Biomedical subjects

E F Coyle

Publications and source records attributed to E F Coyle.

At least 37 records · Page 2Linked to original sources

PubMed1997

Fatty acid oxidation is directly regulated by carbohydrate metabolism during exercise.

We determined whether increased glycolytic flux from hyperglycemia and hyperinsulinemia directly reduces fatty acid oxidation during exercise. Fatty acid oxidation rates were measured during constant-rate intravenous infusion of trace amounts of a long-chain fatty acid ([1-13C]palmitate; Pal) vs. a medium-chain fatty acid ([1-13C]octanoate; Oct). Six endurance-trained men cycled for 40 min at 50% of maximal O2 uptake 1) after an overnight fast ("fasting") and 2) after ingestion of 1.4 g/kg of glucose at 60 min and again 10 min before exercise (Glc). Glc caused hyperinsulinemia, a preexercise blood glucose of 6 mM, and a 34% reduction in total fat oxidation during exercise due to an approximately equal reduction in oxidation of plasma-free fatty acids (FFA) and intramuscular triglycerides (all P < 0.05). Oxidation of Pal was significantly reduced during Glc compared with fast (i.e., 70.0 +/- 4.1 vs. 86.0 +/- 1.9% of tracer infusion rate; P < 0.05). However, Glc had no effect on Oct oxidation, which is apparently not limited by mitochondrial transport. Furthermore, Glc reduced plasma FFA appearance 36% (P < 0.05), indicating a coordination of effects on adipose tissue and muscle. In summary, substrate oxidation during exercise can be regulated by increased glycolytic flux that is accompanied by a direct inhibition of long-chain fatty acid oxidation. These observations indicate that carbohydrate availability can directly regulate fat oxidation during exercise.

Adipose Tissue↗

PubMed1997

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 microU/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 micromol x kg(-1) x min(-1) and fat oxidation was 6.1 +/- 0.2, 4.2 +/- 0.5, and 3.1 +/- 0.3 micromol x kg(-1) x min(-1) during 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 micromol x kg(-1) x 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.

Adult↗

PubMed1997

Dehydration markedly impairs cardiovascular function in hyperthermic endurance athletes during exercise.

We identified the cardiovascular stress encountered by superimposing dehydration on hyperthermia during exercise in the heat and the mechanisms contributing to the dehydration-mediated stroke volume (SV) reduction. Fifteen endurance-trained cyclists [maximal O2 consumption (VO2max) = 4.5 l/min] exercised in the heat for 100-120 min and either became dehydrated by 4% body weight or remained euhydrated by drinking fluids. Measurements were made after they continued exercise at 71% VO2max for 30 min while 1) euhydrated with an esophageal temperature (T(es)) of 38.1-38.3 degrees C (control); 2) euhydrated and hyperthermic (39.3 degrees C); 3) dehydrated and hyperthermic with skin temperature (T(sk)) of 34 degrees C; 4) dehydrated with T(es) of 38.1 degrees C and T(sk) of 21 degrees C; and 5) condition 4 followed by restored blood volume. Compared with control, hyperthermia (1 degrees C T(es) increase) and dehydration (4% body weight loss) each separately lowered SV 7-8% (11 +/- 3 ml/beat; P < 0.05) and increased heart rate sufficiently to prevent significant declines in cardiac output. However, when dehydration was superimposed on hyperthermia, the reductions in SV were significantly (P < 0.05) greater (26 +/- 3 ml/beat), and cardiac output declined 13% (2.8 +/- 0.3 l/min). Furthermore, mean arterial pressure declined 5 +/- 2%, and systemic vascular resistance increased 10 +/- 3% (both P < 0.05). When hyperthermia was prevented, all of the decline in SV with dehydration was due to reduced blood volume (approximately 200 ml). These results demonstrate that the superimposition of dehydration on hyperthermia during exercise in the heat causes an inability to maintain cardiac output and blood pressure that makes the dehydrated athlete less able to cope with hyperthermia.

Adult↗

PubMed1996

Plasma catecholamines and hyperglycaemia influence thermoregulation in man during prolonged exercise in the heat.

