Post-competition blood lactate concentrations in collegiate swimmers

Summary The purpose of this investigation was to quantitate post-competition lactate (LA) concentrations of swimmers during a competitive collegiate meet. Blood LA was measured by an enzymatic method on 23 subjects 5 min after each race event. The largest mean LA concentration of 25.7 mM/L was observed in swimmers after competing in the 200-yd individual medley. Swimmers in the 200-yd butterfly, back, breast and freestyle races had similar mean blood LA concentrations (ranging from 16.4 to 20.6 mM/L). Swimmers in the two longest events, the 500-yd and 1,000-yd free style races, had mean LA concentrations of 15.6 and 10.0 mM/L, respectively. To account for the effects of motivation, LA concentrations were measured following maximal effort noncompetitive 100 and 200-yd swims. LA concentrations were slightly greater in conjunction with faster performances for the competitive as compared to the noncompetitive 100 and 200-yd swims.     

Power and peak blood lactate at 5050 m with 10 and 30 s ‘all out’ cycling

Anecdotal observations suggest that the reduction in peak lactate accumulation in blood ([La]_{b peak}) after exhausting exercise, in chronic hypoxia vs. normoxia, may be related to the duration of the exercise protocol, being less pronounced after short supramaximal exercise than after incremental exercise (IE) lasting several minutes. To test this hypothesis, six healthy male Caucasians (age 36.8 ± 7.3, x¯ ± SD) underwent three exercise protocols on a cycle ergometer, at sea level (SL) and after 21 ± 10 days at 5050 m altitude (ALT): (1) 10 s, (2) 30 s ‘all out’ exercise and (3) IE leading to exhaustion in ～20–25 min. ‘Average’ power output (p¯) was calculated for 10 or 30 s ‘all out’; maximal power output (P_max) was determined for IE. Lactate concentration in arterialized capillary blood ([La]_b) was measured at rest and at different times during recovery; the highest [La]_b during recovery was taken as [La]_{b peak}. No significant differences in p¯ were observed between SL and ALT, for either 10 or 30 s ‘all out’ exercise; P_max during IE was significantly lower at ALT than at SL. [La]_{b peak} after 10 s ‘all out’ was unaffected by chronic hypoxia (7.0 ± 0.9 at ALT vs. 6.3 ± 1.8 mmol L^–1 at SL). After 30 s ‘all out’ the [La]_{b peak} decrease, at ALT (10.6 ± 0.6 mmol L^–1) vs. SL (12.9 ± 1.4 mmol L^–1), was only ～50% of that observed for IE (6.7 ± 1.6 mmol L^–1 vs. 11.3 ± 2.8 mmol L^–1). Muscle power output and blood lactate accumulation during short supramaximal exercise are substantially unaffected by chronic hypoxia.     

Age-Related Changes in Ceruloplasmin Content in W/SSM Rats

We studied enzyme systems (lactate dehydrogenase) of mitochondria in cerebral nerve cells in experimental encephalopathy developing after thermal injury. In animals receiving neuromedin at the early terms after injury, the ratio of forward to reverse lactate dehydrogenase reactions significantly increased over the first day after injury and returned to normal on day 7. __________ Translated from Byulleten' Eksperimental'noi Biologii i Meditsiny, Vol. 145, No. 6, pp. 626–627, June, 2008     

金属硫蛋白对培养神经细胞迟发性损伤的作用和一氧化氮的表达

本文以新生大鼠原代培养皮质神经元为实验材料，造成迟发性神经元损伤模型．在不同时程内，测试培养液中的细胞乳酸脱氢酶漏出量和用还原型尼克酰胺腺嘌呤二核着苷酸脱氢酶染色反应，观察培养细胞中一氧化氮合酶的表达水平．结果表明，缺血组在缺血与再灌流中，细胞乳酸脱氢酶漏出量明显高于对照组，差异显著（Ｐ＜０．００１）．一氧化氮合酶阳性神经元数量在缺血组的缺血时即明显高于对照组（Ｐ＜０．０１），再灌流后一氧化氮合酶表达仍然强烈，与对照组相比有显著差异（Ｐ＜０．０１）．当损伤细胞再灌流时，同时加入金属硫蛋白后，显示一氧化氮合酶表达减弱，和缺血组相比有显著差异（Ｐ＜０．０５～０．００１），细胞乳酸脱氢酶漏出量在再灌流后的早期近似于对照组．结合文献和本实验结果提示：在迟发性神经元损伤形成过程中一氧化氮起着重要作用；金属硫蛋白对脑缺血后迟发性神经元损伤有一定保护作用，是一种细胞保护剂，可望用于临床，控制缺血再灌流损伤。     

