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.     

Energy expenditure during simulated rowing

Metabolic function was measured by open-circuit spirometry for 310 competitive oarsmen during and following a 6-min maximal rowing ergometer exercise. Aerobic and anaerobic energy contributions to exercise were estimated by calculating exercise O2 cost and O2 debt.O2 debt was measured for 30 min of recovery using oxygen consumption (Vo2) during light rowing as the base line. Venous blood lactates were analyzed at rest and at 5 and 30 min of recovery. Maximal ventilation volumes ranged from 175 to 22l 1/min while Vo2 max values averaged 5,950 ml/min and 67.6 ml/kg min. Maximal venous blood lactates ranged from 126 to 240 mg/100 ml. Average O2 debt equaled 13.4 liters. The total energy cost for simulated rowing was calculated at 221.5 kcal assuming 5 kcal/l O2 with aerobic metabolism contributing 70% to the total energy released and anaerobiosis providing the remaining 30%. Vo2 values for each minute of exercise reflect a severe steady state since oarsmen work at 96-98% of maximal aerobic capacity. O2 debt and lactate measurements attest to the severity of exercise and dominance of anaerobic metabolism during early stages of work.     

Intensity-dependent tolerance to exercise after attaining V(O2) max in humans.

The tolerable duration of high-intensity, constant-load cycle ergometry is a hyperbolic function of power, with an asymptote termed critical power (CP) and a curvature constant (W') with units of work. It has been suggested that continued exercise after exhaustion may only be performed below CP, where predominantly aerobic energy transfer can occur and W' can be partially replenished. To test this hypothesis, six volunteers each performed cycle-ergometer exercise with breath-by-breath determination of ventilatory and pulmonary gas exchange variables. Initially, four exercise tests to exhaustion were made: 1). a ramp-incremental and 2). three high-intensity constant-load bouts at different work rates, to estimate lactate (theta(L)) and CP thresholds, W', and maximum oxygen uptake (Vo2 max). Subsequently, subjects cycled to the limit of tolerance (for approximately 360 s) on three occasions, each followed by a work rate reduction to 1). 110% CP, 2). 90% CP, and 3). 80% theta(L) for a 20-min target. W' averaged 20.9 +/- 2.35 kJ or 246 +/- 30 J/kg. After initial fatigue, 110% CP was tolerated for only 30 +/- 12 s. Each subject completed 20 min at 80% theta(L), but only two sustained 20 min at 90% CP; the remaining four subjects fatigued at 577 +/- 306 s, with oxygen consumption at 89 +/- 8% Vo2 max. The results support the suggestion that replenishing W' after fatigue necessitates a sub-CP work rate. The variation in subjects' responses during 90% CP was unexpected but consistent with mechanisms such as reduced CP consequent to prior high-intensity exercise, variation in lactate handling, and/or regional depletion of energy substrates, e.g., muscle glycogen.     

Anaerobic energy provision does not limit Wingate exercise performance in endurance-trained cyclists.

The aim of this study was to evaluate the effects of severe acute hypoxia on exercise performance and metabolism during 30-s Wingate tests. Five endurance- (E) and five sprint- (S) trained track cyclists from the Spanish National Team performed 30-s Wingate tests in normoxia and hypoxia (inspired O(2) fraction = 0.10). Oxygen deficit was estimated from submaximal cycling economy tests by use of a nonlinear model. E cyclists showed higher maximal O(2) uptake than S (72 +/- 1 and 62 +/- 2 ml x kg(-1) x min(-1), P < 0.05). S cyclists achieved higher peak and mean power output, and 33% larger oxygen deficit than E (P < 0.05). During the Wingate test in normoxia, S relied more on anaerobic energy sources than E (P < 0.05); however, S showed a larger fatigue index in both conditions (P < 0.05). Compared with normoxia, hypoxia lowered O(2) uptake by 16% in E and S (P < 0.05). Peak power output, fatigue index, and exercise femoral vein blood lactate concentration were not altered by hypoxia in any group. Endurance cyclists, unlike S, maintained their mean power output in hypoxia by increasing their anaerobic energy production, as shown by 7% greater oxygen deficit and 11% higher postexercise lactate concentration. In conclusion, performance during 30-s Wingate tests in severe acute hypoxia is maintained or barely reduced owing to the enhancement of the anaerobic energy release. The effect of severe acute hypoxia on supramaximal exercise performance depends on training background.     

