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

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

Maximal voluntary hyperpnoea increases blood lactate concentration during exercise

Ventilatory work during heavy endurance exercise has not been thought to influence systemic lactate concentration. We evaluated the effect of maximal isocapnic volitional hyperpnoea upon arterialised venous blood lactate concentration ([lac⁻]_B) during leg cycling exercise at maximum lactate steady state (MLSS). Seven healthy males performed a lactate minimum test to estimate MLSS, which was then resolved using separate 30 min constant power tests (MLSS=207±8 W, mean ± SEM). Thereafter, a 30 min control trial at MLSS was performed. In a further experimental trial, the control trial was mimicked except that from 20 to 28 min maximal isocapnic volitional hyperpnoea was superimposed on exercise. Over 20–28 min minute ventilation, oxygen uptake, and heart rate during the control and experimental trials were 87.3±2.4 and 168.3±7.0 l min⁻¹ (P<0.01), the latter being comparable to that achieved in the maximal phase of the lactate minimum test (171.9±6.8 l min⁻¹), 3.46±0.20 and 3.83 ± 0.20 l min⁻¹ (P<0.01), and 158.5±2.7 and 166.8±2.7 beats min⁻¹ (P<0.05), respectively. From 20 to 30 min of the experimental trial [lac⁻]_B increased from 3.7±0.2 to 4.7±0.3 mmol l⁻¹ (P<0.05). The partial pressure of carbon dioxide in arterialised venous blood increased approximately 3 mmHg during volitional hyperpnoea, which may have attenuated the [lac⁻]_B increase. These results show that, during heavy exercise, respiratory muscle work may affect [lac⁻]_B. We speculate that the changes observed were related to the altered lactate turnover in respiratory muscles, locomotor muscles, or both.     

Extracellular pH defense against lactic acid in untrained and trained altitude residents

The assumption that buffering at altitude is deteriorated by bicarbonate (bi) reduction was investigated. Extracellular pH defense against lactic acidosis was estimated from changes (Δ) in lactic acid ([La]), [HCO₃ ⁻], pH and PCO₂ in plasma, which equilibrates with interstitial fluid. These quantities were measured in earlobe blood during and after incremental bicycle exercise in 10 untrained (UT) and 11 endurance-trained (TR) highlanders (2,600 m). During exercise the capacity of non-bicarbonate buffers (β _nbi = −Δ[La] · ΔpH⁻¹ − Δ[HCO₃ ⁻] · ΔpH⁻¹) amounted to 40 ± 2 (SEM) and 28 ± 2 mmol l⁻¹ in UT and TR, respectively (P < 0.01). During recovery β _nbi decreased to 20 (UT) and 16 (TR) mmol l⁻¹ (P < 0.001) corresponding to values expected from hemoglobin, dissolved protein and phosphate concentrations related to extracellular fluid (ecf). This was accompanied by a larger decrease of base excess after than during exercise for a given Δ[La]. β _bi amounted to 37–41 mmol l⁻¹ being lower than at sea level. The large exercise β _nbi was mainly caused by increasing concentrations of buffers due to temporary shrinking of ecf. Tr has lower β _nbi in spite of an increased Hb mass mainly because of an expanded ecf compared to UT. In highlanders β _nbi is higher than in lowlanders because of larger Hb mass and reduced ecf and counteracts the decrease in [HCO₃ ⁻]. The amount of bicarbonate is probably reduced by reduction of the ecf at altitude but this is compensated by lower maximal [La] and more effective hyperventilation resulting in attenuated exercise acidosis at exhaustion.     

