Cerebral blood flow during static exercise in humans

Cerebral blood flow (CBF) was determined in humans at rest and during four consecutive unilateral static contractions of the knee extensors. Each contraction was maintained for 3 min 15 s with the subjects in a semisupine position. The contractions corresponded to 8, 16, 24, and 32% of the maximal voluntary contraction (MVC) and utilized alternate legs. CBF (measured by the 133Xe clearance technique) was expressed by a noncompartmental flow index (ISI). Heart rate and mean arterial pressure increased from resting values of 73 (55-80) beats/min and 88 (74-104) mmHg to 106 (86-138) beats/min and 124 (102-146) mmHg, respectively (P less than 0.0005), during the contraction at 32% MVC. Arterial PCO2 and central venous pressure did not change. Corrected to the average resting PCO2, CBF during control was 55 (35-73) ml.100 g-1.min-1 and remained constant during contractions. Cerebral vascular resistance increased from 1.5 (1.0-2.2) to 2.4 (1.4-3.0) mmHg. 100 g.min.ml-1 (P less than 0.025) at 32% of MVC. There was no difference in CBF between the two hemispheres at rest or during exercise. In contrast to dynamic leg exercise, static leg exercise is not associated with an increase in global CBF when measured by the 133Xe clearance technique.     

Distribution of blood flow in muscles of miniature swine during exercise

The purpose of this study was to determine how the distribution of blood flow within and among the skeletal muscles of miniature swine (22 +/- 1 kg body wt) varies as a function of treadmill speed. Radiolabeled microspheres were used to measure cardiac output (Q) and tissue blood flows in preexercise and at 3-5 min of treadmill exercise at 4.8, 8.0, 11.3, 14.5, and 17.7 km/h. All pigs (n = 8) attained maximal O2 consumption (VO2max) (60 +/- 4 ml X min-1 X kg-1) by the time they ran at 17.7 km/h. At VO2max, 87% of Q (9.9 +/- 0.5 l/min) was to skeletal muscle, which constituted 36 +/- 1% of body mass. Average total muscle blood flow at VO2max was 127 +/- 14 ml X min-1 X 100 g-1; average limb muscle flow was 135 +/- 17 ml X min-1 X 100 g-1. Within the limb muscles, blood flow was distributed so that the deep red parts of extensor muscles had flows about two times higher than the more superficial white portions of the same muscles; the highest muscle blood flows occurred in the elbow flexors (brachialis: 290 +/- 44 ml X min-1 X 100 g-1). Peak exercise blood flows in the limb muscles were proportional (P less than 0.05) to the succinate dehydrogenase activities (r = 0.84), capillary densities (r = 0.78), and populations of oxidative (slow-twitch oxidative + fast-twitch oxidative-glycolytic) fiber types (r = 0.93) in the muscles. Total muscle blood flow plotted as a function of exercise intensity did not peak until the pigs attained VO2max, although flows in some individual muscles showed a plateau in this relationship at submaximal exercise intensities. The data demonstrate that blood flow in skeletal muscles of miniature swine is distributed heterogeneously and varies in relation to fiber type composition and exercise intensity.     

Effects of prolonged exercise at a similar percentage of maximal oxygen consumption in trained and untrained subjects

Six trained male cyclists and six untrained but physically active men participated in this study to test the hypothesis that the use of percentage maximal oxygen consumption (%VO2max) as a normalising independent variable is valid despite significant differences in the absolute VO2max of trained and untrained subjects. The subjects underwent an exercise test to exhaustion on a cycle ergometer to determine VO2max and lactate threshold. The subjects were grouped as trained (T) if their VO2max exceeded 60 ml.kg-1.min-1, and untrained (UT) if their VO2max was less than 50 ml.kg-1.min-1. The subjects were required to exercise on the ergometer for up to 40 min at power outputs that corresponded to approximately 50% and 70% VO2max. The allocation of each exercise session (50% or 70% VO2max) was random and each session was separated by at least 5 days. During these tests venous blood was taken 10 min before exercise (- 10 min), just prior to the commencement of exercise (0 min), after 20 min of exercise (20 min), at the end of exercise and 10 min postexercise (+ 10 min) and analysed for concentrations of cortisol, [Na+], [K+], [Cl-], glucose, free fatty acid, lactate [la-], [NH3], haemoglobin [Hb] and for packed cell volume. The oxygen consumption (VO2) and related variables were measured at two time intervals (14-15 and 34-35 min) during the prolonged exercise tests. Rectal temperature was measured throughout both exercise sessions. There was a significant interaction effect between the level of training and exercise time at 50% VO2max for heart rate (fc) and venous [la-].(ABSTRACT TRUNCATED AT 250 WORDS)     

Effects of training on lactate production and removal during progressive exercise in humans.

