Fatigue in repeated-sprint exercise is related to muscle power factors and reduced neuromuscular activity

The purpose of this study was (1) to determine the relationship between each individual’s anaerobic power reserve (APR) [i.e., the difference between the maximum anaerobic (P _ana) and aerobic power (P _aer)] and fatigability during repeated-sprint exercise and (2) to examine the acute effects of repeated sprints on neuromuscular activity, as evidenced by changes in the surface electromyogram (EMG) signals. Eight healthy males carried out tests to determine P _ana (defined as the highest power output attained during a 6-s cycling sprint), P _aer (defined as the highest power output achieved during a progressive, discontinuous cycling test to failure) and a repeated cycling sprint test (10 × 6-s max sprints with 30 s rest). Peak power output (PPO) and mean power output (MPO) were calculated for each maximal 6-s cycling bout. Root mean square (RMS) was utilized to quantify EMG activity from the vastus lateralis (VL) muscle of the right leg. Over the ten sprints, PPO and MPO decreased by 24.6 and 28.3% from the maximal value (i.e., sprint 1), respectively. Fatigue index during repeated sprints was significantly correlated with APR (R = 0.87; P < 0.05). RMS values decreased over the ten sprints by 14.6% (±6.3%). There was a strong linear relationship (R ² = 0.97; P < 0.05) between the changes in MPO and EMG RMS from the vastus lateralis muscle during the ten sprints. The individual advantage in fatigue-resistance when performing a repeated sprint task was related with a lower anaerobic power reserve. Additionally, a suboptimal net motor unit activity might also impair the ability to repeatedly generate maximum power outputs.     

The effects of exercise-induced muscle damage on maximal intensity intermittent exercise performance

Exercise-induced muscle damage (EIMD) is a common occurrence following activities with a high eccentric component. Alterations to the torque–velocity relationship following EIMD would appear to have serious implications for athletic performance, particularly as they relate to impairment of maximal intensity exercise. However, this has been studied infrequently. The purpose of this study was to assess the effects of EIMD on maximal intermittent sprint performance. Ten male participants (age 22.4±3.2 years, height 178.6±5.2 cm, mass 80.6±10.7 kg) performed 10×6 s cycle ergometer sprints, interspersed with 24 s recovery against a load corresponding to 0.10 kp/kg and 10×10 m sprints from a standing start, each with 12 s active (walking) recovery. All variables were measured immediately before and at 30 min, 24, 48 and 72 h following a plyometric exercise protocol comprising of 10×10 maximal counter movement jumps. Repeated measures ANOVA showed significant changes over time (all P<0.05) for perceived soreness, plasma creatine kinase activity (CK), peak power output (PPO), sprint time and rate of fatigue. Soreness was significantly higher (P<0.01) than baseline values at all time intervals (3.1, 4.9, 5.5 and 3.2 at 30 min, 24, 48 and 72 h, respectively). CK was significantly elevated (P<0.05) at 24 h (239 IU/l) and 48 h (245 IU/l) compared to baseline (151 IU/l). PPO was significantly lower (P<0.05) than baseline (1,054 W) at all time intervals (888, 946, 852 and 895 W, at 30 min, 24, 48 and 72 h, respectively). The rate of fatigue over the ten cycling sprints was reduced compared to baseline, with the greatest reduction of 48% occurring at 48 h (P<0.01). This was largely attributed to the lower PPO in the initial repetitions, resulting in a lower starting point for the rate of fatigue. Values returned to normal at 72 h. Sprint times over 10 m were higher (P<0.05) at 30 min, 24 h and 48 h compared to baseline (1.96 s) with values corresponding to 2.01, 2.02 and 2.01 at 30 min, 24 h and 48 h, respectively. Values returned to baseline by 72 h. The results provide further evidence that, following a plyometric, muscle-damaging exercise protocol, the ability of the muscle to generate power is reduced for at least 3 days. This is also manifested by a small, but statistically significant reduction in very short-term (2 s) intermittent sprint running performance. These findings have implications for appropriate training strategies in multiple sprint sports.     

