Biomedical subjects

M E Nevill

Publications and source records attributed to M E Nevill.

At least 19 recordsLinked to original sources

PubMed2006

The reliability and validity of a field hockey skill test.

High test retest reliability is essential in tests used for both scientific research and to monitor athletic performance. Thirty-nine (20 male and 19 female) well-trained university field hockey players volunteered to participate in the study. The reliability of the in house designed test was determined by repeating the test (3 - 14 days later) following full familiarisation. The validity was assessed by comparing coaches ranks of players with ranked performance on the skill test. The mean difference and confidence limits in overall skill test performance was 0.0 +/- 1.0 % and the standard error (confidence limits) was 2.1 % (1.7 to 2.8 %). The mean difference and confidence limits for the "decision making" time was 0.0 +/- 1.0 % and the standard error (confidence limits) was 4.5 % (3.6 to 6.2 %). The validity correlation (Pearson) was r = 0.83 and r = 0.73 for female players and r = 0.61 and r = 0.70 for male players for overall time and "decision making" time respectively. We conclude that the field hockey skill test is a reliable measure of skill performance and that it is valid as a predictor of coach-assessed hockey performance, but the validity is greater for female players.

Decision Making↗

PubMed2005

Muscle metabolism, temperature, and function during prolonged, intermittent, high-intensity running in air temperatures of 33 degrees and 17 degrees C.

Nine unacclimatized university sportsmen performed a prolonged, intermittent, high-intensity shuttle running test in hot (HT) (33 degrees C, dry bulb temperature, approximately 28 %, relative humidity) and moderate (MT) (17 degrees C, 63 %) environmental conditions. Subjects performed 60 m of walking, a 15-m sprint, 60 m of cruising ( approximately 85 % V.O (2max)), and 60 m of jogging ( approximately 45 %V.O (2max)) for 14.8 +/- 0.1 min followed by a 3-min rest, repeated until volitional exhaustion. The hot trial was performed first followed, 14 days later, by the moderate trial. During exercise subjects drank water ad libitum. Subjects ran almost twice as far in the moderate as in the hot trial (HT 11216 +/- 1411, MT 21644 +/- 1629, m, p < 0.01), and the decline in average 15-m sprint performance was greater in the heat (HT, 0.17 +/- 0.05, MT, 0.09 +/- 0.03, s, p < 0.05). Average heart rates, blood lactate and glucose, and plasma adrenaline and noradrenaline concentrations were greater in the HT (main effect trial, p < 0.01), as were serum cortisol concentration (main effect trial p < 0.05, n = 5) and muscle temperature (HT exhaustion vs. same time point in MT, 40.2 +/- 0.3 vs. 39.3 +/- 0.2, degrees C, p < 0.01). Peak torque during knee flexion and extension was not different pre-and post-exercise in the HT. Muscle glycogen utilization tended to be greater in the heat (HT 193.2 +/- 19.5, MT 143.8 +/- 23.9, mmol . kg dry wt (-1), p = 0.055, n = 8). In 7 out of the 8 subjects the increase in utilization was between 19 and just over 200 % greater in the HT. Glycogen remaining in the muscle at exhaustion was greater in the hot than moderate trial (HT 207.4 +/- 34.3, MT 126.5 +/- 46.8, mmol . kg dry wt (-1), p < 0.01, n = 8). Rectal temperature (T (rec)) was higher in the HT at exhaustion than at the same point in time in the moderate trial (HT, 39.60 +/- 0.15 vs. MT 38.75 +/- 0.10, degrees C, interaction trial-time, p < 0.01). There was a very strong negative relationship between rate of rise in T (rec) and distance completed in the HT (HT r = - 0.90, p < 0.01, MT r = - 0.76, p < 0.05). Thus, the earlier onset of exhaustion during prolonged intermittent shuttle running in the heat is associated with hyperthermia. However, while muscle glycogen utilization may be elevated by heat stress, low whole muscle glycogen concentrations would not seem to be the cause of this earlier exhaustion.

Adult↗

PubMed2002

The time course of the human growth hormone response to a 6 s and a 30 s cycle ergometer sprint.

