Biomedical subjects

E F Coyle

Publications and source records attributed to E F Coyle.

At least 73 records · Page 4Linked to original sources

PubMed1991

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.

Bicycling↗

PubMed1991

Physiological and biomechanical factors associated with elite endurance cycling performance.

In this study we evaluated the physiological and biomechanical responses of "elite-national class" (i.e., group 1; N = 9) and "good-state class" (i.e., group 2; N = 6) cyclists while they simulated a 40 km time-trial in the laboratory by cycling on an ergometer for 1 h at their highest power output. Actual road racing 40 km time-trial performance was highly correlated with average absolute power during the 1 h laboratory performance test (r = -0.88; P less than 0.001). In turn, 1 h power output was related to each cyclists' VO2 at the blood lactate threshold (r = 0.93; P less than 0.001). Group 1 was not different from group 2 regarding VO2max (approximately 70 ml.kg-1.min-1 and 5.01 l.min-1) or lean body weight. However, group 1 bicycled 40 km on the road 10% faster than group 2 (P less than 0.05; 54 vs 60 min). Additionally, group 1 was able to generate 11% more power during the 1 h performance test than group 2 (P less than 0.05), and they averaged 90 +/- 1% VO2max compared with 86 +/- 2% VO2max in group 2 (P = 0.06). The higher performance power output of group 1 was produced primarily by generating higher peak torques about the center of the crank by applying larger vertical forces to the crank arm during the cycling downstroke. Compared with group 2, group 1 also produced higher peak torques and vertical forces during the downstroke even when cycling at the same absolute work rate as group 2. Factors possibly contributing to the ability of group 1 to produce higher "downstroke power" are a greater percentage of Type I muscle fibers (P less than 0.05) and a 23% greater (P less than 0.05) muscle capillary density compared with group 2. We have also observed a strong relationship between years of endurance training and percent Type I muscle fibers (r = 0.75; P less than 0.001). It appears that "elite-national class" cyclists have the ability to generate higher "downstroke power", possibly as a result of muscular adaptations stimulated by more years of endurance training.

Adolescent↗

PubMed1990

Maximal oxygen uptake relative to plasma volume expansion.

Controversy exists as to whether plasma volume (PV) expansion has the potential to increase maximal oxygen uptake (VO2max). In the present study, VO2max and exercise time to fatigue were measured in nine untrained men when plasma volume (PV) was normal and then again on the next day following two levels of PV expansion. Resting PV was expanded (via intravenous infusion of a 6% dextran solution) by 282 +/- 16 ml (i.e., PVX-1) and then by 624 +/- 26 ml (i.e., PVX-2). PVX-1 increased stroke volume (CO2 rebreathing) during submaximal exercise by 15% (P less than 0.05) above normal levels. VO2max following PVX-1 was increased 4% (P less than 0.05; 3.78 to 3.92 l/min) despite a 4% reduction in hemoglobin concentration. Exercise time to fatigue was also increased (P less than 0.05). PVX-2 resulted in an 11% (P less than 0.05) reduction in hemoglobin concentration during maximal exercise and a return of VO2max and exercise time to normal levels. In summary, we have observed in untrained men that 200-300 ml of PV expansion increases SV, measured during submaximal exercise, yet causes only a small amount of hemodilution. As a result, VO2max is increased slightly and performance is improved. Further PV expansion to levels 500-600 ml above normal results in an excessive hemodilution and a subsequent decline in VO2max and performance to normal levels. There is an optimal PV for eliciting VO2max in untrained men which appears to be approximately 200-300 ml above their normal levels.

Adult↗

PubMed1989

Metabolism and performance following carbohydrate ingestion late in exercise.