Recovery from short term intense exercise: Its relation to capillary supply and blood lactate concentration

Summary Muscle force recovery from short term intense exercise was examined in 16 physically active men. They performed 50 consecutive maximal voluntary knee extensions. Following a 40-s rest period five additional maximal contractions were executed. The decrease in torque during the 50 contractions and the peak torque during the five contractions relative to initial torque were used as indices for fatigue and recovery, respectively. Venous blood samples were collected repeatedly up to 8 min post exercise for subsequent lactate analyses. Muscle biopsies were obtained from m. vastus lateralis and analysed for fiber type composition, fiber area, and capillary density. Peak torque decreased 67 (range 47–82%) as a result of the repeated contractions. Following recovery, peak torque averaged 70 (47–86%) of the initial value. Lactate concentration after the 50 contractions was 2.9±1.3 mmol·l⁻¹ and the peak post exercise value averaged 8.7±2.1 mmol·l⁻¹. Fatigue and recovery respectively were correlated with capillary density (r=−0.71 and 0.69) but not with fiber type distribution. A relationship was demonstrated between capillary density and post exercise/peak post exercise blood lactate concentration (r=0.64). Based on the present findings it is suggested that lactate elimination from the exercising muscle is partly dependent upon the capillary supply and subsequently influences the rate of muscle force recovery. Dr. Tesch was on leave from Department of Clinical Physiology, Karolinska Hospital, Stockholm, Sweden     

Extracellular bicarbonate and non-bicarbonate buffering against lactic acid during and after exercise

Defense of extracellular pH constancy against lactic acidosis can be estimated from changes (Δ) in lactic acid ([La]), [HCO₃⁻], pH and PCO₂ in blood plasma because it is equilibrated with the interstitial fluid. These quantities were measured in earlobe blood during and after incremental bicycle exercise in 13 untrained (UT) and 21 endurance-trained (TR) males to find out if acute and chronic exercise influence the defense. During exercise the capacity of non-bicarbonate buffers (β_nbi = −Δ[La] · ΔpH⁻¹ − Δ[HCO₃⁻] · ΔpH⁻¹) available for the extracellular fluid (mainly hemoglobin, dissolved proteins and phosphates) amounted to 32 ± 2(SEM) and 20 ± 2 mmol l⁻¹ in UT and TR, respectively (P < 0.02). During recovery β_nbi decreased to 14 (UT) and 12 (TR) mmol l⁻¹ (both P < 0.001) corresponding to values previously found at rest by in vivo CO₂ titration. Bicarbonate buffering (β_bi) amounted to 44–48 mmol l⁻¹ during and after exercise. The large exercise β_nbi seems to be mainly caused by an increasing concentration of all buffers due to shrinking of the extracellular volume, exchange of small amounts of HCO₃⁻ or H⁺ with cells and delayed HCO₃⁻ equilibration between plasma and interstitial fluid. Increase of [HCO₃⁻] during titration by these mechanisms augments total β and thus the calculated β_nbi more than β_bi because it reduces ΔpH and Δ[HCO₃⁻] at constant Δ[La]. The smaller rise in exercise β_nbi in TR than UT may be caused by an increased extracellular volume and an improved exchange of La⁻, HCO₃⁻ and H⁺ between trained muscles and blood.     

Lung oxidative stress as related to exercise and altitude. Lipid peroxidation evidence in exhaled breath condensate: a possible predictor of acute mountain sickness

Lung oxidative stress (OS) was explored in resting and in exercising subjects exposed to moderate and high altitude. Exhaled breath condensate (EBC) was collected under field conditions in male high-competition mountain bikers performing a maximal cycloergometric exercise at 670 m and at 2,160 m, as well as, in male soldiers climbing up to 6,125 m in Northern Chile. Malondialdehyde concentration [MDA] was measured by high-performance liquid chromatography in EBC and in serum samples. Hydrogen peroxide concentration [H₂O₂] was analysed in EBC according to the spectrophotometric FOX₂ assay. [MDA] in EBC of bikers did not change while exercising at 670 m, but increased from 30.0±8.0 to 50.0±11.0 nmol l⁻¹ (P<0.05) at 2,160 m. Concomitantly, [MDA] in serum and [H₂O₂] in EBC remained constant. On the other hand, in mountaineering soldiers, [H₂O₂] in EBC under resting conditions increased from 0.30±0.12 μmol l⁻¹ at 670 m to 1.14±0.29 μmol l⁻¹ immediately on return from the mountain. Three days later, [H₂O₂] in EBC (0.93 ±0.23 μmol l⁻¹) continued to be elevated (P<0.05). [MDA] in EBC increased from 71±16 nmol l⁻¹ at 670 m to 128±26 nmol l⁻¹ at 3,000 m (P<0.05). Changes of [H₂O₂] in EBC while ascending from 670 m up to 3,000 m inversely correlated with concomitant variations in HbO2 saturation (r=−0.48, P<0.05). AMS score evaluated at 5,000 m directly correlated with changes of [MDA] in EBC occurring while the subjects moved from 670 to 3,000 m (r=0.51, P<0.05). Lung OS may constitute a pathogenic factor in AMS.     