Determinants of time trial performance and maximal incremental exercise in highly trained endurance athletes

Human endurance performance can be predicted from maximal oxygen consumption (Vo(2max)), lactate threshold, and exercise efficiency. These physiological parameters, however, are not wholly exclusive from one another, and their interplay is complex. Accordingly, we sought to identify more specific measurements explaining the range of performance among athletes. Out of 150 separate variables we identified 10 principal factors responsible for hematological, cardiovascular, respiratory, musculoskeletal, and neurological variation in 16 highly trained cyclists. These principal factors were then correlated with a 26-km time trial and test of maximal incremental power output. Average power output during the 26-km time trial was attributed to, in order of importance, oxidative phosphorylation capacity of the vastus lateralis muscle (P = 0.0005), steady-state submaximal blood lactate concentrations (P = 0.0017), and maximal leg oxygenation (sO(2LEG)) (P = 0.0295), accounting for 78% of the variation in time trial performance. Variability in maximal power output, on the other hand, was attributed to total body hemoglobin mass (Hb(mass); P = 0.0038), Vo(2max) (P = 0.0213), and sO(2LEG) (P = 0.0463). In conclusion, 1) skeletal muscle oxidative capacity is the primary predictor of time trial performance in highly trained cyclists; 2) the strongest predictor for maximal incremental power output is Hb(mass); and 3) overall exercise performance (time trial performance + maximal incremental power output) correlates most strongly to measures regarding the capability for oxygen transport, high Vo(2max) and Hb(mass), in addition to measures of oxygen utilization, maximal oxidative phosphorylation, and electron transport system capacities in the skeletal muscle.     

Effects of exercise on maximal instantaneous muscular power of humans

The maximal instantaneous anaerobic power (w), as determined during a high jump off both feet on a force platform, was measured on eight subjects starting from a resting base line; a base line of steady-state cycloergometric exercise requiring 30, 50, and 70% of individual maximum O2 consumption (VO2max); and a base line of maximal and supramaximal exercise (100 and 120% of VO2max). In addition, w was also measured during the VO2 transients from rest to each of the above work loads. Blood lactate concentration ([Lab]) was determined before and 8 min after the end of each priming load. After the onset of any priming load, w decreases with time reaching in 2 min a steady level that is lower the higher the VO2. For the three lowest work rates, the steady w level is unchanged by increasing the duration of the priming exercise up to 30 min. For low work levels, the decrease of w as a function of VO2 is essentially parallel to that of estimated muscle concentration of ATP ([ATP]). For work levels greater than 60% of VO2max involving a substantial accumulation of lactate, the decrease of w becomes smaller than the estimated drop of muscle [ATP]. This finding is tentatively attributed to an increase of either the mechanical equivalent or of the velocity constant of ATP splitting brought about by the lowering of intracellular muscle pH after lactate accumulation.(ABSTRACT TRUNCATED AT 250 WORDS)     

