Cadence Paradox in Cycling-Part 2: Theory and Simulation of Maximal Lactate Steady State and Carbohydrate Utilization Dependent on Cycling Cadence.

PURPOSE: To develop and evaluate a theory on the frequent observation that cyclists prefer cadences (RPMs) higher than those considered most economical at submaximal exercise intensities via modeling and simulation of its mathematical description. METHODS: The theory combines the parabolic power-to-velocity (v) relationship, where v is defined by crank length, RPM-dependent ankle velocity, and gear ratio, RPM effects on the maximal lactate steady state (MLSS), and lactate-dependent carbohydrate oxidation (CHO). It was tested against recent experimental results of 12 healthy male recreational cyclists determining the v-dependent peak oxygen uptake (VO2PEAKv), MLSS (MLSSv), corresponding power output (PMLSSv), oxygen uptake at PMLSSv (VO2MLSSv), and CHOMLSSv-management at 100 versus 50 per minute, respectively. Maximum RPM (RPMMAX) attained at minimized pedal torque was measured. RPM-specific maximum sprint power output (PMAXv) was estimated at RPMs of 100 and 50, respectively. RESULTS: Modeling identified that MLSSv and PMLSSv related to PMAXv (IPMLSSv) promote CHO and that VO2MLSSv related to VO2PEAKv inhibits CHO. It shows that cycling at higher RPM reduces IPMLSSv. It suggests that high cycling RPMs minimize differences in the reliance on CHO at MLSSv between athletes with high versus low RPMMAX. CONCLUSIONS: The present theory-guided modeling approach is exclusively based on data routinely measured in high-performance testing. It implies a higher performance reserve above IPMLSSv at higher RPM. Cyclists may prefer high cycling RPMs because they appear to minimize differences in the reliance on CHO at MLSSv between athletes with high versus low RPMMAX.

Cadence Paradox in Cycling-Part 1: Maximal Lactate Steady State and Carbohydrate Utilization Dependent on Cycling Cadence.

PURPOSE: To assess (1) whether and how a higher maximal lactate steady state (MLSS) at higher cycling cadence (RPM) comes along with higher absolute and/or fractional carbohydrate combustion (CHOMLSS), respectively, and (2) whether there is an interrelation between potential RPM-dependent MLSS effects and the maximally achievable RPM (RPMMAX). METHODS: Twelve healthy males performed incremental load tests to determine peak power, peak oxygen uptake, and 30-minute MLSS tests at 50 and 100 per minute, respectively, to assess RPM-dependent MLSS, corresponding power output, CHOMLSS responses, and 6-second sprints to measure RPMMAX. RESULTS: Peak power, peak carbon dioxide production, and power output at MLSS were lower (P = .000, ω2 = 0.922; P = .044, ω2 > 0.275; and P = .016, ω2 = 0.373) at 100 per minute than at 50 per minute. With 6.0 (1.5) versus 3.8 (1.2) mmol·L-1, MLSS was higher (P = .000, ω2 = 0.771) at 100 per minute than at 50 per minute. No corresponding RPM-dependent differences were found in oxygen uptake at MLSS, carbon dioxide production at MLSS, respiratory exchange ratio at MLSS, CHOMLSS, or fraction of oxygen uptake used for CHO at MLSS, respectively. There was no correlation between the RPM-dependent difference in MLSS and RPMMAX. CONCLUSIONS: The present study extends the previous finding of a consistently higher MLSS at higher RPM by indicating (1) that at fully established MLSS conditions, respiration and CHOMLSS management do not differ significantly between 100 per minute and 50 per minute, and (2) that linear correlation models did not identify linear interdependencies between RPM-dependent MLSS conditions and RPMMAX.

Lactate response to short term exercise with elevated starting levels.

A model that describes the blood lactate concentration (BLC) dynamics [BLC(t)] of a Wingate Anaerobic Test (WAnT) as a function of (a) BLC at the start of exercise (BLC(0)), (b) extra-vascular increase in lactate (A), (c) two corresponding velocity constants of appearance (k (1)) and disappearance (k (2)) of lactate into and out of the blood requires that BLC(0) is equal to resting BLC (BLC(rest)). We developed a model that considers an elevated BLC(0). 19 males performed WAnTs with warm-ups increasing (p < 0.001) BLC(0). The goodness of each individual fit improved (p < 0.05) if the difference between BLC(rest) and BLC(0) (DeltaBLC) was higher than 1.0 mmol l(-1). All differences between old and new model (p < 0.05) in A, k (1) and k (2) were interrelated with and increased with DeltaBLC (p < 0.05). The new model well describes BLC(t) and prevents substantial errors concerning lactate generation and dynamics if BLC(0) is elevated by more than 1.0 mmol l(-1).