Effect of menstrual cycle phase on sprinting performance

This study examined the effects of menstrual cycle phase (MCP) upon sprinting and recovery as well as upon metabolic responses to such exercise. Eight females performed a repeated 30-s sprint on a non-motorised treadmill interspersed with a 2-min rest in three phases of the MCP, follicular (low 17β-estradiol and progesterone), just prior to ovulation (midcycle trial, highest 17β-estradiol concentration and low progesterone) and in the luteal phase (high 17β-estradiol and high progesterone). MCP was verified later by radioimmunoassay of 17β-estradiol and progesterone. Peak power output (PPO) and mean power output (MPO) were unaltered (P > 0.05) due to MCP [PPO for sprint 1: 463 (18) W vs. 443 (15) W vs. 449 (18) W; PPO for sprint 2: 395 (17) W vs. 359 (16) W vs. 397 (17) W; MPO for sprint 1: 302 (15) W vs. 298 (13) W vs. 298 (14) W; MPO for sprint 2: 252 (10) W vs. 248 (10) W vs. 259 (12) W for follicular, midcycle and luteal trial, mean (SEM), respectively]. Similarly, percentage recovery of PPO and MPO (the PPO or MPO during sprint 2 expressed as a percentage of the PPO or MPO during sprint 1) was also unchanged (P > 0.05). Blood lactate, blood pH and plasma ammonia after sprinting and estimated plasma volume were also unaltered by MCP (P > 0.05). These findings suggest that hormonal fluctuations due to MCP do not interfere with maximal intensity whole body sprinting and the metabolic responses to such exercise.     

Effects of age and mode of exercise on power output profiles during repeated sprints

The aim of this study was to compare power output profiles during repeated cycling and running sprints in children and adults. On two separate visits, 12 boys [11.7 (0.5) years] and 13 men [22.1 (2.9) years] performed ten consecutive 10-s sprints interspersed with 15-s recovery intervals on a non-motorised treadmill and cycle ergometer. Peak (PPO) and mean (MPO) power outputs were measured during each sprint. Capillary fingertip blood samples were drawn at rest and 3 min after the final sprint to measure lactate accumulation ([La]). PPO and MPO decreased significantly more in adults compared to children over the ten sprints irrespective of the mode of exercise (P<0.001). PPO decreased by a similar amount during running and cycling in children (–17.7 versus –14.3%, P>0.05, respectively) and adults (–43.3 versus –40.0%, P>0.05, respectively). In contrast, MPO decreased significantly more during running compared to cycling both in children (–28.9 versus –18.7%, P<0.05) and adults (–47.0 versus –36.7%, P<0.05). The greater decrease in MPO during running compared to cycling was accompanied in children by significantly higher [La] values (7.7 versus 4.1 mmol l^–1, P<0.001). In adults, blood lactate accumulation tended to be higher during running than cycling (12.7 versus 10.8 mmol l^–1, P=0.06). To conclude, adults displayed a greater decrement in power output compared to children over the ten repeated running and cycling sprints. Furthermore, children and adults experienced greater fatigue during running compared to cycling. This last result may be attributed to additional muscle recruitment during sprint running.     

Influence of resistive load on power output and fatigue during intermittent sprint cycling exercise in children

This study examined the effects of two resistive loads on fatigue during repeated sprints in children. Twelve 11.8 (0.2) year old boys performed a force–velocity test to determine the load (Fopt) corresponding to the optimal pedal rate. On two separate occasions, ten 6-s sprints interspersed with 24-s recovery intervals were performed on a friction-loaded cycle ergometer, against a load equal to Fopt or 50%Fopt. Although mean power output (MPO) was higher in the Fopt [397 (24) and 356 (19) W, P < 0.01], the decline in MPO over the 10 sprints was similar in Fopt [8.8 (1.9) %] and 50%Fopt [9.0 (2.4) %]. In contrast, peak power (PPO) was not different in sprint 1 between the two conditions [459 (24) and 460 (28) W], but was decreased only in 50%Fopt [11.4 (3.2) %, P < 0.01], while it was maintained in the Fopt despite the higher total work during each sprint. Fatigue within each sprint (percent drop from peak to end power output) was also higher in the 50%Fopt compared with the Fopt [32 (2.5) vs. 10 (1.6) %, P < 0.01]. Peak and mean pedal rate in Fopt condition were close to the optimum (Vopt), while a large part of the sprint time in 50%Fopt was spent far from Vopt. The present study shows that sprinting against Fopt reduces fatigue within and between repeated short sprints in children. It is suggested that fatigue during repeated sprints is modified when pedal rate is not close to Vopt, according to the parabolic power versus pedal rate relationship.     

