Maximum Phonation Time as a Predictor of Lactate Threshold during Intermittent Incremental Endurance Test.

The aim of the present study was to examine whether the exercise intensity corresponding to the lactate threshold may be predicted by the Maximum Phonation Time task (MPT). Ten Greek amateur football players (age: 18.4 ± 1.0 years), performed a graded cycling exercise test to exhaustion in order to determine lactate threshold. A number of physiological variables were measured including perceived exertion, cardiopulmonary values and blood lactate. The MPT variable was correlated with all of the physiological variables. Also, a binary logistic regression analysis was used to investigate whether MPT could predict lactate threshold. The ROC analysis showed specificity to be 0.90 and sensitivity to be 0.70 (optimal screening cutoff point for MPT 9.5 seconds). The results showed an odds ratio of 1.45 indicating a 45% increase in the probability of passing the threshold for every second there was a reduction in voice duration. MPT may be used as a simple, non-invasive, inexpensive method for monitoring exercise intensity during physical exercise. Further research is needed to measure its efficacy in bigger samples and in different sports.

Effects of high-intensity interval cycling performed after resistance training on muscle strength and hypertrophy.

Aim of the study was to investigate whether high-intensity interval cycling performed immediately after resistance training would inhibit muscle strength increase and hypertrophy expected from resistance training per se. Twenty-two young men were assigned into either resistance training (RE; N = 11) or resistance training plus high-intensity interval cycling (REC; N = 11). Lower body muscle strength and rate of force development (RFD), quadriceps cross-sectional area (CSA) and vastus lateralis muscle architecture, muscle fiber type composition and capillarization, and estimated aerobic capacity were evaluated before and after 8 weeks of training (2 times per week). Muscle strength and quadriceps CSA were significantly and similarly increased after both interventions. Fiber CSA increased significantly and similarly after both RE (type I: 13.6 ± 3.7%, type IIA: 17.6 ± 4.4%, type IIX: 23.2 ± 5.7%, P < 0.05) and REC (type I: 10.0 ± 2.7%, type IIA: 14.8 ± 4.3% type IIX: 20.8 ± 6.0%, P < 0.05). In contrast, RFD decreased and fascicle angle increased (P < 0.05) only after REC. Capillary density and estimated aerobic capacity increased (P < 0.05) only after REC. These results suggest that high-intensity interval cycling performed after heavy-resistance exercise may not inhibit resistance exercise-induced muscle strength/hypertrophy after 2 months of training, while it prompts aerobic capacity and muscle capillarization. The addition of high-intensity cycling after heavy-resistance exercise may decrease RFD partly due to muscle architectural changes.

Knee Extension Strength and Hamstrings-to-Quadriceps Imbalances in Elite Soccer Players.

This study examined the relationship between hamstrings-to-quadriceps strength ratio (H:Q) and relative strength of the knee extensors in elite soccer players. Peak torque was measured during isokinetic knee extension/flexion at angular velocities of 60°·s(-1), 180°·s(-1) and 300°·s(-1). 18 professional players were divided into 2 groups, depending on their H:Q at 60°·s(-1). Players in the lower H:Q group (n=7) had significantly smaller H:Q ratios compared with the higher H:Q group (n=11) at all angular velocities (60°·s(-1): 49.2%; 95% CI: 61.3-57.8% vs. 59.5%; 95% CI: 52.2-46.2%, p=0.001). Players in the lower H:Q group had greater knee-extension peak torque compared with the higher H:Q group (60°·s(-1): 313; 95% CI: 335-291 vs. 269; 95% CI: 289-250 N·m, p=0.01). No differences were found in hamstrings' strength between the 2 groups (60°·s(-1): 156; 95% CI: 170-143 vs. 160; 95% CI: 173-148 N·m, p=0.96). Negative correlations between knee extension peak torque and H:Q ratio were observed at all angular velocities (r=-0.65 to -0.67, p<0.01). In conclusion, a low H:Q strength ratio measured during isokinetic strength testing in professional soccer players, is observed mainly in those with strong quadriceps muscles, while players with lower quadriceps strength have H:Q ratios around the recommended values.

Comparison of inflammatory responses and muscle damage indices following a soccer, basketball, volleyball and handball game at an elite competitive level.