To determine whether the reduced blood lactate concentrations [La] during submaximal exercise in humans after endurance training result from a decreased rate of lactate appearance (Ra) or an increased rate of lactate metabolic clearance (MCR), interrelationships among blood [La], lactate Ra, and lactate MCR were investigated in eight untrained men during progressive exercise before and after a 9-wk endurance training program. Radioisotope dilution measurements of L-[U-14C]lactate revealed that the slower rise in blood [La] with increasing O2 uptake (VO2) after training was due to a reduced lactate Ra at the lower work rates [VO2 less than 2.27 l/min, less than 60% maximum VO2 (VO2max); P less than 0.01]. At power outputs closer to maximum, peak lactate Ra values before (215 +/- 28 mumol.min-1.kg-1) and after training (244 +/- 12 mumol.min-1.kg-1) became similar. In contrast, submaximal (less than 75% VO2max) and peak lactate MCR values were higher after than before training (40 +/- 3 vs. 31 +/- 4 ml.min-1.kg-1, P less than 0.05). Thus the lower blood [La] values during exercise after training in this study were caused by a diminished lactate Ra at low absolute and relative work rates and an elevated MCR at higher absolute and all relative work rates during exercise.     

Determination of maximal oxygen consumption in exercising pregnant sheep.

Previous work with pregnant ewes has shown that acute bouts of exercise may cause changes in plasma hormone concentrations, blood flow distribution, and maternal and fetal temperatures. However, most of these studies do not quantify the chosen exercise intensity through measurement of oxygen consumption (VO2). Therefore the purpose of this study was to statistically model the VO2 response of pregnant sheep to treadmill (TM) exercise to determine the exercise intensities (% maximal VO2) of previous studies. Ewes with either single (n = 9) or twin (n = 5) fetuses were studied from 100 to 130 days of gestation. After 1-2 wk of TM habituation, maximal VO2 (VO2max) was determined by measurements of VO2 (open flow-through method) and blood lactate concentration. VO2 was measured as a function of TM incline (0, 3, 5, and 7 degree) and speed (0.8-3.4 m/s). VO2max averaged 57 +/- 7 (SD) ml.min-1.kg-1, and peak lactate concentration during exercise averaged 22 +/- 2 mmol/l. The relationship between VO2 (ml.min-1.kg-1) and incline (INC) and speed (SP) [VO2 = 0.70(INC) + 13.95(SP) + 1.07(INC x SP) - 1.18] was linear (r2 = 0.94). Our findings suggest that most previous research used exercise intensities less than 60% VO2max and indicate the need for further research that examines the effect of exercise during pregnancy at levels greater than 60% VO2max.     

Exercise training and "ventilation threshold" in elderly

Dynamic exercise training of the elderly increases maximal O2 uptake (VO2max); however, the effects of training on the ventilation threshold (VET) have not been studied. VET was identified as the final point before the ventilatory equivalent for O2 (VE/VO2) increased, without an increase in the ventilatory equivalent for CO2 (VE/VCO2). Inactive elderly males (mean age, 62 yr) were randomly assigned to a control (C, n = 44) or activity (A, n = 45) group. VO2max and VET were determined from an incremental treadmill test. Initial VO2max was not different between the C (2.34 +/- 0.42 l X min-1) and A (2.28 +/- 0.44 l X min-1) groups, nor was there a significant difference in the VO2 at the VET (C = 1.39 +/- 0.26 l X min-1; A = 1.31 +/- 0.23 l X min-1). The activity group trained for 30 min/day, 3 days/wk at an intensity of approximately 65-80% of VO2max. After 1 yr of training the activity group exhibited an 18% increase in VO2max (A = 2.70 +/- 0.54 l X min-1), but the change in VET was not significant (A = 1.39 +/- 0.28 l X min-1). There was no significant change in VO2max (C = 2.45 +/- 0.68 l X min-1) or VET (C = 1.38 +/- 0.31 l X min-1) in the control group. VET/VO2max declined significantly in the activity group (from 58 to 52% of VO2max). Change in VET/VO2max with training was not correlated with the initial VO2max value. We conclude that increases in aerobic capacity are more readily effected than alterations of the VET in elderly subjects.     

