Muscle metabolism, blood lactate and oxygen uptake in steady state exercise at aerobic and anaerobic thresholds

Muscle metabolites and blood lactate concentration were studied in five male subjects during five constant-load cycling exercises. The power outputs were below, equal to and above aerobic (AerT) and anaerobic (AnT) threshold as determined during an incremental leg cycling test. At AerT, muscle lactate had increased significantly (p less than 0.05) from the rest value of 2.31 to 5.56 mmol X kg-1 wet wt. This was accompanied by a significant reduction in CP by 28% (p less than 0.05), whereas only a minor change (9%) was observed for ATP. At AnT muscle lactate had further increased and CP decreased although not significantly as compared with values at AerT. At the highest power outputs (greater than AnT) muscle lactate had increased (p less than 0.01) and CP decreased (p less than 0.01) significantly from the values observed at AnT. Furthermore, a significant reduction (p less than 0.05) in ATP over resting values was recorded. Blood lactate decreased significantly (p less than 0.01) during the last half of the lowest 5 min exercise, remained unchanged at AerT and increased significantly (p less than 0.05-0.01) at power outputs greater than or equal to AnT. It is concluded that anaerobic muscle metabolism is increased above resting values at AerT: at low power outputs (less than or equal to AerT) this could be related to the transient oxygen deficit during the onset of exercise or the increase in power output. At high power outputs (greater than AnT) anaerobic energy production is accelerated and it is suggested that AnT represents the upper limit of power output where lactate production and removal may attain equilibrium during constant load exercise.     

Metabolic and ventilatory responses to steady state exercise relative to lactate thresholds

The metabolic and ventilatory responses to steady state submaximal exercise on the cycle ergometer were compared at four intensities in 8 healthy subjects. The trials were performed so that, after a 10 min adaptation period, power output was adjusted to maintain steady state VO2 for 30 min at values equivalent to: (1) the aerobic threshold (AeT); (2) between the aerobic and the anaerobic threshold (AeTAnT); (3) the anaerobic threshold (AnT); and (4) between the anaerobic threshold and VO2max (AnTmax). Blood lactate concentration and ventilatory equivalents for O2 and CO2 demonstrated steady state values during the last 20 min of exercise at the AeT, AeAnT and AnT intensities, but increased progressively until fatigue in the AnTmax trial (mean time = 16 min). Serum glycerol levels were significantly higher at 40 min of exercise on the AeAnT and the AnT when compared to AeT, while the respiratory exchange ratios were not significantly different from each other. Thus, metabolic and ventilatory steady state can be maintained during prolonged exercise at intensities up to and including the AnT, and fat continues to be a major fuel source when exercise intensities are increased from the AeT to the AnT in steady state conditions. The blood lactate response to exercise suggests that, for the organism as a whole, anaerobic glycolysis plays a minor role in the energy release system at exercise intensities upt to and including the AnT during steady state conditions.     

Effect of prolonged dynamic exercise on plasma adrenomedullin concentration in healthy young men.

The aim of the study was to find out whether prolonged exercise influences plasma adrenomedullin (ADM) concentration and whether it is related to the hormonal, metabolic and cardiovascular changes. Eighteen healthy subjects (age 25+/-1 yrs) were submitted to cycle exercise for 90 min at 70% of maximal oxygen uptake. Heart rate (HR) and blood pressure (BP) were measured continously. Before, at 30(th) min, and at the end of exercise venous blood samples were taken for [ADM], noradrenaline [NA], adrenaline [A], atrial natriuretic peptide [ANP], plasma renin activity PRA, interleukin-6 [IL-6] and lactate [LA] determination. Significant increases in plasma ADM and IL-6 were found at 90(th) min whereas other hormones were elevated already at 30(th) min of exercise. Positive correlations were ascertained between [ADM] and [NA] (r=0.47), [ANP] (r=0.35) or [IL-6] (r=0.35) and between exercise-induced increases in [ADM] and [NA] (r=0.38). PRA correlated positively with [NA] and [ANP]. Negative correlation was found between plasma [ADM] and diastolic BP. The present data suggest that increase in sympathetic nervous activity and cytokine induction during prolonged exercise may be involved in plasma ADM release and that increase in ADM and ANP secretion may be a compensatory mechanism against further elevation of blood pressure.     