Inflammatory responses and muscle damage indices were compared between four popular team sports at an elite level. Seventy two male elite players of four team sports: soccer (n = 18), basketball (n = 18), volleyball (n = 18) and handball (n = 18), completed an official match, while 18 non-athletes served as controls. Blood samples were drawn before, immediately after and 13 and 37 h post-match. Soccer produced the greatest increase in inflammatory cytokines (tumor necrosis factor-alpha and interleukin-6), which were increased by 3-4 fold immediately after the game, as well as in C-reactive protein, which was increased by threefold in the next morning after the match. Metabolic stress (urea, ammonia and cortisol) and muscle damage indices (creatine kinase and lactate dehydrogenase) were also higher after soccer, with creatine kinase responses being almost 2-3 times higher than the other sports. Volleyball showed the smallest increase in inflammation and muscle damage markers compared with the other three sports.

Changes in the lipid profile of elite basketball and soccer players after a match.

The lipid profile of elite basketball and soccer athletes was evaluated and compared with that of inactive individuals. Total cholesterol (T-C), low and high density lipoprotein cholesterol (LDL-C and HDL-C), and triglyceride (TG) concentration were measured in the morning and after a soccer or a basketball match. All parameters of lipid profile measured at a fasted and resting state, except HDL-C, were lower in the athletes compared with the controls (p < 0.01). The soccer match resulted in a greater decrease in TG (78.3 ± 6.7 to 70.7 ± 6.3, p < 0.01), T-C (179.3 ± 10.7 to 171.6 ± 9.6, p < 0.01), LDL-C (110.9 ± 8.9 to 103.5 ± 7.5, p < 0.01) compared with the basketball match that resulted only in a decrease in LDL-C (126.8 ± 9.5 to 117.3 ± 9.1, p < 0.01) and an increase in HDL-C that was similar to that observed after the soccer match (9-12%). These findings support the beneficial effects of basketball and soccer on cardiovascular health.

Short-term high-intensity interval exercise training attenuates oxidative stress responses and improves antioxidant status in healthy humans.

This study investigated the changes in oxidative stress biomarkers and antioxidant status indices caused by a 3-week high-intensity interval training (HIT) regimen. Eight physically active males performed three HIT sessions/week over 3 weeks. Each session included four to six 30-s bouts of high-intensity cycling separated by 4 min of recovery. Before training, acute exercise elevated protein carbonyls (PC), thiobarbituric acid reactive substances (TBARS), glutathione peroxidase (GPX) activity, total antioxidant capacity (TAC) and creatine kinase (CK), which peaked 24h post-exercise (252 ± 30%, 135 ± 17%, 10 ± 2%, 85 ± 14% and 36 ± 13%, above baseline, respectively; p<0.01), while catalase activity (CAT) peaked 30 min post-exercise (56 ± 18% above baseline; p<0.01). Training attenuated the exercise-induced increase in oxidative stress markers (PC by 13.3 ± 3.7%; TBARS by 7.2 ± 2.7%, p<0.01) and CK activity, despite the fact that total work done was 10.9 ± 3.6% greater in the post- compared with the pre-training exercise test. Training also induced a marked elevation of antioxidant status indices (TAC by 38.4 ± 7.2%; CAT by 26.2 ± 10.1%; GPX by 3.0 ± 0.6%, p<0.01). Short-term HIT attenuates oxidative stress and up-regulates antioxidant activity after only nine training sessions totaling 22 min of high intensity exercise, further supporting its positive effect not only on physical conditioning but also on health promotion.

Changes in homocysteine and 8-iso-PGF(2a) levels in football and hockey players after a match.

The aim of the present study was to evaluate the levels of homocysteine and 8-iso PGF(2a) in football and hockey players before and soon after a match, on the predisposition for development of atherosclerosis. We measured 8-iso-PGF(2a) and homocysteine in 21 football athletes aged 21.8 ± 3.7 years old and 18 hockey athletes 22.2 ± 3.3 years old, respectively. All the athletes presented significant increases in serum homocysteine levels following the match (p = 0.001 for football and p = 0.001 for hockey players) Also a statistically significant increase of 8-iso-PGF(2a) levels was found in hockey and football athletes following the match (p < 0.001 and p = 0.071). Our findings suggest that strenuous exercise such as a football or a hockey match causes a marked increase in serum homocysteine and 8-iso-PGF(2a). Due to the fact that homocysteine and 8-iso-PGF(2a) are contributing to atheromatosis, it may be useful to follow a restoration exercise program that involves mild exercise and to pay special attention to folate, vitamin B6, and vitamin B12 balance during the first 24 h after the match.

Immune responses during and after exercise of constant and alternating intensity above the lactate threshold.

