Oxygen consumption, lactate accumulation, and sympathetic response during prolonged exercise under hypoxia

Six men (33 +/- 3 years old) performed 1 h ergocycle exercise (60% VO2 max) at sea level and at a simulated altitude of 3000 m. A similar relative exercise intensity corresponded to a lower absolute work load (139 +/- 4 W) in hypoxic than normoxic (163 +/- 4 W) conditions. Lower oxygen uptake (VO2) with no change in ventilation (VE), respiratory exchange ratio (R), and heart rate (Hr) were observed during exercise under hypoxia compared to normoxia. A slow rise in VO2, after the initial 5 min exercise, was observed in normoxic (+ 230 ml/min) as well as in hypoxic (250 ml/min) conditions that might be, in part, related to oxidative removal of blood lactate. Peak blood lactate concentration reached at 30 min of exercise was similar in normoxia (4.5 +/- 0.4) and in hypoxia (4.7 +/- 0.5). However, while the lactate level decreased during exercise at sea level, it remained elevated throughout exercise in altitude. Blood lactate concentration measured at the end of exercise was significantly (P less than 0.05) higher in hypoxic (4.4 +/- 0.3) than in normoxic (3.2 +/- 0.4) conditions. Catecholamine response to exercise was similar in both conditions. We conclude that during prolonged exercise at a given relative work load, hypoxia does not affect cardiorespiratory and sympathetic responses but tends to increase blood lactate accumulation. Higher blood lactate concentrations during hypoxic exercise seems to reflect alterations in the removal of blood lactate rather than changes in glycolytic flux.     

热脱水对高温及常温环境中渐增负荷运动时血乳酸浓度的影响

本研究旨在探讨在热脱水之后，高温、常温及非脱水条件下运动时血乳酸（ＨＬａ）的变化。１２名身体健康男大学生（非热环境适应者），在以下３种不同环境条件下，进行功率自行车渐增负荷运动，测定吸氧量（ＶＯ２）、通气量（ＶＥ）、心率（ＨＲ）及直肠温度（Ｔｒ）：（１）在常温条件下，不进行桑拿浴（Ｎ２５℃）：（２）进行桑拿浴后，在常温条件下（ｍ５℃）；（３）进行桑拿浴后，在高温条件下（Ｄ４Ｏ℃）。结果如下：（ｕＤ４Ｏ℃渐增负荷运动时，ＨＬａ显著性高于Ｄ２５℃和Ｎ２５℃，并且渐增负荷运动ｍ５℃时Ｍａ也高于Ｎ２５℃。但是３种条件下ＶＯ２却未出现显著性差异；（２）不但Ｎ２５℃时最大吸氧量（Ｖｑｎｔａｘ）要比ｏ２５℃和Ｄ４０℃高，而且Ｄ２５℃时ＶＯ２ｍａｘ也比Ｄ４０℃高。Ｎ２５℃时力竭时间明显长于Ｄ２５℃和ＭＯ℃。结果表明，热脱水之后，高温渐增负荷运动时ＨＩａ上升由于活动肌肉的糖元分解增强，而非局部缺氧所致。肝脏清除ＨＬａ能力下降也可导致ＨＬａ上升。     

