The effects of fasting on metabolism and performance.

An overnight fast of 8-10 h is normal for most people. Fasting is characterised by a coordinated set of metabolic changes designed to spare carbohydrate and increase reliance on fat as a substrate for energy supply. As well as sparing the limited endogenous carbohydrate, and increased rate of gluconeogenesis from amino acids, glycerol and ketone bodies help maintain the supply of carbohydrate. Many individuals undergo periodic fasts for health, religious or cultural reasons. Ramadan fasting, involving 1 month of abstention from food and fluid intake during daylight hours, is practised by a large part of the world population. This period involves a shift in the pattern of intake from daytime to the hours of darkness. There seems to be little effect on overall daily dietary intake and only small metabolic effects, but there may be implications for both physical and cognitive function. The limited evidence suggests that effects of Ramadan-style fasting on exercise performance are generally small. This needs to be balanced, however, against the observation that small differences in performance are critical in determining the outcomes of sporting events. Studies involving challenging sporting events (prolonged sustained or intermittent high-intensity events, hot and humid environments) are needed. Increases in subjective sensations of fatigue may be the result of loss of sleep or disruption of normal sleep patterns. Modifications to the competition timetable may minimise or even eliminate any effect on performance in sport, but there may be negative effects on performance in some events.

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.

Physical activity as a metabolic stressor.

Both physical activity and diet stimulate processes that, over time, alter the morphologic composition and biochemical function of the body. Physical activity provides stimuli that promote very specific and varied adaptations according to the type, intensity, and duration of exercise performed. There is further interest in the extent to which diet or supplementation can enhance the positive stimuli. Prolonged walking at low intensity presents little metabolic, hormonal, or cardiovascular stress, and the greatest perturbation from rest appears to be from increased fat oxidation and plasma free fatty acid mobilization resulting from a combination of increased lipolysis and decreased reesterification. More intense jogging or running largely stimulates increased oxidation of glycogen and triacylglycerol, both of which are stored directly within the muscle fibers. Furthermore, these intramuscular stores of carbohydrate and fat appear to be the primary substrates for the enhanced oxidative and performance ability derived from endurance training-induced increases in muscle mitochondrial density. Weightlifting that produces fatigue in brief periods (ie, in 15-90 s and after 15 repetitive contractions) elicits a high degree of motor unit recruitment and muscle fiber stimulation. This is a remarkably potent stimulus for altering protein synthesis in muscle and increasing neuromuscular function. The metabolic stress of physical activity can be measured by substrate turnover and depletion, cardiovascular response, hormonal perturbation, accumulation of metabolites, or even the extent to which the synthesis and degradation of specific proteins are altered, either acutely or by chronic exercise training.

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.

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.

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.

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.

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.

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.

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.

Influence of the timing of fluid ingestion on temperature regulation during exercise.

The purpose of this investigation was to determine whether the timing of fluid ingestion affects thermoregulation during exercise-heat stress. On four occasions, seven endurance-trained cyclists [age 25 +/- 2 (SE) yr, body weight 70.5 +/- 3.3 kg, maximal O2 uptake (VO2max) 4.69 +/- 0.11 l/min] performed 140 min of cycle ergometer exercise at 62-66% of VO2max in a hot environment (33 degrees C dry bulb, 51% relative humidity, wind speed 2.5 m/s). The subjects drank 1,173 +/- 44 ml of a carbohydrate-electrolyte beverage after 0 min (D0), 40 min (D40), or 80 min (D80) of exercise or consumed the same total volume in small aliquots throughout exercise (DT). The exercise-heat stress resulted in calculated sweating rates of approximately 1,200 ml/h and a body weight loss of 2.9 +/- 0.1% after 140 min of exercise. After fluid intake in the D0, D40, and D80 trials, there was a time period (approximately 40 min) in which the increases in serum osmolality and sodium concentration and the reduction in blood volume were attenuated. During that same time period, there was an attenuated rise in esophageal temperature (Tes; P < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

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)

Influence of graded dehydration on hyperthermia and cardiovascular drift during exercise.