Muscle metabolic profile and oxygen transport capacity as determinants of aerobic and anaerobic thresholds

Aerobic and anaerobic thresholds determined by different methods in repeated exercise tests were correlated with cardiorespiratory variables and variables of muscle metabolic profile in 33 men aged 20-50 years. Aerobic threshold was determined from blood lactate, ventilation, and respiratory gas exchange by two methods (AerT1 and AerT2) and anaerobic threshold from venous lactate (AnTLa), from ventilation and gas exchange (AnTr) and by using the criterion of 4 mmol.1(-1) of venous lactate (AnT4mmol). In addition to ordinary correlative analyses, applications of LISREL models were used. The 8 explanatory variables chosen for the regression analyses were height, relative heart volume, relative diffusing capacity of the lung, muscle fiber composition, citrate synthase (CS) and succinate dehydrogenase activities, the lactate dehydrogenase--CS ratio, and age. They explained 58% of the variation in AerT1, 73.5% that of AerT2, 71% that of AnTr, 74.5% that of AnTLa, and 67.5% that of AnT4mmol.AerT and AnT alone explained 77% of the variation in each other. Both AerT and AnT were determined mainly by a muscle metabolic profile, with the CS activity of vastus lateralis as the strongest determinant. The factor 'submaximal endurance' which was measured with AerT and AnT seemed to be slightly more closely connected to 'muscle metabolic profile' than was 'maximal aerobic power' (= VO2max), but both also correlated strongly with each other (r = 0.92).     

Influence of moderate cold exposure on blood lactate during incremental exercise.

This study examined the effect of exposure of the whole body to moderate cold on blood lactate produced during incremental exercise. Nine subjects were tested in a climatic chamber, the room temperature being controlled either at 30 degrees C or at 10 degrees C. The protocol consisted of exercise increasing in intensity in 35 W increments every 3 min until exhaustion. Oxygen consumption (VO2) was measured during the last minute of each exercise intensity. Blood samples were collected at rest and at exhaustion for the measurement of blood glucose, free fatty acid (FFA), noradrenaline (NA) and adrenaline (A) concentrations and, during the last 15 s of each exercise intensity, for the determination of blood lactate concentration [la-]b. The VO2 was identical under both environments. At 10 degrees C, as compared to 30 degrees C, the lactate anaerobic threshold (Than,la-) occurred at an exercise intensity 15 W higher and [la-]b was lower for submaximal intensities above the Than,la-. Regardless of ambient temperature, glycaemia, A and NA concentrations were higher at exhaustion while FFA was unchanged. At exhaustion the NA concentration was greater at 10 degrees C [15.60 (SEM 3.15) nmol.l-1] than at 30 degrees C [8.64 (SEM 2.37) nmol.l-1]. We concluded that exposure to moderate cold influences the blood lactate produced during incremental exercise. These results suggested that vasoconstriction was partly responsible for the lower [la-]b observed for submaximal high intensities during severe cold exposure.     

Beta-endorphin and corticotropin release is dependent on a threshold intensity of running exercise in male endurance athletes

Relationship between the intensity of running exercise on a treadmill and the changes in the concentrations of beta-endorphin + beta-lipotropin (beta-E + beta-LPH) and adrenocorticotropic hormone (ACTH) in plasma were studied in 10 experienced male endurance athletes. At random order, the subjects run on a treadmill six exercises which required on an average (mean +/- S.E.) 50 +/- 0.8%, 58 +/- 0.8%, 69 +/- 1.1%, 80 +/- 0.7%, 92 +/- 1.0% and 98 +/- 0.5% of their maximal oxygen consumption. Plasma levels of beta-E + beta-LPH and ACTH did not show any significant changes during the 50-80%-tests. During the 92% test, the mean levels (+/- S.E.) of beta-E + beta-LPH and ACTH increased significantly (p less than 0.001), from 3.0 +/- 0.4 to 8.0 +/- 1.2 pmol/l and from 3.1 +/- 0.5 to 8.9 +/- 1.3 pmol/l, respectively, and during the 98% test, from 3.7 +/- 0.6 pmol/l to 20.4 +/- 1.5 pmol/l, and from 3.6 +/- 0.6 to 21.8 +/- 1.5 pmol/l, respectively. Increases in the plasma levels of beta-E + beta-LPH and ACTH were always accompanied by an increase in the blood lactate level. We conclude that intensive running with an anaerobic response causes an increase in the concentrations of beta-endorphin and ACTH in plasma in endurance athletes, whereas slight aerobic exercise did not elicit any response.     

