Intensity of exercise recovery,blood lactate disappearance,and subsequent swimming performance

Abstract

The aim of this study was to examine the effects of active versus passive recovery on blood lactate disappearance and subsequent maximal performance in competitive swimmers. Fourteen male swimmers from the University of Virginia swim team (mean age 20.3 years, s = 4.1; stature 1.85 m, s = 2.2; body mass 81.1 kg, s = 5.6) completed a lactate profiling session during which the speed at the lactate threshold (V_LT), the speed at 50% of the lactate threshold (V_LT.5), and the speed at 150% of the lactate threshold (V_LT1.5) were determined. Participants also completed four randomly assigned experimental sessions that consisted of a 200-yard maximal-effort swim followed by 10 min of recovery (passive, V_LT.5, V_LT, V_LT1.5) and a subsequent 200-yard maximal effort swim. All active recovery sessions resulted in greater lactate disappearance than passive recovery (P < 0.0001 for all comparisons), with the greatest lactate disappearance associated with recovery at V_LT (P = 0.006 and 0.007 vs. V_LT.5 and V_LT1.5 respectively) [blood lactate disappearance was 2.1 mmol · l^?1 (s = 2.0), 6.0 mmol · l^?1 (s = 2.6), 8.5 mmol · l^?1 (s = 1.8), and 6.1 mmol · l^?1 (s = 2.5) for passive, V_LT.5, V_LT, and V_LT1.5 respectively]. Active recovery at V_LT and V_LT1.5 resulted in faster performance on time trial 2 than passive recovery (P = 0.005 and 0.03 respectively); however, only active recovery at V_LT resulted in improved performance on time trial 2 (TT₂) relative to time trial 1 (TT₁) [TT₂?TT₁: passive +1.32 s (s = 0.64), V_LT.5+1.01 s (s = 0.53), V_LT?1.67 s (s = 0.26), V_LT1.5?0.07 s (s = 0.51); P < 0.0001 for V_LT). In conclusion, active recovery at the speed associated with the lactate threshold resulted in the greatest lactate disappearance and in improved subsequent performance in all 14 swimmers. Our results suggest that coaches should consider incorporating recovery at the speed at the lactate threshold during competition and perhaps during hard training sessions.     

Effects of active and passive recovery on performance during repeated-sprint swimming

The effect of active and passive recovery on repeated-sprint swimming bouts was studied in eight elite swimmers. Participants performed three trials of two sets of front crawl swims with 5 min rest between sets. Set A consisted of four 30-s bouts of high-intensity tethered swimming separated by 30 s passive rest, whereas Set B consisted of four 50-yard maximal-sprint swimming repetitions at intervals of 2 min. Recovery was active only between sets (AP trial), between sets and repetitions of Set B (AA trial) or passive throughout (PP trial). Performance during and metabolic responses after Set A were similar between trials. Blood lactate concentration after Set B was higher and blood pH was lower in the PP (18.29 +/- 1.31 mmol x l(-1) and 7.12 +/- 0.11 respectively) and AP (17.56 +/- 1.22 mmol x l(-1) and 7.14 +/- 0.11 respectively) trials compared with the AA (14.13 +/- 1.56 mmol x l(-1) and 7.23 +/- 0.10 respectively) trial (P < 0.01). Performance time during Set B was not different between trials (P > 0.05), but the decline in performance during Set B of the AP trial was less marked than in the AA or PP trials (main effect of sprints, P < 0.05). Results suggest that active recovery (60% of the 100-m pace) could be beneficial between training sets, and may compromise swimming performance between repetitions when recovery durations are short (< 2 min).     