This investigation determined the effect of different rates of dehydration, induced by ingesting different volumes of fluid during prolonged exercise, on hyperthermia, heart rate (HR), and stroke volume (SV). On four different occasions, eight endurance-trained cyclists [age 23 +/- 3 (SD) yr, body wt 71.9 +/- 11.6 kg, maximal O2 consumption 4.72 +/- 0.33 l/min] cycled at a power output equal to 62-67% maximal O2 consumption for 2 h in a warm environment (33 degrees C dry bulb, 50% relative humidity, wind speed 2.5 m/s). During exercise, they randomly received no fluid (NF) or ingested a small (SF), moderate (MF), or large (LF) volume of fluid that replaced 20 +/- 1, 48 +/- 1, and 81 +/- 2%, respectively, of the fluid lost in sweat during exercise. The protocol resulted in graded magnitudes of dehydration as body weight declined 4.2 +/- 0.1, 3.4 +/- 0.1, 2.3 +/- 0.1, and 1.1 +/- 0.1%, respectively, during NF, SF, MF, and LF. After 2 h of exercise, esophageal temperature (Tes), HR, and SV were significantly different among the four trials (P < 0.05), with the exception of NF and SF. The magnitude of dehydration accrued after 2 h of exercise in the four trials was linearly related with the increase in Tes (r = 0.98, P < 0.02), the increase in HR (r = 0.99, P < 0.01), and the decline in SV (r = 0.99, P < 0.01). LF attenuated hyperthermia, apparently because of higher skin blood flow, inasmuch as forearm blood flow was 20-22% higher than during SF and NF at 105 min (P < 0.05). There were no differences in sweat rate among the four trials. In each subject, the increase in Tes from 20 to 120 min of exercise was highly correlated to the increase in serum osmolality (r = 0.81-0.98, P < 0.02-0.19) and the increase in serum sodium concentration (r = 0.87-0.99, P < 0.01-0.13) from 5 to 120 min of exercise. In summary, the magnitude of increase in core temperature and HR and the decline in SV are graded in proportion to the amount of dehydration accrued during exercise.

Fluid ingestion during exercise increases skin blood flow independent of increases in blood volume.

The purpose of this experiment was to determine whether fluid ingestion attenuates the hyperthermia and cardiovascular drift that occurs during exercise dehydration due to increases in blood volume. In addition, forearm blood flow, which is indicative of skin blood flow, was measured to determine whether the attenuation of hyperthermia and cardiovascular drift during exercise with fluid ingestion is due to higher skin blood flow. On three different occasions, seven trained cyclists [mean age, body weight, and maximum oxygen uptake: 23 +/- 3 yr, 73.9 +/- 10.5 kg, and 4.75 +/- 0.34 (SD) l/min, respectively] cycled at a power output equal to 62-67% maximum oxygen uptake for 2 h in a warm environment (33 degrees C, 50% relative humidity, wind speed 2.5 m/s). During exercise, they randomly received no fluid (NF) or a volume of a carbohydrate-electrolyte fluid replacement solution (FR) sufficient to replace 80 +/- 2% of sweat loss or were intravenously infused with 5.3 ml/kg of a blood volume expander (BVX; 6% dextran in saline). The infusion of 398 +/- 23 ml of BVX maintained blood volume at levels similar to that when 2,404 +/- 103 ml of fluid were ingested during FR and greater than that when no fluid was ingested during the 2nd h of exercise (P less than 0.05). However, BVX and NF resulted in similar esophageal and rectal temperatures, forearm blood flow, and elevations in serum osmolality and sodium concentration during 2 h of exercise.(ABSTRACT TRUNCATED AT 250 WORDS)

Cutaneous blood flow during exercise is higher in endurance-trained humans.

This study determined whether cutaneous blood flow during exercise is different in endurance-trained (Tr) compared with untrained (Untr) subjects. Ten Tr and ten Untr men (62.4 +/- 1.7 and 44.2 +/- 1.8 ml. kg(-1). min(-1), respectively; P < 0.05) underwent three 20-min cycling-exercise bouts at 50, 70, and 90% peak oxygen uptake in this order, with 30 min rest in between. The environmental conditions were neutral ( approximately 23-24 degrees C, 50% relative humidity, front and back fans at 2.5 m/s). Because of technical difficulties, only seven Tr and seven Untr subjects completed all forearm blood flow and laser-Doppler cutaneous blood flow (CBF) measurements. Albeit similar at rest, at the end of all three exercise bouts, forearm blood flow was approximately 40% higher in Tr compared with Untr subjects (50%: 4.64 +/- 0.50 vs. 3. 17 +/- 0.20, 70%: 6.17 +/- 0.61 vs. 4.41 +/- 0.37, 90%: 6.77 +/- 0. 62 vs. 5.01 +/- 0.37 ml. 100 ml(-1). min(-1), respectively; n = 7; all P < 0.05). CBF was also higher in Tr compared with Untr subjects at all relative intensities (n = 7; all P < 0.05). However, esophageal temperature was not different in Tr compared with Untr subjects at the end of any of the aforementioned exercise bouts (50%: 37.8 +/- 0.1 vs. 37.9 +/- 0.1 degrees C, 70%: 38.1 +/- 0.1 vs. 38.1 +/- 0.1 degrees C, and 90%: 38.8 +/- 0.1 vs. 38.6 +/- 0.1 degrees C, respectively). We conclude that a higher CBF may allow Tr subjects to achieve an esophageal temperature similar to that of Untr, despite their higher metabolic rates and thus higher heat production rates, during exercise at 50-90% peak oxygen uptake.

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.

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.

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.

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.

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)