in the working musculature when attempts are made to maximize work output during a 4 to 15-minute period. Sodium bicarbonate ingestion may act to buffer the acid produced, provided that blood flow to the muscle is adequate. Prolonged intense exercise can be maintained for approximately two hours before carbohydrate stores become depleted. Carbohydrate feedings delay fatigue during prolonged exercise, especially in subjects who display a decline in blood glucose during exercise in the fasting state. Caffeine ingestion prior to an endurance bout has been reported to allow an individual to exercise somewhat more intensely than he or she would otherwise. Its effect may be mediated by augmenting fat metabolism or by altering the perception of effort. Amphetamines may act in a similar manner. Water ingestion during prolonged exercise that results in dehydration and hyperthermia can offset fluid losses and allow an individual to better maintain work output while substantially reducing the risk of heat-related injuries.

Amphetamines↗

Effects of detraining on enzymes of energy metabolism in individual human muscle fibers.

Muscle biopsies were obtained from three cyclists and four runners at the end of 10-24 mo of intensive training and after intervals of detraining up to 12 wk. Control samples came from four untrained persons and four former athletes. Macro mixed fiber samples were assayed for lactate dehydrogenase, adenylate kinase, glycogen phosphorylase, citrate synthase, malate dehydrogenase, beta-hydroxyacyl-CoA dehydrogenase, succinate dehydrogenase, beta-hydroxybutyrate dehydrogenase, creatine kinase, hexokinase, 1-phosphofructokinase, fructosebisphosphatase, protein, and total creatine. In the case of three trained persons and two controls, the first six of the enzymes were also measured in individual fibers. Before detraining, enzymes of oxidative metabolism were substantially higher than in controls, and differences in levels between type I and type II fibers were smaller. During detraining, oxidative enzymes were decreased in both fiber types but the type II fibers did not fall to control levels even after 12 wk. Phosphorylase increased with detraining in both fiber types. The same is true for lactate dehydrogenase and adenylate kinase, except in the case of the type I fibers of one individual. Among the other six enzymes (measured in mixed fiber samples), only hexokinase was consistently affected (decreased) by detraining.

Adenylate Kinase↗

Blood lactate threshold in some well-trained ischemic heart disease patients.

Six patients with ischemic heart disease who had exercised intensely for longer than 1 yr appeared to have a disproportionately high capacity for endurance exercise relative to VO2 max. They were compared with healthy runners of the same age (mean 55 yr) with similar training programs (6-12 km/day, 5 day/wk). The trained patients had a significantly (P less than 0.05) lower maximal cardiac output (-17%) and VO2 max (-18%, 37 vs. 45 ml . kg-1 . min-1). Despite their lower VO2 max, the trained patients were able to run 8 km at the same speed as the normal runners (approximately 189 m/min). The trained patients' ability to keep pace with the normal subjects was apparently due to a very high lactate threshold (LT) relative to VO2 max. The patients' LT (lactate 1 mM above base line) occurred at a treadmill running speed of 176 m/min, which elicited 100% of their VO2 max, compared with a LT at 178 m/min and 84% of VO2 max in the normal subjects (P less than 0.01). Our results show that some individuals with VO2 max limited by impaired cardiac function can undergo adaptations to training that enable them to maintain close to a metabolic steady state during exercise that elicits VO2 max.

Aged↗

Carbohydrate feeding during prolonged strenuous exercise can delay fatigue.

This study was undertaken to determine whether carbohydrate feeding during exercise can delay the development of fatigue. Ten trained cyclists performed two bicycle ergometer exercise tests 1 wk apart. The initial work rate required 74 +/- 2% of maximum O2 consumption (VO2 max) (range 70-79% of VO2 max). The point of fatigue was defined as the time at which the exercise intensity the subjects could maintain decreased below their initial work rate by 10% of VO2 max. During one exercise test the subjects were fed a glucose polymer solution beginning 20 min after the onset of exercise; during the other they were given a placebo. Blood glucose concentration was 20-40% higher during the exercise after carbohydrate ingestion than during the exercise without carbohydrate feeding. The exercise-induced decrease in plasma insulin was prevented by carbohydrate feeding. The respiratory exchange ratio was unchanged by the glucose feeding. Fatigue was postponed by carbohydrate feeding in 7 of the 10 subjects. This effect appeared to be mediated by prevention of hypoglycemia in only two subjects. The exercise time to fatigue for the 10 subjects averaged 134 +/- 6 min (mean +/- SE) without and 157 +/- 5 min with carbohydrate feeding (P less than 0.01).

Adult↗

Physiological determinants of endurance performance as studied in competitive racewalkers.

