Effect of exercise duration on lactate kinetics after short muscular exercise

Summary Arterial blood lactate concentrations were measured in six normal males before, during and after 3 and 6-min bicycle exercises performed at three different work rates. The lactate recovery curves were fitted to a bi-exponential time function consisting of a rapidly increasing and a slowly decreasing component, which supplied an accurate representation of the changes in lactate concentration. Variations in the parameters of this mathematical model have been studied as a function of the duration of exercise and of the work rate, showing a clear dependence on exercise duration such that increasing exercise length decreases the velocity constants of the fitted curves. In terms of the functional meaning which can be given to these constants, this result indicates that extending exercise duration from 3 to 6 min reduces the ability of the whole body to exchange and remove lactate. This effect did not qualitatively modify the one already described, which is due to increased work rates, but it shifted the ability to exchange and remove lactate towards lower values. The main conclusion of the study is that lactate kinetic data vary as a function of time during exercise. This inference must be accounted for in the interpretation of lactate data obtained during muscular exercise.     

Effect of ageing on the ventilatory response and lactate kinetics during incremental exercise in man

We investigated the effects of age on breathing pattern, mouth occlusion pressure, the ratio of mouth occlusion pressure to mean inspiratory flow, and venous blood lactate kinetics during incremental exercise. Mouth occlusion pressure was used as an index of inspiratory neuromuscular activity, and its ratio to mean inspiratory flow was used as an index of the “effective impedance” of the respiratory system. Nine elderly male subjects [mean (SD) age: 68.1 (4.8) years] and nine young male subjects [mean (SD) age: 23.4 (1.3) years] performed an incremental exercise test on a bicycle ergometer. After a warm-up at 30 W, the power was increased by 30 W every 1.5 min until exhaustion. Our results showed that at maximal exercise, power output, breathing pattern, and respiratory exchange values, with the exception of tidal volume and the “effective impedance” of the respiratory system, were significantly higher in the young subjects. The power output and oxygen consumption values at the anaerobic threshold were also significantly higher in the young men. At the same power output, the elderly subjects showed significantly higher values for minute ventilation, respiratory equivalents for oxygen uptake and carbon dioxide output (CO₂), mean inspiratory flow, occlusion pressure and lactate concentration than the young subjects. At the same CO₂ below the anaerobic threshold (0.5, 0.75, 1.00 and 1.25 l · min⁻¹), minute ventilation and lactate concentration were also significantly higher in the elderly subjects. We observed a significantly higher minute ventilation at CO₂ values of 0.5, 0.75, 1.00 (P < 0.001) and 1.25 l · min⁻¹ (P < 0.05) in the elderly men, and a significantly higher lactate concentration at CO₂ values of 1.00 (P < 0.05) and 1.25 l · min⁻¹ (P < 0.01). In conclusion, the ventilatory response in elderly subjects is elevated in comparison with that in young subjects, both below and above the anaerobic threshold. This study demonstrates for the first time that this ventilatory increase, both below and above the threshold, is partly due to an increased lactate concentration. Received: 30 March 1999 / Accepted: 24 June 1999     

Respiratory alkalosis: no effect on blood lactate decline or exercise performance