The effect of citrate loading on exercise performance,acid-base balance and metabolism

Summary Nine subjects ( 65±2 ml·kg⁻¹·min⁻¹, mean±SEM) were studied on two occasions following ingestion of 500 ml solution containing either sodium citrate (C, 0.300 g·kg⁻¹ body mass) or a sodium chloride placebo (P, 0.045 g·kg⁻¹ body mass). Exercise began 60 min later and consisted of cycle ergometer exercise performed continuously for 20 min each at power outputs corresponding to 33% and 66% , followed by exercise to exhaustion at 95% . Pre-exercise arterialized-venous [H⁺] was lower in C (36.2±0.5 nmol·l⁻¹; pH 7.44) than P (39.4±0.4 nmol·l⁻¹; pH 7.40); the plasma [H⁺] remained lower and [HCO ₃ ⁻ ] remained higher in C than P throughout exercise and recovery. Exercise time to exhaustion at 95% was similar in C (310±69 s) and P (313±74 s). Cardiorespiratory variables (ventilation, , , heart rate) measured during exercise were similar in the two conditions. The plasma [citrate] was higher in C at rest (C, 195±19 μmol·l⁻¹; P, 81±7 μmol·l⁻¹) and throughout exercise and recovery. The plasma [lactate] and [free fatty acid] were not affected by citrate loading but the plasma [glycerol] was lower during exercise in C than P. In conclusion, sodium citrate ingestion had an alkalinizing effect in the plasma but did not improve endurance time during exercise at 95% . Furthermore, citrate loading may have prevented the stimulation of lipolysis normally observed with exercise and prevented the stimulation of glycolysis in muscle normally observed in bicarbonate-induced alkalosis.     

Changes in blood lactate and respiratory gas exchange measures in sports with discontinuous load profiles

This study compares two different sport events (orienteering = OTC; tennis = TEC) with discontinuous load profiles and different activity/recovery patterns by means of blood lactate (LA), heart rate (HR), and respiratory gas exchange measures (RGME) determined via a portable respiratory system. During the TEC, 20 tennis-ranked male subjects [age: 26.0 (3.7) years; height: 181.0 (5.7) cm; weight: 73.2 (6.8) kg; maximal oxygen consumption (V˙O₂max): 57.3 (5.1) ml·kg⁻¹·min⁻¹] played ten matches of 50 min. During the OTC, 11 male members of the Austrian National Team [age: 23.5 (3.9) years; height: 183.6 (6.8) cm; weight: 72.4 (3.9) kg; V˙O₂max: 67.9 (3.8) ml·kg⁻¹·min⁻¹] performed a simulated OTC (six sections; average length: 10.090 m). In both studies data from the maximal treadmill tests (TT) were used as reference values for the comparison of energy expenditure of OTC and TEC. During TEC, the average V˙O₂ was considerably lower [29.1 (5.6) ml^·kg^−1·min⁻¹] or 51.1 (10.9)% of VO₂max and 64.8.0 (13.3)% of V˙O₂ determined at the individual anaerobic threshold (IAT) on the TT. The short high-intensity periods (activity/recovery = 1/6) did not result in higher LA levels [average LA of games: 2.07 (0.9) mmol·l⁻¹]. The highest average V˙O₂ value for a whole game was 47.8 ml·kg^−1·min⁻¹ and may provide a reference for energy demands required to sustain high-intensity periods of tennis predominately via aerobic mechanism of energy delivery. During OTC, we found an average V˙O₂ of 56.4 (4.5) ml·kg⁻¹·min⁻¹ or 83.0 (3.8)% of V˙O₂max and 94.6 (5.2)% of V˙O₂ at IAT. In contrast to TEC, LA were relatively high [5.16 (1.5) mmol·l⁻¹) although the average V˙O₂ was significantly lower than V˙O₂ at IAT. Our data suggest that portable RGEM provides valuable information concerning the energy expenditure in sports that cannot be interpreted from LA or HR measures alone. Portable RGEM systems provide valuable assessment of under- or over-estimation of requirements of sports and assist in the optimization and interpretation of training in athletes. Electronic Publication     