Ammonia and lactate in the blood after short-term sprint exercise

Summary Nine well-trained subjects performed 15-, 30-and 45-s bouts of sprint exercise using a cycle ergometer. There was a significant difference in the mean power between a 15-s sprint (706.0 W, SD 32.5) and a 30-s sprint (627.0 W, SD 27.8;P<0.01). The mean power of the 30-s sprint was higher than that of the 45-s sprint (554.7 W, SD 29.8;P<0.01). Blood ammonia and lactate were measured at rest, immediately after warming-up, and 2.5, 5, 7.5, 10, 12.5 min after each sprint. The peak blood ammonia content was 133.8 mol·1^–1, SD 33.5,- for the 15-s sprint, 130.2 ol·1^–1, SD 44.9, for the 30-s sprint, and 120.8 mol ·1^–1, SD 24.6, for the 45-s sprint. Peak blood lactates after the 15-, 30- and 45-s sprints were 8.1 mmol · 1^–1, SD 1.7, 11.2 mmol · 1^–1, SD 2.4, and 14.7 mmol ·1^–1, SD 2.1, respectively. There was a significant linear relationship between peak blood ammonia and lactate in the 15-s (r, 0.709;P< 0.05), 30-s (r, 0.797;P<0.05) and 45-s (r, 0.696;P<0.05) sprints. Though the peak blood lactate content increased significantly with increasing duration of the sprints (P<0.01), no significant difference was found in peak blood ammonia content among the 15-, 30- and 45-s sprints. These results suggest that the peak value of ammonia in the blood appears in sprints within 15-s and that the blood ammonia level is linked to the lactate in the blood.     

Optimum loading for maximizing muscle power output: the effect of training history

Although the effect of external load on the mechanical output of individual muscle has been well documented, the literature still provides conflicting evidence regarding whether the optimum loading (L_opt) for exerting the maximum muscle power output (MPO) could be different for individuals with different levels of strength and power. The aim of this study was to explore the effect of training history on L_opt that maximizes MPO during the 6-s maximal cycling sprint test. Forty healthy young males (strength-and speed-trained athletes, and physically active and sedentary non-athletes) were tested on maximum strength, and on peak MPO when loaded 5–12% of body weight (BW). As expected, the strength trained and sedentary participants, respectively, revealed the highest and lowest strengths and MPO (p < 0.001). However, the main finding was a significant across-group difference in L_opt (p < 0.001) revealing the values 9.7% (for strength trained), 9.2% (speed trained), 8.7% (active), and 8.0% of BW (sedentary individuals). This suggests that the effects of external loading on maximum MPO in complex functional movements could be training history dependent. In addition to revealing a sensitivity of the 6-s maximal cycling sprint tests (and, perhaps, other maximum cycling tests), the results suggest that the external loading in routine MPO tests should not be solely adjusted to a fixed percentage of subject’s BW (as routinely done in standard tests), but also to their training history. The same phenomenon remains to be evaluated in a number of other routine tests of MPO and other maximum performance tasks.     