Summary It was the purpose of this study to determine the effects of respiratory alkalosis before and after high intensity exercise on recovery blood lactate concentration. Five subjects were studied under three different acid-base conditions before and after 45 s of maximal effort exercise: 1) hyperventilating room air before exercise (Respiratory Alkalosis Before=RALB, 2) hyperventilating room air during recovery (Respiratory Alkalosis After=RALA), and 3) breathing room air normally throughout rest and recovery (Control =C). RALB increased blood pH during rest to 7.65±0.03 while RALA increased blood pH to 7.57±0.03 by 40 min of recovery. Neither alkalosis treatment had a significant effect on blood lactate concentration during recovery. The peak lactate values of 12.3±1.2 mmol · L^–1 for C, 11.8±1.2 mmol · L^–1 for RALB, and 10.2±0.9 mmol · L^–1 for RALA were not significantly different, nor were the half-times (t _1/2) for the decline in blood lactate concentration; C=18.2 min, RALB=19.3 min, and RALA=18.2 min. In C, RALB and RALA, the change in base excess from rest to postexercise was greater than the concomitant increase in blood lactate concentration, suggesting the presence of a significant amount of acid in the blood in addition to lactic acid. There was no significant difference in either the total number of cycle revolutions (C=77±2, RALB=77±1) or power output at 5 s intervals between RALB and C during the 45 s. These results suggest that the possible range of respiratory alkalosis changes in intact humans may be insufficient 1) to affect recovery blood lactate concentrations, or 2) to affect intense, short-term exercise performance.     

Effect of muscle mass on lactate formation during exercise in humans

To elucidate the mechanisms of lactate formation during submaximal exercise, eight men were studied during one- (1-LE) and two-leg (2-LE) exercise (approximately 11-min cycling) using the catheterization technique and muscle biopsies (quadriceps femoris muscle). The absolute exercise intensity and thus the energy demand for the exercising limb was the same [mean 114 (SEM 7) W] during both 1-LE and 2-LE. At the end of exercise partial pressure of O₂ and O₂ saturation in femoral venous blood were lower and arterial adrenaline and noradrenaline were higher during 2-LE than during 1-LE. Mean arterial blood lactate concentration increased to 10.8 (SEM 0.8) (2-LE) and 5.2 (SEM 0.4) mmol · 1^–1 (1-LE) after 10 min of exercise. The intramuscular metabolic response to exercise was attenuated during 1-LE [mean, lactate = 49 (SEM 9); glucose 6-P = 3.3 (SEM 0.3); nicotinamide adenine dinucleotide, reduced = 0.17 (SEM 0.02); adenosine 5-diphosphate 2.7 (SEM 0.1) mmol · kg dry mass^–1] compared to 2-LE [76 (SEM 6); 6.1 (SEM 0.7); 0.21 (SEM 0.02); 3.0 (SEM 0.1) mmol · kg dry mass^–1, respectively]. To elucidate whether the lower plasma adrenaline concentration could contribute to the attenuated metabolic response, additional experiments were performed on four of the eight subjects with infusion of adrenaline during 1-LE (1-LEE). Average plasma adrenaline concentration was increased during 1-LEE and reached 2–4 times higher levels than during 2-LE. Post-exercise muscle lactate and glucose 6-P contents were higher during 1-LEE than during 1-LE and were similar to those during 2-LE. Also, leg lactate release was elevated during 1-LEE versus 1-LE. It was concluded that during submaximal dynamic exercise the intramuscular metabolic response not only depended on the muscle power output, but also on the total muscle mass engaged. Plasma adrenaline concentrations and muscle oxygenation were found to be dependent upon the working muscle mass and both may have affected the metabolic response during exercise.     

Effect of exercise modality on oxygen uptake kinetics during heavy exercise

The mechanisms responsible for the oxygen uptake (V˙O₂) slow component during high-intensity exercise have yet to be established. In order to explore the possibility that the V˙O₂ slow component is related to the muscle contraction regimen used, we examined the pulmonary V˙O₂ kinetics during constant-load treadmill and cycle exercise at an exercise intensity that produced the same level of lactacidaemia for both exercise modes. Eight healthy subjects, aged 22–37 years, completed incremental exercise tests to exhaustion on both a cycle ergometer and a treadmill for the determination of the ventilatory threshold (defined as the lactate threshold, Th_la) and maximum V˙O₂ (V˙O_{2 max}). Subsequently, the subjects completed two “square-wave” transitions from rest to a running speed or power output that required a V˙O₂ that was halfway between the mode-specific Th_la and V˙O_{2 max}. Arterialised blood lactate concentration was determined immediately before and after each transition. The V˙O₂ responses to the two transitions for each exercise mode were time-aligned and averaged. The increase in blood lactate concentration produced by the transitions was not significantly different between cycling [mean (SD) 5.9 (1.5) mM] and running [5.5 (1.6) mM]. The increase in V˙O₂ between 3 and 6?min of exercise; (i.e. the slow component) was significantly greater in cycling than in running, both in absolute terms [290 (102) vs 200 (45) ml?·?min^?1; P<0.05] and as a proportion of the total V˙O₂ response above baseline [10 (3)% vs 6 (1)%; P<0.05]. These data indicate that: (a) a V˙O₂ slow component does exist for high-intensity treadmill running, and (b) the magnitude of the slow component is less for running than for cycling at equivalent levels of lactacidaemia. The greater slow component observed in cycling compared to running may be related to differences in the muscle contraction regimen that is required for the two exercise modes.     