Carbohydrate feeding and exercise: effect of beverage carbohydrate content

Summary The purpose of this study was to determine the effect of ingesting fluids of varying carbohydrate content upon sensory response, physiologic function, and exercise performance during 1.25 h of intermittent cycling in a warm environment (T _db=33.4°C). Twelve subjects (7 male, 5 female) completed four separate exercise sessions; each session consisted of three 20 min bouts of cycling at 65% , with each bout followed by 5 min rest. A timed cycling task (1200 pedal revolutions) completed each exercise session. Immediately prior to the first 20 min cycling bout and during each rest period, subjects consumed 2.5 ml·kg BW⁻¹ of water placebo (WP), or solutions of 6%, 8%, or 10% sucrose with electrolytes (20 mmol·l⁻¹ Na⁺, 3.2 mmol·l⁻¹ K⁺). Beverages were administered in double blind, counterbalanced order. Mean (±SE) times for the 1200 cycling task differed significantly: WP=13.62±0.33 min, *6%=13.03±0.24 min, 8%=13.30±0.25 min, 10%=13.57±0.22 min (*=different from WP and 10%,P<0.05). Compared to WP, ingestion of the CHO beverages resulted in higher plasma glucose and insulin concentrations, and higher RER values during the final 20 min of exercise (P<0.05). Markers of physiologic function and sensory perception changed similarly throughout exercise; no differences were observed among subjects in response to beverage treatments for changes in plasma concentrations of lactate, sodium, potassium, for changes in plasma volume, plasma osmolality, rectal temperature, heart rate, oxygen uptake, rating of perceived exertion, or for indices of gastrointestinal distress, perceived thirst, and overall beverage acceptance. Compared to ingestion of a water placebo, consumption of beverages containing 6% to 10% sucrose resulted in similar physiologic and sensory response, while ingestion of the 6% sucrose beverage resulted in significantly improved end-exercise performance following only 60 min of intermittent cycling exercise.     

Gender differences in sweat lactate

Sweat rate may affect sweat lactate concentration. The current study examined potential gender differences in sweat lactate concentrations because of varying sweat rates. Males (n=6) and females (n=6) of similar age, percentage body fat, and maximal oxygen consumption (VO_2max) completed constant load (CON) cycling (30 min – approximately 40% VO_2max) and interval cycling (INT) (15 1-min intervals each separated by 1 min of rest) trials at 32 (1) °C wet bulb globe temperature (WBGT). Trials were preceded by 15 min of warm-up (0.5 kp, 60 rpms) and followed by 15 min of rest. Blood and sweat samples were collected at 15, 25, 35, 45, and 60 min during each trial. Total body water loss was used to calculate sweat rate. Blood lactate concentrations (CON ≅ 2 mmol · l⁻¹, INT ≅ 6 mmol · l⁻¹) and sweat lactate concentrations (CON and INT ≅ 12 mmol · l⁻¹) were not significantly different (P > 0.05) at any time between genders for CON or INT. Overall sweat rates (ml · h⁻¹) were not significantly different (P > 0.05) between trials but were significantly greater (P ≤ 0.05) for males than for females for CON [779.7 (292.6) versus 450.3 (84.6) ml · h⁻¹] and INT [798.0 (268.3) versus 503.0 (41.4) ml · h⁻¹]. However, correcting for surface area diminished the difference [CON: 390.7 (134.4) versus 277.7 (44.4) ml · h⁻¹, INT: 401.5 (124.1) versus 310.6 (23.4) ml · h⁻¹ (P ≤ 0.07)]. Estimated total lactate secretion was significantly greater (P ≤ 0.05) in males for CON and INT. Results suggest that sweat rate differences do not affect sweat lactate concentrations between genders. Accepted: 7 February 2000     