O2 delivery at VO2max and oxidative capacity in muscles of standardbred horses.

The purpose of this study was to describe the relationships between 16 physiological, biochemical, and morphological variables presumed to relate to the oxidative capacity in quadriceps muscles or muscle parts in Standardbred horses. The variables included O2 delivery (blood flow) and mean capillary transit time (MTT) during treadmill locomotion at whole animal maximal O2 consumption (VO2max, 134 +/- 2 ml.min-1 x kg-1), capillary density and capillary-to-fiber ratio, myoglobin concentration, oxidative enzyme activities, glycolytic enzyme activities, fiber type populations, and fiber size. These components of muscle metabolic capacity were found to be interrelated to varying degrees using correlation matrix analysis, with lactate dehydrogenase activity showing the most significant correlations (n = 14) with other variables. Most of the "oxidative" variables occurred in the highest quantities in the deepest muscle of the group (vastus intermedius) and in the deepest parts of the other quadriceps muscles where the highest proportions of type I fibers were localized. The highest blood flow measured with microspheres in the muscle group during exercise was in vastus intermedius muscle (145 ml.min-1 x 100 g-1), and the lowest was in the superficial part of rectus femoris muscle (32 ml.min-1 x 100 g-1). Average muscle blood flow during exercise at whole animal VO2max was 116 ml.min-1 x 100 g-1. Because skeletal muscle comprised 43% of total body mass (453 +/- 34 kg), total muscle blood flow was estimated at 226 l/min, which was approximately 78% of total cardiac output (288 l/min).(ABSTRACT TRUNCATED AT 250 WORDS)     

Dissociation of maximal O2 uptake from O2 delivery in canine gastrocnemius in situ

To test the hypothesis that maximal O2 uptake (VO2max) can be limited by O2 diffusion in the peripheral tissue, we kept O2 delivery [blood flow X arterial O2 content (CaO2)] to maximally contracting muscle equal between 1) low flow-high CaO2 and 2) high flow-low CaO2 conditions. The hypothesis predicts, because of differences in the capillary PO2 profile, that the former condition will result in both a higher VO2max and muscle effluent venous PO2 (PVO2). We studied the relations among VO2max, PVO2, and O2 delivery during maximal isometric contractions in isolated, in situ dog gastrocnemius muscle (n = 6) during these two conditions. O2 delivery was matched by varying arterial O2 partial pressure and adjusting flow to the muscle accordingly. A total of 18 matched O2 delivery pairs were obtained. As planned, O2 delivery was not significantly different between the two treatments. In contrast, VO2max was significantly higher [10.4 +/- 0.5 (SE) ml.100 g-1.min-1; P = 0.01], as was PVO2 (25 +/- 1 Torr; P less than 0.01) in the low flow-high CaO2 treatment compared with the high flow-low CaO2 treatment (9.1 +/- 0.4 ml.100 g-1.min-1 and 20 +/- 1 Torr, respectively). The rate of fatigue was greater in the high flow-low CaO2 condition, as was lactate output from the muscle and muscle lactate concentration. The results of this study show that VO2max is not uniquely dependent on O2 delivery and support the hypothesis that VO2max can be limited by peripheral tissue O2 diffusion.     

Validity of pulse oximetry during exercise in elite endurance athletes.

