Effect of blood lactate concentration and the level of oxygen uptake immediately before a cycling sprint on neuromuscular activation during repeated cycling sprints

The purpose of this study was to determine whether neuromuscular activation is affected by blood lactate concentration (La) and the level of oxygen uptake immediately before a cycling sprint (preVO(2)). The tests consisted of ten repeated cycling sprints for 10 sec with 35-sec (RCS(35)) and 350-sec recovery periods (RCS(350)). Peak power output (PPO) was not significantly changed despite an increase in La concentration up to 12 mmol/L in RCS(350). Mean power frequency (MPF) of the power spectrum calculated from a surface electromyogram on the vastus lateralis showed a significantly higher level in RCS(350). In RCS(35), preVO(2) level and La were higher than those in RCS(350) in the initial stage of the RCS and in the last half of the RCS, respectively. Thus, neuromuscular activation during exercise with maximal effort is affected by blood lactate concentration and the level of oxygen uptake immediately before exercise, suggesting a cyclic system between muscle recruitment pattern and muscle metabolites.     

Effects of heat exposure in the absence of hyperthermia on power output during repeated cycling sprints

The aim of this study was to investigate the effects of heat exposure in the absence of hyperthermia on power output during repeated cycling sprints. Seven males performed four 10-s cycling sprints interspersed by 30 s of active recovery on a cycle ergometer in hot-dry and thermoneutral environments. Changes in rectal temperature were similar under the two ambient conditions. The mean 2-s power output over the 1st–4th sprints was significantly lower under the hot-dry condition than under the thermoneutral condition. The amplitude of the electromyogram was lower under the hot-dry condition than under the thermoneutral condition during the early phase (0–3 s) of each cycling sprint. No significant difference was observed for blood lactate concentration between the two ambient conditions. Power output at the onset of a cycling sprint during repeated cycling sprints is decreased due to heat exposure in the absence of hyperthermia.     

Blood lactate disappearance at various intensities of recovery exercise

Numerous studies have reported that following intense exercise the rate of blood lactate (La) disappearance is greater during continuous aerobic work than during passive recovery. Recent work indicates that a combination of high- and low-intensity work may be optimal in reducing blood La. We tested this hypothesis by measuring the changes in blood La levels following maximal exercise during four different recovery patterns. Immediately following 50 S of maximal work, subjects (n = 7) performed one of the following recovery treatments for 40 min: 1) passive recovery (PR); 2) cycling at 35% maximal O2 uptake (VO2 max) (35% R); 3) cycling at 65% VO2 max (65% R); 4) cycling at 65% for 7 min followed by cycling at 35% for 33 min (CR). The treatment order was counterbalanced with each subject performing all treatments. Serial blood samples were obtained throughout recovery treatments and analyzed for La. The rate of blood La disappearance was significantly greater (P less than 0.05) in both the 35% R and CR when compared with either the 65% R or PR. No significant difference (P greater than 0.05) existed in the rate of blood La disappearance between the 35% R and CR. These data do not support the hypothesis that exercise recovery at a combination of intensities is superior to a recovery involving continuous submaximal exercise in lowering blood La following maximal work.     

Acid-base balance during repeated cycling sprints in boys and men.

The aim of this study was to investigate the acid-base balance during repeated cycling sprints in children and adults. Eleven boys (9.6 +/- 0.7 yr) and ten men (20.4 +/- 0.8 yr) performed ten 10-s sprints on a cycle ergometer separated by 30-s passive recovery intervals. To measure the time course of lactate ([La]), hydrogen ions ([H(+)]), bicarbonate ions ([HCO(3)(-)]), and base excess concentrations and the arterial partial pressure of CO(2), capillary blood samples were collected at rest and after each sprint. Ventilation and CO(2) output were continuously measured. After the 10th sprint, concentrations of boys vs. men were as follows: [La], 8.5 +/- 2.1 vs. 15.4 +/- 2.0 mmol/l; [H(+)], 43.8 +/- 1.3 vs. 66.9 +/- 9.9 nmol/l (P < 0.001). Significant correlations showed that, for a given [La], [H(+)] was lower in the boys compared with the men (P < 0.001). Significant relationships also indicated that, for a given [La], [HCO(3)(-)] and base excess concentration were similar in the boys compared with the men. Moreover, significant relationships revealed that, for a given [H(+)] or [HCO(3)(-)], arterial partial pressure of CO(2) was lower in the boys compared with the men (P < 0.001). The ventilation-to-CO(2) output ratio was higher in the boys during the first five rest intervals and was then higher in the men during the last five sprints. To conclude, during repeated sprints, the ventilatory regulation related to the change in acid-base balance induced by lactic acidosis was more important during the first rest intervals in the boys compared with the men.     