AIM: Intense and prolonged exercise greatly affects circulating cytokine levels. The purpose of this study was to investigate the possible changes in tumour necrosis factor -a (TNF-a), interleukin 6 (IL-6) and cortisol concentrations during and after prolonged exercise of constant and alternating intensity of the same duration and total work performed. METHODS: Ten male subjects underwent two main cycling exercise trials lasting one hour each. On one occasion, exercise intensity was alternated between 46.5±1.9% of maximal oxygen uptake (VO2max ) for 40 s and 120% of VO2max for 20 s, so that the mean intensity corresponded to 105% of the lactate threshold. On the other occasion, exercise intensity was constant at 105% of the lactate threshold. Levels of TNF-a, IL-6 after lipo polysaccharide (LPS) stimulation as well as cortisol were measured at rest, 30 and 60 minutes of exercise and 1 hour after. RESULTS: No significant differences were observed in TNF-a concentrations between the two exercise protocols (P= 0.75), but there was a significant time effect (P<0.01). TNF-a was increased in both groups from a resting value of 436.1±102.5 to 649.5±187.7 pg/mL (P<0.05) at the end of exercise and was subsequently decreased 1 hour post exercise to 305.9±78.8 pg/mL (P<0.01). No significant difference in IL-6 and cortisol concentrations was observed between the two exercise protocols (P=0.13, P=0.10 accordingly). CONCLUSION: In conclusion, prolonged constant and alternating intensity exercise of the same mean intensity and duration seemed to provoke similar changes in aspects of immune response in healthy subjects.

Changes in the mechanical properties of human quadriceps muscle after eccentric exercise.

Muscular adaptation which occurs following eccentric exercise-induced muscle damage has been associated with changes in the mechanical properties of muscle manifested as a shift in the length-tension relationship towards longer muscle lengths. However, it is not clear whether this shift is a long term adaptation to eccentric exercise. The purpose of this study was to investigate functional adaptations to skeletal muscle damage in humans, tracking such responses several days into muscle recovery. Ten healthy young men performed an eccentric exercise protocol involving the quadriceps muscle and functional measurements were performed before and on days 1, 2, 5, 8, 12 and 16 post-exercise. Blood samples were also withdrawn before and at 6 h, and 2 days, 5 days and 16 days post-exercise. The exercise protocol resulted in muscle damage, indicated by changes in clinical markers including increased serum creatine kinase activity and muscle soreness compared to pre-exercise levels (p<0.05-0.001). An acute, but not sustained shift in the quadriceps isokinetic and isometric angle-torque curves towards longer muscle lengths was observed post-exercise (p<0.05). It was speculated that the functional adaptations following eccentric exercise might be affected by the short resting and functional length of the quadriceps muscle, relative to its optimum. More studies are needed to confirm the hypothesis that a sustained shift in the muscle's length-tension relationship, as an adaptation after lengthening contraction-induced damage, is muscle specific.

Expression of IGF-1 isoforms after exercise-induced muscle damage in humans: characterization of the MGF E peptide actions in vitro.

Different insulin-like growth factor-1 (IGF-1) isoforms, namely IGF-1Ea, IGF-1Eb and IGF-1Ec (MGF), have been proposed to have various functions in muscle repair and growth. To gain insight into the potentially differential actions of IGF-1 isoforms in the regulation of muscle regeneration, we assessed the time course of their expressions at both mRNA and protein levels after exercise-induced muscle damage in humans. In addition, we characterized mature IGF-1 and synthetic MGF E peptide signalling in C2C12 myoblast-like cells in vitro. Ten healthy male volunteers were subjected to exercise-induced muscle damage and biopsy samples were taken from the exercised muscles before and 6 h, 2, 5 and 16 days post exercise. Muscle damage was documented by specific functional and biochemical responses post exercise. PCR-based analyses of muscle biopsy samples revealed a rapid and transient up-regulation of MGF mRNA expression which was followed by a prolonged increase of IGF-1Ea and IGF-1Eb mRNA expression (p<0.05). Patterns similar to those for mRNA expression were detected for MGF and IGF-1Ea expression at the protein level. The action of synthetic MGF E peptide differed from that of mature IGF-1 since its proliferative effect on C2C12 myoblast-like cells was not blocked by an anti-IGF-1 receptor neutralizing antibody and it did not phosphorylate Akt. Therefore, we conclude that the differential expression profile of IGF-1 isoforms in vivo and the possible IGF-1R - independent MGF E peptide signalling in skeletal muscle-like cells in vitro support the notion that tissue-specific mRNA expression of MGF isoform produces mature IGF-1 and MGF E peptides which possibly act as distinct mitogens in skeletal muscle regeneration.