1. We manipulated plasma catecholamines (combined adrenaline and noradrenaline concentrations) to three levels during prolonged exercise to determine their effect on cutaneous and forearm vascular conductance (CVC and FVC), oesophageal temperature (T(oes)) and cardiovascular responses. 2. On three occasions, seven endurance-trained men cycled at 65% VO2, max in the heat (33.1 +/- 0.7 degrees C) for 120-150 min. During the control trial (150 min duration), 0.45% saline was intravenously infused (SI) starting at 30 min, at a rate that replaced a third of the fluid losses. The infusion start time and rate were identical in all three trials. During SI, plasma catecholamine levels increased progressively and were 18.2 +/- 2.7 pmol ml-1 at 150 min. In another trial (120 min duration), adrenaline was infused (AI) at 0.1 microgram kg-1 min-1 and plasma catecholamine levels were elevated 6 pmol ml-1 above SI during the 60-120 min period. In a third trial (150 min duration), an 18% glucose solution was infused (GI) at a rate that maintained plasma glucose levels above 11 mM and plasma catecholamine levels were 5.0-5.5 pmol ml-1 lower (P < 0.05) than SI from 120-150 min. 3. Heat production and sweat rate were not different during the three trials and neither was the decline in stroke volume, cardiac output and mean arterial pressure. 4. Soon after beginning AI, CVC decreased 15%, T(oes) increased by 0.4 +/- 0.1 degree C and heart rate increased by 6 +/- 1 beats min-1; these significant (P < 0.05) differences from SI were maintained throughout the bout. As a result of GI, FVC was 15% higher than SI and T(oes) and heart rate were attenuated by 0.3 +/- 0.1 degree C and 7 +/- 1 beats min-1 at 150 min compared with SI (P < 0.05). 5. In conclusion, large increases in plasma catecholamine levels cause hyperthermia during exercise by vasoconstricting the skin. The mechanisms by which hyperglycaemia (i.e. 11 mM) attenuates hyperthermia are less clear and may be due to others factors besides attenuation of the plasma catecholamine response to exercise.

Adult↗

PubMed1996

Effect of endurance training on glycerol kinetics during strenuous exercise in humans.

Glycerol kinetics were evaluated during high-intensity exercise in five untrained and five endurance-trained subjects. Glycerol rate of appearance (Ra) in plasma was determined by infusing [2H5]glycerol during rest and 60 minutes of cycle ergometer exercise performed at 70% V02 peak. Mean plasma glycerol concentration was greater in trained than untrained subjects throughout exercise (P<.05). The average glycerol Ra during exercise and the integrated lipolytic response to exercise, expressed as total glycerol Ra above baseline, were both greater in trained (7.85 +/- 0.72 micromol x kg(-1) x min(-1) and 289 +/- 50 micromol x kg(-1) x h(-1), respectively) than in untrained (5.68 +/- 0.90 micromol x kg(-1) x min(-1), and 198 +/- 31 micromol x kg(-1) x h(-1), respectively) subjects (P<.05). We conclude that whole-body lipolytic rates are greater in endurance-trained athletes than in sedentary controls during high-intensity exercise performed at the same relative intensity.

Adult↗

PubMed1996

American College of Sports Medicine position stand. Exercise and fluid replacement.

It 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 comprehensive review and interpretation of scientific literature concerning the influence of fluid replacement on exercise performance and the risk of thermal injury associated with dehydration and hyperthermia. Based on available evidence, the American College of Sports Medicine makes the following general recommendations on the amount and composition of fluid that should be ingested in preparation for, during, and after exercise or athletic competition: 1) It is recommended that individuals consume a nutritionally balanced diet and drink adequate fluids during the 24-hr period before an event, especially during the period that includes the meal prior to exercise, to promote proper hydration before exercise or competition. 2) It is recommended that individuals drink about 500 ml (about 17 ounces) of fluid about 2 h before exercise to promote adequate hydration and allow time for excretion of excess ingested water. 3) During exercise, athletes should start drinking early and at regular intervals in an attempt to consume fluids at a rate sufficient to replace all the water lost through sweating (i.e., body weight loss), or consume the maximal amount that can be tolerated. 4) It is recommended that ingested fluids be cooler than ambient temperature [between 15 degrees and 22 degrees C (59 degrees and 72 degrees F])] and flavored to enhance palatability and promote fluid replacement. Fluids should be readily available and served in containers that allow adequate volumes to be ingested with ease and with minimal interruption of exercise. 5) Addition of proper amounts of carbohydrates and/or electrolytes to a fluid replacement solution is recommended for exercise events of duration greater than 1 h since it does not significantly impair water delivery to the body and may enhance performance. During exercise lasting less than 1 h, there is little evidence of physiological or physical performance differences between consuming a carbohydrate-electrolyte drink and plain water. 6) During intense exercise lasting longer than 1 h, it is recommended that carbohydrates be ingested at a rate of 30-60 g.h(-1) to maintain oxidation of carbohydrates and delay fatigue. This rate of carbohydrate intake can be achieved without compromising fluid delivery by drinking 600-1200 ml.h(-1) of solutions containing 4%-8% carbohydrates (g.100 ml(-1)). The carbohydrates can be sugars (glucose or sucrose) or starch (e.g., maltodextrin). 7) Inclusion of sodium (0.5-0.7 g.1(-1) of water) in the rehydration solution ingested during exercise lasting longer than 1 h is recommended since it may be advantageous in enhancing palatability, promoting fluid retention, and possibly preventing hyponatremia in certain individuals who drink excessive quantities of fluid. There is little physiological basis for the presence of sodium in n oral rehydration solution for enhancing intestinal water absorption as long as sodium is sufficiently available from the previous meal.