Human growth hormone responses to repeated bouts of sprint exercise with different recovery periods between bouts.

This study examined the growth hormone (GH) response to repeated bouts of sprint cycling. Eight healthy men completed three trials consisting of two 30-s sprints on a cycle ergometer separated by either 60 min (Trial A) or 240 min (Trial B) of recovery and a single 30-s sprint carried out the day after Trial B (Trial C). Trials A and B were separated by at least 7 days. Blood samples were obtained at rest and during recovery from each sprint. In Trial A, GH was elevated immediately before sprint 2, and there was no further increase in GH following the second sprint [area under the curve: 460 (SD 348) vs. 226 min.mug(-1).l(-1) (SD 182), P = 0.05]. Free insulin-like growth factor I tended to be lower immediately before sprint 2 than sprint 1 (P = 0.06). Serum free fatty acids were not different immediately before each of the sprints. In Trial B, there was a trend for a smaller GH response to the second sprint [GH area under the curve: 512 (SD 396) vs. 242 min.mug(-1).l(-1) (SD 190), P = 0.09]. Free insulin-like growth factor I tended to be lower (P = 0.06), and serum free fatty acids were higher (P = 0.01) immediately before sprint 2 than sprint 1. There was no difference in the GH response to sprinting on consecutive days (Trials B and C). In conclusion, repeated bouts of sprint cycling on the same day result in an attenuation or even ablation of the exercise-induced increase in GH, depending on the recovery interval between sprints.     

Maximal intermittent cycling exercise: effects of recovery duration and gender.

This study aimed to evaluate potential gender differences in recovery of power output during repeated all-out cycling exercise. Twenty men and thirteen women performed four series of two sprints (Sp1 and Sp2) of 8 s, separated by 15-, 30-, 60-, and 120-s recovery. Peak power (Ppeak), power at the 8th s, total mechanical work, and time to Ppeak were calculated for each sprint. Ppeak and mechanical work decreased significantly between Sp1 and Sp2 after 15-s recovery in both men (-6.4 and -9.4%, respectively) and women (-7.4 and -6.8%, respectively). Time to Ppeak did not change between recovery durations, but women reached their peak power more slowly than men (on average 5.15 +/- 1.2 and 3.8 +/- 1.2 s, respectively; P < 0.01). During Sp1 and Sp2, linear regressions from Ppeak to power at the 8th s showed a greater power decrease (%Ppeak) in women compared with men (P < 0.05). In conclusion, patterns of power output recovery between two consecutive short bouts were similar in men and women, despite lower overall performance and greater fatigability during sprints in women.     