Effect of prior heavy exercise on muscle deoxygenation kinetics at the onset of subsequent heavy exercise

This study examines the effect of prior heavy exercise on muscle deoxygenation kinetics at the onset of heavy-intensity cycling exercise. Ten young male adults (20 +/- 2 years) performed two repetitions of step transitions (6 min) from 35 W to heavy-intensity exercise preceded by either no warm-up or by a heavy-intensity exercise. VO2 was measured breath-by-breath, and muscle deoxygenation (HHb) and total hemoglobin (Hb(tot)) were monitored continuously by near-infrared spectroscopy. We used a two-exponential model to describe the VO2 kinetics and a mono-exponential model for the HHb kinetic. The parameters of the phase II VO2 kinetics (TD1 VO2, tau1 VO2 and A1 VO2) were unaffected by prior heavy exercise, while some parameters of local muscle deoxygenation kinetics were significantly faster (TD HHb: 7 +/- 2 vs. 5 +/- 2 s; P < 0.001, MRT HHb: 20 +/- 3 vs. 15+/- 4 s; P < 0.05). Blood lactate, heart rate and Hb(tot) values were significantly higher before the second bout of heavy exercise. These results collectively suggest that the prior heavy exercise probably increased muscle O2 availability and improved O2 utilization at the onset of a subsequent bout of heavy exercise.     

Effect of alkalosis on performance and lactate formation in supramaximal exercise

Summary An increased base binding power of the blood induced by alkali administration to subjects performing a supramaximal exercise has no appreciable effect neither on the maximal performance time nor on the total amount of lactic acid or its rate of appearance in blood.This work has been supported by a grant from the Italian National Research Council. Thanks are due also to Laboratory Glaxo, S.p.A. for facilities and financial support in the course of the experiments.     

Effect of exercise duration during incremental exercise on the determination of anaerobic threshold and the onset of blood lactate accumulation

Summary To determine the effect of the duration of incremental exercise on the point at which arterial blood lactate concentration (HLa) increases above the resting value (anaerobic threshold: AT) and on the point at which HLa reaches a constant value of 4 mM (onset of blood lactate accumulation: OBLA), eight male students performed two different kinds of incremental exercise. A comparison of arterial HLa and venous HLa was made under both conditions of incremental exercise. The incremental bicycle exercise tests consisted of 25 W increase every minute (1-min test) and every 4 min (4-min test). At maximal exercise, there were no significant differences in either gas exchange parameters or HLa values for the two kinds of incremental exercise. However, the peak workloads attained during the two exercises were significantly different (P<0.01). At OBLA and AT, there were no significant differences in gas exchange parameters during the 1-min and 4-min tests except for the workload (at OBLAP<0.01; at ATP<0.05). When venous blood HLa was used instead of arterial HLa for a 4-min test, AT was not significantly different from that obtained by arterial HLa, but OBLA was significantly different from that obtained by arterial HLa (P<0.05). On the other hand, for the 1-min test, venous HLa values yielded significantly higher AT and OBLA compared with those obtained using arterial HLa (P<0.01).It was concluded that when arterial blood was used, there was no effect of duration of workload increase in an incremental exercise test on the determination of the AT and OBLA expressed in . On the other hand, when venous HLa was used instead of arterial blood, these points might be overestimated when a fast increase in workload, such as the 1-min test, is used.     