Exercise is a potent stimulus for the release of human growth hormone (hGH), but the time course of the hGH response to sprint exercise has not been studied. The aim of the present study was to determine the time course of the hGH response to a 6 s and a 30 s maximal sprint on a cycle ergometer. Nine males completed two trials, on one occasion performing a single 6 s sprint and on another a single 30 s sprint. They then rested on a couch for 4 h while blood samples were obtained. Three of the participants completed a further control trial involving no exercise. Metabolic responses were greater after the 30 s sprint than after the 6 s sprint. The highest measured mean serum hGH concentrations after the 30 s sprint were more than 450% greater than after the 6 s sprint (18.5 +/- 3.1 vs 4.0 +/- 1.5 microg l(-1), P < 0.05). Serum hGH also remained elevated for 90-120 min after the 30 s sprint compared with approximately 60 min after the 6 s sprint. There was a large inter-individual variation in the hGH response to the 30 s sprint. In the control trial, serum hGH concentrations were not elevated above baseline at any time. It would appear that the duration of a bout of maximal sprint exercise determines the magnitude of the hGH response, although the mechanism for this is still unclear.

Adolescent↗

PubMed2002

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.

Adult↗

PubMed2000

Physiological and metabolic responses of female games and endurance athletes to prolonged, intermittent, high-intensity running at 30 degrees and 16 degrees C ambient temperatures.

Eight female games players (GP) and eight female endurance athletes (EA) ran intermittently at high-intensity and for prolonged periods in hot (30 degrees C) and moderate (16 degrees C) ambient temperatures. The subjects performed a two-part (A, B) test based on repeated 20-m shuttle runs. Part A comprised 60 m of walking, a maximal 15-m sprint, 60 m of cruising (90% maximal oxygen uptake, VO(2max)) and 60 m of jogging (45% VO(2max)) repeated for 75 min with a 3-min rest every 15 min. Part B involved an exercise and rest pattern of 60-s running at 100% VO(2max) and 60-s rest which was continued until fatigue. Although the GP and EA did not respond differently in terms of distances completed, performance was 25 (SEM 4)% less (main effect trial, P < 0.01) in the hot (HT) compared with the moderate trial (MT). Sprints of 15 m took longer to complete in the heat (main effect, trial, P < 0.01), and sprint performance declined during HT but not MT (interaction, trial x time, P < 0.01). A very high correlation was found between the rate of rise in rectal temperature in HT and the distance completed [GP, r =-0.94, P < 0. 01; EA (n = 7), r = -0.93, P < 0.01]. Blood lactate [La(-) ](b) and plasma ammonia [NH(3)](p1) concentrations were higher for GP than EA, but were similar in HT and MT [La(-) ](b), HT: GP vs EA, 8.0 (SEM 0. 9) vs 4.9 (SEM 1.1) mmol x l(-1); MT: GP vs EA, 8.0 (SEM 1.3) vs 4.4 (SEM 1.2) mmol x l(-1); interaction, group x time, P < 0.01; [NH(3)](p1), HT: GP vs EA, 70.1 (SEM 12.7) vs 43.2 (SEM 6.1) mmol x l(-1); MT: GP vs EA, 76.8 (SEM 8.8) vs 32.5 (SEM 3.8) micromol x l(-1); interaction, group x time, P < 0.01. Ad libitum water consumption was higher in HT [HT: GP vs EA, 18.9 (SEM 2.9) vs 13.5 (SEM 1.7) ml x kg(-1) x h(-1); MT: GP vs EA, 12.7 (SEM 3.7) vs 8.5 (SEM 1.5) ml x kg(-1) x h(-1); main effect, group, n.s.; main effect, trial, P < 0.01]. These results would suggest that elevated body temperature is probably the key factor limiting performance of prolonged, intermittent, high-intensity running when the ambient temperature is high, but not because of its effect on the metabolic responses to exercise.

Adult↗

PubMed1998

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.

Acid-Base Equilibrium↗

PubMed1998

Rapid recovery of power output in females.

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

Adenosine Triphosphate↗

PubMed1998

Modelling the relationship between isokinetic muscle strength and sprint running performance.

Muscle strength is thought to be a major factor in athletic success. However, the relationship between muscle strength and sprint performance has received little attention. The aim of this study was to examine the relationship in elite performers of isokinetic muscle strength across three lower limb joints and sprinting performance, including the use of theoretical models. Eight rugby players, eight track sprinters and eight competitive sportsmen, all elite national or regional competitors, performed sprints over 15 m and 35 m with times recorded over 0-15 m and 30-35 m. Isokinetic torque was measured at the knee, hip and ankle joints at low (1.05 rad s(-1)), intermediate (2.09 or 2.62 rad s(-1)) and high (3.14 or 4.19 rad s(-1)) speeds during concentric and eccentric muscle actions. Using linear regression and expressing sprint performance as time, the strongest relationship, for the joint actions and speeds tested, was between concentric knee extension at 4.19 rad s(-1) and sprint performance (0-15 m times: r=-0.518, P< 0.01; 30-35 m times: r=-0.688, P< 0.01). These relationships were improved for 0-15 m, but not for 30-35 m, by expressing torque relative to body mass (0-15 m times: r=-0.581; 30-35 m times: r=-0.659). When 0-15 m performance was expressed as acceleration rather than time, the correlation was improved slightly (r=0.590). However, when the data (0-15 m times) were fitted to the allometric force model proposed by Gunther, 77% of the variance in concentric knee extension torque at 4.19 rad s(-1) could be explained by 0-15 m times, limb length (knee to buttocks) and body mass. The fitted parameters were similar to those from the theoretical model. These findings suggest that the relationship between isokinetic muscle strength and sprint performance over 0-15 m (during the acceleration phase) is improved by taking limb length and body mass into account.