Plasma catecholamine responses to four resistance exercise tests in men and women

The plasma adrenaline ([A]) and noradrenaline ([NA]) concentration responses of nine men and eight women were investigated in four resistance exercise tests (E80, E60, E40 and E20), in which the subjects had to perform a maximal number of bilateral knee extension-flexion movements at a given cycle pace of 0.5 Hz, but at different load levels (80%, 60%, 40% and 20% of 1 repetition maximum, respectively). The four test sessions were separated by a minimal interval of 3 rest days. The number of repetitions (Repmax), the total work (Wtot) done normalized for the lean body mass and the heart rate (HR) responses were similar in the two groups in each test. In addition, no differences were found between the two groups in [A] and [NA] either before or after the exercise tests. The postexercise [NA], both in the men [10.8 (SD 7.0) nmol x l(-1)] and in the women [11.7 (SD 7.4) nmol x l(-1)], was clearly the highest in E20, where also the Repmax, WtOt, the total amount of integrated electromyograph activity in the agonist muscles and the peak postexercise blood lactate concentration [men 8.3 (SD 1.6) vs women 7.3 (SD 0.9) mmol x l(-1), ns] were significantly higher than in the other tests. Although the postexercise [A] in E20 both in the men [7.1 (SD 6.0) nmol x l(-1)] and in the women [5.2 (SD 2.0) nmol x l(-1)] were higher than in E80 [men 3.1 (SD 4.2), women 2.1 (SD 2.0) nmol x l(-l)] (P < 0.05), they were not significantly different from E60 [men 3.6 (SD 1.9), women 4.0 (SD 3.3) nmol x l(-1)] and E40 [men 3.8 (SD 4.1), women 5.8 (SD 4.0) nmol x l(-1)] in either group. The present study did not indicate any sex differences in performance and in plasma catecholamine responses in different exhausting resistance exercise tests performed with the knee extensor muscles. In both groups the plasma [NA] response was clearly the largest in the longest exercise with the greatest amount of muscle activity and work done, and with the largest blood lactate response. The differences in the plasma [A] responses between the exercises tended to be somewhat smaller.     

Comparison of incremental and steady state tests of endurance training

To compare the results obtained by incremental or constant work load exercises in the evaluation of endurance conditioning, a 20-week training programme was performed by 9 healthy human subjects on the bicycle ergometer for 1 h a day, 4 days a week, at 70-80% VO2max. Before and at the end of the training programme, (1) the blood lactate response to a progressive incremental exercise (18 W increments every 2nd min until exhaustion) was used to determine the aerobic and anaerobic thresholds (AeT and AnT respectively). On a different day, (2) blood lactate concentrations were measured during two sessions of constant work load exercises of 20 min duration corresponding to the relative intensities of AeT (1st session) and AnT (2nd session) levels obtained before training. A muscle biopsy was obtained from vastus lateralis at the end of these sessions to determine muscle lactate. AeT and AnT, when expressed as % VO2max, increased with training by 17% (p less than 0.01) and 9% (p less than 0.05) respectively. Constant workload exercise performed at AeT intensity was linked before training (60% VO2max) to a blood lactate steady state (4.8 +/- 1.4 mmol.l-1) whereas, after training, AeT intensity (73% VO2max) led to a blood lactate accumulation of up to 6.6 +/- 1.7 mmol.l-1 without significant modification of muscle lactate (7.6 +/- 3.1 and 8.2 +/- 2.8 mmol.kg-1 wet weight respectively). It is concluded that increase in AeT with training may reflect transient changes linked to lower early blood lactate accumulation during incremental exercise.(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.     