Beverages↗

PubMed1995

Substrate utilization during exercise in active people.

When people walk at low intensity after fasting, the energy needed is provided mostly by oxidation of plasma fatty acids. As exercise intensity increases (eg, to moderate running), plasma fatty acid turnover does not increase and the additional energy is obtained by utilization of muscle glycogen, blood glucose, and intramuscular triglyceride. Further increases in exercise intensity are fueled mostly by increases in muscle glycogen utilization with some additional increase in blood glucose oxidation. Muscle glycogen and blood glucose contribute equally to carbohydrate energy production over 2-3 h of moderate-intensity exercise; fatigue develops when these substrates are depleted. Active people can deplete muscle glycogen with 30-60 min of high intensity, intermittent exercise. When the ingestion of dietary carbohydrate is optimal, it is possible to resynthesize muscle glycogen to high concentrations in approximately 24 h, which is the major factor in recovery of exercise tolerance. However, this requires that a 70-kg person eat at least 50 g carbohydrate per every 2 h, beginning soon after exercise, and ingest 500-600 g in 24 h (ie; approximately 7-9 g/kg body wt). Carbohydrate foods eliciting high glycemic and insulinemic responses promote more rapid glycogen resynthesis than do foods eliciting lower glycemic responses. Therefore, foods ingested for energy before, during, or after exercise should be classified according to their glycemic index. Although carbohydrate ingestion before and during exercise adds exogenous substrate to the body, it usually attenuates plasma fatty acid mobilization and oxidation.

Dietary Carbohydrates↗

PubMed1995

Effect of exercise on lipolytic sensitivity in endurance-trained athletes.

Studies performed in vitro suggest that an acute bout of exercise increases the lipolytic response to beta-adrenergic stimulation. We evaluated the effect of exercise on lipolytic sensitivity in vivo in five endurance-trained athletes. The rate of appearance (Ra) of glycerol in plasma, an index of whole body lipolysis, was determined during 60 min of epinephrine infusion (0.015 microgram.kg-1.min-1) on two occasions: 1) at basal resting conditions and 2) 90 min after completing 1 h of high-intensity (70% O2 uptake) cycle ergometer exercise. Total glycerol Ra during epinephrine infusion in the basal state (352 +/- 35 mumol.kg-1. 60 min-1) was not significantly different from the value obtained after high-intensity exercise (439 +/- 58 mumol.kg-1. 60 min-1). However, the increase in glycerol Ra above baseline during epinephrine infusion was lower after (30 +/- 16 mumol.kg-1. 60 min-1) than before (148 +/- 28 mumol.kg-1. 60 min-1) exercise because of the high postexercise baseline value (P < 0.05). Mean plasma free fatty acid (FFA) concentration was lower during exercise than during epinephrine infusion despite a greater rate of lipolysis during exercise. The slope of change in plasma FFA with respect to glycerol RA was lower during exercise (0.0171 +/- 0.006) than during epinephrine infusion (0.0835 +/- 0.018) (P < 0.05). We conclude that a single bout of intense exercise does not increase in vivo lipolytic sensitivity to beta-adrenergic stimulation in endurance-trained athletes. In addition, plasma FFA concentration represents the balance between plasma FFA inflow and tissue uptake and cannot be used as an index of lipolytic activity during certain physiological conditions, such as exercise.

