Running economy of elite surf iron men and male runners, on soft dry beach sand and grass

The primary aim of this study was to measure the energetics of six elite surf iron men (who participate in regular sand running training), performing steady-state running trials on grass in shoes at 8, 11 and 14 km·h^–1, and on sand bare foot and in shoes, at both 8 and 11 km·h^–1. The net total energy cost (EC, J·kg^–1·m^–1) was determined from the net steady-state oxygen consumption and respiratory exchange ratio (net aerobic EC) plus net lactate accumulation (net anaerobic EC). For the sand barefoot and sand in shoes running trials at 8 and 11 km·h^–1, net aerobic EC and total net EC (but not anaerobic EC) were significantly greater (P<0.001) than the grass running trial values. No differences (P>0.05) existed between the sand barefoot and sand in shoes trials. These measures were compared with data obtained from eight well-trained male recreational runners who performed the same protocol in a previous study, but who were not accustomed to running on sand. Comparisons of net aerobic EC between the two groups for the surface conditions were not significantly different (P>0.05). For net anaerobic EC, the iron man values were significantly less (P<0.02) than the recreational runner values. For net total EC, the iron man values were less than the recreational runner values, but the differences were only significant when both groups ran on sand barefoot (P<0.03: on grass P=0.158; on sand in shoes P=0.103). The lower lactate accumulation values recorded for the iron men on both grass and sand may indicate that running on sand potentially reduces metabolic fatigue when running on firm or soft surfaces. Electronic Publication     

Blood lactate and sEMG at different knee angles during fatiguing leg press exercise

The purpose of this study was to examine the changes in peak power output, blood lactate concentrations and surface electromyographic activity (sEMG) of the agonist [vastus lateralis (VL) and vastus medialis (VM)] and the antagonist [biceps femoris (BF)] muscles at two angular positions intervals (90–67° and 23–0° of knee flexion), during a set of 10 repetitions leading to failure of bilateral leg press exercise. Fatiguing exercise resulted in increased blood lactate concentrations, the agonist mean rectified voltage (MRV) at 90–67° of flexion, the antagonist average MRV at 23–0° of flexion and the spectral parameter proposed by Dimitrov (FI_nsm5) (P < 0.01–0.05). Significant decreases (P < 0.01–0.05) were observed in power output, median frequency (F_med) of the agonist muscles at both angular position intervals and of the antagonist muscle at 90–67° of flexion. No changes were observed in the antagonist/agonist MRV activation ratio. The present data suggest that the shift of frequency spectrum to lower frequencies and the accumulation of lactate and/or H⁺, but not the antagonist/agonist MRV activation ratio, may be relevant independent factors associated with fatigue.     

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.     

The relationship between critical velocity, maximal lactate steady-state velocity and lactate turnpoint velocity in runners

In cycle exercise, it has been suggested that critical power, maximal lactate steady state, and lactate turnpoint all demarcate the transition between the heavy exercise domain (in which blood lactate is elevated above resting values but remains stable over time) and the very heavy exercise domain (in which blood lactate increases continuously throughout constant-intensity exercise). The purpose of the present study was to assess the level of agreement between critical velocity (CV), maximal lactate steady-state velocity (MLSSV), and lactate turnpoint velocity (LTPV) during treadmill running. Eight male subjects [mean (SD) age 28 (5) years, body mass 71.2 (8.0) kg, maximum oxygen uptake 54.9 (3.2) ml·kg^–1·min^–1) performed an incremental treadmill test for the determination of LTPV (defined as a sudden and sustained increase in blood lactate concentration ([La]) at ≅2.0–5.0 mM). The subjects returned to the laboratory on eight or nine occasions for the determination of CV and MLSSV. The CV was determined from four treadmill runs at velocities that were chosen to result in exhaustion within 2–12 min. The MLSSV was determined from four or five treadmill runs of up to 30 min duration and defined as the highest velocity at which blood [La] increased by no more than 1.0 mM after between 10 and 30 min of exercise. Analysis of variance revealed no significant differences between [mean (SD)] CV [14.4 (1.1) km·h^–1], MLSSV [13.8 (1.1) km·h^–1] and LTPV [13.7 (0.6) km·h^–1]. However, the bias ±95% limits of agreement for comparisons between CV and MLSSV [0.6 (2.2) km·h^–1], CV and LTPV [0.7 (2.7) km·h^–1], and MLSSV and LTPV [0.1 (1.8) km·h^–1] suggest that the extent of disagreement is too great to allow one variable to be estimated accurately from another in individual subjects. Direct determination of MLSSV is necessary if precision is required in experimental studies. Electronic Publication     