Plasma hypoxanthine and ammonia in humans during prolonged exercise

In this study we examined the time course of changes in the plasma concentration of oxypurines [hypoxanthine (Hx), xanthine and urate] during prolonged cycling to fatigue. Ten subjects with an estimated maximum oxygen uptake (VO2(max)) of 54 (range 47-67) ml x kg(-1) x min(-1) cycled at [mean (SEM)] 74 (2)% of VO2(max) until fatigue [79 (8) min]. Plasma levels of oxypurines increased during exercise, but the magnitude and the time course varied considerably between subjects. The plasma concentration of Hx ([Hx]) was 1.3 (0.3) micromol/l at rest and increased eight fold at fatigue. After 60 min of exercise plasma [Hx] was >10 micromol/l in four subjects, whereas in the remaining five subjects it was <5 micromol/l. The muscle contents of total adenine nucleotides (TAN = ATP+ADP+AMP) and inosine monophosphate (IMP) were measured before and after exercise in five subjects. Subjects with a high plasma [Hx] at fatigue also demonstrated a pronounced decrease in muscle TAN and increase in IMP. Plasma [Hx] after 60 min of exercise correlated significantly with plasma concentration of ammonia ([NH(3)], r = 0.90) and blood lactate (r = 0.66). Endurance, measured as time to fatigue, was inversely correlated to plasma [Hx] at 60 min (r = -0.68, P < 0.05) but not to either plasma [NH(3)] or blood lactate. It is concluded that during moderate-intensity exercise, plasma [Hx] increases, but to a variable extent between subjects. The present data suggest that plasma [Hx] is a marker of adenine nucleotide degradation and energetic stress during exercise. The potential use of plasma [Hx] to assess training status and to identify overtraining deserves further attention.     

Plasma adrenomedullin response to maximal exercise in healthy subjects.

The aim of the study was to find out whether maximal exercise performed by healthy young men influences plasma adrenomedullin concentration (ADM) and is the peptide level related to the cardiovascular, metabolic and hormonal changes induced by exercise. Ten subjects (age 24+/-1.0 yr) participated in the study. They performed graded bicycle ergometer exercise until exhaustion. Heart rate (HR) and blood pressure (BP) were measured throughout the test. Before and at the end of exercise venous blood samples were taken for [ADM], noradrenaline [NA], adrenaline [A], growth hormone [hGH], cortisol and lactate [LA] determination. Plasma [ADM] decreased during exercise from 1.71+/-0.09 to 1.53+/-0.10 pmol x l(-1) (p<0.01). This was accompanied by increases in plasma catecholamines and [hGH], while plasma cortisol level did not change. Positive correlation was found between the exercise-induced decreases in plasma ADM and diastolic BP. Blood [LA], systolic and mean BP at the end of exercise correlated negatively with plasma [ADM]. No significant interrelationships were found between plasma ADM, catecholamines or the other hormones measured. The present data suggests, that maximal exercise inhibits ADM secretion in young healthy men. Metabolic acidosis and a decrease in peripheral resistance might be involved in this effect.     

The effects of training on the metabolic and respiratory profile of high-intensity cycle ergometer exercise

The tolerable work duration (t) for high-intensity cycling is well described as a hyperbolic function of power (W): W = (W'.t-1) + Wa, where Wa is the upper limit for sustainable power (lying between maximum W and the threshold for sustained blood [lactate] increase, theta lac), and W' is a constant which defines the amount of work which can be performed greater than Wa. As training increases the tolerable duration of high-intensity cycling, we explored whether this reflected an alteration of Wa, W' or both. Before and after a 7-week regimen of intense interval cycle-training by healthy males, we estimated ( ) theta lac and determined maximum O2 uptake (mu VO2); Wa; W'; and the temporal profiles of pulmonary gas exchange, blood gas, acid-base and metabolic response to constant-load cycling at and above Wa. Although training increased theta lac (24%), mu VO2 (15%) and Wa (15%), W' was unaffected. For exercise at Wa, a steady state was attained for VO2, [lactate] and pH both pre- and post-training, despite blood [norepinephrine] and [epinephrine] ([NE], [E]) and rectal temperature continuing to rise. For exercise greater than Wa, there was a progressive increase in VO2 (resulting in mu VO2 at fatigue), [lactate], [NE], [E] and rectal temperature, and a progressive decrease for pH. We conclude that the increased endurance capacity for high-intensity exercise following training reflects an increased W asymptote of the W-t relationship with no effect on its curvature; consequently, there is no appreciable change in the amount of work which can be performed above Wa.(ABSTRACT TRUNCATED AT 250 WORDS)     