Substrate utilisation during exercise and shivering

It is generally assumed that exercise and shivering are analogous processes with regard to substrate utilisation and that, as a consequence, exercise can be used as a model for shivering. In the present study, substrate utilisation during exercise and shivering at the same oxygen consumption (V˙O₂) were compared. Following an overnight fast, eight male subjects undertook a 2-h immersion in cold water, designed to evoke three different intensities of shivering. At least 1 week later they undertook a 2-h period of bicycle ergometry during which the exercise intensity was varied to match the V˙O₂ recorded during shivering. During both activities hepatic glucose output (HGO), the rate of glucose utilisation (Rd), blood glucose, plasma insulin, free fatty acid (FFA) and beta-hydroxybutyrate (B-HBA) concentrations were measured. The V˙O₂ measured during the different levels of shivering averaged 0.49 l · min⁻¹ (level 1: low), 0.6 l · min⁻¹ (level 2: low-moderate), and 0.9 l · min⁻¹ (level 3: moderate), and corresponded closely to the levels measured during exercise. HGO and Rd were greater (P < 0.05) during exercise than during shivering at the same V˙O₂ (9.5% and 14.7%, respectively). The average (SD) HGO during level 3 exercise was 3.0 (0.91) mg · kg⁻¹ . min⁻¹ compared to 2.76 (1.0) mg · kg⁻¹ . min⁻¹ during shivering. The values for Rd were 3.06 (0.98) mg · kg⁻¹ · min⁻¹ during level 3 exercise and 2.68 (0.82) mg · kg⁻¹ · min⁻¹ during shivering. Blood glucose levels did not differ between conditions, averaging 5.4 (0.3) mmol . l⁻¹ over all levels of shivering and 5.2 (0.3) mmol · l⁻¹ during exercise. Plasma FFA and B-HBA were higher (P < 0.01) during shivering than during corresponding exercise (12.3% and 33.3%, respectively). FFA averaged 0.61 (0.2) mmol · l⁻¹ over all levels of shivering and 0.47 (0.16) mmol · l⁻¹ during exercise. The figures for B-HBA were 0.44 (0.13) mmol · l⁻¹ during all levels of shivering and 0.32 (0.1) mmol · l⁻¹ during exercise. Plasma insulin was higher (P < 0.05) during level 2 and 3 shivering compared to corresponding exercise; at these levels the average value for plasma insulin was 95.9 (21.9) pmol · l⁻¹ during shivering and 80.6 (16.1) pmol · l⁻¹ during exercise. On the basis of the present findings it is concluded that, with regard to substrate utilisation, shivering and exercise of up to 2 h duration should not be regarded as analogous processes. Accepted: 12 February 1997     

Methodological aspects of maximal lactate steady state—implications for performance testing