Intra- and extra-cellular lactate shuttles

The "lactate shuttle hypothesis" holds that lactate plays a key role in the distribution of carbohydrate potential energy that occurs among various tissue and cellular compartments such as between: cytosol and mitochondria, muscle and blood, blood and muscle, active and inactive muscles, white and red muscles, blood and heart, arterial blood and liver, liver and other tissues such as exercising muscle, intestine and portal blood, portal blood and liver, zones of the liver, and skin and blood. Studies on resting and exercising humans indicate that most lactate (75-80%) is disposed of through oxidation, with much of the remainder converted to glucose and glycogen. Lactate transport across cellular membranes occurs by means of facilitated exchange along pH and concentration gradients involving a family of lactate transport proteins, now called monocarboxylate transporters (MCTs). Current evidence is that muscle and other cell membrane lactate transporters are abundant with characteristics of high Km and Vmax. There appears to be long-term plasticity in the number of cell membrane transporters, but short-term regulation by allosteric modulation or phosphorylation is not known. In addition to cell membranes, mitochondria also contain monocarboxylate transporters (mMCT) and lactic dehydrogenase (mLDH). Therefore, mitochondrial monocarboxylate uptake and oxidation, rather than translocation of transporters to the cell surfaces, probably regulate lactate flux in vivo. Accordingly, the "lactate shuttle" hypothesis has been modified to include a new, intracellular component involving cytosolic to mitochondrial exchange. The intracellular lactate shuttle emphasizes the role of mitochondrial redox in the oxidation and disposal of lactate during exercise and other conditions.     

Arterial blood gases, acid-base balance, and lactate and gas exchange variables during hypoxic exercise

To determine the effect of hypoxia on lactate threshold (LT), onset of blood lactate accumulation (OBLA), and gas exchange threshold (GET), the lactate level together with VO2, VCO2, VE, and acid-base status in arterial blood from 12 female distance runners performing a progressive incremental treadmill test under the condition of hypoxic gas inhalation (HC: FIO2 is 16.0% in N2) compared with normoxic conditions (NC: FIO2 is 20.9%; i.e., air) were examined. During exercise, HC shifted LT, GET, and OBLA to a lower VO2 by 12.5%, 12.9%, and 9.3%, respectively. The GET during hypoxic exercise was well correlated with LT (GET = 0.973LT + 0.04; expressed in VO2 l.min-1). The close reciprocal changes in arterial blood lactate and bicarbonate (HCO3-) were observed during hypoxic as well as normoxic exercise. These findings provide evidence for the cause and effect relationship between LT and GET, even in hypoxic exercise. During submaximal exercise below the LT, PaCO2 and HCO3- slightly increased both in NC and HC with pH remaining unchanged. However, during exercise above the LT, the PaCO2, HCO3-, and pH all decreased with pH decreasing more markedly during hypoxia. In conclusion, this study demonstrated a clear increase in arterial lactate during hypoxic exercise above the LT. Both the LT and GET are shifted to a lower work rate by hypoxia in the same manner with the correlation between them remaining high, supporting the cause and effect relationship of these two parameters.     

Blood lactate. Implications for training and sports performance

The blood lactate response to exercise has interested physiologists for over fifty years, but has more recently become as routine a variable to measure in many exercise laboratories as is heart rate. This rising popularity is probably due to: the ease of sampling and improved accuracy afforded by recently developed micro-assay methods and/or automated lactate analysers; and the predictive and evaluative power associated with the lactate response to exercise. Several studies suggest that the strong relationship between exercise performance and lactate-related variables can be attributed to a reflection by lactate during exercise of not only the functional capacity of the central circulatory apparati to transport oxygen to exercising muscles, but also the peripheral capacity of the musculature to utilise this oxygen. For example, several studies contrast the relationship between VO2max and endurance running performance with that between a lactate variable and the same running performance. In every study, the lactate variable is more highly correlated with performance. Similarly, prescribing training intensity as a function of the lactate concentration elicited by the training may prove to be a means of obtaining a more homogeneous adaptation to training in a group of athletes or subjects than is obtained by setting intensity as a function of maximal heart rate or % VO2max. A review of the recent literature shows that the lactate response to supramaximal exercise is a sensitive indicator of adaptation to 'sprint training' and is correlated with supramaximal exercise performance. This review also describes the possible applications of lactate measurements to enhance the rate of recovery from high intensity exercise. Although the lactate response to exercise is reproducible under standardised conditions it can be influenced by the site of blood sampling, ambient temperature, changes in the body's acid-base balance prior to exercise, prior exercise, dietary manipulations, or pharmacological interpretation.     