Cardiorespiratory and metabolic responses to a simulated synchronized swimming routine in senior (>18 years) and comen (13-15 years) national level athletes.

AIM: This study examined the ventilatory responses and blood lactate concentration after a simulated synchronized swimming routine of athletes of two different age categories. METHODS: Sixteen trained female synchronized swimmers, 8 competing at the comen category (age: 13.8+/-0.2 years) and 8 competing at the senior category (age: 22.6+/-0.9 years), performed a maximal 400 m swimming test and a simulated synchronized swimming routine. Oxygen uptake (VO(2)) of the tests was obtained by backward extrapolation of a monoexponential curve fitted to the postexercise oxygen uptake data. RESULTS: There were no differences in VO(2) at the end of the routine (37.4+/-2.7 vs 40.5+/-2 mL . kg(-1) . min(-1), or 81.8+/-3.1% and 85.8+/-2.7% of VO(2peak)) and blood lactate (5.7+/-0.9 vs 4.5+/-0.4 mmol.L(-1)) between senior and comen synchronized swimmers. There was no difference in the half-time of V.O(2) decay (T(1/2)) between the athletes of the two categories, but T(1/2) was significantly higher after the routine compared with the V.O(2peak) test for both categories (senior: 45.2+/-5.9 vs 33.1+/-2.1 s, P<0.05, comen: 38.2+/-6 vs 27.4+/-8.2 s, P<0.05). The mean end-tidal pressure of CO(2) during the second half of the recovery was higher after the routine than after the VO(2peak) test (37.2+/-1.4 vs 34.5+/-1.5 mmHg, P<0.05), possibly due to the prolonged periods of breath holding (55+/-4% of routine time). Breathing frequency was also high (30+/-2.2 breaths . min(-1)) at the later part of recovery after the routine. CONCLUSION: Cardiorespiratory and metabolic responses to a simulated synchronized swimming routine were similar in senior and comen athletes. The slower recovery of V.O(2)after the routine could be related to the elevated cost of ventilation, especially during the later stages of recovery, possibly as a result of the prolonged apnea.

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.

A model for phosphocreatine resynthesis.

A model for phosphocreatine (PCr) resynthesis is proposed based on a simple electric circuit, where the PCr store in muscle is likened to the stored charge on the capacitor. The solution to the second-order differential equation that describes the potential around the circuit suggests the model for PCr resynthesis is given by PCr(t) = R - [d1.exp(-k1.t) +/- d2.exp(-k2.t)], where R is PCr concentration at rest, d1, d2, k1, and k2 are constants, and t is time. By using nonlinear least squares regression, this double-exponential model was shown to fit the PCr recovery data taken from two studies involving maximal exercise accurately. In study 1, when the muscle was electrically stimulated while occluded, PCr concentrations rose during the recovery phase to a level above that observed at rest. In study 2, after intensive dynamic exercise, PCr recovered monotonically to resting concentrations. The second exponential term in the double-exponential model was found to make a significant additional contribution to the quality of fit in both study 1(P < 0.05) and study 2(P < 0.01).

Contribution of phosphocreatine and aerobic metabolism to energy supply during repeated sprint exercise.

This study examined the contribution of phosphocreatine (PCr) and aerobic metabolism during repeated bouts of sprint exercise. Eight male subjects performed two cycle ergometer sprints separated by 4 min of recovery during two separate main trials. Sprint 1 lasted 30 s during both main trials, whereas sprint 2 lasted either 10 or 30 s. Muscle biopsies were obtained at rest, immediately after the first 30-s sprint, after 3.8 min of recovery, and after the second 10- and 30-s sprints. At the end of sprint 1, PCr was 16.9 +/- 1.4% of the resting value, and muscle pH dropped to 6.69 +/- 0.02. After 3.8 min of recovery, muscle pH remained unchanged (6.80 +/- 0.03), but PCr was resynthesized to 78.7 +/- 3.3% of the resting value. PCr during sprint 2 was almost completely utilized in the first 10 s and remained unchanged thereafter. High correlations were found between the percentage of PCr resynthesis and the percentage recovery of power output and pedaling speed during the initial 10 s of sprint 2 (r = 0.84, P < 0.05 and r = 0.91, P < 0.01). The anaerobic ATP turnover, as calculated from changes in ATP, PCr, and lactate, was 235 +/- 9 mmol/kg dry muscle during the first sprint but was decreased to 139 +/- 7 mmol/kg dry muscle during the second 30-s sprint, mainly as a result of a approximately 45% decrease in glycolysis. Despite this approximately 41% reduction in anaerobic energy, the total work done during the second 30-s sprint was reduced by only approximately 18%. This mismatch between anaerobic energy release and power output during sprint 2 was partly compensated for by an increased contribution of aerobic metabolism, as calculated from the increase in oxygen uptake during sprint 2 (2.68 +/- 0.10 vs. 3.17 +/- 0.13 l/min; sprint 1 vs. sprint 2; P < 0.01). These data suggest that aerobic metabolism provides a significant part (approximately 49%) of the energy during the second sprint, whereas PCr availability is important for high power output during the initial 10 s.