To determine whether a single carbohydrate feeding could rapidly restore and maintain plasma glucose availability late in exercise, six trained cyclists were studied on two occasions during exercise to fatigue at 70 +/- 1% of VO2max. After 135 min of exercise, the men were fed either an artificially sweetened placebo or glucose polymers (3 g.kg-1 in a 50% solution). Prolonged exercise led to a decline in plasma glucose from 4.6 +/- 0.1 mM at rest to 3.9 +/- 0.2 mM after 135 min (P less than 0.05). Plasma glucose decreased further (P less than 0.05) to 3.2 +/- 2.0 mM at fatigue following placebo ingestion but increased (P less than 0.05) and was then maintained at 4.5-4.9 mM following carbohydrate ingestion. Respiratory exchange ratio (R) fell gradually during the placebo trial from 0.88 +/- 0.01 after 10 min of exercise to 0.81 +/- 0.01 at fatigue (P less than 0.01). R also reached a minimum of 0.81-0.82 in each subject after 135-180 min of exercise during the carbohydrate feeding trial but increased again to 0.84-0.86 as plasma glucose rose following the carbohydrate feeding. Exercise time to fatigue was 21% longer (205 +/- 17 vs 169 +/- 12 min; P less than 0.01) during the carbohydrate ingestion trial. Plasma insulin did not increase significantly, whereas plasma free fatty acids and blood glycerol plateaued following carbohydrate ingestion. These data indicate that a single carbohydrate feeding late in exercise can supply sufficient carbohydrate to restore euglycemia and increase carbohydrate oxidation, thereby delaying fatigue.

Adult↗

PubMed1988

Salmonella enteritidis phage type 4 infection: association with hen's eggs.

Epidemiological and microbiological investigation of the four outbreaks of Salmonella enteritidis phage type (PT) 4 that occurred in Wales in 1988 implicated foods containing shell eggs from hens as the vehicle of infection. In a case-control study of sporadic cases there was a significant association between infection and egg consumption in the 3 days before illness. These findings provide data to support the warnings from the Departments of Health in the United Kingdom about risks of infection from eating raw or undercooked hens' eggs.

Adult↗

PubMed1988

Exercise stroke volume relative to plasma-volume expansion.

The effects of plasma-volume (PV) expansion on stroke volume (SV) (CO2 rebreathing) during submaximal exercise were determined. Intravenous infusion of 403 +/- 21 ml of a 6% dextran solution before exercise in the upright position increased SV 11% (i.e., 130 +/- 6 to 144 +/- 5 ml; P less than 0.05) in untrained males (n = 7). Further PV expansion (i.e., 706 +/- 43 ml) did not result in a further increase in SV (i.e., 145 +/- 4 ml). SV was somewhat higher during supine compared with upright exercise when blood volume (BV) was normal (i.e., 138 +/- 8 vs. 130 +/- 6 ml; P = 0.08). PV expansion also increased SV during exercise in the supine position (i.e., 138 +/- 8 to 150 +/- 8 ml; P less than 0.05). In contrast to these observations in untrained men, PV expansion of endurance-trained men (n = 10), who were naturally PV expanded, did not increase SV during exercise in the upright or supine positions. When BV in the untrained men was increased to match that of the endurance-trained subjects, SV was observed to be 15% higher (165 +/- 7 vs. 144 +/- 5 ml; P less than 0.05), whereas mean blood pressure and total peripheral resistance were significantly lower (P less than 0.05) in the trained compared with untrained subjects during upright exercise at a similar heart rate. The present findings indicate that exercise SV in untrained men is preload dependent and that increases in exercise SV occur in response to the first 400 ml of PV expansion. It appears that approximately one-half of the difference in SV normally observed between untrained and highly endurance-trained men during upright exercise is due to a suboptimal BV in the untrained men.

Adult↗

PubMed1988

Muscle glycogen synthesis after exercise: effect of time of carbohydrate ingestion.

The time of ingestion of a carbohydrate supplement on muscle glycogen storage postexercise was examined. Twelve male cyclists exercised continuously for 70 min on a cycle ergometer at 68% VO2max, interrupted by six 2-min intervals at 88% VO2max, on two separate occasions. A 25% carbohydrate solution (2 g/kg body wt) was ingested immediately postexercise (P-EX) or 2 h postexercise (2P-EX). Muscle biopsies were taken from the vastus lateralis at 0, 2, and 4 h postexercise. Blood samples were obtained from an antecubital vein before and during exercise and at specific times after exercise. Muscle glycogen immediately postexercise was not significantly different for the P-EX and 2P-EX treatments. During the first 2 h postexercise, the rate of muscle glycogen storage was 7.7 mumol.g wet wt-1.h-1 for the P-EX treatment, but only 2.5 mumol.g wet wt-1.h-1 for the 2P-EX treatment. During the second 2 h of recovery, the rate of glycogen storage slowed to 4.3 mumol.g wet wt-1.h-1 during treatment P-EX but increased to 4.1 mumol.g wet wt-1.h-1 during treatment 2P-EX. This rate, however, was still 45% slower (P less than 0.05) than that for the P-EX treatment during the first 2 h of recovery. This slower rate of glycogen storage occurred despite significantly elevated plasma glucose and insulin levels. The results suggest that delaying the ingestion of a carbohydrate supplement post-exercise will result in a reduced rate of muscle glycogen storage.