Effect of caffeine on LT, VT and HRVT

Caffeine has many diverse physiological effects including central nervous system stimulation. Ventilatory threshold and a recently described heart rate variability threshold both have a relationship with autonomic control that could be altered by caffeine consumption. The purpose of this investigation was to determine the influence of caffeine on lactate, ventilatory, and heart rate variability thresholds during progressive exercise. Using a randomized placebo controlled, double-blind study design, 10 adults performed 2 graded maximal cycle ergometry tests with and without caffeine (5 mg·kg?1). Respiratory gas exchange, blood lactate concentrations, and heart rate variability data were obtained at baseline and throughout exercise. RESULTS: At rest, caffeine (p<0.05) increased blood lactate, oxygen consumption, carbon dioxide production, and minute ventilation. For indices of heart rate variability at rest, caffeine increased (p<0.05) the coefficient of variation, while standard deviation, and mean successive difference displayed non-significant increases. During progressive exercise, minute ventilation volumes were higher in caffeine trials but no other parameters were significantly different compared to placebo tests. CONCLUSION: These data demonstrate the robustness of the lactate, ventilatory and heart rate variability thresholds when challenged by a physiological dose of caffeine.     

Influence of caffeine on blood lactate response during incremental exercise

To test the hypothesis that caffeine ingestion prior to exercise would delay the onset of blood lactate accumulation, eight male subjects were studied during incremental exercise to maximal work rates on a cycle ergometer under two conditions: 1 h after ingestion of 200 ml of either decaffeinated, calorie-free cola (control trial) or the same cola drink with 5 mg caffeine/kg body weight added (caffeine trial). Maximal exercise values for oxygen consumption (VO2 max), ventilation, heart rate, respiratory exchange ratio (R), work rate, and blood lactate were not affected by caffeine. Submaximal exercise VO2, ventilation, and R also were unaffected by caffeine. During the caffeine trial, submaximal exercise blood lactate was significantly higher and heart rate significantly lower than during the control trial (P less than 0.05). The lower exercise heart rate at the same VO2 resulted in a significantly greater O2 pulse during all submaximal exercise intensities for the caffeine trial (P less than 0.05). Data on R indicated that caffeine had no effect on substrate utilization during exercise. Data on exercise blood lactate response suggested that caffeine does not delay and may accelerate the onset of blood lactate accumulation during incremental exercise. When defined as either a "breakpoint," delta l mM (above resting lactate), or fixed level of 4 mM, the lactate threshold (LT) did not differ between caffeine and control trials. However, in using a 2 mM lactate level as a criterion, the LT during the caffeine trial (2.13 +/- 0.22 l X min-1) was significantly (P less than 0.05) lower than during the control trial (2.71 +/- 0.17 l X min-1).(ABSTRACT TRUNCATED AT 250 WORDS)     

Prolonged exercise at a constant load on a bicycle ergometer: ratings of perceived exertion and leg aches and pain as well as measurements of blood lactate accumulation and heart rate

To study changes over time during prolonged exercise on a bicycle ergometer at a constant load, 22 healthy males rated perceived exertion as well as aches and pain in the legs, and measurements were taken on blood lactate accumulation and heart rate (HR). The prolonged exercise was carried out at WOBLA (the power level eliciting a blood lactate concentration of 4 mmol X l-1). All four measured variables, ratings of perceived exertion, ratings of aches and pain in the legs, blood lactate accumulation, and HR, grew systematically according to negatively accelerating functions. HR showed more of a steady state, whereas all the other three variables grew continuously over time. Three subgroups were identified related to the blood lactate response after 15 min at WOBLA: elevated (greater than 5 mmol X l-1), intermediate (3.5-4.9 mmol X l-1), and low (less than 3.4 mmol X l-1). It was suggested that a major contribution to the discrepancies in blood lactate between the subgroups after 15 min was partly due to insufficient warming up, which was 5 min at 20 W as compared with the final power level (WOBLA), which differed between 140 and 260 W. After 15 min both rated perceived exertion and rated aches and pain in the legs were related to the corresponding blood lactates. It was suggested that rated perceived exertion and rated aches and pain in the legs partly reflected the degree of "anaerobic" metabolism measured as blood lactate.     