Eleven highly trained male cyclists [maximal aerobic power (VO2max) = 70.6 +/- 4.2 ml.kg-1.min-1] performed both high intensity constant load (90-95% VO2max) and incremental cycle exercise tests with arterial blood sampling to evaluate the accuracy of pulse oximeter estimates (%SpO2) of arterial oxyhemoglobin fraction of total hemoglobin (%HbO2). Three subjects also performed an incremental exercise test in hypoxic conditions (inspired partial pressure of O2 = 89, 93, or 100 Torr). Arterial %HbO2 was determined via CO-oximetry and ranged from 72 to 99%. Three Ohmeda 3740 pulse oximeters were used to estimate %HbO2, one on each ear lobe and a finger probe. The finger probe tended to provide the best estimate of %HbO2 during exercise: the mean %SpO2 - %HbO2 difference for 232 exercise observations was 0.52 +/- 1.36% (SD). Finger probe %SpO2 and %HbO2 were highly correlated [r = 0.98, standard error of the estimate (SEE) = 1.32%, P less than 0.0001]. The accuracy of pulse oximeters has been questioned during high-intensity exercise. When aerobic power was greater than 81% of VO2max (n = 75), the finger probe's mean error was -0.01 +/- 1.40%. Finger probe %SpO2 and %HbO2 were highly correlated (r = 0.97, SEE = 1.32%, P less than 0.0001). These results indicate that this pulse oximeter is a valid predictor of %HbO2 in elite athletes during cycle exercise.     

Effects of endurance training on hyperammonaemia during a 45-min constant exercise intensity

Eleven laboratory-pretrained subjects (initial VO2max = 54 ml.kg-1.min-1) took part in a study to evaluate the effect of a short endurance training programme [8-12 sessions, 1 h per session, with an intensity varying from 60% to 90% maximal oxygen consumption (VO2max)] on the responses of blood ammonia (b[NH+4]) and lactate (b[la]) concentrations during progressive and constant exercise intensities. After training, during which VO2max did not increase, significant decreases in b[NH+4], b[la] and muscle proton concentration were observed at the end of the 80% VO2max constant exercise intensity, although b[NH+4] and b[la] during progressive exercise were unchanged. On the other hand, no correlations were found between muscle fibre composition and b[NH+4] in any of the exercise procedures. This study demonstrated that a constant exercise intensity was necessary to reveal the effect of training on muscle metabolic changes inducing the decrease in b[NH+4] and b[la]. At a relative power of exercise of 80% VO2max, there was no effect of muscle fibre composition on b[NH+4] accumulation.     

Linear relationship between VO2max and VO2max decrement during exposure to acute hypoxia

The purpose of these experiments is to test the hypothesis that exercise-induced hypoxemia at sea level in highly trained athletes might be exacerbated during acute hypoxia and therefore result in correspondingly larger decrements in maximal O2 uptake (VO2max) compared with less trained individuals. Thirteen healthy male volunteers were divided into two groups according to their level of fitness: 1) trained endurance athletes (T) (n = 7), with a VO2max range of 56-75 ml.kg-1.min-1 and 2) untrained individuals (UT) (n = 6), with a VO2max range of 33-49 ml.kg-1.min-1. Subjects performed two incremental cycle ergometry tests to determine VO2max under hypoxic conditions [14% O2-86% N2, barometric pressure (PB) = 760 Torr] and normoxic conditions (21% O2-79% N2, PB = 760 Torr). Tests were single blind, randomly administered, and separated by at least 72 h. Mean percent oxyhemoglobin saturation (%SaO2) during maximal exercise under hypoxic conditions was significantly (P less than 0.05) lower in the T group (77%) compared with the UT group (86%). Furthermore, the T group exhibited larger decrements (P less than 0.05) in VO2max (normoxic-hypoxic) compared with the UT group. Finally, a significant linear correlation (r = 0.94) existed between normoxic VO2max (ml.kg-1.min-1) and delta VO2max (normoxic-hypoxic). These data suggest that highly T endurance athletes suffer more severe gas exchange impairments during acute exposure to hypoxia than UT individuals, and this may explain a portion of the observed variance in delta VO2max among individuals during acute altitude or hypoxia exposure.     

NADH content in type I and type II human muscle fibres after dynamic exercise.

The effect of dynamic exercise on the NADH content of human type I (slow-twitch) and II (fast-twitch) muscle fibres was investigated. Muscle biopsy samples were obtained from the quadriceps femoris of seven healthy subjects at rest and after bicycle exercise at 40, 75 and 100% of the maximal oxygen uptake [VO2(max.)]. At rest and after exercise at 100% VO2(max.), muscle NADH content was significantly higher (P less than 0.05) in type I than in type II fibres. After exercise at 40% VO2(max.), muscle NADH decreased in type I fibres (P less than 0.01), but was not significantly changed in type II fibres. After exercise at 75 and 100% VO2(max.), muscle NADH increased above the value at rest in both type I and II fibres (P less than 0.05). Muscle lactate was unchanged at 40% VO2(max.), but increased 20- and 60-fold after exercise at 75 and 100% VO2(max.) respectively. The finding that NADH decreased only in type I fibres at 40% VO2(max.) supports the idea that type I is the fibre type predominantly recruited during low-intensity exercise. The increase of NADH in both fibre types after exercise at 75% and 100% VO2(max.) suggests that the availability of oxygen relative to the demand is decreased in both fibre types at high exercise intensities.     