Carbohydrate and fat metabolism of unacclimatized men during and after submaximal exercise in cool and hot environments

Summary Changes in levels of plasma lactate, pyruvate, glucose, free fatty acids (FFA), glycerol and 3-hydroxybutyrate during muscular exercise and recovery in cool (ambient temperature T _a = 23 C and water vapor pressure P _w = 13 mb) and hot environments (T _a = 40 C, P _w = 30 mb) were measured in six subjects. Arterial blood samples were collected at fixed time intervals during an initial resting phase of 75 min, an exercise period of 20 min and a recovery period of 125 min. Exercise consisted in pedaling a bicycle ergometer in the supine position at a work load that raised the heart pulse rate to nearly 140 beats min^–1 in the cool condition. Heart rate and rectal temperature were significantly higher during exercise and recovery in the hot environment. For samples collected at corresponding times in the cool and the hot conditions, the deviations of the observed blood parameters from their mean values during the whole resting phase seldom differed. However, for the exercise phase as a whole, the mean increases of lactate, pyruvate and glycerol were significantly greater and the mean decrease of glucose significantly smaller, in the hot condition, while the mean decreases of FFA and 3-hydroxybutyrate did not differ significantly. Related to their corresponding mean resting values, the mean changes in all six blood parameters measured were significantly larger during recovery in the hot condition than in the cool. These results verify the enhanced anaerobic metabolism in hot environment already described by previous authors, and show an adipokinetic and hyperglycemic effect of acute exposure to heat.     

Non-invasive prediction of blood lactate response to constant power outputs from incremental exercise tests

We determined the ability of gas exchange analyses during incremental exercise tests (IXT) to predict blood lactate levels associated with a range of constant power output cycle ergometer tests. Twenty-seven healthy young men performed duplicate IXT and four 15-min constant power output tests at intensities ranging from moderate to very severe, before and after a training program. End-exercise blood lactate levels were approximated from superficial venous samples obtained 60 s after each constant power output test. From IXT, the power outputs corresponding to peak oxygen uptake (W _max) and lactic acidosis threshold (W _LAT), were determined. We examined the ability of four measures of exercise intensity to predict blood lactate levels for power outputs above the LAT: (1) power output (W), (2) power difference (W – W _LAT), (3) power fraction (W/W _max) and (4) power difference to delta ratio [(W – W _LAT)/(W _max – W _LAT)]. Correlation coefficients were r = 0.38, 0.69, 0.75, and 0.81, respectively. The best linear regression prediction equation was: lactate (mmol · l^–1) = 12.2[(W – W _LAT)/(W _max –W _LAT)] + 0.7 mmol · l^–1. This relationship was not significantly affected by training, despite increased values of LAT and peak oxygen uptake. Normalizing exercise intensity to the range of power outputs between W _LAT and W _max provided an estimate of blood lactate response to constant power outputs with a standard error of the estimate of 1.66 mmol · l^–1.     

Influence of moderate cold exposure on blood lactate during incremental exercise

Summary 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°C or at 10°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. TheVO₂ was identical under both environments. At 10°C, as compared to 30°C, the lactate anaerobic threshold (Th_{an, la} ^–) occurred at an exercise intensity 15 W higher and [Th_{an, la} ^–]_b was lower for submaximal intensities above the Th_{an, 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°C [15.60 (SEM 3.15) nmol·l^–1] than at 30°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.     