Anaerobic threshold and maximal steady-state blood lactate in prepubertal boys

To elucidate further the special nature of anaerobic threshold in children, 11 boys, mean age 12.1 years (range 11.4-12.5 years), were investigated during treadmill running. Oxygen uptake, including maximal oxygen uptake (VO2max), ventilation and the "ventilatory anaerobic threshold" were determined during incremental exercise, with determination of maximal blood lactate following exercise. Within 2 weeks following this test four runs of 16-min duration were performed at a constant speed, starting with a speed corresponding to about 75% of VO2max and increasing it during the next run by 0.5 or 1.0 km.h-1 according to the blood lactate concentrations in the previous run, in order to determine maximal steady-state blood lactate concentration. Blood lactate was determined at the end of every 4-min period. "Anaerobic threshold" was calculated from the increase in concentration of blood lactate obtained at the end of the runs at constant speed. The mean maximal steady-state blood lactate concentration was 5.0 mmol.l-1 corresponding to 88% of the aerobic power, whereas the mean value of the conventional "anaerobic threshold" was only 2.6 mmol.l-1, which corresponded to 78% of the VO2max. The correlations between the parameters of "anaerobic threshold", "ventilatory anaerobic threshold" and maximal steady-state blood lactate were only poor. Our results demonstrated that, in the children tested, the point at which a steeper increase in lactate concentrations during progressive work occurred did not correspond to the true anaerobic threshold, i.e. the exercise intensity above which a continuous increase in lactate concentration occurs at a constant exercise intensity.     

Blood lactate responses in incremental exercise as predictors of constant load performance

Seven trained male cyclists (VO2max = 4.42 +/- 0.23 l.min-1; weight 71.7 +/- 2.7 kg, mean +/- SE) completed two incremental cycling tests on the cycle ergometer for the estimation of the "individual anaerobic threshold" (IAT). The cyclists completed three more exercises in which the work rate incremented by the same protocol, but upon reaching selected work rates of approximately 40, 60 and 80% VO2max, the subjects cycled for 60 min or until exhaustion. In these constant load studies, blood lactate concentration was determined on arterialized venous ([La-]av) and deep venous blood ([La-]v) of the resting forearm. The av-v lactate gradient across the inactive forearm muscle was -0.08 mmol.l-1 at rest. After 3 min at each of the constant load work rates, the gradients were +0.05, +0.65* and +1.60* mmol.l-1 (*P less than 0.05). The gradients after 10 min at these same work rates were -0.09, +0.24 and +1.03* mmol.l-1. For the two highest work rates taken together, the lactate gradient was less at 10 min than 3 min constant load exercise (P less than 0.05). The [La-]av was consistently higher during prolonged exercise at both 60 and 80% VO2max than that observed at the same work rate during progressive exercise. At the highest work rate (at or above the IAT), time to exhaustion ranged from 3 to 36 min in the different subjects. These data showed that [La-] uptake across resting muscle continued to increase to work rates above the IAT. Further, the greater av-v lactate gradient at 3 min than 10 min constant load exercise supports the concept that inactive muscle might act as a passive sink for lactate in addition to a metabolic site.     

Leukocyte, lymphocyte and platelet response to dynamic exercise. Duration or intensity effect?

The influence of work intensity and duration on the white blood cell (WBC), lymphocyte (L) and platelet (P) count response to exercise was studied in 16 trained subjects (22 +/- 5.4 years, means +/- SD). They performed three cyclo-ergospirometric protocols: A) 10 min at 150 W followed by a progressive test (30 W/3 min) till exhaustion; B) constant maximal work (VO2max); C) a 45 min Square-Wave Endurance Exercise Test (SWEET), (n = 5). Arterial blood samples were taken: at rest, submaximal and maximal exercise in A; maximal exercise in B; 15th, 30th and 45th min in the SWEET. Lactate, [H+], PaCO2, PaO2, [Hct], Hb, cortisol, ACTH, total platelet volume (TPV), total blood red cell (RBC), WBC, L and P were measured. At 150 W, WBC, L, P, and TPV increased. VO2max did not differ between A and B, but a difference was found in total exercise time (A = 25 +/- 3 min; B = 7 +/- 2 min, p less than 0.001). In A, at VO2max, the increase was very small for Hct, [Hb], and RBC (10%), in contrast with large changes for WBC (+93%), L (+137%), P (+32%), TPV (+35%), [H+] (+39%), lactate (+715%), and ACTH (+95%). At VO2max there were no differences in these variables between A and B. During the SWEET: WBC, L, P, TPV and ACTH increased at the 15th min as much as in VO2max, but no difference was observed between the 15th, 30th and 45th min, except for ACTH which continued to rise; the lactate increase during the SWEET was about half (+341%) the value observed at VO2max, and [H+] did not vary with respect to values at rest.(ABSTRACT TRUNCATED AT 250 WORDS)     