Adult↗

PubMed1995

Dehydration reduces cardiac output and increases systemic and cutaneous vascular resistance during exercise.

This investigation determined the manner in which the cardiovascular system copes with the dehydration-induced reductions in cardiac output (Q) during prolonged exercise in the heat. On two separate occasions, seven endurance-trained subjects (maximal O2 consumption 4.70 +/- 0.41 l/min) cycled in the heat (35 degrees C) for 2 h, beginning at 62 +/- 2% maximal O2 consumption. During exercise, they randomly received either 0.2 liter of fluid and became dehydrated by 4.9 +/- 0.2% of their body weight [i.e., dehydration trial (DE)] or 3.6 +/- 0.4 liter of fluid and replaced 95% of fluid losses [i.e., euhydration trial (EU)]. During the 10- to 120-min period of EU, Q, mean arterial pressure (MAP), systemic vascular resistance (SVR), cutaneous vascular resistance (CVR), and plasma catecholamines did not change while esophageal temperature stabilized at 38.0 +/- 0.1 degrees C. Conversely, after 120 min of DE, Q and MAP were reduced 18 +/- 3 and 5 +/- 2%, respectively, compared with EU (P < 0.05). This was associated with a significantly higher SVR (17 +/- 6%) and plasma norepinephrine concentration (50 +/- 19%, P < 0.05). In addition, CVR was also significantly higher (126 +/- 16 vs. 102 +/- 6% of 20-min value; P < 0.05) during DE despite a 1.2 +/- 0.1 degrees C greater esophageal temperature (P < 0.05). In conclusion, significant reductions in Q are accompanied by significant increases in SVR and plasma norepinephrine and a slight although significant decline in MAP. The cutaneous circulation participates in this systemic vasoconstriction as indicated by increases in CVR despite significant hyperthermia.

Adult↗

PubMed1995

Relationship between fatty acid delivery and fatty acid oxidation during strenuous exercise.

To evaluate the extent to which decreased plasma free fatty acid (FFA) concentration contributes to the relatively low rates of fat oxidation during high-intensity exercise, we studied FFA metabolism in six endurance-trained cyclists during 20-30 min of exercise [85% of maximal O2 uptake (VO2max)]. They were studied on two occasions: once during a control trial when plasma FFA concentration is normally low and again when plasma FFA concentration was maintained between 1 and 2 mM by intravenous infusion of lipid (Intralipid) and heparin. During the 20-30 min of exercise, fat and carbohydrate oxidation were measured by indirect calorimetry, and the rates of appearance (Ra) of plasma FFA and glucose were determined by the constant infusion of [6,6-2H2]glucose and [2H2]palmitate. Lipid-heparin infusion did not influence the Ra or rate of disappearance of glucose. During exercise in the control trial, Ra FFA failed to increase above resting levels (11.0 +/- 1.2 and 12.4 +/- 1.7 mumol.kg-1.min-1 for rest and exercise, respectively) and plasma FFA concentration dropped from a resting value of 0.53 +/- 0.08 to 0.29 +/- 0.02 mM. The restoration of plasma FFA concentration resulted in a 27% increase in total fat oxidation (26.7 +/- 2.6 vs. 34.0 +/- 4.4 mumol.kg-1.min-1, P < 0.05) with a concomitant reduction in carbohydrate oxidation, apparently due to a 15% (P < 0.05) reduction in muscle glycogen utilization. However, the elevation of plasma FFA concentration during exercise at 85% VO2max only partially restored fat oxidation compared with the levels observed during exercise at 65% VO2max. These findings indicate that fat oxidation is normally impaired during exercise at 85% VO2max because of the failure of FFA mobilization to increase above resting levels, but this explains only part of the decline in fat oxidation when exercise intensity is increased from 65 to 85% VO2max.

Adult↗

PubMed1995

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 patient's 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 muscle's Aerobic Enzyme Activity or mitochondrial respiratory capacity, as discussed in previous reviews [29, 30].(ABSTRACT TRUNCATED AT 400 WORDS)

Bicycling↗

PubMed1995

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.

Adult↗

PubMed1994

Hypohydration causes cardiovascular drift without reducing blood volume.