Muscle oxygenation kinetics at the onset of exercise do not depend on exercise intensity

The purpose of this study was to determine whether the onset kinetics of muscle oxygenation in localized working muscle (mOxy) was affected by differences in exercise intensity. Five healthy male subjects exercised for 6 min at 125 W, 150 W, and 175 W, and 1 min at 300 W on a cycle ergometer. mOxy was estimated by near-infrared spectroscopy (NIRS) with a continuous wave photometer. The NIRS probe was positioned on the vastus lateralis muscle of the right leg. The relative change in mOxy was calculated from the relative change of the oxygenated hemoglobin (OxyHb) and deoxygenated hemoglobin (DeoxyHb) concentration from their resting values ([mOxy]=[OxyHb]–[DeoxyHb]). Assuming an exponential time course with time delay, the time constants of the mOxy were 5.7 (SD 2.2) s at 125 W, 5.6 (SD 1.9) s at 150 W, 6.0 (SD 2.2) s at 175 W, and 5.6 (SD 2.1) s at 300 W. The time delays of the mOxy were 6.7 (SD 4.2) s at 125 W, 8.6 (SD 1.6) s at 150 W, 6.4 (SD 3.0) s at 175 W, and 5.4 (SD 2.9) s at 300 W. The mean response times of the mOxy were 12.5 (SD 2.7) s at 125 W, 14.2 (SD 2.4) s at 150 W, 12.4 (SD 4.4) s at 175 W, and 11.0 (SD 3.1) s at 300 W. These results indicate that the kinetics of mOxy were not affected by differences in exercise intensity.     

Influence of cold exposure on blood lactate response during incremental exercise

Summary This study examined the effect of acute exposure of the whole body to cold on blood lactate response during incremental exercise. Eight subjects were tested with a cycle ergometer in a climatic chamber, room temperature being controlled either at 24° C (MT) or at –2° C (CT). The protocol consisted of a step increment in exercise intensity of 30 W every 2 min until exhaustion. Oxygen consumption ( ) was measured at rest and during the last minute of each exercise intensity. Blood samples were collected at rest and at exhaustion for estimations of plasma norepinephrine (NE), epinephrine (E), free fatty acid (FFA) and glucose concentrations, during the last 15 s of each exercise step and also during the 1^st, 4^th, 7^th, and the 10^th min following exercise for the determination of blood lactate (LA) concentration. The , was higher during CT than during MT at rest and during nearly every exercise intensity. At CT, lactate anaerobic threshold (LAT), determined from a marked increase of LA above resting level, increased significantly by 49% expressed as absolute , and 27% expressed as exercise intensity as compared with MT. The LA tended to be higher for light exercise intensities and lower for heavy exercise intensities during CT than during MT. The E and NE concentrations increased during exercise, regardless of ambient temperature. Furthermore, at rest and at exhaustion E concentrations did not differ between both conditions, while NE concentrations were greater during CT than during MT. Moreover, an increase of FFA was found only during CT. The difference in FFA level suggests that alterations in fat metabolism, possibly initiated by an enhanced secretion of NE, may have contributed to a decrease in lactate production.     

Effect of prolonged exercise on the level of triglycerides in the rat liver

Summary This study examined the effect of prolonged exercise on the level of triglycerides (TG) in rat liver. The rats were divided into groups: 1-control, 2-treated with nicotinic acid, 3-fed with glucose during exercise, 4-fasted, 5-adrenalectomized, 6-adrenalectomized and fed with oil. In the control group, there was gradual accumulation of TG in the liver and their level was doubled at exhaustion as compared to the resting value. Nicotinic acid lowered the resting level of TG and prevented their accumulation during exercise. Administration of glucose during exercise partially prevented the increase in TG level in the liver. In rats fasted for 24 h before exercise, the net increase in liver TG level during exercise was similar to that in the controls. Adrenalectomy, like nicotinic acid, lowered TG level at rest and prevented its increase during exercise. Feeding the adrenalectomized rats with oil elevated the plasma free fatty acid level but did not result in accumulation of TG in the liver, either at rest or during exercise. It is concluded that prolonged exercise results in accumulation of TG in the liver and that the process depends on the supply of free fatty acids and glucose and requires the presence of glucocorticoids.This work was supported by the Polish Central Programme for Basic Research 06-02.     