Neural control of force output during maximal and submaximal exercise

A common belief in exercise physiology is that fatigue during exercise is caused by changes in skeletal muscle metabolism. This 'peripheral' fatigue results either from substrate depletion during submaximal exercise or metabolite accumulation during maximal exercise in the exercising muscles. However, if substrate depletion alone caused fatigue, intracellular ATP levels would decrease and lead to rigor and cellular death. Alternatively, metabolite accumulation would prevent any increase in exercise intensity near the end of exercise. At present, neither of these effects has been shown to occur, which suggests that fatigue may be controlled by changes in efferent neural command, generally described as 'central' fatigue. In this review, we examine neural efferent command mechanisms involved in fatigue, including the concepts of muscle wisdom during short term maximal activity, and muscle unit rotation and teleoanticipation during submaximal endurance activity. We propose that neural strategies exist to maintain muscle reserve, and inhibit exercise activity before any irreparable damage to muscles and organs occurs. The finding that symptoms of fatigue occur in the nonexercising state in individuals with chronic fatigue syndrome indicates that fatigue is probably not a physiological entity, but rather a sensory manifestation of these neural regulatory mechanisms.     

The influence of pacing during 6-minute supra-maximal cycle ergometer performance

The aim of this study was to evaluate the influence of pacing on performance, oxygen uptake (VO2), oxygen deficit and blood lactate accumulation during a 6-minute cycle ergometer test. Six recreational cyclists completed three 6-minute cycling tests using fast-start, even-pacing and slow-fast pacing conditions. Cycle ergometer performance was measured as the mean power output produced for each cycling test. Energy system contribution during each cycling trial was estimated using a modified accumulated oxygen deficit (AOD) method. Blood lactate concentration was analysed from blood sampled using a catheter in a forearm vein prior to exercise, at 2 minutes, 4 minutes and 6 minutes during exercise, and at 2 minutes, 5 minutes and 10 minutes post-exercise. There was no significant difference between the pacing conditions for mean power output (P = 0.09), peak VO2 (P = 0.92), total VO2 (P = 0.76), AOD (P = 0.91), the time-course of VO2 (P = 0.22) or blood lactate accumulation (P= 0.07). There was, however, a significant difference between the three pacing conditions in the oxygen deficit measured over time (P = 0.02). These changes in the time-course of oxygen deficit during cycling trials did not, however, significantly affect the mean power output produced by each pacing condition.     

Lactate accumulation in response to supramaximal exercise in rowers

The aim of this study was to test (a) three methods to estimate the quantity of lactate accumulated (Q_LaA) in response to supramaximal exercise and (b) correlations between Q_LaA and the nonoxidative energy supply assessed by the accumulated oxygen deficit (AOD). Nine rowers performed a 3‐min all‐out test on a rowing ergometer to estimate AOD and lactate accumulation in response to exercise. Peak blood lactate concentration [(La)_peak] during recovery was assessed, allowing Q_LaA(m1) to be estimated by the method of Margaria et al. Application of a bicompartmental model of lactate distribution space to the blood lactate recovery curves allowed estimation of (a) the net amount of lactate released during recovery from the active muscles (NALR_max), and (b) Q_LaA according to two methods (Q_LaA(m2) and Q_LaA(m3)). (La)_peak did not correlate with AOD. Q_LaA(m1), Q_LaA(m2) and Q_LaA(m3) correlated with AOD (r = 0.70, r = 0.85 and r = 0.92, respectively). These results confirm that (La)_peak does not provide reliable information on nonoxidative energy supply during supramaximal exercise. The correlations between AOD and Q_LaA(m2) and Q_LaA(m3) support the concept of studying blood lactate recovery curves to estimate lactate accumulation and thus the contribution of nonoxidative pathway to energy supply during supramaximal exercise.     