EFFECT OF THE NUMBER OF SPRINT REPETITIONS ON THE VARIATION OF BLOOD LACTATE CONCENTRATION IN REPEATED SPRINT SESSIONS

The aim of the present study was to examine the effect of number of sprint repetitions on the variation of blood lactate concentration (blood [La]) during different repeated-sprint sessions in order to find the appropriate number of sprint repetitions that properly simulates the physiological demands of team sport competitions. Twenty male team-sport players (age, 22.2 ± 2.9 years) performed several repeated-sprint sessions (RSS) consisting of 1, 2, 3, 4, 5, 9, or 10 repetitions of 30 m shuttle sprints (2 × 15 m) with 30 s recovery in between. The blood [La] was obtained after 3 min of recovery at the end of each RSS. The present study showed that for RSS of 3 sprints (RSS3) there was a high increase (p<0.001) in blood [La], which reached approximately fivefold resting values (9.4±1.7 mmol · l⁻¹) and then remained unchanged for the RSS of 4 and 5 sprints (9.6±1.4 and 10.5±1.9 mmol · l⁻¹, p=0.96 and 0.26, respectively). After RSS9 and RSS10 blood [La] further significantly increased to 12.6 and 12.7 mmol · l⁻¹, p<0.001, respectively. No significant difference was found between RSS3, RSS4 and RSS5 for the percentage of sprint speed decrement (Sdec) (1.5±1.2; 2.0±1.1 and 2.6±1.4%, respectively). There was also no significant difference between RSS9 and RSS10 for Sdec (3.9±1.3% and 4.5±1.4%, respectively). In conclusion, the repeated-sprint protocol composed of 5 shuttle sprint repetitions is more representative of the blood lactate demands of the team sports game intensity.     

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

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 less than 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 less than 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 mumol.l-1, SD 33.5, for the 15-s sprint, 130.2 mumol.l-1, SD 44.9, for the 30-s sprint, and 120.8 mumol.l-1, SD 24.6, for the 45-s sprint. Peak blood lactates after the 15-, 30- and 45-s sprints were 8.1 mmol.l-1, SD 1.7, 11.2 mmol.l-1, SD 2.4, and 14.7 mmol.l-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 less than 0.05), 30-s (r, 0.797; P less than 0.05) and 45-s (r, 0.696; P less than 0.05) sprints. Though the peak blood lactate content increased significantly with increasing duration of the sprints (P less than 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.     

The influence of recovery duration after heavy resistance exercise on sprint cycling performance

ABSTRACT: Thatcher, R, Gifford, R, and Howatson, G. The influence of recovery duration after heavy resistance exercise on sprint cycling performance. J Strength Cond Res 26(11): 3089-3094, 2012-The aim of this study was to determine the optimal recovery duration after prior heavy resistance exercise (PHRE) when performing sprint cycling. On 5 occasions, separated by a minimum of 48 hours, 10 healthy male subjects (mean ± SD), age 25.5 ± 7.7 years, body mass 82.1 ± 9.0 kg, stature 182.6 ± 87 cm, deadlift 1-repetition maximum (1RM) 142 ± 19 kg performed a 30-second sprint cycling test. Each trial had either a 5-, 10-, 20-, or 30-minute recovery after a heavy resistance activity (5 deadlift repetitions at 85% 1RM) or a control trial with no PHRE in random order. Sprint cycling performance was assessed by peak power (PP), fatigue index, and mean power output over the first 5 seconds (MPO5), 10 seconds (MPO10), and 30 seconds (MPO30). One-way analysis of variance with repeated measures followed by paired t-tests with a Bonferroni adjustment was used to analyze data. Peak power, MPO5, and MPO10 were all significantly different during the 10-minute recovery trial to that of the control condition with values of 109, 112, and 109% of control, respectively; no difference was found for the MPO30 between trials. This study supports the use of PHRE as a strategy to improve short duration, up to, or around 10-second, sprint activity but not longer duration sprints, and a 10-minute recovery appears to be optimal to maximize performance.     

Impaired interval exercise responses in elite female cyclists at moderate simulated altitude.

The effect of hypoxia on the response to interval exercise was determined in eight elite female cyclists during two interval sessions: a sustained 3 x 10-min endurance set (5-min recovery) and a repeat sprint session comprising three sets of 6 x 15-s sprints (work-to-relief ratios were 1:3, 1:2, and 1:1 for the 1st, 2nd, and 3rd sets, respectively, with 3 min between each set). During exercise, cyclists selected their maximum power output and breathed either atmospheric air (normoxia, 20.93% O(2)) or a hypoxic gas mix (hypoxia, 17.42% O(2)). Power output was lower in hypoxia vs. normoxia throughout the endurance set (244+/-18 vs. 226+/-17, 234+/-18 vs. 221+/-25, and 235+/-18 vs. 221+/-25 W for 1st, 2nd, and 3rd sets, respectively; P< 0.05) but was lower only in the latter stages of the second and third sets of the sprints (452+/-56 vs. 429+/-49 and 403+/-54 vs. 373+/- 43 W, respectively; P<0.05). Hypoxia lowered blood O(2) saturation during the endurance set (92.9+/-2.9 vs. 95.4+/-1.5%; P<0.05) but not during repeat sprints. We conclude that, when elite cyclists select their maximum exercise intensity, both sustained (10 min) and short-term (15 s) power are impaired during hypoxia, which simulated moderate ( approximately 2,100 m) altitude.     