The maximal lactate steady state (MLSS) is the highest blood lactate concentration (BLC) that can be identified as maintaining a steady-state during a prolonged submaximal constant workload. Comparative interpretation of published data about MLSS is complicated by the fact that different methods of testing have been utilized. Thus, three methods, corresponding to the time course of changes in BLC incurred during either 30 min (MLSS I) or 20 min (MLSS II and III) of constant submaximal workload exercise, were compared in 26 male subjects [mean (SD) age 24.6 (5.6) years, height 181.6 (4.9) cm, body mass 74.4 (5.2) kg]. MLSS I [5.1 (1.3) mmol·l^-1], II [4.9 (1.3) mmol·l^-1], and III [4.3 (1.3) mmol·l^-1] were different (P<0.01). The workload corresponding to MLSS III [244.8 (44.0) W] was lower (P<0.01) than that at MLSS I [254.0 (40.8) W] and II [251.9 (40.4) W]. No difference could be confirmed between the workloads established for MLSS I and MLSS II. The differences between MLSS I, MLSS II, and MLSS III and corresponding workloads reflect insufficient contribution to lactate kinetics by testing procedures that depend strongly upon the time course of changes in BLC during the initial 20–25 min of constant-workload exercise. Based on the present findings, constant-load tests lasting at least 30 min and a BLC increase of no more than 1.0 mmol·l^-1 after the 10th testing minute appear to be the most reasonable with respect to valid testing results. Electronic Publication     

Plasma norepinephrine and heart rate dynamics during recovery from submaximal exercise in man

Summary The time course of heart rate (HR) and venous blood norepinephrine concentration [NE], as an expression of the sympathetic nervous activity (SNA), was studied in six sedentary young men during recovery from three periods of cycle ergometer exercise at 21%±2.8%, 43%±2.1% and 65%±2.3% of respectively (mean±SE). The HR decreased mono-exponentially withτ values of 13.6±1.6 s, 32.7±5.6 s and 55.8±8.1s respectively in the three periods of exercise. At the low exercise level no change in [NE] was found. At medium and high exercise intensity: (a) [NE] increased significantly at the 5th min of exercise (Δ[NE]=207.7±22.5 pg·ml⁻¹ and 521.3±58.3 pg·ml⁻¹ respectively); (b) after a time lag of 1 min [NE] decreased exponentially (τ=87 s and 101 s respectively); (c) in the 1st min HR decreased about 35 beats · min⁻¹; (d) from the 2nd to 5th min of recovery HR and [NE] were linearly related (100 pg·ml⁻¹ Δ[NE]5 beats ·min⁻¹). In the 1st min of recovery, independent of the exercise intensity, the adjustment of HR appears to have been due mainly to the prompt restoration of vagal tone. The further decrease in HR toward the resting value could then be attributed to the return of SNA to the pre-exercise level.     

Heart rate is lower during ergometer rowing than during treadmill running

This study evaluated whether the heart rate (HR) response to exercise depends on body position and on the active muscle mass. The HR response to ergometer rowing (sitting and using both arms and legs) was compared to treadmill running (upright exercise involving mainly the legs) using a progressive exercise intensity protocol in 55 healthy men [mean (SD) height 176 (5) cm, body mass 71 (6) kg, age 21 (3) years]. During rowing HR was lower than during running at a blood lactate concentration of 2 mmol·l^–1 [145 (13) compared to 150 (11) beat·min^–1, P<0.05], 4 mmol·l^–1 [170 (10) compared to 177 (13) beat·min^–1, P<0.05], and 6 mmol·l^–1 [182 (10) compared to 188 (10) beat·min^–1, P<0.05]. Also during maximal intensity rowing, HR was lower than during maximal intensity running [194 (9) compared to 198 (11) beat·min^–1, P<0.05]. These results were accompanied by a higher maximal oxygen uptake during rowing than during running [rowing compared to running, 4.50 (0.5) and 4.35 (0.4) l·min^–1, respectively, P<0.01]. Thus, the oxygen pulse, as an index of the stroke volume of the heart, was higher during rowing than during running at any given intensity. The results suggest that compared to running, the seated position and/or the involvement of more muscles during rowing facilitate venous return and elicit a smaller HR response for the same relative exercise intensity. Electronic Publication     

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 (Rep_max), the total work (W _tot) 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?·?l^?1] and in the women [11.7 (SD 7.4) nmol?·?l^?1], was clearly the highest in E20, where also the Rep_max, W _tot, 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?·?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?·?l^?1] and in the women [5.2 (SD 2.0) nmol?·?l^?1] were higher than in E80 [men 3.1 (SD 4.2), women 2.1 (SD 2.0) nmol?·?l^?1] (P??1] and E40 [men 3.8 (SD 4.1), women 5.8 (SD 4.0) nmol?·?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.     