Blood lactate response and critical speed in swimmers aged 10-12 years of different standards

It has previously been shown that measurement of the critical speed is a non-invasive method of estimating the blood lactate response during exercise. However, its validity in children has yet to be demonstrated. The aims of this study were: (1) to verify if the critical speed determined in accordance with the protocol of Wakayoshi et al. is a non-invasive means of estimating the swimming speed equivalent to a blood lactate concentration of 4 mmol x l(-1) in children aged 10-12 years; and (2) to establish whether standard of performance has an effect on its determination. Sixteen swimmers were divided into two groups: beginners and trained. They initially completed a protocol for determination of speed equivalent to a blood lactate concentration of 4 mmol x l(-1). Later, during training sessions, maximum efforts were swum over distances of 50, 100 and 200 m for the calculation of the critical speed. The speeds equivalent to a blood lactate concentration of 4 mmol x l(-1) (beginners = 0.82 +/- 0.09 m x s(-1), trained = 1.19 +/- 0.11 m x s(-1); mean +/- s) were significantly faster than the critical speeds (beginners = 0.78 +/- 0.25 m x s(-1), trained = 1.08 +/- 0.04 m x s(-1)) in both groups. There was a high correlation between speed at a blood lactate concentration of 4 mmol x l(-1) and the critical speed for the beginners (r= 0.96, P < 0.001), but not for the trained group (r= 0.60, P> 0.05). The blood lactate concentration corresponding to the critical speed was 2.7 +/- 1.1 and 3.1 +/- 0.4 mmol x l(-1) for the beginners and trained group respectively. The percent difference between speed at a blood lactate concentration of 4 mmol x l(-1) and the critical speed was not significantly different between the two groups. At all distances studied, swimming performance was significantly faster in the trained group. Our results suggest that the critical speed underestimates swimming intensity corresponding to a blood lactate concentration of 4 mmol x l(-1) in children aged 10-12 years and that standard of performance does not affect the determination of the critical speed.     

Urea production during prolonged swimming

Male interscholastic swimmers (n = 8) completed a 4572 m training swim in in 62 +/- 1.1 min (means +/- S.E.) with terminal heart rate and blood lactate of 152 +/- 6 beats min-1 and 6.9 +/- 0.89 mM, respectively. Sweat rate (0.48 +/- 0.095 l. h-1) was lower than similar intensity cycling (1.5 +/- 0.13 l. h-1) or running (1.1 +/- 0.14 l. h-1). Post-swim serum urea N (11.6 +/- 0.71 mM) was elevated (P less than 0.05) vs pre-swim (4.6 +/- 0.39 mM). Post-swim urine volume (860 +/- 75 ml 24 h-1) was reduced (P less than 0.07) and resulted in an elevated (P less than 0.05), but delayed (24-84 h), post-exercise urea N excretion. Although the reduced urine and sweat production during the swim undoubtedly contributed to the elevated serum urea, there must be another explanation because together they could only account for 38% of the observed increase. On the basis of the magnitude of serum urea increase, it appears that the swim caused an increase in urea production (amino acid oxidation). The failure to observe larger increases in urinary urea during recovery indicates that either urea excretion following exercise continues for prolonged periods of time (greater than 48 h) or another significant mode of nitrogen excretion exists.     

Changes in blood lactate and pyruvate concentrations and the lactate-to-pyruvate ratio during the lactate minimum speed test

The aim of this study was to assess the responses of blood lactate and pyruvate during the lactate minimum speed test. Ten participants (5 males, 5 females; mean +/- s: age 27.1+/-6.7 years, VO2max 52.0+/-7.9 ml x kg(-1) x min(-1)) completed: (1) the lactate minimum speed test, which involved supramaximal sprint exercise to invoke a metabolic acidosis before the completion of an incremental treadmill test (this results in a 'U-shaped' blood lactate profile with the lactate minimum speed being defined as the minimum point on the curve); (2) a standard incremental exercise test without prior sprint exercise for determination of the lactate threshold; and (3) the sprint exercise followed by a passive recovery. The lactate minimum speed (12.0+/-1.4 km x h(-1)) was significantly slower than running speed at the lactate threshold (12.4+/-1.7 km x h(-1)) (P < 0.05), but there were no significant differences in VO2, heart rate or blood lactate concentration between the lactate minimum speed and running speed at the lactate threshold. During the standard incremental test, blood lactate and the lactate-to-pyruvate ratio increased above baseline values at the same time, with pyruvate increasing above baseline at a higher running speed. The rate of lactate, but not pyruvate, disappearance was increased during exercising recovery (early stages of the lactate minimum speed incremental test) compared with passive recovery. This caused the lactate-to-pyruvate ratio to fall during the early stages of the lactate minimum speed test, to reach a minimum point at a running speed that coincided with the lactate minimum speed and that was similar to the point at which the lactate-to-pyruvate ratio increased above baseline in the standard incremental test. Although these results suggest that the mechanism for blood lactate accumulation at the lactate minimum speed and the lactate threshold may be the same, disruption to normal submaximal exercise metabolism as a result of the preceding sprint exercise, including a three- to five-fold elevation of plasma pyruvate concentration, makes it difficult to interpret the blood lactate response to the lactate minimum speed test. Caution should be exercised in the use of this test for the assessment of endurance capacity.     