Lactate disposal in resting trained and untrained forearm skeletal muscle during high intensity leg exercise

Summary At a given oxygen uptake ( O₂) and exercise intensity blood lactate concentrations are lower following endurance training. While decreased production of lactate by trained skeletal muscle is the commonly accepted cause, the contribution from increased lactate removal, comprising both uptake and metabolic disposal, has been less frequently examined. In the present study the role of resting skeletal muscle in the removal of an arterial lactate load (approximately 11 mmol·-l^–1) generated during high intensity supine leg exercise (20 min at approximately 83% maximal oxygen uptake) was compared in the untrained (UT) and trained (T) forearms of five male squash players. Forearm blood flow and the venoarterial lactate concentration gradient were measured and a modified form of the Fick equation used to determine the relative contributions to lactate removal of passive uptake and metabolic disposal. Significant lactate uptake and disposal were observed in both forearms without any change in forearm O₂. Neither the quantity of lactate taken up [UT, 344.2 (SEM 118.8) mol·100 ml^–1; T, 330.3 (SEM 85.3) mol·100 ml^–1] nor the quantity disposed of [UT, 284.0 (SEM 123.3) mol·100 ml^–1, approximately 83% of lactate uptake; T, 300.8 (SEM 77.7) mol·100 ml^–1, approximately 91% of lactate uptake] differed between the two forearms. It is concluded that while significant lactate disposal occurs in resting skeletal muscle during high intensity exercise the lower blood lactate concentrations following endurance training are unlikely to result from an increase in lactate removal by resting trained skeletal muscle.     

Cardiovascular reflexes during sustained handgrip exercise: role of muscle fibre composition,potassium and lactate

Summary Six healthy men performed sustained static handgrip exercise for 2 min at 40% maximal voluntary contraction followed by a 6-min recovery period. Heart rate (f _c), arterial blood pressures, and forearm blood flow were measured during rest, exercise, and recovery. Potassium ([K⁺]) and lactate concentrations in blood from a deep forearm vein were analysed at rest and during recovery. Mean arterial pressure (MAP) andf _c declined immediately after exercise and had returned to control levels about 2 min into recovery. The time course of the changes in MAP observed during recovery closely paralleled the changes in [K⁺] (r=0.800,P<0.01), whereas the lactate concentration remained elevated throughout the recovery period. The close relationship between MAP and [K⁺] was also confirmed by experiments in which a 3-min arterial occlusion period was applied during recovery to the exercised arm by an upper arm cuff. The arterial occlusion affected MAP whilef _c recovered at almost the same rate as in the control experiment. Muscle biopsies were taken from the brachioradialis muscle and analysed for fibre composition and capillary supply. The MAP at the end of static contraction and the [K⁺] appearing in the effluent blood immediately after contraction were positively correlated to the relative content of fast twitch (% FT) fibres (r=0.886 for MAP vs %FT fibres,P<0.05 andr=0.878 for [K⁺] vs %FT fibres,P<0.05). Capillary to fibre ratio showed an inverse correlation to % FT fibres (r=–0.979,P<0.01). These results indicated that activation of FT rather than slow twitch fibres during static contraction induced a more marked arterial pressure reflex. It was concluded that the arterial pressure reflex would seem to be mediated through stimulation of unmyelinized free nerve endings in the contracted muscle. The [K⁺] would appear to be a more likely candidate than lactate as a mediator for this pressure reflex.     