Extracellular pH defense against lactic acid in normoxia and hypoxia before and after a Himalayan expedition

The extracellular pH defense against the lactic acidosis resulting from exercise can be estimated from the ratios −Δ[La] · ΔpH⁻¹ (where Δ[La] is change in lactic acid concentration and ΔpH is change in pH) and Δ[HCO₃ ⁻] · ΔpH⁻¹ (where Δ[HCO₃ ⁻] is change in bicarbonate concentration) in blood plasma. The difference between −Δ[La] · ΔpH⁻¹ and Δ[HCO₃ ⁻] · ΔpH⁻¹ yields the capacity of available non-bicarbonate buffers (mainly hemoglobin). In turn, Δ[HCO₃ ⁻] · ΔpH⁻¹ can be separated into a pure bicarbonate buffering (as calculated at constant carbon dioxide tension) and a hyperventilation effect. These quantities were measured in 12 mountaineers during incremental exercise tests before, and 7–8 days (group 1) or 11–12 days (group 2) after their return from a Himalayan expedition (2800–7600 m altitude) under conditions of normoxia and acute hypoxia. In normoxia −Δ[La] · ΔpH⁻¹ amounted to [mean (SEM)] 92 (6) mmol · l⁻¹ before altitude, of which 19 (4), 48 (1) and 25 (3) mmol · l⁻¹ were due to hyperventilation, bicarbonate and non-bicarbonate buffering, respectively. After altitude −Δ[La] · ΔpH⁻¹ was increased to 128 (12) mmol · l⁻¹ (P < 0.01) in group 1 and decreased to 72 (5) mmol · l⁻¹ in group 2 (P < 0.05), resulting mainly from apparent large changes of non-bicarbonate buffer capacity, which amounted to 49 (14) mmol · l⁻¹ in group 1 and to 10 (2) mmol · l⁻¹ in group 2. In acute hypoxia the apparent increase in non-bicarbonate buffers of group 1 was even larger [140 (18) mmol · l⁻¹]. Since the hemoglobin mass was only modestly elevated after descent, other factors must play a role. It is proposed here that the transport of La⁻ and H⁺ across cell membranes is differently influenced by high-altitude acclimatization. Accepted: 14 September 2000     

Effects of anaemia and stepwise-induced polycythaemia on maximal aerobic power in individuals with high and low haemoglobin concentrations

Increasing the haemoglobin concentration ([Hb]) improves the oxygen transport capacity but it also increases the viscosity of the blood. The influence of changes in [Hb] and viscosity on submaximal exercise capacity and maximal aerobic power was investigated in eight healthy males in varying states of training and with a normal resting [Hb] ([Hb]_r), ranging from 123 to 178 g]^-1. The subjects were venesected five times (450 ml per unit) and exercise tests were performed in the anaemic state. After 5–7 weeks, when [Hb] had returned to the ‘normal’ value, a stepwise re-transfusion of three to five units of blood was performed with exercise tests after each transfusion. The [Hb]_r was 137 ± 15 g l^-1 in the anaemic state (A) and 170 ± 16 g l^-1 after the last re-transfusion (LT). The V_o2max rose from 3.94 ± 0.35 in A to 4.68 ± 0.30 1 min^-1 after LT. Individual regression lines for [Hb] and V_o2max revealed a mean increase in V_o2max of 19 ± 6 ml min^-1 per g l^-1 change in [Hb]. This value did not differ between individuals with high and low normal [Hb]. Furthermore, in intra-individual comparisons the relationship between [Hb] and V_o2max in high and low individual [Hb] ranges was not found to be statistically different despite a 40% increase in the in vitro viscosity from the anaemic to the polycythaemic state. The average individual correlation (based on five to seven measurements) between [Hb] at rest and after exercise and V_o2max was r= 0.89 (P > 0.01) in the former case and r= 0.92 (P > 0.01) in the latter. The running velocity corresponding to a blood lactate concentration of 4 mM (V_Hla4.0) increased from 15.3 ± 2.3 in the control state to 15.6±2.3 km h¹ after the last transfusion (P > 0.01). A leftward shift of the blood lactate curve, expressed as a percentage of V_o2max, was found. In conclusion, the results obtained indicate a close relationship between V_o2max and [Hb] up to at least 170 g l^-1. Furthermore, both inter-and intra-individual comparisons suggest that the influence of viscosity as such on V_o2max does not differ at high and low [Hb] levels.     