Lactate acidosis and the increase in VE/VO2 during incremental exercise

The purpose of this investigation was to determine whether the onset of lactate acidosis is responsible for the increase in ventilatory equivalent (VE/VO2) during exercise of increasing intensity. Eight male subjects performed maximal incremental exercise tests on a cycle ergometer on two separate occasions. For the control (C) treatment, the initial work rates consisted of 4 min of unloaded pedaling (60 rpm) and 1 min of pedaling at a work rate of 30 W. Thereafter, the work rate was increased each minute by 22 W until volitional fatigue. Venous blood samples were taken before the onset of exercise and at the end of each work rate for determination of pH and lactate. Ventilatory parameters at each work rate were also monitored. Before the experimental treatment (E), the subjects performed two 3-min work bouts at high intensity (210-330 W) on the cycle ergometer in order to prematurely raise blood lactate levels and lower blood pH. The same incremental exercise test as C was then performed. The results indicated that the increase in VE/VO2 occurred at similar work rates and %VO2max although the venous H+ and lactate concentrations were significantly elevated during the E treatment. These results suggest that a decrease in the blood pH resulting from blood lactate accumulation is not responsible for the increase in VE/VO2 during incremental exercise.     

A comparison of blood gases and acid-base measurements in arterial, arterialized venous, and venous blood during short-term maximal exercise

The purpose of this study was to determine the relationship between blood gases and acid-base measurements in arterial, arterialized venous, and venous blood measured simultaneously during short-term maximal exercise. Ten well-trained male cyclists performed a graded maximal exercise test on a cycle ergometer to determine the power output corresponding to their peak oxygen consumption (test I), and a short-term maximal test on a cycle ergometer at peak power output (test II). During test II arterial, arterialized venous and venous blood were sampled simultaneously for determination of partial pressures of oxygen and carbon dioxide, pH, bicarbonate (HCO3-), base excess (BE), and lactate (La). Samples were taken at rest, the end of 1 min of exercise (1 ME), at the end of exercise (EE), and at 2 min of recovery (REC). During test II, subjects maintained a peak power output of 370.6 (62.1) W [mean (SD)] for 4.5, SD 1.6 min. Except at rest venous and arterialized venous measurements tended to be the same at all sampling intervals, but differed significantly from measurements in arterial blood (P less than 0.05). BE was the only variable that rendered consistently significant correlations between arterial and arterialized venous blood at each sampling interval. The pooled correlation coefficient between arterial and arterialized venous BE was r = 0.83 [regression equation: BEa = (0.84 BEav)-0.51]. Arterial La was significantly higher than venous La at 1 ME (2.8, 0.7 vs 0.8, 0.3 mmol.l-1) and higher than both venous and arterialized venous La at EE.(ABSTRACT TRUNCATED AT 250 WORDS)     

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)     