Myocardial lactate metabolism during exercise

The heart consumes lactate under resting conditions in normal healthy people. A limited number of studies have measured lactate exchange across the heart during exercise by using simultaneous arterial and coronary sinus catheterization. In general, exercise results in an increase in the rate of lactate uptake, which is due both to the increases in myocardial blood flow and lactate extraction from rest to exercise. Lactate extraction by the myocardium during submaximal exercise (40-60% VO2max) is largely dependent upon the concentration of lactate in arterial blood. Studies using a continuous infusion of 14C-lactate tracer have demonstrated that essentially all of the lactate taken up during exercise is immediately oxidized to CO2 in the myocardium. In addition, lactate tracer studies indicate that healthy myocardium simultaneously consumes and produces lactate under conditions of net lactate consumption. Moderate intensity exercise (40% VO2max) does not result in an increase in the rate of myocardial lactate production above resting values. Thus, the heart takes up lactate in proportion to the rate of lactate delivery to the myocardium both at rest and during exercise. Exercise that elicits an increase in the arterial lactate concentration above resting values results in an increase in the relative contribution of lactate oxidation to myocardial oxidative metabolism.     

Changes in beta-endorphin levels in response to aerobic and anaerobic exercise.

Exercise-induced increases in the peripheral beta-endorphin concentration are mainly associated both with changes in pain perception and mood state and are possibly of importance in substrate metabolism. A more precise understanding of opioid function during exercise can be achieved by investigating the changes in beta-endorphin concentrations dependent upon intensity and duration of physical exercise and in comparison to other stress hormones. Published studies reveal that incremental graded and short term anaerobic exercise lead to an increase in beta-endorphin levels, the extent correlating with the lactate concentration. During incremental graded exercise beta-endorphin levels increase when the anaerobic threshold has been exceeded or at the point of an overproportionate increase in lactate. In endurance exercise performed at a steady-state between lactate production and elimination, blood beta-endorphin levels do not increase until exercise duration exceeds approximately 1 hour, with the increase being exponential thereafter. beta-Endorphin and ACTH are secreted simultaneously during exercise, followed by a delayed release of cortisol. It is not yet clear whether a relationship exists between the catecholamines and beta-endorphin. These results support a possible role of beta-endorphin in changes of mood state and pain perception during endurance sports. In predominantly anaerobic exercise the behaviour of beta-endorphin depends on the degree of metabolic demand, suggesting an influence of endogenous opioids on anaerobic capacity or acidosis tolerance. Further investigations are necessary to determine the role of beta-endorphin in exercise-mediated physiological and psychological events.     

Muscle as a consumer of lactate

Historically, muscle has been viewed primarily as a producer of lactate but is now considered also to be a primary consumer of lactate. Among the most important factors that regulate net lactate uptake and consumption are metabolic rate, blood flow, lactate concentration ([La]), hydrogen ion concentration ([H+]), fiber type, and exercise training. Muscles probably consume more lactate during steady state exercise or contractions because of increased lactate oxidation since enhancements in lactate transport due to acute activity are small. For optimal lactate consumption, blood flow should be adequate to maintain ideal [La] and [H+] gradients from outside to inside muscles. However, it is not clear that greater than normal blood flow will enhance lactate exchange. A widening of the [La] gradient from outside to inside muscle cells along with an increase in muscle [La] enhances both lactate utilization and sarcolemmal lactate transport. Similarly, a significant outside to inside [H+] gradient will stimulate sarcolemmal lactate influx, whereas an increased intramuscular [H+] may stimulate exogenous lactate utilization by inhibiting endogenous lactate production. Oxidative muscle fibers are metabolically suited for lactate oxidation, and they have a greater capacity for sarcolemmal lactate transport than do glycolytic muscle fibers. Endurance training improves muscle capacity for lactate utilization and increases membrane transport of lactate probably via an increase in Type I monocarboxylate transport protein (MCT1) and perhaps other MCT isoforms as well. The future challenge is to understand the regulatory roles of both lactate metabolism and membrane transport of lactate.     