The effect of citrate loading on exercise performance, acid-base balance and metabolism

Nine subjects (VO2max 65 +/- 2 ml.kg-1.min-1, mean +/- SEM) were studied on two occasions following ingestion of 500 ml solution containing either sodium citrate (C, 0.300 g.kg-1 body mass) or a sodium chloride placebo (P, 0.045 g.kg-1 body mass). Exercise began 60 min later and consisted of cycle ergometer exercise performed continuously for 20 min each at power outputs corresponding to 33% and 66% VO2max, followed by exercise to exhaustion at 95% VO2max. Pre-exercise arterialized-venous [H+] was lower in C (36.2 +/- 0.5 nmol.l-1; pH 7.44) than P (39.4 +/- 0.4 nmol.l-1; pH 7.40); the plasma [H+] remained lower and [HCO3-] remained higher in C than P throughout exercise and recovery. Exercise time to exhaustion at 95% VO2max was similar in C (310 +/- 69 s) and P (313 +/- 74 s). Cardiorespiratory variables (ventilation, VO2, VCO2, heart rate) measured during exercise were similar in the two conditions. The plasma [citrate] was higher in C at rest (C, 195 +/- 19 mumol.l-1; P, 81 +/- 7 mumol.l-1) and throughout exercise and recovery. The plasma [lactate] and [free fatty acid] were not affected by citrate loading but the plasma [glycerol] was lower during exercise in C than P. In conclusion, sodium citrate ingestion had an alkalinizing effect in the plasma but did not improve endurance time during exercise at 95% VO2max. Furthermore, citrate loading may have prevented the stimulation of lipolysis normally observed with exercise and prevented the stimulation of glycolysis in muscle normally observed in bicarbonate-induced alkalosis.     

Lymphocyte proliferation responses after exercise in men: fitness, intensity, and duration effects

This study investigated the effects of intensity and duration of exercise on lymphocyte proliferation as a measure of immunologic function in men of defined fitness. Three fitness groups--low [maximal O2 uptake (VO2max) = 44.9 +/- 1.5 ml O2.kg-1.min-1 and sedentary], moderate (VO2max = 55.2 +/- 1.6 ml O2.kg-1.min-1 and recreationally active), and high (VO2max = 63.3 +/- 1.8 ml O2.kg-1.min-1 and endurance trained)--and a mixed control group (VO2max = 52.4 +/- 2.3 ml O2.kg-1.min-1) participated in the study. Subjects completed four randomly ordered cycle ergometer rides: ride 1, 30 min at 65% VO2max; ride 2, 60 min at 30% VO2max; ride 3, 60 min at 75% VO2max; and ride 4, 120 min at 65% VO2max. Blood samples were obtained at various times before and after the exercise sessions. Lymphocyte responses to the T cell mitogen concanavalin A were determined at each sample time through the incorporation of radiolabeled thymidine [( 3H]TdR). Despite differences in resting levels of [3H]TdR uptake, a consistent depression in mitogenesis was present 2 h after an exercise bout in all fitness groups. The magnitude of the reduction in T cell mitogenesis was not affected by an increase in exercise duration. A trend toward greater reduction was present in the highly fit group when exercise intensity was increased. The reduction in lymphocyte proliferation to the concanavalin A mitogen after exercise was a short-term phenomenon with recovery to resting (preexercise) values 24 h after cessation of the work bout. These data suggest that single sessions of submaximal exercise transiently reduce lymphocyte function in men and that this effect occurs irrespective of subject fitness level.     