Growth resistance-sized arteries in response to bladder hypertrophy in the rat: time-course,DNA-synthesis and LDH-isoform pattern

Bladder growth was induced by partial urethral obstruction. Bladder hypertrophy was evident at 53 h after obstruction and continued over a 6 weeks period. Small bladder arteries were taken from fixed anatomical locations of the bladder circulation, mounted in a small vessel myograph and the optimal diameter for maximal isometric force development was determined (L_max, K⁺=125 mm stimulation). Bladder hypertrophy was associated with an enlarged L_max from 53 h onward (compared with sham-operated controls) and L_max continued to increase until 10 days after urethral obstruction. Between 10 days and 6 weeks no further increase of the diameter was observed. Increased diameters in vitro were accompanied by a transiently increased [³H]Thymidine uptake in the small arteries which peaked at 53 h after obstruction but was still above background at 10 days. At this time point, small arterial growth was associated with a significant relative increase in the M isoform of LDH as determined with agarose electrophoresis on tissue homogenates. Thus organ growth induced small vessel growth in the rat is characterized by a rapid onset, increased but transient DNA-turnover and LDH-isoform changes. The latter mimic changes seen in other types of smooth muscle growth.     

Energy turnover and lactate dehydrogenase activity in detrusor smooth muscle from rats with streptozotocin-induced diabetes

Force generation and tissue glucose metabolism were measured in the urinary bladder smooth muscle from rats with streptozotocin-induced diabetes (7–8 wk duration). Bladder wet wt was almost 4–fold higher in the diabetic animals compared with the untreated controls. Morphological analysis showed that the growth was associated with hypertrophy of the smooth muscle component in the bladder wall. Force generation of isolated bladder strip preparations was measured in vitro at different ambient oxygen tensions. Activation of intramural nerves, with electrical field stimulation, induced contractions that were unaffected by reduction of oxygen tension down to Po₂ 100 mmHg for both control and diabetic muscle strips. At zero Po₂ force was reduced by approximately 10–20% in both groups. High-K⁺ solution induced ‘tonic’ contractions that were slightly more inhibited by lowering Po₂. At intermediate Po₂ (between 100 and 20 mmHg) the diabetic muscle gave slightly higher force. At zero Po₂ no significant difference could be detected between strips from control and diabetic animals. Oxygen consumption and lactate production in the preparations were determined at a Po₂ of 290 mmHg and related to the volume of smooth muscle. At zero Po₂ lactate formation increased 3- to 4-fold. The metabolic tension cost was lower at zero Po₂ No differences in basal and contraction related metabolic rates could be detected between the two groups under normoxic and anoxic conditions. The maximal activity of lactate dehydrogenase (LDH) determined in tissue sampIes was about 2-fold higher in the diabetic bladder muscle. This increased enzymatic activity could thus not be correlated with any altered metabolic properties of the smooth muscle in the urinary bladder from diabetic rats.     

Blood lactate response to overtraining in male endurance athletes

Many physiological markers vary similarly during training and overtraining. This is the case for the blood lactate concentration ([La⁻]_b), since a right shift of the lactate curve is to be expected in both conditions. We examined the possibility of separating the changes in training from those of overtraining by dividing [La⁻]_b by the rating of perceived exertion ([La⁻]_b/RPE) or by converting [La⁻]_b into a percentage of the peak blood lactate concentration ([La⁻]_b,peak). Ten experienced endurance athletes increased their usual amount of training by 100% within 4 weeks. An incremental test and a time trial were performed before (baseline) and after this period of overtraining, and after 2 weeks of recovery (REC). The [La⁻]_b and RPE were measured during the recovery of each stage of the incremental test. We diagnosed overtraining in seven athletes, using both physiological and psychological criteria. We found a decrease in mean [La⁻]_b,peak from baseline to REC [9.64 (SD 1.17), 8.16 (SD 1.31) and 7.69 (SD 1.84) mmol · l⁻¹, for the three tests, respectively; P < 0.05] and a right shift of the lactate curve. Above 90% of maximal aerobic speed (MAS) there was a decrease of mean [La⁻]_b/RPE from baseline to REC [at 100% of MAS of 105.41 (SD 17.48), 84.61 (SD 12.56) and 81.03 (SD 22.64) arbitrary units, in the three tests, respectively; P < 0.05), but no difference in RPE, its variability accounting for less than 25% of the variability of [La⁻]_b/RPE (r=0.49). Consequently, [La⁻]_b/RPE provides little additional information compared to [La⁻]_b alone. Expressing [La⁻]_b as a %[La⁻]_b,peak resulted in a suppression of the right shift of the lactate curve, suggesting it was primarily the consequence of a decreased production of lactate by the muscle. Since the right shift of the curve induced by optimal training is a result of improved lactate utilization, the main difference between the two conditions is the decrease of [La⁻]_b,peak during overtraining. We propose retaining it as a marker of overtraining for long duration events, and repeating its measurement after a sufficient period of rest to make the distinction with overreaching. Accepted: 26 September 2000     