Adult↗

PubMed1988

Determinants of endurance in well-trained cyclists.

Fourteen competitive cyclists who possessed a similar maximum O2 consumption (VO2 max; range, 4.6-5.0 l/min) were compared regarding blood lactate responses, glycogen usage, and endurance during submaximal exercise. Seven subjects reached their blood lactate threshold (LT) during exercise of a relatively low intensity (group L) (i.e., 65.8 +/- 1.7% VO2 max), whereas exercise of a relatively high intensity was required to elicit LT in the other seven men (group H) (i.e., 81.5 +/- 1.8% VO2 max; P less than 0.001). Time to fatigue during exercise at 88% of VO2 max was more than twofold longer in group H compared with group L (60.8 +/- 3.1 vs. 29.1 +/- 5.0 min; P less than 0.001). Over 92% of the variance in performance was related to the % VO2 max at LT and muscle capillary density. The vastus lateralis muscle of group L was stressed more than that of group H during submaximal cycling (i.e., 79% VO2 max), as reflected by more than a twofold greater (P less than 0.001) rate of glycogen utilization and blood lactate concentration. The quality of the vastus lateralis in groups H and L was similar regarding mitochondrial enzyme activity, whereas group H possessed a greater percentage of type I muscle fibers (66.7 +/- 5.2 vs. 46.9 +/- 3.8; P less than 0.01). The differing metabolic responses to submaximal exercise observed between the two groups appeared to be specific to the leg extension phase of cycling, since the blood lactate responses of the two groups were comparable during uphill running. These data indicate that endurance can vary greatly among individuals with an equal VO2 max.(ABSTRACT TRUNCATED AT 250 WORDS)

3-Hydroxyacyl CoA Dehydrogenases↗

PubMed1988

Effect of carbohydrate feedings during high-intensity exercise.

To determine the upper limits of steady-state exercise performance and carbohydrate oxidation late in exercise, seven trained men were studied on two occasions during prolonged cycling that alternated every 15 min between approximately 60% and approximately 85% of VO2max. When fed a sweet placebo throughout exercise, plasma glucose and respiratory exchange ratio (R) declined (P less than 0.05) from 5.0 +/- 0.1 mM and 0.91 +/- 0.01 after 30 min (i.e., at 85% VO2max) to 3.7 +/- 0.3 mM and 0.79 +/- 0.01 at fatigue (i.e., when the subjects were unable to continue exercise at 60% VO2max). Carbohydrate feeding throughout exercise (1 g/kg at 10 min, then 0.6 g/kg every 30 min) increased plasma glucose to approximately 6 mM and partially prevented this decline in carbohydrate oxidation, allowing the men to perform 19% more work (2.74 +/- 0.13 vs. 2.29 +/- 0.09 MJ, P less than 0.05) before fatiguing. Even when fed carbohydrate, however, by the 3rd h of exercise, R had fallen from 0.92 to 0.87, accompanied by a reduction in exercise intensity from approximately 85% to approximately 75% VO2max (both P less than 0.05). These data indicate that carbohydrate feedings enable trained cyclists to exercise at up to 75% VO2max and to oxidize carbohydrate at up to 2 g/min during the later stages of prolonged intense exercise.

Adult↗

PubMed1987

Reversal of fatigue during prolonged exercise by carbohydrate infusion or ingestion.