Changes in blood lactate and pyruvate concentrations and the lactate-to-pyruvate ratio during the lactate minimum speed test

The aim of this study was to assess the responses of blood lactate and pyruvate during the lactate minimum speed test. Ten participants (5 males, 5 females; mean +/- s: age 27.1 +/- 6.7 years, VO 2max 52.0 +/- 7.9 ml kg -1 min -1 ) completed: (1) the lactate minimum speed test, which involved supramaximal sprint exercise to invoke a metabolic acidosis before the completion of an incremental treadmill test (this results in a ‘U-shaped’ blood lactate profile with the lactate minimum speed being defined as the minimum point on the curve); (2) a standard incremental exercise test without prior sprint exercise for determination of the lactate threshold; and (3) the sprint exercise followed by a passive recovery. The lactate minimum speed (12.0 +/- 1.4 km h -1 ) was significantly slower than running speed at the lactate threshold (12.4 +/- 1.7 km h -1 ) (P < 0.05), but there were no significant differences in VO 2 , heart rate or blood lactate concentration between the lactate minimum speed and running speed at the lactate threshold. During the standard incremental test, blood lactate and the lactate-topyruvate ratio increased above baseline values at the same time, with pyruvate increasing above baseline at a higher running speed. The rate of lactate, but not pyruvate, disappearance was increased during exercising recovery (early stages of the lactate minimum speed incremental test) compared with passive recovery. This caused the lactate-to-pyruvate ratio to fall during the early stages of the lactate minimum speed test, to reach a minimum point at a running speed that coincided with the lactate minimum speed and that was similar to the point at which the lactate-to-pyruvate ratio increased above baseline in the standard incremental test. Although these results suggest that the mechanism for blood lactate accumulation at the lactate minimum speed and the lactate threshold may be the same, disruption to normal submaximal exercise metabolism as a result of the preceding sprint exercise, including a three- to five-fold elevation of plasma pyruvate concentration, makes it difficult to interpret the blood lactate response to the lactate minimum speed test. Caution should be exercised in the use of this test for the assessment of endurance capacity.     

Effect of 6 weeks of endurance training on the lactate minimum speed

The aim of this study was to assess the sensitivity of the lactate minimum speed test to changes in endurance fitness resulting from a 6 week training intervention. Sixteen participants (mean +/- s :age 23 +/- 4 years;body mass 69.7 +/- 9.1 kg) completed 6 weeks of endurance training. Another eight participants (age 23 +/- 4 years; body mass 72.7 +/-12.5 kg) acted as non-training controls. Before and after the training intervention, all participants completed: (1) a standard multi-stage treadmill test for the assessment of VO 2max , running speed at the lactate threshold and running speed at a reference blood lactate concentration of 3 mmol.l -1 ; and (2) the lactate minimum speed test, which involved two supramaximal exercise bouts and an 8 min walking recovery period to increase blood lactate concentration before the completion of an incremental treadmill test. Additionally, a subgroup of eight participants from the training intervention completed a series of constant-speed runs for determination of running speed at the maximal lactate steady state. The test protocols were identical before and after the 6 week intervention. The control group showed no significant changes in VO 2max , running speed at the lactate threshold, running speed at a blood lactate concentration of 3 mmol.l -1 or the lactate minimum speed.In the training group, there was a significant increase in VO 2max (from 47.9 +/- 8.4 to 52.2 +/- 2.7 ml.kg -1 .min -1 ), running speed at the maximal lactate steady state (from 13.3 +/- 1.7 to 13.9 +/- 1.6 km.h -1 ), running speed at the lactate threshold (from 11.2 +/- 1.8 to 11.9 +/- 1.8 km.h -1 ) and running speed at a blood lactate concentration of 3 mmol.l -1 (from 12.5 +/- 2.2 to 13.2 +/- 2.1 km.h -1 ) (all P ? 0.05). Despite these clear improvements in aerobic fitness, there was no significant difference in lactate minimum speed after the training intervention (from 11.0 +/- 0.7 to 10.9 +/- 1.7 km.h -1 ). The results demonstrate that the lactate minimum speed,when assessed using the same exercise protocol before and after 6 weeks of aerobic exercise training, is not sensitive to changes in endurance capacity.     