Venous blood lactate increase after vertical jumping in volleyball athletes

The aim of this study was to test the hypothesis that venous blood lactate concentrations ([La^–]) would vary from the beginning of brief exercise. Maximal vertical jumping was used as a model of brief intense exercise. Eleven healthy male volleyball players, aged [mean (SE)] 18.5 (0.7) years, performed three exercise tests with different protocols, each separated by quiet seated recovery periods of 45 min. After the first test, consisting of a single maximal jump [lasting ≅0.6 s for the pushing phase, and in which the subjects jumped 64 (2.2) cm], forearm venous [La^–] increased significantly with respect to rest at 1 min (t ₁), 3 min (t ₃), and 5 min (t ₅) of recovery. The second test, comprising six maximal jumps, each separated by 20-s recovery periods, resulted in an unchanged [La^–] with respect to the baseline value. After the third test [i.e., six consecutive maximal jumps that lasted a total of 7.36 (0.33) s], [La^–] increased significantly at t ₃ and t ₅ with respect to the pre-test value (F=10.3, P<0.001). We conclude that a significant venous [La^–] increase occurs after vertical jumping. This result may be explained by the activation of lactic anaerobic metabolism at the very onset of exercise, which participates in energy production and/or in the resynthesis of the phosphocreatine that was used during such brief exercise. Electronic Publication     

Rowing prevents muscle wasting in older men

We evaluated the effects of rowing on the morphology and function of the leg extensor muscle in old people. The area and the power of the leg extensor muscle were measured in 15 oarsmen – age [mean (SD)] 65 (3) years; height 171 (4) cm, body mass 68 (6) kg – and in 15 sedentary men – age 66 (4) years, height 170 (4) cm, body mass 67 (7) kg – who were matched on the basis of their body size. The leg extensor muscle area of the oarsmen was larger than that of the sedentary men [77.8 (5.4) vs 68.4 (5.1) cm², P<0.05]. Also the bilateral leg extension power of the oarsmen was larger than that of the sedentary men [1,624 (217) vs 1,296 (232) W, P<0.05]. Thus, the leg extension power per the leg extensor muscle area was not significantly different between two groups [20.9 (2.0) vs 19.9 (2.1) W·cm^–2) and leg extension power was correlated to the leg extensor muscle area (59–89 cm², r=0.74, P<0.001). Also the 2,000-m rowing ergometer time of the oarsmen [495 (14) s; range 479–520 s] was related to leg extensor muscle area (68–89 cm², r=0.63, P<0.01). The results suggest that rowing prevents age-related muscle wasting and weakness. Electronic Publication     

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     

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.     

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     

Effects of high-altitude exposure on vascular endothelial growth factor levels in man

Vascular endothelial growth factor (VEGF) is an endothelial cell mitogen and permeability factor that is inducible by hypoxia. Its contribution to high-altitude illness in man is unknown. We measured VEGF levels in 14 mountaineers at low altitude (490 m) and 24 h after their arrival at high altitude (4,559 m). At high altitude, VEGF increased from [mean (SEM)] 32.5 (9.2) to 60.9 (18.5) pg·ml^–1 (P<0.004) in the arterial blood, and from 15.9 (2.9) to 49.3 (15.9) pg·ml^–1 (P=0.0001) in the mixed venous blood. Whereas at low altitude venous and arterial VEGF levels were not statistically different from each other (P=0.065), the VEGF concentration was significantly lower in venous than in arterial blood samples at high altitude (P=0.004). The pulmonary capillary VEGF concentration remained unchanged at high altitude [14.8 (2.5) vs 17.1 (5.4) pg·ml^–1, P=0.85]. VEGF levels in the nine mountaineers who developed symptoms of acute mountain sickness (AMS), and in the six subjects who had radiographic evidence of high-altitude pulmonary edema were similar to those in subjects without symptoms. VEGF was not correlated with either AMS scores, mean pulmonary arterial pressures, arterial partial pressure of O₂, or alveolar-arterial O₂ gradients. We conclude that VEGF release is stimulated at high altitude, but that VEGF is probably not related to high-altitude illness. Electronic Publication     

Influence of prolonged continuous exercise on hormone responses to subsequent exercise in humans