Continuous intramuscular pH measurement during the recovery from brief, maximal exercise in man

Muscle pH and temperature were measured before, and continuously for 30 min after, a 30-s maximal sprint exercise in ten subjects. These measurements were made with a needle-tipped pH electrode and a thermocouple placed in vastus lateralis. Venous blood samples were collected for pH, lactate and catecholamine estimations and measurements were also made of the arterial blood pressure and heart rate. The muscle and venous pH decreased from 7.17 +/- 0.01 (mean +/- SEM) and 7.39 +/- 0.01 to 6.57 +/- 0.04 and 7.04 +/- 0.03, respectively, in response to the exercise. No significant recovery occurred in either pH measurement for 10 min, after which muscle pH increased to 7.03 +/- 0.03 and venous pH to 7.29 +/- 0.01 by 30 min. Muscle temperature increased by 2.1 degrees C with exercise and also failed to return to pre-exercise values by 30 min. Blood lactate concentration increased from 0.75 +/- 0.04 mmol l-1 before exercise to a peak value of 15.76 +/- 0.35 mmol l-1 5 min after completion of the exercise, and then declined slowly to 10.30 +/- 0.61 mmol l-1 by 30 min. Arterial blood pressure increased transiently with exercise but recovered rapidly, whereas the exercise-induced tachycardia was sustained throughout the recovery period. The recovery from the metabolic and cardiovascular responses to maximal sprint exercise in man is incomplete 30 min after cessation of the exercise.     

The growth hormone response to repeated bouts of sprint exercise with and without suppression of lipolysis in men.

A single 30-s sprint is a potent physiological stimulus for growth hormone (GH) release. However, repeated bouts of sprinting attenuate the GH response, possibly due to negative feedback via elevated systemic free fatty acids (FFA). The aim of the study was to use nicotinic acid (NA) to suppress lipolysis to investigate whether serum FFA can modulate the GH response to exercise. Seven nonobese, healthy men performed two trials, consisting of two maximal 30-s cycle ergometer sprints separated by 4 h of recovery. In one trial (NA), participants ingested NA (1 g 60 min before, and 0.5 g 60 and 180 min after sprint 1); the other was a control (Con) trial. Serum FFA was not significantly different between trials before sprint 1 but was significantly lower in the NA trial immediately before sprint 2 [NA vs. Con: mean (SD); 0.08 (0.05) vs. 0.75 (0.34) mmol/l, P < 0.05]. Peak and integrated GH were significantly greater following sprint 2 compared with sprint 1 in the NA trial [peak GH: 23.3 (7.0) vs. 7.7 (11.9) microg/l, P < 0.05; integrated GH: 1,076 (350) vs. 316 (527) microg.l(-1).60 min(-1), P < 0.05] and compared with sprint 2 in the Con trial [peak GH: 23.3 (7.0) vs. 5.2 (2.3) microg/l, P < 0.05; integrated GH: 1,076 (350) vs. 206 (118) microg.l(-1).60 min(-1), P < 0.05]. In conclusion, suppressing lipolysis resulted in a significantly greater GH response to the second of two sprints, suggesting a potential role for serum FFA in negative feedback control of the GH response to repeated exercise.     