Effect of 6 weeks of endurance training on the lactate minimum speed

The aim of this study was to assess the sensitivity of the lactate minimum speed test to changes in endurance fitness resulting from a 6 week training intervention. Sixteen participants (mean +/- s: age 23+/-4 years; body mass 69.7+/-9.1 kg) completed 6 weeks of endurance training. Another eight participants (age 23+/-4 years; body mass 72.7+/-12.5 kg) acted as non-training controls. Before and after the training intervention, all participants completed: (1) a standard multi-stage treadmill test for the assessment of VO2max, running speed at the lactate threshold and running speed at a reference blood lactate concentration of 3 mmol x l(-1); and (2) the lactate minimum speed test, which involved two supramaximal exercise bouts and an 8 min walking recovery period to increase blood lactate concentration before the completion of an incremental treadmill test. Additionally, a subgroup of eight participants from the training intervention completed a series of constant-speed runs for determination of running speed at the maximal lactate steady state. The test protocols were identical before and after the 6 week intervention. The control group showed no significant changes in VO2max, running speed at the lactate threshold, running speed at a blood lactate concentration of 3 mmol x l(-1) or the lactate minimum speed. In the training group, there was a significant increase in VO2max (from 47.9+/-8.4 to 52.2+/-2.7 ml x kg(-1) x min(-1)), running speed at the maximal lactate steady state (from 13.3+/-1.7 to 13.9+/-1.6 km x h(-1)), running speed at the lactate threshold (from 11.2+/-1.8 to 11.9+/-1.8 km x h(-1)) and running speed at a blood lactate concentration of 3 mmol x l(-1) (from 12.5+/-2.2 to 13.2+/-2.1 km x h(-1)) (all P < 0.05). Despite these clear improvements in aerobic fitness, there was no significant difference in lactate minimum speed after the training intervention (from 11.0+/-0.7 to 10.9+/-1.7 km x h(-1)). The results demonstrate that the lactate minimum speed, when assessed using the same exercise protocol before and after 6 weeks of aerobic exercise training, is not sensitive to changes in endurance capacity.     

Urea production during prolonged swimming

Male interscholastic swimmers (n = 8) completed a 4572 m training swim in 62 ±1.1 min (x ± s.e.) with terminal heart rate and blood lactate of 152 ± 6 beats min^‐1 and 6.9±0.89 mM, respectively. Sweat rate (0.48±0.0951. h^‐1) was lower than similar intensity cycling (1.5±0.13 1. h^‐1) or running (1.1 ± 0.14 l.h^‐1). Post‐swim serum urea N (11.6±0.71 mM) was elevated (P<0.05) vs pre‐swim (4.6±0.39 mM). Post‐swim urine volume (860±75 ml 24 h^‐1) was reduced (P<0.07) and resulted in an elevated (P<0.05), but delayed (24–84 h), post‐exercise urea N excretion. Although the reduced urine and sweat production during the swim undoubtedly contributed to the elevated serum urea, there must be another explanation because together they could only account for 38% of the observed increase. On the basis of the magnitude of serum urea increase, it appears that the swim caused an increase in urea production (amino acid oxidation). The failure to observe larger increases in urinary urea during recovery indicates that either urea excretion following exercise continues for prolonged periods of time (>48 h) or another significant mode of nitrogen excretion exists.     