To determine the effect of hydration on cardiovascular drift (i.e.; increased heart rate and reduced stroke volume) during exercise in a 21 degrees C environment, nine subjects were studied while cycling at 65% of peak oxygen consumption when euhydrated and while still hypohydrate, following exercise-induced dehydration and a 2 h rest/rehydration period. Subjects dehydrated by exercising in the heat (32 degrees C) until body weight was reduced 2.5%. On two separate occasions following exercise, subjects either received no fluid or ingested a volume of water equal to 100% of the fluid lost during exercise. Following the 2 h rest/rehydration period, 65 +/- 6% of the ingested water was retained and thus the subjects were hypohydrated by 0.9 +/- 0.1%, compared to being hypohydrated by 2.8 +/- 0.1% when no fluid was ingested. Despite these differences in whole body hydration, blood volume during exercise remained at euhydrated levels when hypohydrated by 0.9% and 2.8%. However, the degree of cardiovascular drift was graded in proportion to hypohydration. Compared to the responses when euhydrated, heart rate was elevated 10 +/- 2 and 18 +/- 2 bt/min, whereas stroke volume was reduced 9 +/- 3 and 18 +/- 2 ml/bt, respectively, when hypohydrated by 0.9% and 2.8% during the water and no fluid trials (p < 0.05 for all comparisons). These observations indicate that cardiovascular drift during exercise in a 21 degrees C environment is graded in proportion to hydration and, under these conditions, not due to reductions in blood volume.

Adolescent↗

PubMed1994

High efficiency of type I muscle fibers improves performance.

We have recently demonstrated that people with a high percentage of Type I muscle fibers display a relatively high muscular efficiency when cycling. These individuals generate a relatively high muscular power output at a given steady-state level of oxygen consumption and caloric expenditure. The purpose of this study was to directly determine the extent to which differences in muscle fiber composition and efficiency influence endurance performance in competitive cyclists. The percentage of Type I and II muscle fibers was determined from several biopsies from the vastus lateralis which were histochemically stained for ATPase activity. During a laboratory performance test, 14 endurance trained cyclists (mean +/- SE; VO2max, 5.2 +/- 0.11/min; body weight, 74 +/- 1 kg) cycled an ergometer for 1 h at the highest work rate they could tolerate. VO2 and RER were simultaneously measured using open circuit spirometry for calculating caloric expenditure. Subjects were divided into two groups of seven according to their muscle fiber type composition: High % Type I Group (> 56% Type I fibers); Normal % Type I Group (38-55% Type I fibers). Each subject from High % Type I Group was paired with a subject from the Normal % Type I Group according to their similarity in VO2max, blood lactate threshold and average VO2 maintained during the 1 h performance test. Both groups averaged 4.5 +/- 0.11/min during the 1 h performance test (i.e., 86-88% VO2max).(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine Triphosphatases↗

PubMed1994

Fat metabolism during low-intensity exercise in endurance-trained and untrained men.

Whole body lipid kinetics were evaluated during basal resting conditions, 4 h of treadmill exercise eliciting an oxygen uptake of 20 ml.kg-1.min-1, and 1 h of recovery in five untrained and five endurance-trained men. Glycerol and free fatty acid (FFA) rate of appearance (Ra) values in plasma were determined by infusing [2H5]glycerol and [1-13C]palmitate, respectively, and lipid oxidation was determined by indirect calorimetry. The lipolytic response to 4 h of exercise, expressed as the average glycerol and FFA Ra values, was similar in both trained (9.85 +/- 1.02 and 24.64 +/- 3.76 mumol.kg-1.min-1, respectively) and untrained subjects (11.29 +/- 0.99 and 24.13 +/- 0.39 mumol.kg-1.min-1, respectively). However, mean triglyceride oxidation was greater during exercise in the trained than in the untrained group (7.51 +/- 0.26 and 5.67 +/- 0.51 mumol.kg-1.min-1, respectively; P < 0.001). During recovery, glycerol and FFA Ra values decreased more rapidly in trained than in untrained subjects. We conclude that highly trained male endurance runners use more fat as a fuel during low-intensity exercise than do untrained healthy men despite similar rates of lipolysis and FFA uptake from plasma. Therefore, the increase in fat oxidation must be related to an increased percentage of FFA uptake oxidized, a greater contribution from intramuscular triglyceride stores, or both. Additionally, lipid kinetics return to baseline more rapidly in trained than in untrained subjects after completing an exercise bout of the same absolute intensity.