This study examined the possibility that fatigue may modify the hormone responses to exercise. A group of 12 endurance trained athletes ran for 2 h (blood lactate concentrations of approximately 2 mmol·l^–1) in order to induce fatigue. The subjects exercised for 10 min at 70% maximal oxygen uptake before (1st test) and after (2nd test) the 2 h run to assess hormone responsiveness. A 1 min anaerobic power test was performed to assess muscle power. Cortisol, growth hormone, testosterone and insulin concentrations were determined before and after the 1st and 2nd tests. The 1st test resulted in increases in concentrations (P<0.05) of cortisol and growth hormone, a decrease in insulin concentration (P<0.01) and no change in testosterone concentration. The 2 h run caused decreases of insulin, increases of growth hormone concentration and variable responses in the concentrations of cortisol and testosterone. The 2nd test decreased insulin concentration further (P<0.05), but responses of the concentrations of testosterone, growth hormone and cortisol were variable. In 6 subjects (group A) cortisol displayed an increase [mean (SD)] from baseline concentrations [+304.0 (60.0) nmol·l^–1], while in the other 6 subjects (group B) a decrease or no change was seen [+3.1 (5.3) nmol·l^–1 ,between groups, P<0.05]. Growth hormone concentration was substantially higher in group A [+14.7 (4.8) ng·ml^–1] than group B [+6.0 (2.9) ng·ml^–1] following the 2nd test. In group A anaerobic muscle power was higher, while in group B it was lower, after the 2 h run than before the 2 h run (P<0.05). The findings suggest that fatigue from prolonged endurance activity may introduce a resetting in the pituitary-adrenocortical component of the endocrine system, expressed either by intensified or by suppressed endocrine functions. Electronic Publication     

Effect of short-term endurance training on exercise capacity,haemodynamics and atrial natriuretic peptide secretion in heart transplant recipients

Exercise tolerance of heart transplant patients is often limited. Central and peripheral factors have been proposed to explain such exercise limitation but, to date, the leading factors remain to be determined. We examined how a short-term endurance exercise training programme may improve exercise capacity after heart transplantation, and whether atrial natriuretic peptide (ANP) release may contribute to the beneficial effects of exercise training by minimizing ischaemia and/or cardiac and circulatory congestion through its vasodilatation and haemoconcentration properties. Seven heart transplant recipients performed a square-wave endurance exercise test before and after 6 weeks of supervised training, while monitoring haemodynamic parameters, ANP and catecholamine concentrations. After training, the maximal tolerated power and the total mechanical work load increased from 130.4 (SEM 6.5) to 150.0 (SEM 6.0) W (P < 0.05) and from 2.05 (SEM 0.1) to 3.58 (SEM 0.14) kJ · kg⁻¹ (P < 0.001). Resting heart rate decreased from 100.0 (SEM 3.4) to 92.4 (SEM 3.5) beats · min⁻¹ (P < 0.05) but resting and exercise induced increases in cardiac output, stroke volume, right atrial, pulmonary capillary wedge, systemic and pulmonary artery pressures were not significantly changed by training. Exercise-induced decrease of systemic vascular resistance was similar before and after training. After training arterio-venous differences in oxygen content were similar but maximal lactate concentrations decreased from 6.20 (SEM 0.55) to 4.88 (SEM 0.6) mmol · 1⁻¹ (P < 0.05) during exercise. Similarly, maximal exercise noradrenaline concentration tended to decrease from 2060 (SEM 327) to 1168 (SEM 227) pg · ml⁻¹. A significant correlation was observed between lactate and catecholamines concentrations. The ANP concentration at rest and the exercise-induced ANP concentration did not change throughout the experiment [104.8 (SEM 13.1) pg · ml⁻¹ vs 116.0 (SEM 13.5) pg · ml⁻¹ and 200.0 (SEM 23.0) pg · ml⁻¹ vs 206.5 (SEM 25.9) pg · ml⁻¹ respectively]. The results of this study suggested that the significant improvement in exercise capacity observed after this short-term endurance training period may have arisen mainly through peripheral mechanisms, associated with the possible decrease in plasma catecholamine concentrations and reversal of muscle deconditioning and/or prednisone-induced myopathy.     