Analysis of Variance↗

PubMed1998

The effects of oral creatine supplementation on performance in single and repeated sprint swimming.

We studied the effects of oral creatine supplementation on sprint swimming performance in 14 elite competitive male swimmers. The subjects performed a single sprint (1 x 50 yards [45.72 m]) and repeated sprint set (8 x 50 yards at intervals of 1 min 30 s) before and after a 5 day period of either creatine (9 g creatine + 4.5 g maltodextrin + 4.5 g glucose day(-1)) or placebo (18 g glucose day(-1); double-blind protocol) supplementation. Venous and capillary blood samples were taken for the determination of plasma ammonia, blood pH and lactate. Mean times recorded for the single 50 yard sprint were unchanged as a result of supplementation (creatine vs control, N.S.). During the repeated sprint test, mean times increased (P< 0.01, main effect time) during all trials, but performance was improved as a result of creatine supplementation (sprints 1-8: control pre-, 23.35+/-0.68 to 26.32+/-1.34 s; control post-, 23.59+/-0.66 to 26.19+/-1.48 s; creatine pre-, 23.20+/-0.67 to 26.85+/-0.42 s; creatine post-, 23.39+/-0.54 to 25.73+/-0.26 s; P < 0.03, group x trial interaction). Thus the percentage decline in performance times was reduced after creatine supplementation (control, 12.7+/-5.7% vs 11.0+/-5.5%; creatine, 15.7+/-4.3% vs 10.0+/-2.5%; P< 0.05, group x trial interaction). The metabolic response was similar before and after supplementation, with no differences in the blood lactate or pH response. Plasma ammonia was lower on the second trial (P< 0.05, main effect trial), but this could not be attributed to the effect of supplementation (group x trial interaction, N.S.). A further urinary analysis study supported these findings by demonstrating an approximately 67% (approximately 26 g) retention of the administered creatine in this group of swimmers after an identical supplementation regimen. In summary, our results suggest that ingesting 9 g creatine per day for 5 days can improve swimming performance in elite competitors during repeated sprints, but appears to have no effect on a single 50 yard sprint.

Adult↗

PubMed1997

Constant external work cycle exercise--the performance and metabolic effects of all-out and even-paced strategies.

The purpose of the present study was to establish whether the performance of an all-out sprint could be replicated and the metabolic responses moderated in two further trials involving pre-set constant average pedalling rates. A total of 24 subjects (12 males and 12 females) completed a 30-s high-speed maximal all-out effort on a cycle ergometer against an applied resistance equal to 7.5% of their body mass. On two further occasions the applied resistance was increased so that the external work of the all-out effort could be replicated by adopting a pre-determined constant average pedal rate. When the required pedal rate was within the range of 60-90 rev.min-1 the subjects were able to maintain the rate for the full 30-s and so could replicate the external work of the all-out effort. They were unable to sustain a faster constant rate within the range of 97-150 rev.min-1 for the full 30 s, resulting in approximately 7% less external work being achieved (P < 0.05). A lower level of fatigue, reflected by less of a reduction in peak power output in a subsequent 6-s sprint (P < 0.05), arose as a result of similar work produced under constant paced conditions compared with the all-out effort. Also, post-exercise blood lactate, pH and ammonia were less disturbed (P < 0.05) following the paced trial compared with similar work produced in the all-out effort. A possible explanation for these findings is that there may be a partial sparing of some type II fibres as a consequence of an initial submaximal intensity of exercise during the paced trial.

Adult↗

PubMed1997

Effect of the number of preceding muscle actions on subsequent peak power output.