Assessment of post-competition peak blood lactate in male and female master swimmers aged 40–79 years and its relationship with swimming performance

The main purpose of this study was to measure the post-competition blood lactate concentration ([La]_b) in master swimmers of both sexes aged between 40 and 79 years in order to relate it to age and swimming performance. One hundred and eight swimmers participating in the World Master Championships were assessed for [La]_b and the average rate of lactate accumulation (La′; mmol l⁻¹ s⁻¹) was calculated. In addition, 77 of them were also tested for anthropometric measures. When the subjects were divided into 10-year age groups, males exhibited higher [La]_b than women (factorial ANOVA, P < 0.01) and a steeper decline with ageing than female subjects. Overall, mean values (SD) of [La]_b were 10.8 (2.8), 10.3 (2.0), 10.3 (1.9), 8.9 (3.2) mmol l⁻¹ in women, and 14.2 (2.5), 12.4 (2.5), 11.0 (1.6), 8.2 (2.0) mmol l⁻¹ in men for, respectively, 40–49, 50–59, 60–69, 70–79 years’ age groups. When, however, [La]_b values were normalised for a “speed index”, which takes into account swimming speed as a percentage of world record, these sex-related differences, although still present, were considerably attenuated. Furthermore, the differences in La′ between males and females were larger in the 40–49 age group (0.34 vs 0.20 mmol l⁻¹ s⁻¹ for 50-m distance) than in the 70–79 age group (0.12 vs 0.14 mmol l⁻¹ s⁻¹ for 50-m distance). Different physiological factors, supported by the considered anthropometric measurements, are suggested to explain the results.     

Influence of recovery manipulation after hyperlactemia induction on the lactate minimum intensity

This study analyzed the influence of recovery phase manipulation after hyperlactemia induction on the lactate minimum intensity during treadmill running. Twelve male runners (24.6 ± 6.3 years; 172 ± 8.0 cm and 62.6 ± 6.1 kg) performed three lactate minimum tests involving passive (LMT_P) and active recoveries at 30%vVO_2max (LMT_A30) and 50%vVO_2max (LMT_A50) in the 8-min period following initial sprints. During subsequent graded exercise, lactate minimum speed and VO₂ in LMT_A50 (12.8 ± 1.5 km h⁻¹ and 40.3 ± 5.1 ml kg⁻¹ min⁻¹) were significantly lower (P < 0.05) than those in LMT_A30 (13.3 ± 1.6 km h⁻¹ and 42.9 ± 5.3 ml kg⁻¹ min⁻¹) and LMT_P (13.8 ± 1.6 km h⁻¹ and 43.6 ± 6.1 ml kg⁻¹ min⁻¹). In addition, lactate minimum speed in LMT_A30 was significantly lower (P < 0.05) than that in LMT_P. These results suggest that lactate minimum intensity is lowered by active recovery after hyperlactemia induction in an intensity-dependent manner compared to passive recovery.