Carbohydrate and fat metabolism related to blood lactate in boys and male adolescents.

The half maximal constant (k (el)) of the relative rate of carbohydrate oxidation (relCHO) was individually approximated (relCHO = 100/(1 + k (el)/BLC(2)) as a function of the blood lactate concentration (BLC) in 11 pre-pubertal boys and 11 male adolescents (age: 11.6 +/- 0.1 vs. 16.4 +/- 0.2 years, height: 151.6 +/- 1.7 vs. 182.4 +/- 2.3 cm, body mass: 38.2 +/- 1.1 vs. 68.7 +/- 2.3 kg, all P < 0.001) during incremental cycle ergometry. k (el) explained 89.0 +/- 2.2 and 91.9 +/- 2.2% of the variance of the reliance on CHO in boys and adolescents respectively (both P < 0.001). No difference in k (el) [1.34 +/- 0.40 vs. 1.48 +/- 0.30 (mmol l(-1))(2)] was found between boys and adolescents. The BLC was lower (P < 0.05) in boys when relCHO was higher than 91.2 +/- 2.1 and 92.1 +/- 1.3% in boys and adolescents respectively. This seems to explain why the reliance on CHO and the BLC are independent of maturation in the moderate and heavy exercise intensity domain and the BLC but not the relCHO which is higher under severe and maximal exercise conditions in more mature subjects.

The Effects of Maximally Achievable Cycling Cadence on Carbohydrate Management at Moderate and Heavy Exercise Intensity.

Effects of different cycling cadences (revolutions/min [rpm]) on metabolic rate, blood lactate concentration (BLC), and reliance on carbohydrate (CHO) defined as the fraction of oxygen uptake used for CHO oxidation (relCHO) are highly individual. Whether this depends on the individually maximal achievable rpm obtained at minimized cycling resistance (rpmmax) is unknown. The authors tested the hypotheses that the individual freely chosen rpm in an incremental cycle-ergometer test (ILT) and relCHO at given BLC levels both depend on rpmmax. Seven master cyclists and 8 not specifically trained leisure athletes performed an ILT at individually freely chosen rpm and an rpmmax test. Respiratory data and BLC were measured; relCHO was plotted as a function of the BLC for the determinations of the individual BLC at relCHO of 75% and 95% (BLC75% and BLC95%). With 16.7%, the between-subjects variability of individual rpm was high but independent from rpmmax. In the master athletes, rpmmax explained 59.3% and 95.2% of BLC75% (P = .043) and BLC95% (P = .001), respectively. Irrespective of cycling experience, the individually preferred average rpm at submaximal stages of an ILT is highly variable and independent of rpmmax. In experienced cyclists, carbohydrate management defined as the ratio between substrate availability as indicated by BLC and relCHO depends on rpmmax.

Exercise-induced hemolysis is caused by protein modification and most evident during the early phase of an ultraendurance race.

Whether structural changes of the erythrocyte membrane increase the susceptibility to hemolysis particularly of the relatively older cell population during the early phase of a 216-km ultrarace was tested in six male runners (age 53.6 +/- 10.4 yr, height 175.8 +/- 11.1 cm, body mass 75.9 +/- 8.4 kg). Erythrocyte membrane spectrins were lowest (P < 0.001) after 42 km (75.59 +/- 5.25% of prerace) and increased (P < 0.001) toward 216 km (88.27 +/- 3.37%). Susceptibility to osmotic hemolysis was highest (P < 0.01) after 42 km (107.34 +/- 3.02 mOsm sodium phosphate buffer) with almost identical (P > 0.05) values prerace (97.98 +/- 3.41 mOsm) and postrace (98.61 +/- 3.26 mOsm). Haptoglobin indicated intravascular hemolysis of 9.27 x 10(9) cells/l (P < 0.05) during the initial 84 km. Changes in hematocrit and plasma proteins indicated an estimated total net erythrocyte loss of 3.47 x 10(11) cells/l (P < 0.05) after 21 km. This was compensated by a gain in erythrocytes (P < 0.05) of 3.31 x 10(11) cells/l during the final 132 km. A main effect (P < 0.05) on erythropoietin suggests increased erythropoiesis throughout the race. Exercise-induced hemolysis reflects alterations in erythrocyte membrane spectrins and occurs particularly in the early phase of an ultraendurance race because of a relative older cell population.