Adenine nucleotide degradation in the thoroughbred horse with increasing exercise duration

Adenine nucleotide (AN) degradation has been shown to occur during intense exercise in the horse and in man, at or close to the point of fatigue. The aim of the study was to compare the concentrations of muscle inosine 5'-monophosphate (IMP) and plasma ammonia (NH3) during intense exercise with the concentrations of muscle and blood lactate. Seven trained thoroughbred horses were used in the study. Each exercised on a treadmill for periods of between 30 s and 150 s, at 11 and/or 12 m.s-1. Blood and muscle samples were taken and analysed for lactate and NH3 and adenosine 5'-triphosphate (ATP), phosphorylcreatine (PCr), IMP, creatine, lactate and glycerol-3-phosphate respectively. Horses showed varying degrees of AN degradation as indicated by plasma [NH3] and muscle [ATP] and [IMP]. Comparisons of [IMP] with muscle [lactate], and plasma [NH3] with that of blood [lactate] indicated a threshold to the start of AN degradation. This threshold corresponded to a lactate content of around 80 mmol.kg-1 dry muscle and 15 mmol.l-1 in blood. We discuss the mechanisms which have been proposed to account for AN degradation and suggest that IMP formation occurs as a result of a sudden rise in the concentration of adenosine 5'-diphosphate (ADP) and consequently the concentration of adenosine 5'-monophosphate. The data suggest a critical pH below which there may be a substantial reduction in the kinetics of ADP rephosphorylation provided by PCr resulting in an increase in [ADP], which is the stimulus to AN degradation during intense exercise.     

Anaerobic threshold and lactate turnpoint

Venous lactate concentration and ventilatory responses to progressively increased work rates were studied in 16 men who performed an incremental exercise test to exhaustion on an electrically braked cycle ergometer. In this test the characteristic curvilinear increase in venous lactate concentrations was observed. In addition to the anaerobic threshold (AT), a second breakpoint was observed and named the lactate turnpoint (LTP). Eight of the 16 subjects performed a second incremental exercise test initiated during lactic acidosis. In this test the direction of change in venous lactate concentrations was different. The work rate at which lactate concentrations again increased, after a steady decline (previously described as the AT2), was similar to the work rate established for the LTP in the first test. In the second test removal of lactate was demonstrated at work rates exceeding the AT. Although the lactate response to the two tests was different the pattern of change was similar, with the two breakpoints occurring at the same work rates. Collectively these results lend a measure of support to the hypothesis of a positive relationship between the AT, LTP, and a pattern of recruitment of motor units with different enzyme profiles. Both the AT and LTP were predictable from the ventilatory response to incremental exercise.     

Effects of exercise in normoxia and acute hypoxia on respiratory muscle metabolites

We determined changes in rat plantaris, diaphragm, and intercostal muscle metabolites following exercise of various intensities and durations, in normoxia and hypoxia (FIO2 = 0.12). Marked alveolar hyperventilation occurred during all exercise conditions, suggesting that respiratory muscle motor activity was high. [ATP] was maintained at rest levels in all muscles during all normoxic and hypoxic exercise bouts, but at the expense of creatine phosphate (CP) in plantaris muscle and diaphragm muscle following brief exercise at maximum O2 uptake (VO2max) in normoxia. In normoxic exercise plantaris [glycogen] fell as exercise exceeded 60% VO2max, and was reduced to less than 50% control during exhaustive endurance exercise (68% VO2max for 54 min and 84% for 38 min). Respiratory muscle [glycogen] was unchanged at VO2max as well as during either type of endurance exercise. Glucose 6-phosphate (G6P) rose consistently during heavy exercise in diaphragm but not in plantaris. With all types of exercise greater than 84% VO2max, lactate concentration ([LA]) in all three muscles rose to the same extent as arterial [LA], except at VO2max, where respiratory muscle [LA] rose to less than half that in arterial blood or plantaris. Exhaustive exercise in hypoxia caused marked hyperventilation and reduced arterial O2 content; glycogen fell in plantaris (20% of control) and in diaphragm (58%) and intercostals (44%). We conclude that respiratory muscle glycogen stores are spared during exhaustive exercise in the face of substantial glycogen utilization in plantaris, even under conditions of extreme hyperventilation and reduced O2 transport. This sparing effect is due primarily to G6P inhibition of glycogen phosphorylase in diaphragm muscle. The presence of elevated [LA] in the absence of glycogen utilization suggests that increased lactate uptake, rather than lactate production, occurred in the respiratory muscles during exhaustive exercise.     