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 (W) during sprint 2, compared with passive recovery [W] 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) mumol .l-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) l.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.

Recovery of power output and muscle metabolites following 30 s of maximal sprint cycling in man.

1. The recovery of power output and muscle metabolites was examined following maximal sprint cycling exercise. Fourteen male subjects performed two 30 s cycle ergometer sprints separated by 1.5, 3 and 6 min of recovery, on three separate occasions. On a fourth occasion eight of the subjects performed only one 30 s sprint and muscle biopsies were obtained during recovery. 2. At the end of the 30 s sprint phosphocreatine (PCr) and ATP contents were 19.7 +/- 1.2 and 70.5 +/- 6.5% of the resting values (rest), respectively, while muscle lactate was 119.0 +/- 4.6 mmol (kg dry wt)-1 and muscle pH was 6.72 +/- 0.06. During recovery, PCr increased rapidly to 65.0 +/- 2.8% of rest after 1.5 min, but reached only 85.5 +/- 3.5% of rest after 6 min of recovery. At the same time ATP and muscle pH remained low (19.5 +/- 0.9 mmol (kg dry wt)-1 and 6.79 +/- 0.02, respectively). Modelling of the individual PCr resynthesis using a power function curve gave an average half-time for PCr resynthesis of 56.6 +/- 7.3 s. 3. Recovery of peak power output (PPO), peak pedal speed (maxSp) and mean power during the initial 6 s (MPO6) of sprint 2 did not reach the control values after 6 min of rest, and occurred in parallel with the resynthesis of PCr, despite the low muscle pH. High correlations (r = 0.71-0.86; P < 0.05) were found between the percentage resynthesis of PCr and the percentage restoration of PPO, maxSp and MPO6 after 1.5 and 3 min of recovery. No relationship was observed between muscle pH recovery and power output restoration during sprint 2 (P > 0.05). 4. These data suggest that PCr resynthesis after 30 s of maximal sprint exercise is slower than previously observed after dynamic exercise of longer duration, and PCr resynthesis is important for the recovery of power during repeated bouts of sprint exercise.

Effects of previous dynamic arm exercise on power output during repeated maximal sprint cycling.

This study examined the effects of elevating blood lactate concentration by arm exercise on subsequent performance during repeated 30 s sprints with the legs. Eight male students performed two 30 s cycle ergometer sprints separated by 6 min of recovery, on two occasions. On one occasion the subjects performed only the two 30 s cycle ergometer sprints ('legs'), while on the other occasion 5 min of heavy arm cranking preceded the two sprints ('arms and legs'). Blood lactate concentration was determined from capillary samples at rest, after a standardized warm-up and 3 and 5 min following each exercise bout. In the 'legs' condition, the peak power output (PPO) and mean power output (MPO) in the second sprint were 92% (P < 0.05) and 85% (P < 0.01) of the values attained during the first sprint, respectively. Prior arm exercise, which increased blood lactate to 11.0 +/- 0.6 mM, had no effect on PPO and MPO during the first cycle ergometer sprint (approximately 4% drop, N.S.). However, in the second sprint after prior arm exercise, PPO was 10% lower than the PPO attained during the corresponding sprint in the 'legs' condition (sprint 2 'arms and legs' 963 +/- 42 W, sprint 2 'legs' 1074 +/- 60 W, P < 0.05), while MPO was better maintained (sprint 2 'arms and legs' 517 +/- 17 W, sprint 2 'legs' 549 +/- 24 W, N.S.). The rate of blood lactate accumulation after both cycle ergometer sprints was considerably decreased (by approximately 50%) when blood lactate levels were pre-elevated by arm crank exercise.(ABSTRACT TRUNCATED AT 250 WORDS)