Seven cyclists exercised at 70% of maximal O2 uptake (VO2max) until fatigue (170 +/- 9 min) on three occasions, 1 wk apart. During these trials, plasma glucose declined from 5.0 +/- 0.1 to 3.1 +/- 0.1 mM (P less than 0.001) and respiratory exchange ratio (R) fell from 0.87 +/- 0.01 to 0.81 +/- 0.01 (P less than 0.001). After resting 20 min the subjects attempted to continue exercise either 1) after ingesting a placebo, 2) after ingesting glucose polymers (3 g/kg), or 3) when glucose was infused intravenously ("euglycemic clamp"). Placebo ingestion did not restore euglycemia or R. Plasma glucose increased (P less than 0.001) initially to approximately 5 mM and R rose (P less than 0.001) to approximately 0.83 with glucose infusion or carbohydrate ingestion. Plasma glucose and R then fell gradually to 3.9 +/- 0.3 mM and 0.81 +/- 0.01, respectively, after carbohydrate ingestion but were maintained at 5.1 +/- 0.1 mM and 0.83 +/- 0.01, respectively, by glucose infusion. Time to fatigue during this second exercise bout was significantly longer during the carbohydrate ingestion (26 +/- 4 min; P less than 0.05) or glucose infusion (43 +/- 5 min; P less than 0.01) trials compared with the placebo trial (10 +/- 1 min). Plasma insulin (approximately 10 microU/ml) and vastus lateralis muscle glycogen (approximately 40 mmol glucosyl U/kg) did not change during glucose infusion, with three-fourths of total carbohydrate oxidation during the second exercise bout accounted for by the euglycemic glucose infusion rate (1.13 +/- 0.08 g/min).(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Oral↗

PubMed1986

Effects of physical deconditioning after intense endurance training on left ventricular dimensions and stroke volume.

To determine the role of preload in maintaining the enhanced stroke volume of upright exercise-trained endurance athletes after deconditioning, six highly trained subjects undergoing upright and supine bicycle ergometry were characterized before and after 3, 8 and 12 weeks of inactivity that reduced oxygen uptake by 20%. During exercise, oxygen uptake, cardiac output by carbon dioxide rebreathing, cardiac dimensions by M-mode echocardiography, indirect arterial blood pressure and heart rate were studied simultaneously. Two months of inactivity resulted in a reduction in stroke volume, calculated as cardiac output/heart rate, during upright exercise (p less than 0.005) without a significant change during supine exercise. A concomitant decrease in the left ventricular end-diastolic dimension from the trained to the deconditioned state was observed in the upright posture (5.1 +/- 0.3 versus 4.6 +/- 0.3 cm; p = 0.02) but not with recumbency (5.4 +/- 0.2 versus 5.1 +/- 0.3 cm; p = NS). There was a strong correlation between left ventricular end-diastolic dimension and stroke volume (r greater than 0.80) in all subjects. No significant changes in percent fractional shortening or left ventricular end-systolic dimension occurred in either position after cessation of training. Estimated left ventricular mass was 20% lower after 3 and 8 weeks of inactivity than when the subjects were conditioned (p less than 0.05 for both). Thus, the endurance-trained state for upright exercise is associated with a greater stroke volume during upright exercise because of augmented preload. Despite many years of intense training, inactivity for only a few weeks results in loss of this adaptation in conjunction with regression of left ventricular hypertrophy.

Adult↗

PubMed1986

Effects of detraining on cardiovascular responses to exercise: role of blood volume.

In this study we determined whether the decline in exercise stroke volume (SV) observed when endurance-trained men stop training for a few weeks is associated with a reduced blood volume. Additionally, we determined the extent to which cardiovascular function could be restored in detrained individuals by expanding blood volume to a similar level as when trained. Maximal O2 uptake (VO2max) was determined, and cardiac output (CO2 rebreathing) was measured during upright cycling at 50-60% VO2max in eight endurance-trained men before and after 2-4 wk of inactivity. Detraining produced a 9% decline in blood volume (5,177 to 4,692 ml; P less than 0.01) during upright exercise, due primarily to a 12% lowering (P less than 0.01) of plasma volume (PV; Evans blue dye technique). SV was reduced by 12% (P less than 0.05) and VO2max declined 6% (P less than 0.01), whereas heart rate (HR) and total peripheral resistance (TPR) during submaximal exercise were increased 11% (P less than 0.01) and 8% (P less than 0.05), respectively. When blood volume was expanded to a similar absolute level in the trained and detrained state (approximately 5,500 +/- 200 ml) by infusing a 6% dextran solution in saline, the effects of detraining on cardiovascular response were reversed. SV and VO2max were increased (P less than 0.05) by PV expansion in the detrained state to within 2-4% of trained values. Additionally, HR and TPR during submaximal exercise were lowered to near trained values. These findings indicate that the decline in cardiovascular function following a few weeks of detraining is largely due to a reduction in blood volume, which appears to limit ventricular filling during upright exercise.