Maximal lactate steady-state independent of recovery period during intermittent protocol

Barbosa, LF, de Souza, MR, Corrêa Caritá, RA, Caputo, F, Denadai, BS, and Greco, CC. Maximal lactate steady-state independent of recovery period during intermittent protocol. J Strength Cond Res 25(12): 3385-3390, 2011-The purpose of this study was to analyze the effect of the measurement time for blood lactate concentration ([La]) determination on [La] (maximal lactate steady state [MLSS]) and workload (MLSS during intermittent protocols [MLSSwi]) at maximal lactate steady state determined using intermittent protocols. Nineteen trained male cyclists were divided into 2 groups, for the determination of MLSSwi using passive (VO(2)max = 58.1 ± 3.5 ml·kg·min; N = 9) or active recovery (VO(2)max = 60.3 ± 9.0 ml·kg·min; N = 10). They performed the following tests, in different days, on a cycle ergometer: (a) Incremental test until exhaustion to determine (VO(2)max and (b) 30-minute intermittent constant-workload tests (7 × 4 and 1 × 2 minutes, with 2-minute recovery) to determine MLSSwi and MLSS. Each group performed the intermittent tests with passive or active recovery. The MLSSwi was defined as the highest workload at which [La] increased by no more than 1 mmol·L between minutes 10 and 30 (T1) or minutes 14 and 44 (T2) of the protocol. The MLSS (Passive-T1: 5.89 ± 1.41 vs. T2: 5.61 ± 1.78 mmol·L) and MLSSwi (Passive-T1: 294.5 ± 31.8 vs. T2: 294.7 ± 32.2 W; Active-T1: 304.6 ± 23.0 vs. T2: 300.5 ± 23.9 W) were similar for both criteria. However, MLSS was lower in T2 (4.91 ± 1.91 mmol·L) when compared with in T1 (5.62 ± 1.83 mmol·L) using active recovery. We can conclude that the MLSSwi (passive and active conditions) was unchanged whether recovery periods were considered (T1) or not (T2) for the interpretation of [La] kinetics. In contrast, MLSS was lowered when considering the active recovery periods (T2). Thus, shorter intermittent protocols (i.e., T1) to determine MLSSwi may optimize time of the aerobic capacity evaluation of well-trained cyclists.     

Growth hormone responses to repeated maximal cycle ergometer exercise at different pedaling rates.

The present study examined the growth hormone (GH) response to repeated bouts of maximal sprint cycling and the effect of cycling at different pedaling rates on postexercise serum GH concentrations. Ten male subjects completed two 30-s sprints, separated by 1 h of passive recovery on two occasions, against an applied resistance equal to 7.5% (fast trial) and 10% (slow trial) of their body mass, respectively. Blood samples were obtained at rest, between the two sprints, and for 1 h after the second sprint. Peak and mean pedal revolutions were greater in the fast than the slow trial, but there were no differences in peak or mean power output. Blood lactate and blood pH responses did not differ between trials or sprints. The first sprint in each trial elicited a serum GH response (fast: 40.8 +/- 8.2 mU/l, slow: 20.8 +/- 6.1 mU/l), and serum GH was still elevated 60 min after the first sprint. The second sprint in each trial did not elicit a serum GH response (sprint 1 vs. sprint 2, P < 0.05). There was a trend for serum GH concentrations to be greater in the fast trial (mean GH area under the curve after sprint 1 vs. after sprint 2: 1,697 +/- 367 vs. 933 +/- 306 min x mU(-1) x l(-1); P = 0.05). Repeated sprint cycling results in an attenuation of the GH response.     

Muscle metabolic status and acid-base balance during 10-s work:5-s recovery intermittent and continuous exercise

Gastrocnemius muscle phosphocreatine ([PCr]) and hydrogen ion ([H(+)]) were measured using (31)P-magnetic resonance spectroscopy during repeated bouts of 10-s heavy-intensity (HI) exercise and 5-s rest compared with continuous (CONT) HI exercise. Recreationally active male subjects (n = 7; 28 yr ± 9 yr) performed on separate occasions 12 min of isotonic plantar flexion (0.75 Hz) CONT and intermittent (INT; 10-s exercise, 5-s rest) exercise. The HI power output in both CONT and INT was set at 50% of the difference between the power output associated with the onset of intracellular acidosis and peak exercise determined from a prior incremental plantar flexion protocol. Intracellular concentrations of [PCr] and [H(+)] were calculated at 4 s and 9 s of the work period and at 4 s of the rest period in INT and during CONT exercise. [PCr] and [H(+)] (mean ± SE) were greater at 4 s of the rest periods vs. 9 s of exercise over the course of the INT exercise bout: [PCr] (20.7 mM ± 0.6 vs. 18.7 mM ± 0.5; P < 0.01); [H(+)] (370 nM ± 13.50 vs. 284 nM ± 13.6; P < 0.05). Average [H(+)] was similar for CONT vs. INT. We therefore suggest that there is a glycolytic contribution to ATP recovery during the very short rest period (<5 s) of INT and that the greater average power output of CONT did not manifest in greater [H(+)] and greater glycolytic contribution compared with INT exercise.     