Variable effects of β-adrenoceptor blockade on muscle blood flow during exercise

The role of β-adrenoceptors in exercise-induced muscle hyperaemia was investigated. Exercise was performed with a small and a large muscle mass: knee extension (KE) and bicycle exercise (BE). Seven healthy subjects performed light and maximal KE and eight subjects performed stepwise dynamic BE to exhaustion before and after acute i.v. administration of propranolol (0.15 mg kg^-1). Leg blood flow was measured by a bolus dye dilution technique. During KE at low and high power leg blood flow was reduced by 8.7 and 10.5% after propranolol was administered, mean arterial blood pressure (MAP) was reduced at low, but not at high power resulting in increased leg vascular resistance (LVR) during high intensity. During BE propranolol reduced leg blood flow and increased LVR at low power, but not at high power. At high BE intensity LVR did not change with increasing power and was slightly decreased after propranolol was administered. In this situation oxygen uptake was close to maximum and the concentration of catecholamines was 3–5 times higher compared with KE. There was no significant effect of propranolol on lactate release or arterial-femoral venous (a-fv) differences for adrenaline or noradrenaline. We conclude that β-adrenoceptors modulate local vasodilation in skeletal muscles during exercise independently of local muscle energy demand, but that the effect is highly dependent on active muscle mass since a-adrenergic activity during maximal BE seemed to disguise any effect of propranolol on LVR.     

Effects of order of presentation of exercise intensities and of sauna baths on perceived exertion during treadmill running

Summary Thirteen male subjects performed a running test on the treadmill consisting of four standard exercise intensities [65%, 75%, 85%, 95% maximal O₂ uptake (VO_2max)] presented in ascending, descending or random order. At the end of each exercise intensity, O₂ consumption, heart rate (f _c), venous blood lactate concentration ([la]_b) and perceived exertion were assessed. This last variable was determined according to the Borg nonlinear CR-20 scale. The same variables were also determined during exercise at a standard intensity (65% or 95%VO_2max) performed before and after a Finnish sauna bath. Ratings of perceived exertion showed a good test-retest reliability (r=0.77); they were the same when the exercise intensity was expressed in relative (%VO_2max) or absolute (speed) terms, and were independent of the order of presentation of the exercise. The latter had no effect onf _c either but it did, however, influence [la]_b, which was significantly higher in the descending, as compared to the ascending or random modes of presentation. The sauna bath increasedf _c at a given exercise intensity, but left perceived exertion and [la]_b unchanged. It was concluded that at least under the present experimental conditions,f _c and venous [la]_b do not play a major role as determinants of perceived exertion.     

Blood lactate in trained cyclists during cycle ergometry at critical power

Summary The purposes of this investigation were to determine the validity of critical power (CP) as a measure of the work rate that can be maintained for a very long time without fatigue and to determine whether this corresponded with the maximal lactate steady-state (la_ss,max). Eight highly trained endurance cyclists (maximal oxygen uptake 74.1 ml · kg^–1 · min^–1, SD 5.3) completed four cycle ergometer tests to exhaustion at predetermined work rates (360, 425, 480 and 520 W). From these four co-ordinates of work and time to fatigue the regression of work limit on time limit was calculated for each individual (CP). The cyclists were then asked to exercise at their CP for 30 min. If CP could not be maintained, the resistance was reduced minimally to allow the subject to complete the test and maintain a blood lactate plateau. Capillary blood was sampled at 0, 5, 10, 20 and 30 min into exercise for the analysis of lactate. Six of the eight cyclists were unable to maintain CP for 30 min without fatigue. In these subjects, the mean power attained was 6.4% below that estimated by CP. Mean blood lactates (n = 8) reached a steady-state (8.9 mmol · l^–1, SD 1.6) during the last 20 min of exercise indicating that CP slightly overestimated la_{ss, max}. Individual blood lactates during the last 20 min of exercise were more closely related to the y-intercept of the CP curve (r=0.78, P<0.05) than either CP (0.34, NS) or mean power output (r=0.42, NS). The present investigation has shown that highly trained endurance cyclists can tolerate previously unreported levels of blood lactate during 30 min of exercise at or near their CP. Blood lactates during continuous exercise are higher than at the same work rate during an incremental test. The CP provides a simple and inexpensive means of assessing the exercise intensity which can be maintained continuously, while avoiding the methodological difficulties associated with ventilatory and lactate thresholds.