Adult↗

PubMed1986

Muscle glycogen utilization during prolonged strenuous exercise when fed carbohydrate.

The purpose of this study was to determine whether the postponement of fatigue in subjects fed carbohydrate during prolonged strenuous exercise is associated with a slowing of muscle glycogen depletion. Seven endurance-trained cyclists exercised at 71 +/- 1% of maximal O2 consumption (VO2max), to fatigue, while ingesting a flavored water solution (i.e., placebo) during one trial and while ingesting a glucose polymer solution (i.e., 2.0 g/kg at 20 min and 0.4 g/kg every 20 min thereafter) during another trial. Fatigue during the placebo trial occurred after 3.02 +/- 0.19 h of exercise and was preceded by a decline (P less than 0.01) in plasma glucose to 2.5 +/- 0.5 mM and by a decline in the respiratory exchange ratio (i.e., R; from 0.85 to 0.80; P less than 0.05). Glycogen within the vastus lateralis muscle declined at an average rate of 51.5 +/- 5.4 mmol glucosyl units (GU) X kg-1 X h-1 during the first 2 h of exercise and at a slower rate (P less than 0.01) of 23.0 +/- 14.3 mmol GU X kg-1 X h-1 during the third and final hour. When fed carbohydrate, which maintained plasma glucose concentration (4.2-5.2 mM), the subjects exercised for an additional hour before fatiguing (4.02 +/- 0.33 h; P less than 0.01) and maintained their initial R (i.e., 0.86) and rate of carbohydrate oxidation throughout exercise. The pattern of muscle glycogen utilization, however, was not different during the first 3 h of exercise with the placebo or the carbohydrate feedings. The additional hour of exercise performed when fed carbohydrate was accomplished with little reliance on muscle glycogen (i.e., 5 mmol GU X kg-1 X h-1; NS) and without compromising carbohydrate oxidation. We conclude that when they are fed carbohydrate, highly trained endurance athletes are capable of oxidizing carbohydrate at relatively high rates from sources other than muscle glycogen during the latter stages of prolonged strenuous exercise and that this postpones fatigue.

Adult↗

PubMed1985

Substrate usage during prolonged exercise following a preexercise meal.

The effect of a high-carbohydrate meal 4 h before 105 min of exercise at 70% of maximal O2 uptake was determined in seven endurance-trained cyclists and compared with exercise following a 16-h fast. The preexercise meal produced a transient elevation of plasma insulin and blood glucose, which returned to fasting basal levels prior to the initiation of exercise. The meal also resulted in a 42% elevation (P less than 0.05) of glycogen within the vastus lateralis at the beginning of exercise. The 1st h of exercise when subjects were fed was characterized by a 13-25% decline (P less than 0.05) in blood glucose concentration, a suppression of the normal increase in plasma free fatty acids and blood glycerol, and a 45% (P less than 0.05) greater rate of carbohydrate oxidation compared with exercise when subjects were fasted. After 105 min of exercise, there were no significant differences when subjects were fed or fasted regarding blood glucose levels, rate of carbohydrate oxidation, or muscle glycogen concentration. The greater muscle glycogen utilization (97 +/- 18 vs. 64 +/- 8 mmol glucosyl units X kg-1; P less than 0.05) and carbohydrate oxidation when subjects were fed appeared to be derived from the glycogen synthesized following the meal. These results indicate that preexercise feedings alter substrate availability despite a return of plasma insulin to fasting levels prior to exercise and that these effects persist until the 2nd h of exercise.

Bicycling↗

PubMed1985

Effects of detraining on responses to submaximal exercise.