Effect of liver disease on the kinetics of lactate removal after heavy exercise

Summary Recovery from heavy exercise requires clearance of lactic acid from the blood and body tissues. Although it has long been felt that the liver plays the major role in lactate removal, it has more recently been asserted that skeletal muscle plays the dominant role. We felt it relevant to this controversy to determine whether patients with liver dysfunction have slowed lactate removal following heavy exercise. Eight patients with alcoholic liver disease and 5 normal subjects were studied. Liver function was measured by the¹⁴C-aminopyrine breath test; the results were expressed as the rate of appearance of¹⁴CO₂ in the breath two hours after ingestion, as a fraction of the ingested¹⁴C dose (%·h⁻¹). Each participant exercised on a cycle ergometer for 7 min at a work rate which was moderately heavy for that subject (mean peak lactate=5.3 mmol·L⁻¹). During, and for 45 minutes after exercise, blood was drawn from a hand vein catheter. The time required for blood lactate to decrease halfway toward resting levels (t_1/2LA) was determined. Compared to the normal subjects and historical controls, seven of the patients had distinctly slowed lactate removal. The t_1/2LA was as long as 46 min (as compared to approximately 15 min seen normally). Further, among the patients the 2 h breath excretion of¹⁴C was well correlated with the rate constant of lactate removal (r=0.82,P<0.01). Four of the patients with severe liver dysfunction performed a second exercise test in which, instead of resting after heavy exercise, low level exercise was continued. The t_1/2LA of the averaged responses decreased by 29%. We conclude that liver disease slows lactate removal at rest. Lactate removal during continued exercise is less severely impaired.     

Beta-endorphin immunoreactivity during high-intensity exercise with and without opiate blockade

Nine highly fit men [mean (SE) maximum oxygen uptake, : 63.9 (1.7) ml·kg^–1·min^–1; age 27.6 (1.6) years] were studied during two treadmill exercise trials to determine plasma β-endorphin immunoreactivity during intense exercise (80% ). A double-blind experimental design was used, and subjects performed the two exercise trials in counterbalanced order. Exercise trials were 30 min in duration and were conducted 7 days apart. One exercise trial was undertaken following administration of naloxone (1.2 mg; 3 cm³) and the other after receiving a placebo (0.9% NaCl saline; 3 cm³). Prior to each experimental trial, a flexible catheter was placed into an antecubital vein and baseline blood samples were collected. Thereafter, each subject received either a naloxone or placebo bolus injection. Blood samples were also collected after 10, 20 and 30 min of continuous exercise. β-Endorphin was higher (P<0.05) during exercise when compared to pre-exercise in both trials. However, no statistically significant difference was found (P>0.05) between exercise time points within either experimental trial. β-endorphin immunoreactivity was greater (P<0.05) in the naloxone than in the placebo trial during each exercise sampling time point [10 min: 63.7 (3.9) pg·ml^–1 vs 78.7 (3.8) pg·ml^–1; 20 min: 68.7 (4.1) pg·ml^–1 vs 83.8 (4.3) pg·ml^–1; 30 min: 71.0 (4.3) pg·ml^–1 vs 82.5 (3.2) pg·ml^–1]. These data suggest that intense exercise induces significant increases in β-endorphin that are maintained over time during steady-rate exercise. Exercise and naloxone had an interactive effect on β-endorphin release that warrants further investigation. Electronic Publication     

Local and systemic effects on blood lactate concentration during exercise with small and large muscle groups

To evaluate the relationship between lactate release and [lac]_art and to investigate the influence of the catecholamines on the lactate release, 14 healthy men [age 25±3 (SE) year] were studied by superimposing cycle on forearm exercise, both at 65% of their maximal power reached in respective incremental tests. Handgrip exercise was performed for 30 min at 65% of peak power. In addition, between the tenth and the 22nd minute, cycling with the same intensity was superimposed. The increase in venous lactate concentration ([lac]_ven) (rest: 1.3±0.4 mmol·l⁻¹; 3rd min: 3.9±0.8 mmol·l⁻¹) begins with the forearm exercise, whereas arterial lactate concentration ([lac]_art) remains almost unchanged. Once cycling has been added to forearm exercise (COMB), [lac]_art increases with a concomitant increase in [lac]_ven (12th min: [lac]_art, 3.2±1.3 mmol·l⁻¹; [lac]_ven, 5.7±2.2 mmol·l⁻¹). A correlation between oxygen tension (P_vO₂) and [lac]_ven cannot be detected. There is a significant correlation between [lac]_art and norepinephrine ([NE]) (y=0.25x+1.2; r=0.815; p<0.01) but no correlation between lactate release and epinephrine ([EPI]) at moderate intensity. Our main conclusion is that lactate release from exercising muscles at moderate intensities is neither dependent on P_vO₂ nor on [EPI] in the blood.     