Power output and muscle metabolism during and following recovery from 10 and 20 s of maximal sprint exercise in humans

On two separate days eight male subjects performed a 10- or 20-s cycle ergometer sprint (randomized order) followed, after 2 min of recovery, by a 30-s sprint. Muscle biopsies were obtained from the vastus lateralis at rest, immediately after the first sprint and after the 2 min of recovery on both occasions.The anaerobic ATP turnover during the initial 10 s of sprint 1 was 129 ± 12 mmol kg dry weight^?1 and decreased to 63 ± 10 mmol kg dry weight^?1 between the 10th and 20th s of sprint 1. This was a result of a 300% decrease in the rate of phosphocreatine breakdown and a 35% decrease in the glycolytic rate. Despite this 51% reduction in anaerobic ATP turnover, the mean power between 10 and 20 s of sprint 1 was reduced by only 28%. During the same period, oxygen uptake increased from 1.30 ± 0.15 to 2.40 ± 0.23 L min^?1, which partially compensated for the decreased anaerobic metabolism. Muscle pH decreased from 7.06 ± 0.02 at rest to 6.94 ± 0.02 after 10 s and 6.82 ± 0.03 after 20 s of sprinting (for all changes P < 0.01). Muscle pH did not change following a 2-min recovery period after both the 10- and 20-s sprints, but phosphocreatine was resynthesized to 86 ± 3 and 76 ± 3% of the resting value, respectively (n.s. 10- vs. 20-s sprint). Following 2 min of recovery after the 10-s sprint subjects were able to reproduce peak but not mean power. Restoration of both mean and peak power following the 20-s sprint was 88% of sprint 1, and was lower compared with that after the 10-s sprint (P < 0.01). Total work during the second 30-s sprint after the 10- and the 20-s sprint was 19.3 ± 0.6 and 17.8 ± 0.5 kJ, respectively (P < 0.01). As oxygen uptake was the same during the 30-s sprints (2.95 ± 0.15 and 3.02 ± 0.16 L min^?1), and [Phosphocreatine] before the sprint was similar, the lower work may be related to a reduced glycolytic ATP regeneration as a result of the higher muscle acidosis.     

Ergometric and metabolic adaptation to a 5-s sprint training programme

Summary The effects of 7 weeks of sprint training (repeated 5-s all-out sprints) on maximal power output (W _{, max}) determined during a force-velocity test and a 30-s Wingate test (W _peak) were studied in ten students [22 (SD 2) years] exercising on a cycle ergometer. Before and after training, muscle biopsies were taken from vastus lateralis muscle at rest for the ten subjects and immediately after a training session for five of them. Sprint training induced an improvement both in peak performances by 25% (W _{, max} and W _peak) and in the 30-s total work by 16%. Before sprint training, the velocity reached with no load (₀) was related to the resting muscle phosphocreatine (PCr) stores (r=0.87, P < 0.001). The training-induced changes in ₀ were observed only when these PCr stores were lowest. This pointed to a possible limiting role of low PCr concentrations in the ability to reach a high velocity. The improvement in performances was linked to an increase in the energy production from anaerobic glycolysis. This result was suggested in muscle by the increase in lactate production measured after a training session associated with the 20% higher activity of both phosphofructokinase and lactate dehydrogenase. The sprint training also increased the proportion of slow twitch fibres closely related to the decrease in fast twitch b fibres. This result would appear to demonstrate an appropriate adaptive reaction following high-intensity intermittent training for the slow twitch fibres which exhibit a greater oxidative capacity.     