Ammonia and lactate in the blood after short-term sprint exercise

Nine well-trained subjects performed 15-, 30- and 45-s bouts of sprint exercise using a cycle ergometer. There was a significant difference in the mean power between a 15-s sprint (706.0 W, SD 32.5) and a 30-s sprint (627.0 W, SD 27.8; P less than 0.01). The mean power of the 30-s sprint was higher than that of the 45-s sprint (554.7 W, SD 29.8; P less than 0.01). Blood ammonia and lactate were measured at rest, immediately after warming-up, and 2.5, 5, 7.5, 10, 12.5 min after each sprint. The peak blood ammonia content was 133.8 mumol.l-1, SD 33.5, for the 15-s sprint, 130.2 mumol.l-1, SD 44.9, for the 30-s sprint, and 120.8 mumol.l-1, SD 24.6, for the 45-s sprint. Peak blood lactates after the 15-, 30- and 45-s sprints were 8.1 mmol.l-1, SD 1.7, 11.2 mmol.l-1, SD 2.4, and 14.7 mmol.l-1, SD 2.1, respectively. There was a significant linear relationship between peak blood ammonia and lactate in the 15-s (r, 0.709; P less than 0.05), 30-s (r, 0.797; P less than 0.05) and 45-s (r, 0.696; P less than 0.05) sprints. Though the peak blood lactate content increased significantly with increasing duration of the sprints (P less than 0.01), no significant difference was found in peak blood ammonia content among the 15-, 30- and 45-s sprints. These results suggest that the peak value of ammonia in the blood appears in sprints within 15-s and that the blood ammonia level is linked to the lactate in the blood.     

Physiological responses of young and elderly men to prolonged exercise at critical power

The critical power (CP) of a muscle group or individual may represent the highest rate of work which can be performed for an extended period. We investigated this concept in young (n = 13, 24.5 years) and elderly (n = 12, 70.7 years) active men by first determining CP and then comparing responses elicited by 24 min of cycle exercise at power outputs (omega) corresponding to CP. Values from the final 2 min of the 24-min ride were expressed relative to maximal values established in a ramp test. CP for the elderly was only 65% that for the young, but on a relative basis, it was significantly higher both in terms of omega (67 vs 62% of omega max) and oxygen consumption (VO2) (91.5 vs 85.2% of maximum oxygen consumption). There were no group differences in relative values for ventilation (VE), heart rate or respiratory exchange ratio (R). During the 24-min ride, VO2 and R achieved a plateau in both groups, while VE, blood lactate and arterial PCO2 continued to change in the young. It was concluded that CP can be determined in active elderly men, but that CP may not represent a true non-fatiguing work rate in either young or elderly men.     

Comparison of a field-based test to estimate functional threshold power and power output at lactate threshold

It has been proposed that field-based tests (FT) used to estimate functional threshold power (FTP) result in power output (PO) equivalent to PO at lactate threshold (LT). However, anecdotal evidence from regional cycling teams tested for LT in our laboratory suggested that PO at LT underestimated FTP. It was hypothesized that estimated FTP is not equivalent to PO at LT. The LT and estimated FTP were measured in 7 trained male competitive cyclists (VO2max = 65.3 ± 1.6 ml O2·kg(-1)·min(-1)). The FTP was estimated from an 8-minute FT and compared with PO at LT using 2 methods; LT(Δ1), a 1 mmol·L(-1) or greater rise in blood lactate in response to an increase in workload and LT(4.0), blood lactate of 4.0 mmol·L(-1). The estimated FTP was equivalent to PO at LT(4.0) and greater than PO at LT(Δ1). VO2max explained 93% of the variance in individual PO during the 8-minute FT. When the 8-minute FT PO was expressed relative to maximal PO from the VO2max test (individual exercise performance), VO2max explained 64% of the variance in individual exercise performance. The PO at LT was not related to 8-minute FT PO. In conclusion, FTP estimated from an 8-minute FT is equivalent to PO at LT if LT(4.0) is used but is not equivalent for all methods of LT determination including LT(Δ1).     

Uniqueness of interval and continuous training at the same maintained exercise intensity.