不同无氧阈测定方法比较及其在中长跑训练中的应用

本文比较了各种无氧阈测值:通气阈(VT),4mmol乳酸阈(LT_4),血乳酸开始升高(LT_(OBLA)),个体无氧阈(IAT),血乳酸最大稳态(maxLass)和心率拐点(HRd)。发现各测值之间高度相关,但是maxLass与其它测值之间存在不同程度的差异,为AT在训练中的应用提供了有价值的生理依据。继而探讨了LT_4百分比强度对控制中长跑训练,改善运动员肌肉氧化代射能力,提高运动成绩的意义。     

Ability of test measures to predict competitive performance in elite swimmers

The purpose of this study was to quantify the relationship between changes in test measures and changes in competition performance for individual elite swimmers. The 24 male and 16 female swimmers, who were monitored for 3.6 years (s = 2.5), raced in a major competition at the end of each 6-month season (3.6 competitions, s = 2.2). A 7 x 200-m incremental swimming step-test and anthropometry were conducted in up to four training phases each season. Correlations of changes in step-test and anthropometry measures between training phases and seasons with changes in competition performance between seasons were derived with repeated-measures mixed-modelling and linear regression. Changes in competition performance were best tracked by changes in test measures between taper phases. The best single predictor of competition performance was skinfolds for females (r = -0.53). The best predictor from the step-test was stroke rate at a blood lactate concentration of 4 mmol x l(-1) (females: r = 0.46; males: r = 0.41); inclusion of the second-best step-test predictor in a multiple linear regression improved the correlations (females: r = 0.52 with speed in the seventh step included; males: r = 0.58 with peak lactate concentration included). In conclusion, a combination of fitness and technique factors is important for competitive performance. The step-test is a useful adjunct in a swimmer's training preparation for tracking large changes in performance.     

The effects of work-rest duration on intermittent exercise and subsequent performance

This study examined the effects of different work - rest durations during 40 min intermittent treadmill exercise and subsequent running performance. Eight males (mean +/- s: age 24.3 +/- 2.0 years, body mass 79.4 +/- 7.0 kg, height 1.77 +/- 0.05 m) undertook intermittent exercise involving repeated sprints at 120% of the speed at which maximal oxygen uptake (nu-VO2max) was attained with passive recovery between each one. The work - rest ratio was constant at 1:1.5 with trials involving short (6:9 s), medium (12:18 s) or long (24:36 s) work - rest durations. Each trial was followed by a performance run to volitional exhaustion at 150% nu-VO2max. After 40 min, mean exercise intensity was greater during the long (68.4 +/- 9.3%) than the short work - rest trial (54.9 +/- 8.1% VO2max; P < 0.05). Blood lactate concentration at 10 min was higher in the long and medium than in the short work - rest trial (6.1 +/- 0.8, 5.2 +/- 0.9, 4.5 +/- 1.3 mmol x l(-1), respectively; P < 0.05). The respiratory exchange ratio was consistently higher during the long than during the medium and short work - rest trials (P < 0.05). Plasma glucose concentration was higher in the long and medium than in the short work - rest trial after 40 min of exercise (5.6 +/- 0.1, 6.6 +/- 0.2 and 5.3 +/- 0.5 mmol x l(-1), respectively; P < 0.05). No differences were observed between trials for performance time (72.7 +/- 14.9, 63.2 +/- 13.2, 57.6 +/- 13.5 s for the short, medium and long work - rest trial, respectively; P = 0.17), although a relationship between performance time and 40 min plasma glucose was observed (P < 0.05). The results show that 40 min of intermittent exercise involving long and medium work - rest durations elicits greater physiological strain and carbohydrate utilization than the same amount of intermittent exercise undertaken with a short work-rest duration.     