Rapid recovery of power output in females

The purpose of the present study was to examine whether the magnitude of the changes in the concentration of muscle metabolites influences the recovery of power output following short-term maximal intensity cycle exercise performed at different average pedalling rates. In part A of the study eight female subjects performed four trials on a cycle ergometer. Two trials involved maximal sprints of 30- and 6-s duration separated by a very short (2–3 s) recovery period. Average pedal rate during the first 30-s sprint was manipulated by employing resistances of either 7.5 or 10.1% of body weight; the second sprint always being performed against 7.5% BW. In two further trials subjects performed only a single 30-s sprint against the two resistances with pre- and post-exercise muscle biopsies and blood samples being taken. Peak power in the second sprint was significantly higher (442 ± 31W vs. 402 ± 33W; P < 0.05) following prior exercise against the greater resistance during which average pedal rate was lower (≈ 26%; P < 0.01) compared with the lesser resistance. However, despite this the muscle metabolite responses to the first sprint were similar (ΔPCr (7.5 vs. 10.1% applied resistance) –55 vs. –59 mmol kg dry muscle^?1: ΔLactate + 104 vs. +107 mmol kg dry muscle^?1: both P > 0.05). In part B of the study six female subjects performed 19 trials in which the recovery interval between a maximal 30-s sprint (where average pedalling rate was manipulated in a manner similar to part A) and a 6-s sprint ranged from 0 to 300 s. The rate of restoration of power output was influenced by the average pedal rate in sprint 1 only for recovery durations of up to 3 s. These findings suggest that the recovery of power is not exclusively determined by muscle metabolites, in particular PCr, when the recovery duration is very short (≤ 3 s). As it has been previously shown that the pattern of muscle activation influences ionic balance it is speculated that ionic factors may be very important in the early and rapid recovery of power.     

Oxygen deficits incurred during 45, 60, 75 and 90-s maximal cycling on an air-braked ergometer

Summary The aims of this study were to determine the most appropriate duration for the measurement of the maximal accumulated O₂ deficit (MAOD), which is analogous to the anaerobic capacity, to ascertain the effects of mass, fat free mass (FFM), leg volume (V _leg) and lower body volume (V _1b) on anaerobic test performance, to examine the reproducibility for peak power output ( ) or maximal anaerobic power using an air-braked cycle ergometer and to produce approximations for the percentages of aerobic and anaerobic metabolism during exercise of short duration but high intensity. A group of 12 endurance trained cyclists [mean age 25.1 (SD 4.6) years; mean body mass 73.43 (SD 7.12) kg; mean maximal oxygen consumption 5.12 (SD 0.35) l·min^–1; mean body fat 12.5 (SD 4.1) %] accordingly performed four counterbalanced treatments of 45, 60, 75 and 90 s of maximal cycling on an air-braked ergometer. The mean O₂ deficit of 3.52 l for the 45-s treatment was significantly less (P < 0.01) than those for the 60 (3.75 l), 75 (3.80 l) and 90-s (3.75 l) treatments. These data therefore indicate that in predominantly aerobically trained subjects the O₂ deficit attains a plateau after 60 s of maximal cycling on an air-braked ergometer. Statistically significant interclass correlation coefficients (P<0.05) between the anthropometric variables (mass, FFM, V _leg and V_1b) and or maximal anaerobic power (0.624–0.748) and MAOD (ml) or anaerobic capacity (0.666–0.772) furthermore would suggest the relevance of taking into account muscle mass during anaerobic tests. Intraclass correlation coefficients (0.935–0.946; all P<0.001) would indicate a high degree of reliability for the measurement of . The relative importance of anaerobic work decreased from 60% for the 45-s test to 40% for the 90-s one. Hence our study showed that both aerobic and anaerobic metabolism contributed significantly during all-out tests of 45–90 s duration.     

Performance and metabolism in repeated sprint exercise: effect of recovery intensity

This study investigated the effects of a moderate (MI) and a low intensity (LI) active recovery (both compared to a passive recovery) on repeated-sprint performance and muscle metabolism. Nine, male, subjects performed three repeated-sprint cycle tests (6 x 4 s sprints, every 25 s) in a semi-randomized, counter-balanced order. Recovery after each sprint for the MI and LI trials, respectively, was 60 W (approximately 35% VO(2max)) and 20 W (approximately 20% VO(2max). Biopsies were taken from the vastus lateralis pre- and immediately post-test during the MI and LI trials to determine adenosine triphosphate (ATP), phosphocreatine (PCr) and lactate (MLa(-)) content. Compared to passive, significant reductions in peak power of 3.4-6.0% were recorded in the MI trial (4 of 6 sprints; P < 0.05) and reductions of 3.5-3.7% in the LI trial (2 of 6 sprints; P < 0.05), with no differences between the two active trials. No significant differences were evident in ATP, PCr and MLa(-) between the two active recovery trials. In summary, peak power indices during the repeated-sprint test were inferior in the MI and LI active recovery trials, compared to passive. The minimal differences in performance and muscle metabolites between the MI and LI trials suggest that any low-to-moderate level of muscle activation will attenuate the resynthesis of PCr and the recovery of power output during repeated short-sprint exercise.     