Effect of increased Hb-O2 affinity on VO2max at constant O2 delivery in dog muscle in situ

We investigated the effect of increasing hemoglobin- (Hb) O2 affinity on muscle maximal O2 uptake (VO2max) while muscle blood flow, [Hb], HbO2 saturation, and thus O2 delivery (muscle blood flow X arterial O2 content) to the working muscle were kept unchanged from control. VO2max was measured in isolated in situ canine gastrocnemius working maximally (isometric tetanic contractions). The muscles were pump perfused, in alternating order, with either normal blood [O2 half-saturation pressure of hemoglobin (P50) = 32.1 +/- 0.5 (SE) Torr] or blood from dogs that had been fed sodium cyanate (150 mg.kg-1.day-1) for 3-4 wk (P50 = 23.2 +/- 0.9). In both conditions (n = 8) arterial PO2 was set at approximately 200 Torr to fully saturate arterial blood, which thereby produced the same arterial O2 contents, and muscle blood flow was set at 106 ml.100 g-1.min-1, so that O2 delivery in both conditions was the same. VO2max was 11.8 +/- 1.0 ml.min-1.100 g-1 when perfused with the normal blood (control) and was reduced by 17% to 9.8 +/- 0.7 ml.min-1.100 g-1 when perfused with the low-P50 blood (P less than 0.01). Mean muscle effluent venous PO2 was also significantly less (26 +/- 3 vs. 30 +/- 2 Torr; P less than 0.01) in the low-P50 condition, as was an estimate of the capillary driving pressure for O2 diffusion, the mean capillary PO2 (45 +/- 3 vs. 51 +/- 2 Torr). However, the estimated muscle O2 diffusing capacity was not different between conditions.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effect of previous supramaximal work on lacticaemia during supra-anaerobic threshold exercise

Twelve male and female subjects (eight trained, four untrained) exercised for 30 min on a treadmill at an intensity of maximal O2 consumption (% VO2max) 90.0%, SD 4.7 greater than the anaerobic threshold of 4 mmol.l-1 (Than = 83.6% VO2max, SD 8.9). Time-dependent changes in blood lactate concentration [( lab]) during exercise occurred in two phases: the oxygen uptake (VO2) transient phase (from 0 to 4 min) and the VO2 steady-state phase (4-30 min). During the transient phase, [lab] increased markedly (1.30 mmol.l-1.min-1, SD (0.13). During the steady-state phase, [lab] increased slightly (0.02 mmol.l-1.min-1, SD 0.06) and when individual values were considered, it was seen that there were no time-dependent increases in [lab] in half of the subjects. Following hyperlacticaemia (8.8 mmol.l-1, SD 2.0) induced by a previous 2 min of supramaximal exercise (120% VO2max), [lab] decreased during the VO2 transient (-0.118 mmol.l-1.min-1, SD 0.209) and steady-state (-0.088 mmol.l-1.min-1, SD 0.103) phases of 30 min exercise (91.4% VO2max, SD 4.8). In conclusion, it was not possible from the Than to determine the maximal [lab] steady state for each subject. In addition, lactate accumulated during previous supramaximal exercise was eliminated during the VO2 transient phase of exercise performed at an intensity above the Than. This effect is probably largely explained by the reduction in oxygen deficit during the transient phase. Under these conditions, the time-course of changes in [lab] during the VO2 steady state was also affected.     

Evidence of O2 supply-dependent VO2 max in the exercise-trained human quadriceps.