Modelling the lactate response to short-term all out exercise.

BACKGROUND: The maximum post exercise blood lactate concentration (BLCmax) has been positively correlated with maximal short-term exercise (MSE) performance. However, the moment when BLCmax occurs (TBLCmax) is rather unpredictable and interpretation of BLC response to MSE is therefore difficult. METHODS: We compared a 3- and a 4-parameter model for the analysis of the dynamics of BLC response to MSEs lasting 10 (MSE10) and 30 s (MSE30) in eleven males (24.6 +/- 2.3 yrs; 182.4 +/- 6.8 cm; 75.1 +/- 9.4 kg). The 3-parameter model uses BLC at MSE-start, extra-vascular increase (A) and rate constants of BLC appearance (k1) and disappearance (k2). The 4-parameter model includes BLC at MSE termination and amplitudes and rate constants of increase (A1, y1) and decrease (A2, y2) of post MSE-BLC. RESULTS: Both models consistently explained 93.69 % or more of the variance of individual BLC responses. Reduction of the number of parameters decreased (p < 0.05) the goodness of the fit in every MSE10 and in 3 MSE30. A (9.1 +/- 2.1 vs. 15.3 +/- 2.1 mmol l-1) and A1 (7.1 +/- 1.6 vs. 10.9 +/- 2.0 mmol l-1) were lower (p < 0.05) in MSE10 than in MSE30. k1 (0.610 +/- 0.119 vs. 0.505 +/- 0.107 min-1), k2 (4.21 10-2 +/- 1.06 10-2 vs. 2.45 10-2 +/- 1.04 10-2 min-1), and A2 (-563.8 +/- 370.8 vs. -1412.6 +/- 868.8 mmol l-1), and y1 (0.579 +/- 0.137 vs. 0.489 +/- 0.076 min-1) were higher (p < 0.05) in MSE10 than in MSE30. No corresponding difference in y2 (0.41 10-2 +/- 0.82 10-2 vs. 0.15 10-2 +/- 0.42 10-2 min-1) was found. CONCLUSION: The 3-parameter model estimates of lactate appearance and disappearance were sensitive to differences in test duration and support an interrelation between BLC level and halftime of lactate elimination previously found. The 4-parameter model results support the 3-parameter model findings about lactate appearance; however, parameter estimates for lactate disappearance were unrealistic in the 4-parameter model. The 3-parameter model provides useful information about the dynamics of the lactate response to MSE.

Maximal Lactate Steady State's Dependence on Cycling Cadence.

The maximal lactate steady state (MLSS) depicts the highest blood lactate concentration (BLC) that can be maintained over time without a continual accumulation at constant prolonged workload. In cycling, no difference in the MLSS was combined with lower power output related to peak workload (IMLSS) at 100 than at 50 rpm. MLSS coincides with a respiratory exchange ratio (RER) close to 1. Recently, at incremental exercise, an RER of 1 was found at similar workload and similar intensity but higher BLC at 100 than at 50 rpm. Therefore, the authors reassessed a potential effect of cycling cadences on the MLSS and tested the hypothesis that the MLSS would be higher at 105 than at 60 rpm with no difference in IMLSS in a between-subjects design (n = 16, age 25.1 ± 1.9 y, height 178.4 ± 6.5 cm, body mass 70.3 ± 6.5 kg vs n = 16, 23.6 ± 3.0 y, 181.4 ± 5.6 cm, 72.5 ± 6.2 kg; study I) and confirmed these findings in a within-subject design (n = 12, 25.3 ± 2.1 y, 175.9 ± 7.7 cm, 67.8 ± 8.9 kg; study II). In study I, the MLSS was lower at 60 than at 105 rpm (4.3 ± 0.7 vs 5.4 ± 1.0 mmol/L; P = .003) with no difference in IMLSS (68.7% ± 5.3% vs 71.8% ± 5.9%). Study II confirmed these findings on MLSS (3.4 ± 0.8 vs 4.5 ± 1.0 mmol/L; P = .001) and IMLSS (65.0% ± 6.8% vs 63.5% ± 6.3%; P = .421). The higher MLSS at 105 than at 60 rpm combined with an invariance of IMLSS and RER close to 1 at MLSS supports the hypothesis that higher cadences can induce a preservation of carbohydrates at given BLC levels during low-intensity, high-volume training sessions.

Enhancement on Wingate Anaerobic Test Performance With Hyperventilation.