Performance and fatigue during repeated sprints: what is the appropriate sprint dose?

When testing the ability of sportsmen to repeat maximal intensity efforts, or when designing specific training exercises to improve it, fatigue during repeated sprints is usually investigated through a number of sprints identical for all subjects, which induces a high intersubject variability in performance decrement in a typical heterogeneous group of athletes (e.g., team sport group, students, and research protocol volunteers). Our aim was to quantify the amplitude of the reduction in this variability when individualizing the sprint dose, that is, when requiring subjects to perform the number of sprints necessary to reach a target level of performance decrement. Fifteen healthy men performed 6-second sprints on a cycle ergometer with 24 seconds of rest until exhaustion or until 20 repetitions in case no failure occurred. Peak power output (PPO) was measured and a fatigue index (FI) computed. The variability in PPO decrement was compared between the 10th sprint and the sprint at which subject reached the target FI of 10%. Individual FI values after the 10th sprint were 14.6 ± 6.9 vs. 11.1 ± 1.2%, when individualizing the sprint dose, which corresponded to coefficients of interindividual variability of ～47.3 and ～10.8%, respectively. Individualizing the sprint dose substantially reduced intersubject variability in performance decrement, enabling a more standardized state of fatigue in repeated-sprints protocols designed to induce fatigue and test or train this specific repeated-sprint ability in a heterogeneous group of athletes. A direct feedback on the values of performance parameters is necessary between each sprint for the experimenter to set this individualized sprint dose.     

Myosin phosphorylation, twitch potentiation, and fatigue in human skeletal muscle

Twitch tension and phosphate incorporation into the phosphorylatable light chains (P-light chains) of myosin were studied during a 10-min recovery period following a 10- or 60-s maximal voluntary isometric contraction (MVC) in 18 subjects. Analysis of muscle biopsy samples obtained before, immediately after, 1 min, and 10 min following the 10-s MVC revealed that the 10-s MVC produced a modest but transient metabolic displacement from rest, a 35% decrease in phosphocreatine, and a threefold elevation in lactate concentration. Immediately after the 60-s MVC, ATP was decreased by 20%, phosphocreatine decreased by 84%, and lactate was elevated by 15-fold. Lactate remained elevated over the 10-min recovery period. Twitch force was maximally potentiated following the 10-s MVC and declined to rest by 10 min of recovery. Twitch force was 0.66 of rest value immediately after the 60-s MVC, then increased over the next 4 min to reach a potentiated value 21% greater than rest, before declining. Significant phosphate incorporation into P-light chains was observed immediately after both contractions, but dephosphorylation to rest values at the end of recovery was only noted for the 60-s condition. These results demonstrate an inconsistent relationship between twitch tension enhancement and P-light chain phosphorylation in the in vivo human model.     

The relationship between plasma potassium concentration and muscle torque during recovery following intense exercise