Maximal lactate steady state in trained adolescent runners

The aims of this study were: (1) to identify the exercise intensity that corresponds to the maximal lactate steady state in adolescent endurance-trained runners; (2) to identify any differences between the sexes; and (3) to compare the maximal lactate steady state with commonly cited fixed blood lactate reference parameters. Sixteen boys and nine girls volunteered to participate in the study. They were first tested using a stepwise incremental treadmill protocol to establish the blood lactate profile and peak oxygen uptake (VO2). Running speeds corresponding to fixed whole blood lactate concentrations of 2.0, 2.5 and 4.0 mmol x l(-1) were calculated using linear interpolation. The maximal lactate steady state was determined from four separate 20-min constant-speed treadmill runs. The maximal lactate steady state was defined as the fastest running speed, to the nearest 0.5 km x h(-1), where the change in blood lactate concentration between 10 and 20 min was < 0.5 mmol x l(-1). Although the boys had to run faster than the girls to elicit the maximal lactate steady state (15.7 vs 14.3 km x h(-1), P < 0.01), once the data were expressed relative to percent peak VO2 (85 and 85%, respectively) and percent peak heart rate (92 and 94%, respectively), there were no differences between the sexes (P > 0.05). The running speed and percent peak VO2 at the maximal lactate steady state were not different to those corresponding to the fixed blood lactate concentrations of 2.0 and 2.5 mmol x l(-1) (P > 0.05), but were both lower than those at the 4.0 mmol x l(-1) concentration (P < 0.05). In conclusion, the maximal lactate steady state corresponded to a similar relative exercise intensity as that reported in adult athletes. The running speed, percent peak VO2 and percent peak heart rate at the maximal lactate steady state are approximated by the fixed blood lactate concentration of 2.5 mmol x l(-1) measured during an incremental treadmill test in boys and girls.     

Parasympathetic activity delayed after self-paced exercise

The main purpose of this study was to compare the effect of the constant load and self-paced exercise with similar total work on autonomic control after endurance exercise. Ten physically active men were submitted to (i) a maximal incremental exercise test, (ii) a 4-km cycling time trial (4-km TT), and (iii) a constant workload test with identical total external work performed at 4-km TT. Gas exchange was measured throughout the tests, while blood lactate, heart rate, and heart rate variability (HRV) were measured during the passive recovery. Power output measured at the last lap (i.e. 3600–4000?m) of 4-km TT (316?±?89?W) was statistically higher than power output measured at the end of the constant workload exercise (211?±?42?W). The 4-km TT produced higher values of blood lactate concentration (8.8?±?2.1?mmol?L^?1) than the constant workload test (7.8?±?2.1?mmol?L^?1). The heart rate recovery measured at 60?s (constant workload: 37?±?7?bpm; 4-km TT: 30?±?6) and 120?s (constant workload: 57?±?9?bpm; 4-km TT: 51?±?9?bpm) were higher in the constant workload than in the self-paced exercise. The HRV (i.e. RMSSD30s) was statistically higher in the constant load exercise measured at 120, 420, 450, 480, 540, and 570?s than the self-paced exercise. These findings suggest that the autonomic control responses were dependent of the endurance exercise modalities, with parasympathetic activity being delayed after self-paced exercise, as evidenced by post-exercise heart rate indices.     

Kinematic analysis of butterfly turns of international and national swimmers

The aims of this study were (1) to evaluate the different turn phases of 200 m butterfly during competition in a 50 m pool, (2) to determine if wall contact times are related to swim speed and (3) to compare the turn variables of a European Champion with other swimmers. In the first part of the study, we assessed the turns of 22 swimmers ranked in three groups according to 200 m butterfly swim performance (fast group = 121.73 - 3.03 s, intermediate group = 126.25 - 0.55 s, slow group = 129.24 - 2.30 s). Two turn times were recorded: the first before the turn (i.e. the time it takes the swimmer's head to reach the wall from 7.5 m away) and the second after the turn (i.e. the time from the wall to the point at which the swimmer's head passes 7.5 m away). The third turn was performed significantly faster by the fast group than by the slow group, both before ( P ? 0.01) and after ( P ? 0.02) the turn. In the second part of the study, objectives (2) and (3) were evaluated among 15 swimmers based on a specific protocol. Three cameras (50 Hz) simultaneously recorded the turn; these were placed above the water 10 m before the wall, 5 m before and just above the wall. Longer contact times of the feet on the wall were associated with a faster push-off speed ( P ? 0.02). The European Champion achieved an improved contact time while performing a rapid pull-out speed.     