UNLABELLED: Relatively long-lasting metabolic alkalizing procedures such as bicarbonate ingestion have potential for improving performance in long-sprint to middle-distance events. Within a few minutes, hyperventilation can induce respiratory alkalosis. However, corresponding performance effects are missing or equivocal at best. PURPOSE: To test a potential performance-enhancing effect of respiratory alkalosis in a 30-s Wingate Anaerobic Test (WAnT). METHODS: 10 men (mean ± SD age 26.6 ± 4.9 y, height 184.4 ± 6.1 cm, body-mass test 1 80.7 ± 7.7 kg, body-mass test 2 80.4 ± 7.2 kg, peak oxygen uptake 3.95 ± 0.43 L/min) performed 2 WAnTs, 1 with and 1 without a standardized 15-min hyperventilation program pre-WAnT in randomized order separated by 1 wk. RESULTS: Compared with the control condition, hyperventilation reduced (all P < .01) pCO2 (40.5 ± 2.8 vs 22.5 ± 1.6 mm Hg) and HCO3 - (25.5 ± 1.7 vs 22.7 ± 1.6 mmol/L) and increased (all P < .01) pH (7.41 ± 0.01 vs 7.61 ± 0.03) and actual base excess (1.4 ± 1.4 vs 3.2 ± 1.6 mmol/L) pre-WAnT with an ergogenic effect on WAnT average power (681 ± 41 vs 714 ± 44 W) and total metabolic energy (138 ± 12 vs. 144 ± 13 kJ) based on an increase in glycolytic energy (81 ± 13 vs 88 ± 13 kJ). CONCLUSION: Hyperventilation-induced respiratory alkalosis can enhance WAnT cycling sprint performance well in the magnitude of what is seen after successful bicarbonate ingestion.

Modeling the blood lactate kinetics at maximal short-term exercise conditions in children, adolescents, and adults.

Whether age-related differences in blood lactate concentrations (BLC) reflect specific BLC kinetics was analyzed in 15 prepubescent boys (age 12.0 +/- 0.6 yr, height 1.54 +/- 0.06 m, body mass 40.0 +/- 5.2 kg), 12 adolescents (16.3 +/- 0.7 yr, 1.83 +/- 0.07 m, 68.2 +/- 7.5 kg), and 12 adults (27.2 +/- 4.5 yr, 1.83 +/- 0.06 m, 81.6 +/- 6.9 kg) by use of a biexponential four-parameter kinetics model under Wingate Anaerobic Test conditions. The model predicts the lactate generated in the extravasal compartment (A), invasion (k(1)), and evasion (k(2)) of lactate into and out of the blood compartment, the BLC maximum (BLC(max)), and corresponding time (TBLC(max)). BLC(max) and TBLC(max) were lower (P < 0.05) in boys (BLC(max) 10.2 +/- 1.3 mmol/l, TBLC(max) 4.1 +/- 0.4 min) than in adolescents (12.7 +/- 1.0 mmol/l, 5.5 +/- 0.7 min) and adults (13.7 +/- 1.4 mmol/l, 5.7 +/- 1.1 min). No differences were found in A related to the muscle mass (A(MM)) and k(1) between boys (A(MM): 22.8 +/- 2.7 mmol/l, k(1): 0.865 +/- 0.115 min(-1)), adolescents (22.7 +/- 1.3 mmol/l, 0.692 +/- 0.221 min(-1)), and adults (24.7 +/- 2.8 mmol/l, 0.687 +/- 0.287 min(-1)). The k(2) was higher (P < 0.01) in boys (2.87 10(-2) +/- 0.75 10(-2) min(-1)) than in adolescents (2.03 x 10(-2) +/- 0.89 x 10(-2) min(-1)) and adults (1.99 x 10(-2) +/- 0.93 x 10(-2) min(-1)). Age-related differences in the BLC kinetics are unlikely to reflect differences in muscular lactate or lactate invasion but partly faster elimination out of the blood compartment.

Effect of test interruptions on blood lactate during constant workload testing.