Distinctive effects of three different modes of exercise on oxygen uptake, heart rate and blood lactate and pyruvate.

We intended to investigate the effects of different modes of exercise on oxygen uptake (VO2), the heart rate and the levels of lactate and pyruvate in venous blood. For this, untrained male subjects performed three modes of exercise with a treadmill (TR), a bicycle ergometer (UP) and a supine leg ergometer (SU). The percentage of maximal oxygen uptake (% VO2max) and VO2/weight for TR were significantly higher than those for UP or SU at lactate levels of 2, 3 and 4 mmol/l. The heart rate was also higher for TR than for SU at these lactate levels. The correlations of blood lactate with % VO2max, VO2/weight and the heart rate were significant for TR and SU, but not for UP. Blood lactate levels were lower for TR than for SU or UP at 60, 70, 80% VO2max, whereas the values for UP were lower than those for SU only at 60% VO2max. Blood pyruvate levels were always lower for TR than for SU. The ratios of lactate/pyruvate differed for TR and SU only at 60% VO2max. For a given mode of exercise, blood lactate and the ratio of lactate/pyruvate increased with an increase in % VO2max, but those of pyruvate did not. These results reveal that the relationships between any two of lactate, pyruvate, VO2 and the heart rate are different at different modes of exercise, and that blood lactate depends on adaptation of muscles to a mode of exercise rather than on the quantity of muscles mobilized.     

Regulation of hepatic lactate balance during exercise

The rate of exchange of lactate across the liver gives important insights into intracellular processes during muscular work. At the onset of exercise hepatic glycogenolysis increases rapidly, resulting in high rates of glycolytic flux and a transient rise in lactate output. With increasing exercise duration, gluconeogenesis is accelerated and the liver gradually shifts from a lactate-producing to a lactate-consuming state. Exercise-induced changes in hormone levels are critical in the regulation of hepatic glycogenolysis and gluconeogenesis and, therefore, net hepatic lactate balance. The fall in insulin stimulates hepatic glycogenolysis, glycolytic flux, and, as a result, hepatic lactate output. On the other hand, the stimulatory effects of glucagon on gluconeogenesis elicit an increase in hepatic lactate uptake. The rise in epinephrine may regulate gluconeogenesis during prolonged exercise by stimulating peripheral lactate mobilization, thereby providing gluconeogenic substrate to the liver. Chronic hepatic-denervation leads to an increase in gluconeogenesis and net hepatic lactate uptake at rest without altering total glucose production. However, the response to exercise is unaffected by the absence of hepatic nerves. Hence, the direction and magnitude of the hepatic lactate balance during exercise yields important information regarding flux through the gluconeogenic and glycolytic pathways, such that high rates of gluconeogenesis correspond to accelerated rates of hepatic lactate uptake and high rates of hepatic glycolytic flux lead to increased rates of hepatic lactate output.     

Relationship of ergometer-specific VO2 max and muscle enzymes to blood lactate during submaximal exercise.

This study compared the relationship of maximum oxygen uptake and skeletal muscle enzyme activities to the submaximal exercise intensity eliciting 4 mM blood lactate (OBLA). Twelve subjects performed both cycle (Cy) and treadmill (Tr) submaximal exercise with step-wise increments each fourth minute. Blood lactate concentration and oxygen uptake (VO2) were determined during the final minute of each step. Peak VO2 during exhaustive exercise was also measured on each ergometer. Biopsies were taken from the gastrocnemius (gast) and vastus lateralis (vl) muscles as representatives of muscles recruited during Tr and Cy exercise, respectively. Citrate synthase (CS), phosphofructokinase (PFK), and lactate dehydrogenase (LDH) activities were assayed. Peak VO2 was 10% greater and the VO2 at OBLA was 16% greater during Tr compared to Cy exercise. The percent of peak VO2 at OBLA was 85% and 79% for Tr and Cy exercise, respectively. The absolute enzyme activities were not different in the two muscles, however the ratio LDH/CS was greater in the vl than in the gast. The results indicate that the absolute differences between Cy and Tr exercise in peak VO2 are not commensurate with the differences in the relative exercise intensity at which OBLA occurs.     