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     

Cardiac output and oxygen uptake relationship during physical effort in men and women over 60 years old

This study investigated the relationship between oxygen uptake (VO₂), cardiac output (Q), stroke volume (SV), and heart rate (HR) in 54 men and 77 women (age = 69 ± 5 years) during incremental effort. Subjects performed a maximal cycle-ergometer test and VO₂ was directly measured. HR and SV were assessed by ECG and cardiograph impedance. Regression equations were calculated for Q–VO₂, HR–VO₂, and Q–HR relationships. The equations obtained for women were (a) Q (l min⁻¹) = 2.61 + 4.67 VO₂ (l min⁻¹)(r ² = 0.84); (b) HR (bpm) = 62.03 + 46.55 VO₂ (l min⁻¹) (r ² = 0.72); (c) \textSV \text(ml)=100.6[1- \texte^{-2.6  \textVO₂  (1 \textmin-1)}]{\text{SV}\,{\text{(ml)}}}=100.6[1- {\text{e}}^{-2.6\; {\text{VO}_2}\;{(1\,{\text{min}}^{-1})}}] (r ² = 0.41); (d) HR (bpm) = 41.48 + 9.24 Q (l min⁻¹) (r ² = 0.73). Equations for men were (a) Q (l min⁻¹) = 2.52 + 5.70 VO₂ (l min⁻¹) (r ² = 0.89); (b) HR (bpm) = 66.31 + 32.35 VO₂ (l min⁻¹) (r ² = 0.72); (c) \textSV \text(ml)=143.7[1- \texte^{-1.7  \textVO₂  (1 \textmin-1)}]{\text{SV}\,{\text{(ml)}}}=143.7[1- {\text{e}}^{-1.7\; {\text{VO}_2}\;{(1\,{\text{min}}^{-1})}}] (r ² = 0.47); (d) HR (bpm) = 56.33 + 5.25 Q (l min⁻¹) (r ² = 0.69). The intercepts for Q–VO₂ and HR–VO₂ equations were similar for both genders, but the slopes were different (P < 0.05). The SV increased from baseline to 50–60% of VO₂ peak in both groups. No gender effect was found in SV increasing pattern, but the absolute values were in general higher for men (P > 0.05). A significant difference between men and women was observed for both slopes and intercepts in the Q–HR relationship (P < 0.05). In conclusion, (a) Q–VO₂ relation was linear during progressive effort; (b) regression intercepts were similar, but the slopes were higher for men compared to women; (c) SV–VO₂ relationship was nonlinear and maximum SV was reached at very submaximal workload; (d) older men exhibited higher Q upward potential as well higher SV but lower HR for a given submaximal workload than women of similar age.     

Delayed reoxygenation after maximal isometric handgrip exercise in high oxidative capacity muscle

We hypothesized that after maximal short-term isometric exercise, when O₂ demand is still high and O₂ supply is not fully activated, higher oxidative capacity muscle may exhibit slower muscle reoxygenation after the exercise than low oxidative capacity muscle. Seven healthy male subjects performed a maximal voluntary isometric handgrip exercise for 10 s. The reoxygenation rate after the exercise (Reoxy-rate) in the finger flexor muscle was determined by near infrared continuous wave spectroscopy (NIRcws) while phosphocreatine (PCr) was measured simultaneously by ³¹P magnetic resonance spectroscopy. Muscle oxygen consumption (muscle V˙O₂) and muscle oxidative capacity were evaluated using the rate of PCr resynthesis post-exercise. The forearm blood flow (FBF) index at the end of exercise was measured using NIRcws. There was a significant positive correlation between the Reoxy-rate, which ranged between 0.53% s⁻¹ and 12.47% s⁻¹, and the time constant for PCr resynthesis, which ranged between 17.8 s and 38.3 s (r ²=0.939, P<0.001). At the end of the exercise, muscle V˙O₂ exceeded the resting level by approximately 25-fold, while the FBF index exceeded the resting level by only 3-fold on average. The Reoxy-rate closely correlated with muscle V˙O₂ (r ²=0.727, P<0.05), but not with the FBF index. Also, the estimated O₂ balance (muscle V˙O₂ index/FBF index) was negatively correlated with the Reoxy-rate (r ²=0.820, P<0.001). These results support our hypothesis that higher oxidative capacity muscle shows slower muscle reoxygenation after maximal short-term isometric exercise because the Reoxy-rate after this type of exercise may be influenced more by muscle V˙O₂ than by O₂ supply. Electronic Publication