Growth hormone responses to treadmill sprinting in sprint- and endurance-trained athletes

The purpose of the present study was to examine the growth hormone (GH) response to treadmill sprinting in male (M) and female (F) sprint- and endurance-trained atheletes. A group of 11 sprint-trained (ST; 6M, 5F) and 12 endurance-trained (ET; 6M, 6F) athletes performed a maximal 30-s sprint on a nonmotorized treadmill. Peak power and mean power expressed in watts or in watts per kilogram body mass were higher in ST than in ET (P < 0.01) and in the men compared to the women (P < 0.01). Serum GH was greater in ST than in ET athletes, but was not statistically significantly different between the men and the women [mean peak GH: ST 72.4 (SEM 12.5) compared to ET 26.3 (SEM 4.9) mU · I^–1, P < 0.01; men 59.8 (SEM 13.3) compared to the women 35.8 (SEM 7.4) mU · l^–1, n.s.]. Plasma ammonia and blood lactate concentrations were higher and blood pH lower during 1 h of recovery after the sprint in ST compared to ET (all P < 0.01). Multiple log linear regression showed that 82% of the variation in the serum peak GH response was explained by the peak power output and peak blood lactate response to the sprint. As serum GH was still approximately ten times the basal value in ST athletes after 1 h of recovery, it is suggested that the exercise-induced increase in GH could have important physiological effects in this group of athletes, including increased protein synthesis and sparing of protein degradation leading to maintained or increased muscle mass.This work was completed at Department of Physical Education, Sports Science and Recreation Management, Loughborough University     

Acute heat exposure increases high-intensity performance during sprint cycle exercise

The purpose of this study was to investigate the effects of acute heat exposure at thermal balance on high-intensity performance during sprint cycle exercise. Nine healthy male subjects were tested in three different, well-controlled environments in an environmental chamber: T (22°C, 65% RH), H1 (30°C, 55% RH) and H2 (35°C, 62% RH), each test being carried out on a different day following a randomized sequence. After 30 min of exposure to the set environment, subjects performed the 30-s sprint cycle exercise. Heart rate, rectal and skin temperatures were measured prior to exercise, at rest, before and after environmental exposure, and after exercise. There were no differences in subjects’ core temperature or heart rate prior to exercise. However, skin temperature was significantly higher in hot trials compared with the control throughout the experimental session (P < 0.05). Peak power was significantly higher in the hot environments compared with the control. Mean power was higher only in H2 compared with T (P < 0.05). This difference in power output was the consequence of a faster pedaling cadence in the hot trials (P < 0.05). Plasma ammonia was higher in the hot trials versus control at 4 min post-sprint. No differences in blood lactate levels at 3 min post-sprint were observed between tests. The results of this study suggest that the exposure to hot environment caused an improvement in power output for a single 30-s sprint. This increase in power output was associated with an elevation in plasma ammonia suggestive of an increase in adenine nucleotide loss.     

Effects of active recovery on power output during repeated maximal sprint cycling