Recognition,diagnosis, and treatment of mitochondrial myopathies in endurance athletes

Endurance athletes complaining of muscle pains concomitant with fatigue and exercise intolerance provide a diagnostic challenge. When the most common causes have been ruled out, the presence of metabolic myopathies, including mitochondrial myopathies (MMs), should be considered. MMs are a group of diseases characterized by inadequate mitochondrial ATP production needed for the energetic requirement of the exercising muscles. Athletes with myalgia, fatigue, dyspnea, and muscular cramping should be questioned for history of rhabdomyolysis or myoglobinuria as well as detailed family history, given the predominant matrilinear inheritance of MMs. In all suspected cases, blood lactate and ventilatory response on effort plus muscle biospy for histologic and molecular studies are recommended. Therapeutic recommendations consist of a set of instructions including genetic counseling, awareness of possible myoglobinuric episodes, and controlled exercise training.     

Incremental exercise test design and analysis: implications for performance diagnostics in endurance athletes

Physiological variables, such as maximum work rate or maximal oxygen uptake (VO2max), together with other submaximal metabolic inflection points (e.g. the lactate threshold [LT], the onset of blood lactate accumulation and the pulmonary ventilation threshold [VT]), are regularly quantified by sports scientists during an incremental exercise test to exhaustion. These variables have been shown to correlate with endurance performance, have been used to prescribe exercise training loads and are useful to monitor adaptation to training. However, an incremental exercise test can be modified in terms of starting and subsequent work rates, increments and duration of each stage. At the same time, the analysis of the blood lactate/ventilatory response to incremental exercise may vary due to the medium of blood analysed and the treatment (or mathematical modelling) of data following the test to model the metabolic inflection points. Modification of the stage duration during an incremental exercise test may influence the submaximal and maximal physiological variables. In particular, the peak power output is reduced in incremental exercise tests that have stages of longer duration. Furthermore, the VT or LT may also occur at higher absolute exercise work rate in incremental tests comprising shorter stages. These effects may influence the relationship of the variables to endurance performance or potentially influence the sensitivity of these results to endurance training. A difference in maximum work rate with modification of incremental exercise test design may change the validity of using these results for predicting performance, and prescribing or monitoring training. Sports scientists and coaches should consider these factors when conducting incremental exercise testing for the purposes of performance diagnostics.     

Lactate distribution in the blood compartments of sickle cell trait carriers during incremental exercise and recovery

Whether or not whole blood lactate concentration is the same during a ramp exercise test in subjects with sickle cell trait (AS) as in normal subjects remains a point of controversy in the literature. Some studies have shown that the ability to produce or clear circulating lactate might differ between AS and subjects with normal haemoglobin (AA). If this is indeed so, the lactate distribution in the blood compartments should also differ. To test this hypothesis, lactate concentrations in the whole blood, plasma and red blood cells of AS and AA were compared at rest and in response to exercise. Eight AS and 8 AA performed an incremental exercise test. Whole blood, plasma and red blood cell lactate concentrations, the red blood cell : plasma lactate concentration ratio, the plasma-to-red blood cell lactate gradient, haematocrit and cardiorespiratory variables were analysed at rest and during an incremental exercise test and active recovery. Maximal oxygen uptake and ventilatory thresholds were similar in the two groups. No significant difference in whole blood, plasma or red blood cell lactate concentrations was observed between the two groups at rest, during exercise, or during the immediate recovery. Neither the red blood cell : plasma lactate concentration ratio nor the plasma-to-red blood cell lactate gradient differed between groups. Lactate distribution in the blood compartments did not differ between the two groups and this finding suggests that lactate production and/or clearance is quite similar during exercise in AS and AA.