Maximal O2 delivery and O2 uptake (VO2) per 100 g of active muscle mass are far greater during knee extensor (KE) than during cycle exercise: 73 and 60 ml. min-1. 100 g-1 (2.4 kg of muscle) (R. S. Richardson, D. R. Knight, D. C. Poole, S. S. Kurdak, M. C. Hogan, B. Grassi, and P. D. Wagner. Am. J. Physiol. 268 (Heart Circ. Physiol. 37): H1453-H1461, 1995) and 28 and 25 ml. min-1. 100 g-1 (7.5 kg of muscle) (D. R. Knight, W. Schaffartzik, H. J. Guy, R. Predilleto, M. C. Hogan, and P. D. Wagner. J. Appl. Physiol. 75: 2586-2593, 1993), respectively. Although this is evidence of muscle O2 supply dependence in itself, it raises the following question: With such high O2 delivery in KE, are the quadriceps still O2 supply dependent at maximal exercise? To answer this question, seven trained subjects performed maximum KE exercise in hypoxia [0.12 inspired O2 fraction (FIO2)], normoxia (0.21 FIO2), and hyperoxia (1.0 FIO2) in a balanced order. The protocol (after warm-up) was a square wave to a previously determined maximum work rate followed by incremental stages to ensure that a true maximum was achieved under each condition. Direct measures of arterial and venous blood O2 concentration in combination with a thermodilution blood flow technique allowed the determination of O2 delivery and muscle VO2. Maximal O2 delivery increased with inspired O2: 1.3 +/- 0.1, 1.6 +/- 0.2, and 1.9 +/- 0.2 l/min at 0.12, 0.21, and 1.0 FIO2, respectively (P < 0.05). Maximal work rate was affected by variations in inspired O2 (-25 and +14% at 0.12 and 1.0 FIO2, respectively, compared with normoxia, P < 0.05) as was maximal VO2 (VO2 max): 1.04 +/- 0.13, 1. 24 +/- 0.16, and 1.45 +/- 0.19 l/min at 0.12, 0.21, and 1.0 FIO2, respectively (P < 0.05). Calculated mean capillary PO2 also varied with FIO2 (28.3 +/- 1.0, 34.8 +/- 2.0, and 40.7 +/- 1.9 Torr at 0.12, 0.21, and 1.0 FIO2, respectively, P < 0.05) and was proportionally related to changes in VO2 max, supporting our previous finding that a decrease in O2 supply will proportionately decrease muscle VO2 max. As even in the isolated quadriceps (where normoxic O2 delivery is the highest recorded in humans) an increase in O2 supply by hyperoxia allows the achievement of a greater VO2 max, we conclude that, in normoxic conditions of isolated KE exercise, KE VO2 max in trained subjects is not limited by mitochondrial metabolic rate but, rather, by O2 supply.     

Exercise intensity and glucose tolerance in trained and nontrained subjects

The improved glucose tolerance and increased insulin sensitivity associated with regular exercise appear to be the result, in large part, of the residual effects of the last bout of exercise. To determine the effects of exercise intensity on this response, glucose tolerance and the insulin response to a glucose load were determined in seven well-trained male subjects [maximal O2 uptake (VO2max) = 58 ml.kg-1.min-1] and in seven nontrained male subjects (VO2max = 49 ml.kg-1.min-1) in the morning after an overnight fast 1) 40 h after the last training session (control), 2) 14 h after 40 min of exercise on a cycle ergometer at 40% VO2max, and 3) 14 h after 40 min of exercise at 80% VO2max. Subjects replicated their diets for 3 days before each test and ate a standard meal the evening before the oral glucose tolerance test. No differences in the 3-h insulin or glucose response were observed between the control trial and before exercise at either 40 or 80% VO2max in the trained subjects. In the nontrained subjects the plasma insulin response was decreased by 40% after a single bout of exercise at either 40 or 80% VO2max (7.0 X 10(3) vs. 5.0 X 10(3), P less than 0.05; 3.8 X 10(3) microU.ml-1.180 min-1, P less than 0.01). The insulin response after a single bout of exercise in the nontrained subjects was comparable with the insulin responses found in the trained subjects for the control and exercise trials.(ABSTRACT TRUNCATED AT 250 WORDS)     

Slow upward drift of VO2 during constant-load cycling in untrained subjects

The oxygen uptake kinetics during constant-load exercise when sitting on a bicycle ergometer were determined in 7 untrained subjects by measuring breath-by-breath VO2 during continuous exercise to volitional exhaustion (mean endurance time = 1160 +/- 172 s) at a pedal frequency of 70 revolutions.min-1. The power output, averaging 189.5 W, was set at 82.5% of that eliciting the individual VO2max during a 5 min incremental exercise test. Throughout the exercise period, the VO2 kinetics could be appropriately described by a two-component exponential equation of the form: VO2(t) = Ya[1 - exp(-kat)] + Yb[1 - exp(-kbt)] where VO2 is net oxygen consumption and t the time from work onset. VO2 measured at the end of exercise was close to VO2max (98% VO2max) and the mean values of Ya, ka, Yb and kb amounted to 1195 ml O2.min-1, 0.034 s-1, 1562 ml O2.min-1, and 0.005 s-1 respectively. The initial rate of increase in VO2 predicted from the above equation is slower than that calculated, for the same work intensity, on the basis of the data obtained by Morton (1985) in trained subjects. For t greater than 480 s, however, the two models yield substantially equal results.