Blood lactate accumulation in intermittent supramaximal exercise

Blood lactate accumulation rate and oxygen consumption have been studied in six trained male runners, aged 20 to 30 years. Subjects ran on a treadmill at a rate representing 172 +/- 5% VO2max for four 45 s sessions, separated by 9 min rest periods. Oxygen consumption was measured throughout. Blood lactate was determined in samples taken from the ear and VO2 was measured at the end of each exercise session, and two, five and nine minutes later. After the fourth exercise session, the same measurements were made every five min for 30 min. 4 subjects repeated a single exercise of the same type, duration and intensity and the same measurements were taken. With repetitive intermittent exercise, gradual increases in blood lactate concentration [( LA]b) occurred, whereas its rate of accumulation (delta[LA]b) decreased. The amount of oxygen consumed during each 45 s exercise session remained unchanged for a given subject. After cessation of intermittent exercise, the half-time of blood lactate was 26 min, whereas it was only 15 min after a single exercise session. VO2 values, on the other hand, returned to normal after 15 to 20 min. All other conditions being equal, the gradual decrease in delta[LA]b during intermittent exercise could be explained if the lactate produced during the first exercise session is used during the second period, and/or if the diffusion space of lactate increases. The diffusion space seems to be multi-compartmental on the basis of half-time values noted for [LA]b after intermittent exercise, compared with those noted after a single exercise session.(ABSTRACT TRUNCATED AT 250 WORDS)     

Glucose transport and metabolism in rat renal proximal tubules: multicomponent effects of insulin

Glucose transport and metabolism, and the effect of insulin thereon, was studied using suspensions of rat renal tubules enriched in the proximal component. [U-14C]Glucose oxidation is a saturable process (Km 3.1 +/- 0.2 mM; Vmax 14 +/- 0.2 mumole 14CO2 formed/g tissue protein per h). Glucose oxidation and [14C]lactate formation from glucose are inhibited in part by phlorizin and phloretin: the data suggest that the rate-limiting entry of glucose into the cell metabolic pool occurs by both the Na-glucose cotransport system (at the brush border) and the equilibrating, phloretin-sensitive system (at the basal-lateral membrane). Raising external glucose from 5 to 30 mM markedly increases aerobic and anaerobic lactate formation. Gluconeogenesis from lactate is not affected by variations of glucose concentrations. 24 h after streptozotocin administration, aerobic lactate formation is enhanced, as is the uptake of methyl alpha-D-glucoside by the tubules, while anaerobic glycolysis is depressed. Streptozotocin treatment (ST) increases both the Km and Vmax of glucose oxidation; gluconeogenesis and lactate oxidation are not affected. The effect of streptozotocin treatment on lactate formation are abolished by 1 mU/ml insulin. Streptozotocin treatment increases tissue hexokinase activity, decreases glucose-6-phosphatase, but has no significant effect on fructose-1,6-diphosphatase; phosphoenolpyruvate carboxykinase and pyruvate dehydrogenase. The data demonstrate fast streptozotocin-induced changes in cellular enzymes of carbohydrate metabolism. The enhancing effect of streptozotocin on methyl alpha-glucoside uptake is transient: 8 days after administration of the agent, no significant difference from controls is found. It is concluded that under the given experimental conditions insulin enhances the equilibrating glucose entry by the phloretin-sensitive pathway at the basal-lateral membrane, and transiently inhibits the Na-glucose cotransport system.     