Effects of the menstrual cycle phase on the blood lactate responses to exercise

The effects of menstrual cycle phase on the blood lactate response to exercise were examined in eumenorrheic women (n=9). Exercise tests were performed at the mid-follicular and mid-luteal points in the menstrual cycle (confirmed by basal body temperature records and hormone levels). Blood lactates were measured at rest and during the recovery from exercise. Resting lactates were not different between the exercise tests; however, recovery lactates were significantly (p < 0.05) lower in the luteal compared to the follicular phase. The mechanism for these differences is unclear, but may be related to an estrogen mediated increased lipid metabolism inducing a concurrent reduction in carbohydrate metabolism. The present findings question the use of blood lactate monitoring as a suitable technique to measure exercise intensity in eumenorrheic women.     

Variations in serum myoglobin after a 2-min isokinetic exercise test and the effects of training

Summary Serum-myoglobin was measured after the completion of three different types of exercise i.e., dynamic, isometric, and isokinetic. The maximal rises in serum-myoglobin levels were 20%, 70%, and 300%, respectively. On the basis of this finding a 2-min isokinetic test was developed and standardized for the purpose of studying conditions in vivo that may affect myoglobin leakage from skeletal muscle cells.Fourteen healthy men performed the 2-min isokinetic test. Blood lactate increased on average eight times with maximal levels obtained 4 min after completed work. S-Myoglobin was raised approximately five times after 2 h. The rise in S-myoglobin was significantly (P<0.01) related to the loss in muscle strength (torque decline) during the test. After a training period of 3 weeks comprising 4 min of maximal isokinetic exercise three times a week the rise in S-myoglobin after a 2-min isokinetic test was reduced from on average 240 g·l^–1 to 96 g·l^–1 (P<0.001). The rise in blood lactate was not related to the variations in S-myoglobin or affected by training.The 2-min isokinetic exercise test is an easily standardized exercise test which in combination with measurements of serum-myoglobin should prove valuable in the study of conditions affecting leakage from muscle cells.     

Changes in ventilation at the end of heavy exercise of different durations

Summary The purpose of this study was to examine the effects of duration and the concomitant ventilatory drift of heavy exercise on the changes in ventilation following the cessation of exercise. Seven male subjects ran on a motor-driven treadmill at a constant work-rate of 90% of for either 5 min or 7 min on 60 occasions. The exercise was terminated abruptly by stopping the treadmill with a remote switch while recording inspired minute ventilation breath by breath. The fast drop in at the end of exercise is significantly less than the corresponding increase at the onset of exercise (P<0.05) and this difference is greater with longer duration of exercise. The time constants of the slow ventilatory decline are significantly increased following 7 min of exercise (P<0.05). They are also positively related to the drift in that occurs with the continuation of heavy exercise beyond 3 min. This relationship is however not statistically significant (P>0.05). These results indicate that the rate of ventilatory decline is slower after the end of a longer duration of exercise and this is caused by mechanism/s that also contribute/s to the ventilatory drift of heavy exercise. As, of the many different possibilities, only the respiratory after-discharge (central neural reverberatory) mechanism is likely to be more activated with a longer duration of exercise and on the basis of our previous observations (Jeyaranjan et al. 1988, 1989), the results suggest that the mechanism of after-discharge is an important mediator of ventilatory response during as well as after the cessation of heavy exercise.     