Seven endurance-trained subjects were studied 12, 21, 56, and 84 days after cessation of training. Heart rate, ventilation, respiratory exchange ratio, and blood lactate concentration during submaximal exercise of the same absolute intensity increased (P less than 0.05) progressively during the first 56 days of detraining, after which a stabilization occurred. These changes paralleled a 40% decline (P less than 0.001) in mitochondrial enzyme activity levels and a 21% increase in total lactate dehydrogenase (LDH) activity (P less than 0.05) in trained skeletal muscle. After 84 days of detraining, the experimental subjects' muscle mitochondrial enzyme levels were still 50% above, and LDH activity was 22% below, sedentary control levels. The blood lactate threshold of the detrained subjects occurred at higher absolute and relative (i.e., 75 +/- 2% vs. 62 +/- 3% of maximal O2 uptake) exercise intensities in the subjects after 84 days of detraining than in untrained controls (P less than 0.05). Thus it appears that a portion of the adaptation to prolonged and intense endurance training that is responsible for the higher lactate threshold in the trained state persists for a long time (greater than 85 days) after training is stopped.

Blood Glucose↗

PubMed1984

Cardiovascular sensitivity to epinephrine in the trained and untrained states.

Heart rate (HR), blood pressure (BP) and inotropic responses to acute exercise are partially mediated by sympathetic stimulation. Physical conditioning reduces exercise HR and improves maximal stroke volume and cardiac output. Uncertainty exists regarding the role of altered catecholamine sensitivity in producing these changes in man. In 6 highly trained men, noninvasive methods were used to serially assess the effect of cessation of training on the resting HR, BP and left ventricular contractile function in response to constant epinephrine infusion. Plasma epinephrine concentration during infusion did not vary with inactivity and was similar to that attained with strenuous exercise. Two subjects showed an increase in chronotropic sensitivity to epinephrine and 4 showed no consistent change. Despite a significant decline in exercise capacity and no apparent change in cardiac loading conditions, there was no persistent effect of inactivity on BP or left ventricular function as assessed by echocardiography and systolic time intervals. Therefore, an alteration in sensitivity to epinephrine is unlikely to account for the hemodynamic adaptations to endurance exercise training in healthy men.

Adaptation, Physiological↗

PubMed1984

Effect of prolonged intense endurance training on systolic time intervals in patients with coronary artery disease.

We studied the effect of exercise training (ET) on systolic time intervals (STI) in 13 patients with coronary artery disease (CAD). All patients trained for at least 10 months. They exercised three times/week at 50% to 70% of maximal oxygen uptake (VO2max) for the initial 3 months and at least four times/week for approximately 50 minutes at 70% to 90% of VO2max thereafter. A significant training effect was documented by an increase in VO2max from 26.0 +/- 4.3 to 37.2 +/- 5.8 ml/kg/min (p less than 0.01), a lower heart rate (HR) at rest, and a lower blood pressure and HR during submaximal work. The indices of total electromechanical systole (QS2I) and left ventricular ejection time (LVETI) did not change. However, pre-ejection period index (PEPI) decreased from 137 +/- 9 msec to 129 +/- 9 msec (p less than 0.01). PEP/LVET decreased from 0.373 +/- 0.028 to 0.342 +/- 0.032 (p less than 0.01). Left ventricular end-diastolic dimension and posterior wall thickness, measured echocardiographically, were increased after training. We conclude that exercise training may improve myocardial performance in some patients with CAD.

Adult↗

PubMed1984

Physiologic comparison of competitive racewalking and running.

Eight competitive racewalkers were studied to determine a) the speed where running and racewalking become equally efficient, b) if, at a similar VO2, the physiologic responses to submaximal exercise differ between running and racewalking, and c) if VO2 max can be attained during racewalking. The speed at which running and racewalking elicited the same VO2 (approximately 30 ml X kg-1 X min-1) was between 8 and 9 km X h-1. Racewalking was more efficient at slower speeds, and running was more efficient at faster velocities. When running and racewalking were compared at similar oxygen consumptions, heart rate, ventilation, perceived exertion, and respiratory exchange ratio responses were identical. During maximal exercise, running and racewalking resulted in a similar VO2 max (60.4 +/- 1.3 vs. 58.1 +/- 1.5 ml X kg-1 X min-1), heart rate (193 +/- 4 vs. 188 +/- 4 bpm), ventilation (130.6 +/- 5.9 vs. 126.3 +/- 6.6 l X min-1), and post-exercise blood lactic acid concentration (9.8 +/- 0.6 vs. 9.6 +/- 0.7 mM). These results indicate that the speed where racewalking and running become equally efficient is similar to the crossover speed for conventional walking and running. Cardiovascular, respiratory, and perceptual responses during running and racewalking are the same during maximal exercise and during submaximal exercise at the same VO2.

Adult↗