狗在运动中的肌糖原消耗与无氧阈的关系

本实验测定了5条狗的无氧阈值,运动耐受时间、衰竭时的血乳酸浓度及运动中的肌糖原消耗量。结果如下:无氧阈值,1.与运动耐受时间呈正相关(r=0.947,P<0.02);2.与运动中肌糖原消耗量呈负相关(r=-0.959,P<0.01);3.与衰竭时的血乳酸浓度呈负相关(r=-0.942,P<0.02)。实验结果提示,无氧阈值是反映机体耐力的可靠指标。而运动中肌糖原消耗少,血乳酸积累程度轻,可能是无氧阈值之所以能够反映机体耐力的物质基础。     

Plasma catecholamine and serum testosterone responses to four units of resistance exercise in young and adult male athletes

The plasma noradrenaline (NA) and adrenaline (A) concentration responses of seven young male athletes [15 (SD 1) years] and seven adult male athletes [25 (SD 6) years] were investigated together with the serum testosterone (Tes) concentration responses in four different half-squatting exercises. The loads, number of repetitions, exercise intensity and recovery between the sets were manipulated such that different types of metabolic demand could be expected. However, the amount of work done was kept equal in each kind of exercise. After the most exhausting unit of exercise (E3; two sets of 30 repetitions with 50% of 1 repetition maximum and with 2-min recovery between the sets) the plasma NA concentration was significantly lower in the younger than in the adult subjects [15.7 (SD 7.8) vs 32.7 (SD 13.2) nmol · l⁻¹, P < 0.05], while the A concentrations were similar. In the other three exercises no differences in the plasma catecholamine concentration responses among the groups were observed. The postexercise Tes concentrations, however, were significantly lower in the younger than in the adult subjects in every exercise unit. No correlations between the plasma catecholamine and serum Tes concentration responses were observed in any of the exercise units in either group. The results of the present study may suggest reduced sympathetic nervous activity in the younger subjects compared to the adults in response to exhausting resistance exercise. The results may also suggest that the catecholamines were less involved in eliciting an increase in Tes secretion in these resistance exercises. Accepted: 11 November 1997     

Muscle accounts for glucose disposal but not blood lactate appearance during exercise after acclimatization to 4,300 m.

We hypothesized that the increased blood glucose disappearance (Rd) observed during exercise and after acclimatization to high altitude (4,300 m) could be attributed to net glucose uptake (G) by the legs and that the increased arterial lactate concentration and rate of appearance (Ra) on arrival at altitude and subsequent decrease with acclimatization were caused by changes in net muscle lactate release (L). To evaluate these hypotheses, seven healthy males [23 +/- 2 (SE) yr, 72.2 +/- 1.6 kg], on a controlled diet were studied in the postabsorptive condition at sea level, on acute exposure to 4,300 m, and after 3 wk of acclimatization to 4,300 m. Subjects received a primed-continuous infusion of [6,6-D2]glucose (Brooks et al., J. Appl. Physiol. 70: 919-927, 1991) and [3-13C]lactate (Brooks et al., J. Appl. Physiol. 71:333-341, 1991) and rested for a minimum of 90 min, followed immediately by 45 min of exercise at 101 +/- 3 W, which elicited 51.1 +/- 1% of the sea level peak O2 uptake (65 +/- 2% of both acute altitude and acclimatization peak O2 uptake). Glucose and lactate arteriovenous differences across the legs and arms and leg blood flow were measured. Leg G increased during exercise compared with rest, at altitude compared with sea level, and after acclimatization. Leg G accounted for 27-36% of Rd at rest and essentially all glucose Rd during exercise. A shunting of the blood glucose flux to active muscle during exercise at altitude is indicated. With acute altitude exposure, at 5 min of exercise L was elevated compared with sea level or after acclimatization, but from 15 to 45 min of exercise the pattern and magnitude of L from the legs varied and followed neither the pattern nor the magnitude of responses in arterial lactate concentration or Ra. Leg L accounted for 6-65% of lactate Ra at rest and 17-63% during exercise, but the percent Ra from L was not affected by altitude. Tracer-measured lactate extraction by legs accounted for 10-25% of lactate Rd at rest and 31-83% during exercise. Arms released lactate under all conditions except during exercise with acute exposure to high altitude, when the arms consumed lactate. Both active and inactive muscle beds demonstrated simultaneous lactate extraction and release. We conclude that active skeletal muscle is the predominant site of glucose disposal during exercise and at high altitude but not the sole source of blood lactate during exercise at sea level or high altitude.