索拉菲尼对肝硬化大鼠部分肝切除术后肝脏再生的影响

目的: 在大鼠肝硬化模型的基础上行肝脏部分切除(PH),研究索拉菲尼(sorafenib)对大鼠肝脏再生的影响。方法: 使用二乙基亚硝胺(DEN)诱导Wistar大鼠肝硬化,成功建立30只肝硬化大鼠PH模型后,随机分2组,每组15只。术后第1 d开始,分别给予实验组索拉菲尼(30 mg·kg^-1·d^-1)、对照组生理盐水灌胃10 d后处死。留取PH后及实验结束后的血液及肝脏标本,检测2组肝脏再生率(LRR),增殖细胞核抗原(PCNA),生化指标: 丙氨酸转移酶(ALT)和血清白蛋白(ALB)、血清总胆红素(TBIL)和血清直接胆红素(DBIL)的变化,血管生成相关因子:血管内皮生长因子(VEGF)、血管内皮生长因子受体2(VEGFR-2)、血小板源性生长因子受体β(PDGFR-β),以及肝脏微血管密度(MVD)的变化。结果: (1)LRR在实验组及对照组分别为45.43%±3.36%和44.21%±2.77%,无显著差异(P>0.05);(2)免疫组织化学(IHC)没有检测到PCNA;(3)2组的生化指标无显著差异(P>0.05);(4)实验组VEGFR-2和PDGFR-β的表达受到抑制,MVD降低,并且实验组与对照组差异有统计学意义(P<0.01)。结论: 索拉菲尼虽然对肝硬化血管再生相关因子有抑制作用,但是对肝细胞再生和肝功能没有明显影响。     

Effect of exercise to rest ratio on plasma lactate concentration at work rates above and below maximum oxygen uptake

Summary The metabolic and physiological responses to different exercise to rest ratios (E: R) (2:1, 1: l, 1:2) of eight subjects exercising at work rates approximately 10% above and below maximum oxygen uptake ( ) were assessed. Each of the six protocols consisted of 15 1-min-long E : R intervals. Total work (kJ), oxygen uptake ( ), heart rate (f _c and plasma lactate concentrations were monitored. With increases in either E : R or work rate, andf _c increased (P <0.05). The average (15 min) andf _c ranged from 40 to 81 %, and from 62 to 91% of maximum, respectively. Plasma lactate concentrations nearly doubled at each E : R when work rate was increased from 90 to 110% of and ranged from a low of 1.8 mmol -I^–1 (1: 2–90) to a high of 10.7 mmol·1^–1 (2:1–110). The 2:1–110 protocol elicited plasma lactate concentrations which were approximately 15 times greater than that of rest. These data suggest that plasma lactate concentrations during intermittent exercise are very sensitive to both work rate and exercise duration.     

Hemodynamic mechanisms of the attenuated blood pressure response to mental stress after a single bout of maximal dynamic exercise in healthy subjects

To determine the hemodynamic mechanisms responsible for the attenuated blood pressure response to mental stress after exercise, 26 healthy sedentary individuals (age 29 ± 8 years) underwent the Stroop color-word test before and 60 min after a bout of maximal dynamic exercise on a treadmill. A subgroup (N = 11) underwent a time-control experiment without exercise. Blood pressure was continuously and noninvasively recorded by infrared finger photoplethysmography. Stroke volume was derived from pressure signals, and cardiac output and peripheral vascular resistance were calculated. Perceived mental stress scores were comparable between mental stress tests both in the exercise (P = 0.96) and control (P = 0.24) experiments. After exercise, the systolic blood pressure response to mental stress was attenuated (pre: 10 ± 13 vs post: 6 ± 7 mmHg; P < 0.01) along with lower values of systolic blood pressure (pre: 129 ± 3 vs post: 125 ± 3 mmHg; P < 0.05), stroke volume (pre: 89.4 ± 3.5 vs post: 76.8 ± 3.8 mL; P < 0.05), and cardiac output (pre: 7.00 ± 0.30 vs post: 6.51 ± 0.36 L/min; P < 0.05). Except for heart rate, the hemodynamic responses and the mean values during the two mental stress tests in the control experiment were similar (P > 0.05). In conclusion, a single bout of maximal dynamic exercise attenuates the blood pressure response to mental stress in healthy subjects, along with lower stroke volume and cardiac output, denoting an acute modulatory action of exercise on the central hemodynamic response to mental stress.