Many sports events require participants to exert a maximal effort in the closing stages-that is, after prior fatiguing exercise. Peak and mean pedalling rate during 30 s of high-intensity cycle ergometer exercise was manipulated by altering the applied resistance or the initial exercise intensity so that the effect of three contrasting strategies on subsequent peak power output could be examined. Seven female students cycled for 30 s in one of three conditions: (1) all-out effort against an applied resistance of 7.5% of body weight (test 1); (2) at a constant pace of 55% of the peak pedal rate of test 1 against a resistance of 10.9 +/- 0.4% of body weight (test 2); (3) all-out effort against the greater resistance (test 3). A 6 s sprint against the lesser resistance was performed 3 s after each test. Total work was greater (P < 0.01) in test 3 than in test 1, while mean pedal rate was higher (P < 0.01) in test 1 (mean +/- S.E.: 10.0 +/- 0.4 rad s-1) than in tests 2 and 3 (7.2 +/- 0.4 and 7.8 +/- 0.3 rad s-1 respectively). The peak power output in the subsequent 6 s sprint was similar following tests 2 and 3 (516 +/- 37 and 534 +/- 41 W respectively), but was lower following test 1 (420 +/- 37 W) (P < 0.01, test 1 vs tests 2 and 3). These results indicate that the number of muscle actions during 30 s of fatiguing exercise may exert a considerable influence on one's ability to subsequently produce peak power output. In sports such as cycling where the same external velocity is attainable at different muscle action speeds, then appropriate gear selection during the race will impact on the rider's ability to sprint in the latter stages.

Adult↗

PubMed1997

Accumulated oxygen deficit and shuttle run performance in physically active men and women.

The aim of this study was to establish the validity of using shuttle run performance over 20 m to predict accumulated oxygen deficit. A new high-intensity shuttle run test (HIST) was devised, during which subjects ran to exhaustion at a speed equivalent to 120% of their performance attained during a progressive shuttle run test. The reliability of the new test was examined and found to be acceptable for 18 subjects who performed the test twice on separate days (r = 0.84, P < 0.01, study I). The discriminating ability of the new test was examined by comparing the distance covered by eight sprint- and eight endurance-trained athletes at 120% of their respective progressive shuttle run performances (615 +/- 111 vs 273 +/- 84 m, P < 0.01, study II). The strongest predictor of accumulated oxygen deficit for 27 subjects was found to be the geometric mean of the performances on the new test and on the progressive shuttle run test (r = 0.74, study III). The regression equation for this relationship was then used to estimate the accumulated oxygen deficit for a second group of 16 subjects (study IV). The correlation between the estimated and measured accumulated oxygen deficits was significant (r = 0.79, P < 0.01). The results from studies III and IV were therefore combined with the data from six new subjects to give a regression equation for predictive purposes based on 49 subjects.

Adult↗

PubMed1997

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).

Humans↗

PubMed1996

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

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

Adult↗

PubMed1996

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.

Adult↗

PubMed1996

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.

Adenosine Triphosphate↗

PubMed1995

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.

Adenosine Triphosphate↗

PubMed1994

The metabolic responses of human type I and II muscle fibres during maximal treadmill sprinting.

1. Muscle biopsy samples were obtained from the vastus lateralis of six healthy volunteers before and after 30 s of treadmill sprinting. A portion of each biopsy sample was used for mixed-fibre metabolite analysis. Single fibres were dissected from the remaining portion of each biopsy and were used for ATP, phosphocreatine (PCr) and glycogen determination. 2. Before exercise, PCr and glycogen contents were higher in type II fibres (79.3 +/- 2.7 and 472 +/- 35 mmol (kg dry matter (DM)-1, respectively) compared with type I fibres (71.3 +/- 3.0 mmol (kg DM)-1, P < 0.01 and 375 +/- 25 mmol (kg DM)-1, P < 0.001, respectively). 3. Peak power output was 885 +/- 66 W and declined by 65 +/- 3% during exercise. Phosphocreatine and glycogen degradation in type II fibres during exercise (74.3 +/- 2.5 and 126.3 +/- 15.8 mmol (kg DM)-1, respectively) was greater than the corresponding degradation in type I fibres (59.1 +/- 2.9 mmol (kg DM)-1, P < 0.001 and 77.0 +/- 14.3 mmol (kg DM)-1, P < 0.01, respectively). The decline in ATP during exercise was similar when comparing fibre types (P > 0.05). 4. Compared with previous studies involving similar durations of maximal cycling exercise, isokinetic knee extension and intermittent isometric contraction, the rates of substrate utilization recorded in type I fibres were extremely high, being close to the rapid rates observed in this fibre type during intense contraction with limb blood flow occluded.

Adenosine Triphosphate↗