The effects of active recovery on metabolic and cardiorespiratory responses and power output were examined during repeated sprints. Male subjects (n = 13) performed two maximal 30-s cycle ergometer sprints, 4 min apart, on two separate occasions with either an active [cycling at 40 (1)% of maximal oxygen uptake; mean (SEM)] or passive recovery. Active recovery resulted in a significantly higher mean power output ( ) during sprint 2, compared with passive recovery [ ] 603 (17) W and 589 (15) W, P < 0.05]. This improvement was totally attributed to a 3.1 (1.0)% higher power generation during the initial 10 s of sprint 2 following the active recovery (P < 0.05), since power output during the last 20 s sprint 2 was the same after both recoveries. Despite the higher power output during sprint 2 after active recovery, no differences were observed between conditions in venous blood lactate and pH, but peak plasma ammonia was significantly higher in the active recovery condition [205 (23) vs 170 (20) μmol · 1⁻¹;P < 0.05]. No differences were found between active and passive recovery in terms of changes in plasma volume or arterial blood pressure throughout the test. However, heart rate between the two 30-s sprints and oxygen uptake during the second sprint were higher for the active compared with passive recovery [148 (3) vs 130 (4) beats · min⁻¹;P < 0.01) and 3.3 (0.1) vs 2.8 (0.1) 1 · min⁻¹;P < 0.01]. These data suggest that recovery of power output during repeated sprint exercise is enhanced when low-intensity exercise is performed between sprints. The beneficial effects of an active recovery are possibly mediated by an increased blood flow to the previously exercised muscle.     

Blend encapsulation by random copolymers: C/B/A-ran-B and C/D/A-ran-B systems

Random copolymers with the same monomeric units as blended homopolymers A and B have a strong tendency to encapsulate the minor phase in A/B/A-ran-B ternary systems. In this study we investigate encapsulation when one or both monomeric units in the random copolymer are chemically distinct from, but completely or partially miscible with, the other blend components, i.e., a C/D/A-ran-B blend. As model polymers, a styrene/methyl methacrylate random copolymer (70% styrene by weight) (SMMA), and polystyrene (PS), poly(methyl methacrylate) (PMMA), polycarbonate (PC), and poly(phenylene oxide) (PPO) homopolymers are chosen; PPO is completely miscible with PS and PC is partially miscible with PMMA. Three blend systems were prepared by melt mixing: PS/PC/SMMA, PPO/PMMA/SMMA, and PPO/PC/SMMA. Transmission electron microscopy demonstrated that for all cases SMMA moves to the interface between the matrix and dispersed phases during melt mixing, and forms an encapsulating layer. However, the resulting average size of a dispersed phase droplet is not significantly decreased by the addition of SMMA. Moreover, this size increased significantly upon further annealing, except for the blend with a PPO matrix which has a very high melt viscosity, demonstrating that encapsulation by SMMA does not provide stability against static coalescence.     

Blood lactate and glycerol after 400-m and 3,000-m runs in sprint and long distance runners

Summary Lactate, glycerol, and catecholamine in the venous blood after 400-m and 3,000-m runs were determined in eight sprint runners, eight long distance runners, and seven untrained students. In 400-m sprinting, average values of velocity, peak blood lactate, and adrenaline were significantly higher in the sprint group than in the long distance and untrained groups. The mean velocity of 400-m sprinting was significantly correlated with peak blood lactate in the untrained (r=0.76,P<0.05) and long distance (r=0.71,P<0.05) groups, but not in the sprint group. In the 3,000-m run, on the other hand, average values of velocity and glycerol were significantly higher in the long distance group than in the sprint and untrained groups, but there are no significant differences in lactate levels between the three groups. These results suggest that 1) performance in 400-m sprinting may depend mainly upon an energy supply from glycolysis in the long distance and untrained group, but in the sprinters is influenced not only by glycolysis, but also by other factors such as content of ATP or force per unit muscle cross-sectional area; 2) peak blood lactate obtained after 400-m sprinting may be used as a useful indication of anaerobic work capacity in the long distance and untrained groups, but not in the sprinters. 3) high speed in the 3,000-m run could be maintained in the long distance runners by means of a greater energy supply from lipid metabolism as compared with sprinters or untrained subjects.This study was supported by grants from the Japanese Ministry of Education (No. 58780102)     

Effects of hyperthermia on the metabolic responses to repeated high-intensity exercise