The present study investigated the relationship between plasma potassium ion concentration ([K⁺]) and skeletal muscle torque during three different 15-min recovery periods after fatigue induced by four 30-s sprints. Four males and one female completed the multiple sprint exercise on three separate days; recovery was passive, i.e. no cycling exercise (PRec), active cycling at 30% peak oxygen consumption O_2peak (30% Rec) and active cycling at 60% O_2peak (60% Rec). Plasma [K⁺] was measured from blood sampled from an antecubital vein of subjects at rest and at 0, 3, 5, 10 and 15 min into each recovery. Isokinetic leg strength was measured at rest and at 1, 6, 11 and 16 min during each recovery. Following the exhaustive sprints, [K⁺] increased significantly from an average mean (SEM) resting value of 3.81 (0.07) mmol · l⁻¹ to 4.48 (0.19) mmol · l⁻¹ (P < 0.01). In all recovery conditions, plasma [K⁺] returned to resting levels within 3 min following the fourth sprint. However, in the two active recovery conditions plasma [K⁺] increased over the remainder of the recovery periods to 4.36 (0.12) mmol · l⁻¹ in the 30% Rec condition and 4.62 (0.12) mmol · l⁻¹ in the 60% Rec condition, the latter being significantly higher than the former (P < 0.01). The maximum torque measured following the sprints decreased significantly, on average, to 61.1 (8.36)% of peak levels (P < 0.01). After 15 min of recovery, maximum torque was highest in the 30% Rec condition at 92.13 (3.06)% of peak levels (P < 0.01), compared to 85.23 (3.64)% and 85.71 (0.82)% for the PRec and 60% Rec conditions, respectively. In contrast to the significant differences in plasma [K⁺] across all three recovery conditions, muscle torque recovery was significantly different in only the 30% Rec condition. In summary, recovery of peak levels of muscle torque following fatiguing exercise does not appear to follow changes in plasma [K⁺]. Accepted: 18 October 1996     

Relationship between hyperventilation and excessive CO2 output during recovery from repeated cycling sprints

The purpose of the present study was to examine whether excessive CO2 output (VCO2excess) is dominantly attributable to hyperventilation during the period of recovery from repeated cycling sprints. A series of four 10-sec cycling sprints with 30-sec passive recovery periods was performed two times. The first series and second series of cycle sprints (SCS) were followed by 360-sec passive recovery periods (first recovery and second recovery). Increases in blood lactate (DeltaLa) were 11.17+/-2.57 mM from rest to 5.5 min during first recovery and 2.07+/-1.23 mM from the start of the second SCS to 5.5 min during second recovery. CO2 output (VCO2) was significantly higher than O2 uptake (VO2) during both recovery periods. This difference was defined as VCO2excess. VCO2excess was significantly higher during first recovery than during second recovery. VCO2excess was added from rest to the end of first recovery and from the start of the second SCS to the end of second recovery (CO2excess). DeltaLa was significantly related to CO2excess (r=0.845). However, ventilation during first recovery was the same as that during second recovery. End-tidal CO2 pressure (PETCO2) significantly decreased from the resting level during the recovery periods, indicating hyperventilation. PETCO2 during first recovery was significantly higher than that during second recovery. It is concluded that VCO2excess is not simply determined by ventilation during recovery from repeated cycle sprints.     

Respiratory alkalosis: no effect on blood lactate decline or exercise performance

It was the purpose of this study to determine the effects of respiratory alkalosis before and after high intensity exercise on recovery blood lactate concentration. Five subjects were studied under three different acid-base conditions before and after 45 s of maximal effort exercise: 1) hyperventilating room air before exercise (Respiratory Alkalosis Before = RALB, 2) hyperventilating room air during recovery (Respiratory Alkalosis After = RALA), and 3) breathing room air normally throughout rest and recovery (Control = C). RALB increased blood pH during rest to 7.65 +/- 0.03 while RALA increased blood pH to 7.57 +/- 0.03 by 40 min of recovery. Neither alkalosis treatment had a significant effect on blood lactate concentration during recovery. The peak lactate values of 12.3 +/- 1.2 mmol.L-1 for C, 11.8 +/- 1.2 mmol.L-1 for RALB, and 10.2 +/- 0.9 mmol.L-1 for RALA were not significantly different, nor were the half-times (t 1/2) for the decline in blood lactate concentration; C = 18.2 min, RALB = 19.3 min, and RALA = 18.2 min. In C, RALB and RALA, the change in base excess from rest to postexercise was greater than the concomitant increase in blood lactate concentration, suggesting the presence of a significant amount of acid in the blood in addition to lactic acid. There was no significant difference in either the total number of cycle revolutions (C = 77 +/- 2, RALB = 77 +/- 1) or power output at 5 s intervals between RALB and C during the 45 s.(ABSTRACT TRUNCATED AT 250 WORDS)