The physiological factors that relate to 20-km performance were studied in eight competitive racewalkers. The racewalking velocity at the blood lactate threshold (LT) during steady-state exercise was highly correlated to racewalking pace (r = 0.94) and predicted performance times to within 0.6%, which agrees with previous observations on runners. The two factors that contribute to velocity at LT are O2 uptake at LT (VO2 at LT) and submaximal racewalking economy (measured as the VO2 at a standard velocity). Oxygen uptake at LT was significantly correlated (r = 0.89) to performance in the racewalkers in the present investigation, which agrees with previous observations of runners. Submaximal economy was significantly correlated to performance in the racewalkers (r = -0.82). Maximal oxygen uptake measured during racewalking was not significantly correlated (r = 0.62) to performance. These data indicate that the velocity at LT correlates closely to performance in racewalkers and that the factor of submaximal economy, which partly determines velocity at LT, is related more to performance ability in racewalking than was previously observed in running.

Adult↗

Effect of glycerol feeding on endurance and metabolism during prolonged exercise in man.

This study evaluated the effectiveness of pre-exercise glycerol feeding in protecting against development of hypoglycemia and sparing muscle glycogen during prolonged, intense exercise. Thirty minutes after ingesting either glycerol (1 gm X kg-1 body weight) or a placebo, 10 cyclists performed as much exercise on a cycle ergometer as they were able in 150 min. The average exercise intensity was 72% of VO2max during both trials. Glycerol ingestion increased blood glycerol concentration 100-fold, but did not alter the respiratory exchange ratio (R), plasma levels of insulin and free-fatty acids, or blood lactate and beta-hydroxybutyrate. The only significant effect of glycerol feeding was to postpone the decline in blood glucose by about 30 min. This suggests that glycerol served, to a limited extent, as a gluconeogenic substrate; however, glycerol ingestion did not spare muscle glycogen during 90 min of treadmill exercise at 71% VO2max. It appears that man cannot utilize glycerol as gluconeogenic substrate rapidly enough to serve as a major energy source during strenuous exercise.

Administration, Oral↗

Cardiac effects of prolonged and intense exercise training in patients with coronary artery disease.

The effects of intense and prolonged exercise training on the heart were studied with echocardiography in eight men with coronary artery disease with a mean age (+/- standard error of the mean) of 52 +/- 3 years. Training consisted of endurance exercise 3 times/week at 50 to 60 percent of the measured maximal oxygen uptake for 3 months followed by exercise 4 to 5 days/week at 70 to 80 percent of maximal oxygen uptake for 9 months. Maximal oxygen uptake capacity increased by 42 percent (26 +/- 1 versus 37 +/- 2 ml/kg per min; p less than 0.001). Heart rate at rest and submaximal heart rate and systolic blood pressure at a given work rate were significantly lower after training. Systolic blood pressure at the time of maximal exercise increased (145 +/- 9 before versus 166 +/- 8 mm Hg after training; probability [p] less than 0.01). Left ventricular end-diastolic diameter was increased after 12 months of training (from 47 +/- 1 to 51 +/- 1 mm; p less than 0.01). Left ventricular fractional shortening and mean velocity of circumferential shortening decreased progressively in response to graded isometric handgrip exercise before training but not after training. At comparable levels of blood pressure during static exercise, mean velocity of circumferential shortening was significantly higher after training (0.76 +/- 0.04 versus 0.98 +/- 0.07 diameter/sec, p less than 0.01). No improvement in echocardiographic or exercise variables was observed over a 12 month period in another group of five patients who did not exercise. Thus the data suggest that prolonged and vigorous exercise training in selected patients with coronary artery disease can elicit cardiac adaptations.

Adaptation, Physiological↗

Exercise hyperventilation in patients with McArdle's disease.

This study was undertaken to determine if patients who lack muscle phosphorylase (i.e., McArdle's disease), and therefore the ability to produce lactic acid during exercise, demonstrate a normal hyperventilatory response during progressive incremental exercise. As expected these patients did not increase their blood lactate above resting levels, whereas the blood lactate levels of normal subjects increased 8- to 10-fold during maximal exercise. The venous pH of the normal subjects decreased markedly during exercise that resulted in hyperventilation. The patients demonstrated a distinct increase in ventilation with respect to O2 consumption similar to that seen in normal individuals during submaximal exercise. However their hyperventilation resulted in an increase in pH because there was no underlying metabolic acidosis. End-tidal partial pressures of O2 and CO2 also reflected a distinct hyperventilation in both groups at approximately 70-85% maximal O2 consumption. These data show that hyperventilation occurs during intense exercise, even when there is no increase in plasma [H+]. Since arterial CO2 levels were decreasing and O2 levels were increasing during the hyperventilation, it is possible that nonhumoral stimuli originating in the active muscles or in the brain elicit the hyperventilation observed during intense exercise.