OBJECTIVE: To determine whether repetitive test interruptions (TI) during constant load testing influence blood lactate concentration (BLC), maximal lactate steady state (MLSS), MLSS workload (P-MLSS), and relative MLSS intensity (Int-MLSS). METHODS: Nineteen males participated in this study. In experiment A, 10 subjects (27.5 +/- 2.9 yr; 183.7 +/- 5.2 cm; 77.4 +/- 3.7 kg) performed 30-min constant load tests: one without TI, one with TI of 30 s, and one with TI of 90 s after every 5 min of cycling at a given workload. In experiment B, nine subjects (28.0 +/- 2.7 yr; 182.9 +/- 6.8 cm; 76.2 +/- 4.5 kg) performed 30-min constant load tests at different workloads until MLSS had been determined for all three TI protocols. RESULTS: In experiment A, the BLC after 30 min net working time (BLC30) was higher (P < 0.001) without TI (6.0 +/- 1.3 mmol.l(-1)) than with TI of 30 s (4.9 +/- 1.4 mmol.l(-1)) or 90 s (4.5 +/- 1.1 mmol.l(-1)). The change in BLC during the final 20 min (DeltaBLC10-30) was greater (P < 0.01) without TI (1.2 +/- 1.0 mmol.l(-1)) than with TI of 30 s (0.2 +/- 0.7 mmol.l(-1)) or 90 s (-0.3 +/- 0.7 mmol.l(-1)). In experiment B, the MLSS was not affected, but P-MLSS and Int-MLSS were lower (P < 0.01) without TI (277.8 +/- 24.4W and 73.7 +/- 7.6%) than with TI of 30 s (300.4 +/- 30.4W and 79.2 +/- 8.0%) or 90 s (310.0 +/- 31.2W and 81.5 +/- 7.1%). Approximately 35% of the variance of BLC30 and DeltaBLC10-30, and 70% of the variance of P-MLSS and Int-MLSS were explained by TI duration (P < 0.001). CONCLUSIONS: TI decreased BLC30 and DeltaBLC10-30 but has no effect on MLSS. Consequently, with TI, the MLSS is achieved at higher P-MLSS and Int-MLSS.

The energetics of semicontact 3 x 2-min amateur boxing.

UNLABELLED: The energy expenditure of amateur boxing is unknown. PURPOSE: Total metabolic cost (Wtot) as an aggregate of aerobic (Waer), anaerobic lactic (W[lactate]), and anaerobic alactic (WPCr) energy of a 3 × 2-min semicontact amateur boxing bout was analyzed. METHODS: Ten boxers (mean ± SD [lower/upper 95% confidence intervals]) age 23.7 ± 4.1 (20.8/26.6) y, height 180.2 ± 7.0 (175.2/185.2) cm, body mass 70.6 ± 5.7 (66.5/74.7) kg performed a semicontact bout against handheld pads created from previously analyzed video footage of competitive bouts. Net metabolic energy was calculated using respiratory gases and blood [lactate]. RESULTS: Waer, 526.0 ± 57.1 (485.1/566.9) kJ, was higher (P < .001) than WPCr, 58.1 ± 13.6 (48.4/67.8) kJ. W[lactate], 26.2 ± 7.1 (21.1/31.3) kJ, was lower (P < .001) than Waer and WPCr. An ~70-kJ fraction of the aerobic energy expenditure reflects rephosphorylation of high-energy phosphates during the breaks between rounds, which elevated Wtot to ~680 kJ with relative contributions of 77% Waer, 19% WPCr, and 4% W[lactate]. CONCLUSIONS: The results indicate that the metabolic profile of amateur boxing is predominantly aerobic. They also highlight the importance of a highly developed aerobic capacity as a prerequisite of a high activity rate during rounds and recovery of the high-energy phosphate system during breaks as interrelated requirements of successful boxing.

Blood lactate diagnostics in exercise testing and training.

A link between lactate and muscular exercise was seen already more than 200 years ago. The blood lactate concentration (BLC) is sensitive to changes in exercise intensity and duration. Multiple BLC threshold concepts define different points on the BLC power curve during various tests with increasing power (INCP). The INCP test results are affected by the increase in power over time. The maximal lactate steady state (MLSS) is measured during a series of prolonged constant power (CP) tests. It detects the highest aerobic power without metabolic energy from continuing net lactate production, which is usually sustainable for 30 to 60 min. BLC threshold and MLSS power are highly correlated with the maximum aerobic power and athletic endurance performance. The idea that training at threshold intensity is particularly effective has no evidence. Three BLC-orientated intensity domains have been established: (1) training up to an intensity at which the BLC clearly exceeds resting BLC, light- and moderate-intensity training focusing on active regeneration or high-volume endurance training (Intensity < Threshold); (2) heavy endurance training at work rates up to MLSS intensity (Threshold ≤ Intensity ≤ MLSS); and (3) severe exercise intensity training between MLSS and maximum oxygen uptake intensity mostly organized as interval and tempo work (Intensity > MLSS). High-performance endurance athletes combining very high training volume with high aerobic power dedicate 70 to 90% of their training to intensity domain 1 (Intensity < Threshold) in order to keep glycogen homeostasis within sustainable limits.