Adult↗

PubMed1993

Metabolic responses to preexercise meals containing various carbohydrates and fat.

After a 12-h fast six different meals (potatoes, rice, sucrose solution, potatoes+margarine, rice+margarine, and a confectionery bar), each containing 0.7 g carbohydrate/kg body wt, were consumed 30 min before exercise (n = 9). During the 30 min immediately after ingestion, the glycemic and insulinemic responses to the meals distinguished these foods into two groups: 1) high glycemic (ie, potatoes, sucrose, confectionery bar) and 2) moderate glycemic (ie, rice, potatoes+margarine, rice+margarine). After 20 min of moderate-intensity exercise, plasma glucose declined in all carbohydrate trials to values of 3.4 +/- 0.1 mmol/L, which were significantly (P < 0.05) lower than values after subjects fasted (4.2 +/- 0.2 mmol/L). Therefore, the glycemic and insulinemic responses to these meals were independent of their carbohydrate classification of simple or complex and the addition of fat reduced the glycemic and insulinemic responses. However, despite these different responses before exercise, all of the meals caused plasma glucose to decline to equally low concentrations early in exercise.

Adult↗

PubMed1993

Histochemical and physiological correlates of training- and detraining-induced changes in the recovery from a fatigue test.

BACKGROUND AND PURPOSE: The primary purpose of this study was to evaluate the effects of endurance training and detraining on the development of and recovery from fatigue induced by isokinetic exercise. It was our hypothesis that the rate of recovery from fatigue would correlate with maximal oxygen uptake (VO2max). A secondary purpose was to determine whether changes in the development of fatigue and in the time course of recovery that occur with alterations in training status correlate with shifts in the proportions of type IIa and type IIb muscle fibers. SUBJECTS AND METHODS: Four subjects with no regular endurance exercise training participated in a 12-week program of intense endurance exercise training, and 6 endurance-trained subjects stopped all exercise training for 12 weeks. In addition, 11 subjects performed a single isokinetic fatigue test with recovery and a graded treadmill or bicycle ergometer test to determine VO2max. RESULTS: Maximal oxygen uptake increased 24% (SD = 10%) in response to the exercise training program and decreased 17% (SD = 6%) with detraining. The percentage of type IIa and type IIb muscle fibers changed with endurance training and detraining. The percentage of decline in torque during a 60-second isokinetic exercise test was unaffected by endurance training or detraining; however, there was a significant change in recovery of torque. CONCLUSION AND DISCUSSION: The results demonstrate a positive correlation (r = .75) between the percentage of reduction in torque at 30 seconds of recovery and the change in the proportion of type IIb fibers with both training and detraining. The results also demonstrate a high, negative correlation (r = -.84) between the percentage of reduction in torque at 30 seconds of recovery and VO2max. These results suggest the recovery of muscle torque reflects both the training- and detraining-induced changes in the proportion of type IIa and type IIb muscle fibers and maximal aerobic exercise capacity.

Adult↗

PubMed1993

Regulation of endogenous fat and carbohydrate metabolism in relation to exercise intensity and duration.

Stable isotope tracers and indirect calorimetry were used to evaluate the regulation of endogenous fat and glucose metabolism in relation to exercise intensity and duration. Five trained subjects were studied during exercise intensities of 25, 65, and 85% of maximal oxygen consumption (VO2max). Plasma glucose tissue uptake and muscle glycogen oxidation increased in relation to exercise intensity. In contrast, peripheral lipolysis was stimulated maximally at the lowest exercise intensity, and fatty acid release into plasma decreased with increasing exercise intensity. Muscle triglyceride lipolysis was stimulated only at higher intensities. During 2 h of exercise at 65% VO2max plasma-derived substrate oxidation progressively increased over time, whereas muscle glycogen and triglyceride oxidation decreased. In recovery from high-intensity exercise, although the rate of lipolysis immediately decreased, the rate of release of fatty acids into plasma increased, indicating release of fatty acids from previously hydrolyzed triglycerides. We conclude that, whereas carbohydrate availability is regulated directly in relation to exercise intensity, the regulation of lipid metabolism seems to be more complex.

Adult↗