Adult↗

An automated, indirect assessment of cardiac output during rest and exercise.

The present study describes a modification of the equilibration CO2-rebreathing technique for determining cardiac output (Q), utilizing the Beckman Metabolic Measurement Cart (MMC) to provide partial automation of the procedures described by Jones et al. (Clinical Exercise Testing. Philadelphia, PA: Saunders, 1975). Q was determined in six normal healthy males to establish the reliability of the technique at rest, and during exercise at power outputs of 49 and 98 W, or 300 and 600 kpm/min. An additional 11 patients, who were symptomatic for coronary artery disease and scheduled for right and left heart catheterization, were used in validating these procedures against Q determined by the thermodilution method. The automated CO2-rebreathing procedure was found to be reliable at rest and during exercise, and demonstrated a direct linear relationship with VO2 (r = 0.90). Also, this procedure correlated (r = 0.87) with the thermodilution method during supine rest, and both methods were quite consistent between trials within the same subject. It was concluded that the CO2-rebreathing procedure used in this study, as interfaced with the Beckman MMC, provides reasonable estimates of Q, both in patients during supine rest, and in normal healthy subjects at rest and during low to moderate levels of exercise.

Adult↗

Specificity of power improvements through slow and fast isokinetic training.

College age males performed maximal two-legged isokinetic knee extensions three times per week for 6 wk at either 60 degrees/s (slow) or 300 degrees/s (fast) or both 60 and 300 degrees/s (mixed). The velocity specific and action specific (two-leg vs. one leg) improvements in peak torque (PT) were compared to a placebo group receiving low-level muscle stimulation. The slow group improved PT significantly (P less than 0.05) more than the placebo group only at its training velocity (60 degrees/s) and more so when the specific two-legged training action was mimicked (+32% with two legs vs. +19% with one leg). The mixed group enhanced PT by 24 and 16% at their respective training velocities of 60 and 300 degrees/s. These improvements were significantly larger than placebo and also significantly larger than the 9% improvement observed at the midvelocity of 180 degrees/s. The training specificity demonstrated by the slow and mixed groups suggest that neural mechanisms contributed to their improvements in power. This is supported by their unchanging muscle morphology. Training solely at 300 degrees/s (fast) however improved PT significantly more than placebo not only at the training velocity (+18%), but also at a slower velocity of 180 degrees/s (+17%). The fast group demonstrated a significant enlargement (+11%) of type II muscle fibers. These data suggest type II fiber hypertrophy to be a plausible mechanism for the nonspecific improvement of the fast group; however, a neurological adaptation that enhances power at and below the training velocity cannot be excluded.

Adult↗

Adaptations in skeletal muscle following strength training.

Five men were studied before and after 7 wk of isokinetic strength training to determine its effects on muscle enzyme activities and fiber composition. One of the subject's legs was trained using 10 repeated 6-s maximal work bouts, while the other leg performed repeated 30-s maximal knee extension exercise. The total work accomplished by each leg was constant. Training 4 times/wk achieved similar gains in peak torque for both legs at the training velocity (3.14 rad/s) and at slower speeds. Fatigability of the knee extensor muscles, as measured by a 60-s exercise test, was similar in both legs after training. Biopsy specimens showed significant changes in the % of the muscle area composed of type I and IIa fibers as a result of both strength training programs. In terms of muscle enzymes, only the 30 s exercise program resulted in elevated glycolytic, ATP-CP and mitochondrial activities. Despite these changes, none of the parameters measured were found to be related to the gains in either muscle strength or fatigability during maximal isokinetic contractions.

Adaptation, Physiological↗

Leg extension power and muscle fiber composition.

The purpose of this investigation was to relate muscle fiber composition to the isokinetic measure of peak torque production through a range of leg extension velocities. Twenty-one males were biopsied from the vastus lateralis muscle to determine their percent distribution of slow twitch (%ST) and fast twitch (%FT) muscle fibers as identified through myofibrillar adenosine triphosphatase activity. All subjects showed a decline in peak torque with increasing velocities. Subjects with predominantly FT fibers were able to generate 11, 16, 23 and 47 percent greater relative peak torque than could predominantly ST subjects at lever arm velocities of 115, 200, 287 and 400 degrees/second respectively. Likewise the correlation between relative torque production and % FT were significant (p less than .05) and increased from r = 0.44 to r = 0.75 as velocity increased from 115 to 400 degrees/second respectively. These data suggest that muscle fiber composition becomes increasingly more related to power performance as the velocity of movement increases.

Adenosine Triphosphatases↗

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.

Adult↗