Biomechanics,energetics and coordination during extreme swimming intensity: effect of performance level

The present study aimed to examine how high- and low-speed swimmers organise biomechanical, energetic and coordinative factors throughout extreme intensity swim. Sixteen swimmers (eight high- and eight low-speed) performed, in free condition, 100-m front crawl at maximal intensity and 25, 50 and 75-m bouts (at same pace as the previous 100-m), and 100-m maximal front crawl on the measuring active drag system (MAD-system). A 3D dual-media optoelectronic system was used to assess speed, stroke frequency, stroke length, propelling efficiency and index of coordination (IdC), with power assessed by MAD-system and energy cost by quantifying oxygen consumption plus blood lactate. Both groups presented a similar profile in speed, power output, stroke frequency, stroke length, propelling efficiency and energy cost along the effort, while a distinct coordination profile was observed (F_{(3, 42)} = 3.59, P = 0.04). Speed, power, stroke frequency and propelling efficiency (not significant, only a tendency) were higher in high-speed swimmers, while stroke length and energy cost were similar between groups. Performing at extreme intensity led better level swimmers to achieve superior speed due to higher power and propelling efficiency, with consequent ability to swim at higher stroke frequencies. This imposes specific constraints, resulting in a distinct IdC magnitude and profile between groups.     

Effects of active, passive or no warm-up on metabolism and performance during high-intensity exercise

The aim of this study was to determine the influence of type of warm-up on metabolism and performance during high-intensity exercise. Eight males performed 30 s of intense exercise at 120% of their maximal power output followed, 1 min later, by a performance cycle to exhaustion, again at 120% of maximal power output. Exercise was preceded by active, passive or no warm-up (control). Muscle temperature, immediately before exercise, was significantly elevated after active and passive warm-ups compared to the control condition (36.9 +/- 0.18 degrees C, 36.8 +/- 0.18 degrees C and 33.6 +/- 0.25 degrees C respectively; mean +/- sx) (P< 0.05). Total oxygen consumption during the 30 s exercise bout was significantly greater in the active and passive warm-up trials than in the control trial (1017 +/- 22, 943 +/- 53 and 838 +/- 45 ml O2 respectively). Active warm-up resulted in a blunted blood lactate response during high-intensity exercise compared to the passive and control trials (change = 5.53 +/- 0.52, 8.09 +/- 0.57 and 7.90 +/- 0.38 mmol x l(-1) respectively) (P < 0.05). There was no difference in exercise time to exhaustion between the active, passive and control trials (43.9 +/- 4.1, 48.3 +/- 2.7 and 46.9 +/- 6.2 s respectively) (P= 0.69). These results indicate that, although the mechanism by which muscle temperature is elevated influences certain metabolic responses during subsequent high-intensity exercise, cycling performance is not significantly affected.     