In this study, we investigated the metabolic and performance responses to hyperthermia during high-intensity exercise. Seven males completed two 30-s cycle sprints (SpI and SpII) at an environmental temperature of 20.6 (0.3) °C [mean (SD)] with 4 min recovery between sprints. A hot or control treatment preceded the sprint exercise. For the hot trial, subjects were immersed up to the neck in hot water [43°C for 16.0 (3.2) min] prior to entering an environmental chamber [44.2 (0.8)°C for 30.7 (7.1) min]. For the control trial, subjects were seated in an empty bath (15 min) and thereafter in a normal environment [20.2 (0.6)°C for 29.0 (1.9) min]. Subjects core temperature prior to exercise was 38.1 (0.3)°C in the hot trial and 37.1 (0.3)°C in the control trial. Mean power output (MPO) was significantly higher in the hot condition for SpI [683 (130) W hot vs 646 (119) W control (P<0.025)]. Peak power output (PPO) tended to be higher in the hot trial compared with the control trial for SpI [1057 (260) W hot vs 990 (245) W control (P=0.03, NS)]. These differences in power output were a consequence of a faster pedal cadence in the hot trial (P<0.025). There were no differences in sprint performance in SpII in the hot trial compared to the control trial; however, MPO was significantly reduced from SpI to SpII in the hot condition but not in the control condition (P<0.025). Plasma ammonia was higher in the hot trial at 2 min post-SpI [169 (65) mol l^-1 hot vs 70 (26) mol l^-1 control (P<0.01)], immediately and at 2 min post-SpII [231 (76) mol l^-1 hot vs 147 (72) mol l^-1 control (P<0.01)]. Blood lactate was higher in the hot trial compared with the control trial at 5 min post-SpII (P<0.025). The results of this study suggest that an elevation in core body temperature by 1°C can improve performance during an initial bout of high-intensity cycle exercise but has no further beneficial effect on subsequent power production following a 4-min recovery period.     

Effects of fatigue and sprint training on electromechanical delay of knee extensor muscles

Electromechanical delay (EMD) of knee extensors in isometric contraction was investigated in six healthy men before and after four periods of 30-s all-out sprint cycling exercise, conducted pre and post a 7-week sprint cycling training programme. The EMD was lengthened from 40.4 (SEM 3.46) ms at rest to 63.4 (SEM 7.80) ms after the fatiguing exercise (P 0.05) in the pre-training test. During maximal voluntary contractions (MVC) conducted after the fatiguing exercise, the peak contraction force (F _peak) and peak rate of force development (RFD_peak) were reduced by 51%–56% and 38%–50%, respectively (both P 0.05). The mechanisms of EMD lengthening during fatigue could have been due to the deterioration in muscle conductive, contractile or elastic properties and require further study. The training programme increased the total work performed during the four periods of sprint exercise (P 0.05). However, no significant training effects were found in the resting or postexercise EMD, F _peak and RFD_peak during isometric MVC. These unchanged isometric contraction variables but enhanced dynamic performance suggest that isometric tests of muscle are insensitive to the neuromuscular adaptations to sprint training.     

Metabolic transition in the development of Hymenolepis diminuta (Cestoda)

Cysticercoids as well as 6-, 10-, and 14-day Hymenolepis diminuta were evaluated in terms of enzymatic activities related to phosphoenolpyruvate (PEP) utilization and mitochondrial succinate accumulation. The data obtained support a transition toward anaerobic electron-transport-dependent succinate accumulation, characteristic of adult H. diminuta, with development from cysticercoid to adult. This transition was reflected most prominently in the increasing activities of PEP carboxykinase (PEPCK), malate dehydrogenase, NADPH → NAD⁺ transhydrogenase, and fumarate reductase. Developmental increases in PEPCK/pyruvate kinase (PK), fumarate reductase (FR)/NADH oxidase (NO), and FR/succinate dehydrogenase (SDH) activity ratios were also apparent. Evaluations of “egg-free” immature, mature, and pregravid-gravid segments of adult H. diminuta revealed that in general the greater levels of activity were associated with the immature and mature segments. Whereas FR/NO and FR/SDH ratios remained relatively constant in segment comparisons, the greatest PEPCK/PK ratio was associated with the pregravid-gravid segment. Received: 2 December 1997 / Accepted: 5 June 1998