The present study sought to evaluate the inconsistencies previously observed regarding the predominance of continuous or interval training for improving fitness. The experimental design initially equated and subsequently maintained the same relative exercise intensity by both groups throughout the program. Twelve subjects were equally divided into continuous (CT, exercise at 50% maximal work) or interval (IT, 30 s work, 30 s rest at 100% maximal work) training groups that cycled 30 min day-1, 3 days.week-1, for 8 weeks. Following training, aerobic power (VO2max), exercising work rates, and peak power output were all higher (9-16%) after IT than after CT (5-7%). Vastus lateralis muscle citrate synthase activity increased 25% after CT but not after IT. A consistent increase in adenylate kinase activity (25%) was observed only after IT. During continuous cycling testing the CT group had reduced blood lactate (lab) levels and respiratory quotient at both the same absolute and relative (70% VO2max) work rates after training, while the IT group displayed similar changes only at the same absolute work rates. By contrast, both groups responded similarly during intermittent cycling testing with lower lab concentrations seen only at absolute work rates. These results show that, of the two types of training programs currently employed, IT produces higher increases in VO2max and in maximal exercise capacity. Nevertheless, CT is more effective at increasing muscle oxidative capacity and delaying the accumulation of lab during continuous exercise.     

Age and training effects on the lactate kinetics of master athletes during maximal exercise

To study the effects of age and training on lactate production in older trained subjects, the lactate kinetics of highly trained cyclists [HT, n = 7; 65 (SEM 1.2) years] and control subjects with low training (LT, n = 7) and of similar age were compared to those of young athletes [YA, n = 7; 26 (SEM 0.7) years], during an incremental exercise test to maximum power. The results showed that the lactacidaemia at maximal oxygen uptake (VO2max) was lower for HT than for LT (P < 0.05) and, in both cases, lower than that of YA (P < 0.001). The respective values were HT: 3.9 (SEM 0.51), LT: 5.36 (SEM 1.12), and YA: 10.3 (SEM 0.63) mmol.l-1. At submaximal powers, however, the difference in lactacidaemia was not significant between HT and YA, although the values for lactacidaemia at VO2max calculated per watt and per watt normalized by body mass were significantly lower for HT (P < 0.001) and LT (P < 0.02). These results would indicate that the decline in power with age induced a decline in lactacidaemia. Yet this loss in power was not the only causative factor; indeed, our results indicated a complementary metabolic influence. In the older subjects training decreased significantly the lactacidaemia for the same submaximal power (P < 0.01) and from 60% of VO2max onwards (P < 0.05); as for YA it postponed the increase and accumulation of lactates. The lactate increase threshold (Thla-,1) was found at 46% VO2max for LT and at 56% VO2max for HT.(ABSTRACT TRUNCATED AT 250 WORDS)     

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)     

Effect of beta-adrenergic blockade on plasma lactate concentration during exercise at high altitude

When unacclimatized lowlanders exercise at high altitude, blood lactate concentration rises higher than at sea level, but lactate accumulation is attenuated after acclimatization. These responses could result from the effects of acute and chronic hypoxia on beta-adrenergic stimulation. In this investigation, the effects of beta-adrenergic blockade on blood lactate and other metabolites were studied in lowland residents during 30 min of steady-state exercise at sea level and on days 3, 8, and 20 of residence at 4300 m. Starting 3 days before ascent and through day 15 at high altitude, six men received propranolol (80 mg three times daily) and six received placebo. Plasma lactate accumulation was reduced in propranolol- but not placebo-treated subjects during exercise on day 3 at high altitude compared to sea-level exercise of the same percentage maximal oxygen uptake (VO2max). Plasma lactate accumulation exercise on day 20 at high altitude was reduced in both placebo- and propranolol-treated subjects compared to exercise of the same percentage VO2max performed at sea level. The blunted lactate accumulation during exercise on day 20 at high altitude was associated with reduced muscle glycogen utilization. Thus, increased plasma lactate accumulation in unacclimatized lowlanders exercising at high altitude appears to be due to increased beta-adrenergic stimulation. However, acclimatization-induced changes in muscle glycogen utilization and plasma lactate accumulation are not adaptations to chronically increased beta-adrenergic activity.