Effects of dynamic upper-body exercise on lower-limb isometric endurance

Following preliminary indications that in some individuals arm exercise enhanced rather than reduced simultaneous leg endurance, ten young men and women performed three forms of intermittent work to volitional exhaustion, under duty cycles of 45 s work, 15 s rest. The protocols were as follows: (A) knee extensions at 30% maximum voluntary contraction (MVC); (B) 30% MVC knee extensions combined with arm cranking at 130% of their own lactate threshold; (C) combined 30% MVC knee extensions and arm cranking at 20% of their own lactate threshold. Heart rate, oxygen uptake (VO(2)), and blood lactate concentration were among the variables recorded throughout. All physiological indicators of demand were substantially higher in protocol B than in protocols A or C [heart rate: (A) 154 beats . min(-1), (B) 171 beats . min(-1), (C) 150 beats . min(-1); VO(2): (A) 11.9 ml . kg(-1) . min(-1), (B) 21.7 ml . kg(-1) . min(-1), (C) 14.2 ml . kg(-1) . min(-1); blood lactate concentration: (A) 3.3 mmol . l(-1), (B) 5.1 mmol . l(-1), (C) 2.8 mmol . l(-1)], yet there were no significant differences (P > 0.05) in the endurance times between the three conditions [(A) 11.43 min, (B) 11.1 min, (C) 10.57 min] and seven participants endured longest in protocol B. Results from protocol (C) cast doubt on explanations in terms of psychological distraction. We suggest that lactic acid produced by the arms is shuttled to the legs and acts there either as a supplementary fuel source or as an antagonist to the depressing effects of increased potassium concentration.     

Kinematic analysis of butterfly turns of international and national swimmers

The aims of this study were (1) to evaluate the different turn phases of 200 m butterfly during competition in a 50 m pool, (2) to determine if wall contact times are related to swim speed and (3) to compare the turn variables of a European Champion with other swimmers. In the first part of the study, we assessed the turns of 22 swimmers ranked in three groups according to 200 m butterfly swim performance (fast group = 121.73+/-3.03 s, intermediate group = 126.25+/-0.55 s, slow group = 129.24+/-2.30 s). Two turn times were recorded: the first before the turn (i.e. the time it takes the swimmer's head to reach the wall from 7.5 m away) and the second after the turn (i.e. the time from the wall to the point at which the swimmer's head passes 7.5 m away). The third turn was performed significantly faster by the fast group than by the slow group, both before (P< 0.01) and after (P< 0.02) the turn. In the second part of the study, objectives (2) and (3) were evaluated among 15 swimmers based on a specific protocol. Three cameras (50 Hz) simultaneously recorded the turn; these were placed above the water 10 m before the wall, 5 m before and just above the wall. Longer contact times of the feet on the wall were associated with a faster push-off speed (P < 0. 02). The European Champion achieved an improved contact time while performing a rapid pull-out speed.     

Prediction of 2000 m indoor rowing performance using a 30 s sprint and maximal oxygen uptake

The aim of this study was to predict indoor rowing performance in 12 competitive female rowers (age 21.3 - 3.6 years, height 1.68 - 0.54 m, body mass 67.1 - 11.7 kg; mean - s ) using a 30 s rowing sprint, maximal oxygen uptake and the blood lactate response to submaximal rowing. Blood lactate and oxygen uptake ( V O 2 ) were measured during a discontinuous graded exercise test on a Concept II rowing ergometer incremented by 25 W for each 2 min stage; the highest V O 2 measured during the test was recorded as V O 2max (mean = 3.18 - 0.35 l· min -1 ). Peak power (380 - 63.2 W) and mean power (368 - 60.0 W) were determined using a modified Wingate test protocol on the Concept II rowing ergometer. Rowing performance was based on the results of the 2000 m indoor rowing championship in 1997 (466.8 - 12.3 s). Laboratory testing was performed within 3 weeks of the rowing championship. Submitting mean power (Power), the highest and lowest five consecutive sprint power outputs (Maximal and Minimal), percent fatigue in the sprint test (Fatigue), V O 2max (l· min -1 ), V O 2max (ml·kg -1 ·min -1 ), V O 2 at the lactate threshold, power at the lactate threshold (W), maximal lactate concentration, lactate threshold (percent V O 2max ) and V E max (l·min -1 ) to a stepwise multiple regression analysis produced the following model to predict 2000 m rowing performance: Time 2000 =- 0.163 (Power)14.213 ·( V O 2max l· min -1 ) + 0.738· (Fatigue) + 567.259 ( R 2 = 0.96, standard error = 2.89). These results indicate that, in the women studied, 75.7% of the variation in 2000 m indoor rowing performance time was predicted by peak power in a rowing Wingate test, while V O 2max and fatigue during the Wingate test explained an additional 12.1% and 8.2% of the variance, respectively.