Effect of creatine supplementation on sprint exercise performance and muscle metabolism

The aim of the present study was to examine the effect of creatine supplementation (CrS) on sprint exercise performance and skeletal muscle anaerobic metabolism during and after sprint exercise. Eight active, untrained men performed a 20-s maximal sprint on an air-braked cycle ergometer after 5 days of CrS [30 g creatine (Cr) + 30 g dextrose per day] or placebo (30 g dextrose per day). The trials were separated by 4 wk, and a double-blind crossover design was used. Muscle and blood samples were obtained at rest, immediately after exercise, and after 2 min of passive recovery. CrS increased the muscle total Cr content (9.5 +/- 2.0%, P < 0.05, mean +/- SE); however, 20-s sprint performance was not improved by CrS. Similarly, the magnitude of the degradation or accumulation of muscle (e.g., adenine nucleotides, phosphocreatine, inosine 5'-monophosphate, lactate, and glycogen) and plasma metabolites (e.g. , lactate, hypoxanthine, and ammonia/ammonium) were also unaffected by CrS during exercise or recovery. These data demonstrated that CrS increased muscle total Cr content, but the increase did not induce an improved sprint exercise performance or alterations in anaerobic muscle metabolism.     

Metabolic profile of high intensity intermittent exercises

To evaluate the magnitude of the stress on the aerobic and the anaerobic energy release systems during high intensity bicycle training, two commonly used protocols (IE1 and IE2) were examined during bicycling. IE1 consisted of one set of 6-7 bouts of 20-s exercise at an intensity of approximately 170% of the subject's maximal oxygen uptake (VO2max) with a 10-s rest between each bout. IE2 involved one set of 4-5 bouts of 30-s exercise at an intensity of approximately 200% of the subject's VO2max and a 2-min rest between each bout. The accumulated oxygen deficit of IE1 (69 +/- 8 ml.kg-1, mean +/- SD) was significantly higher than that of IE2 (46 +/- 12 ml.kg-1, N = 9, p < 0.01). The accumulated oxygen deficit of IE1 was not significantly different from the maximal accumulated oxygen deficit (the anaerobic capacity) of the subjects (69 +/- 10 ml.kg-1), whereas the corresponding value for IE2 was less than the subjects' maximal accumulated oxygen deficit (P < 0.01). The peak oxygen uptake during the last 10 s of the IE1 (55 +/- 6 ml.kg-1.min-1) was not significantly less than the VO2max of the subjects (57 +/- 6 ml.kg-1.min-1). The peak oxygen uptake during the last 10 s of IE2 (47 +/- 8 ml.kg-1.min-1) was lower than the VO2max (P < 0.01). In conclusion, this study showed that intermittent exercise defined by the IE1 protocol may tax both the anaerobic and aerobic energy releasing systems almost maximally.     

Muscle performance and enzymatic adaptations to sprint interval training

Our purpose was to examine the effects of sprint interval training on muscle glycolytic and oxidative enzyme activity and exercise performance. Twelve healthy men (22 +/- 2 yr of age) underwent intense interval training on a cycle ergometer for 7 wk. Training consisted of 30-s maximum sprint efforts (Wingate protocol) interspersed by 2-4 min of recovery, performed three times per week. The program began with four intervals with 4 min of recovery per session in week 1 and progressed to 10 intervals with 2.5 min of recovery per session by week 7. Peak power output and total work over repeated maximal 30-s efforts and maximal oxygen consumption (VO2 max) were measured before and after the training program. Needle biopsies were taken from vastus lateralis of nine subjects before and after the program and assayed for the maximal activity of hexokinase, total glycogen phosphorylase, phosphofructokinase, lactate dehydrogenase, citrate synthase, succinate dehydrogenase, malate dehydrogenase, and 3-hydroxyacyl-CoA dehydrogenase. The training program resulted in significant increases in peak power output, total work over 30 s, and VO2 max. Maximal enzyme activity of hexokinase, phosphofructokinase, citrate synthase, succinate dehydrogenase, and malate dehydrogenase was also significantly (P < 0.05) higher after training. It was concluded that relatively brief but intense sprint training can result in an increase in both glycolytic and oxidative enzyme activity, maximum short-term power output, and VO2 max.     

Prognostic factors for musculoskeletal sickness absence and return to work among welders and metal workers

The effect of creatine loading on endurance capacity and sprint performance was investigated in elite cyclists according to a double-blind cross-over study design. Subjects (n = 12) underwent on 3 occasions and separated by 5 week wash-out periods, a 2 h 30 min standardized endurance protocol on their own race bicycle, which was mounted on an electromagnetically braked roller-system, whereupon they cycled to exhaustion at their predetermined 4 mmol lactate threshold. Immediately thereafter they performed 5 maximal 10 second sprints, separated by 2 min recovery intervals, on a Monark bicycle ergometer at 6 kg resistance on the flywheel. Before the exercise test, subjects were either creatine loaded (C: 25 g creatine monohydrate/day, 5 days) or were creatine loaded plus ingested creatine during the exercise test (CC: 5 g/h), or received placebo (P). Compared with P, C but not CC increased (p<0.05) peak and mean sprint power output by 8-9% for all 5 sprints. Endurance time to exhaustion was not affected by either C or CC. It is concluded that creatine loading improves intermittent sprint capacity at the end of endurance exercise to fatigue. This ergogenic action is counteracted by high dose creatine intake during exercise.     

The relationship between aerobic fitness and recovery from high-intensity exercise in infantry soldiers

The relationship between aerobic fitness and recovery from high-intensity exercise was examined in 197 infantry soldiers. Aerobic fitness was determined by a maximal-effort, 2,000-m run (RUN). High-intensity exercise consisted of three bouts of a continuous 140-m sprint with several changes of direction. A 2-minute passive rest separated each sprint. A fatigue index was developed by dividing the mean time of the three sprints by the fastest time. Times for the RUN were converted into standardized T scores and separated into five groups (group 1 had the slowest run time and group 5 had the fastest run time). Significant differences in the fatigue index were seen between group 1 (4.9 +/- 2.4%) and groups 3 (2.6 +/- 1.7%), 4 (2.3 +/- 1.6%), and 5 (2.3 +/- 1.3%). It appears that recovery from high-intensity exercise is improved at higher levels of aerobic fitness (faster time for the RUN). However, as the level of aerobic fitness improves above the population mean, no further benefit in the recovery rate from high-intensity exercise is apparent.     

A metabolism study of human masseter muscle by 31P magnetic resonance spectroscopy during long periods of exercise and recovery

The metabolism of the human masseter muscle was investigated using phosphorus (31p) magnetic resonance spectroscopy (MRS) during long periods of exercise and recovery. Eleven subjects aged 19 to 28 yr were examined by 31p MRS during four consecutive periods of 13 min each: rest, exercise, recovery 1 and 2. For each subject, a biting force equal to 20% of maximum voluntary biting force was applied and controlled during the exercise period to produce maximum fatigue. 31p MR spectra were localized from a 24 cm3 volume of interest using an image selected in vivo spectroscopy (ISIS) sequence and a 6 cm diameter surface coil placed on the left masseter. Compared to the resting level, the phosphocreatine (PCr) content decreased by 26% during exercise, while the inorganic phosphate (Pi) concentration increased by 65%. During the two recovery periods, the Pi content remained decreased compared with the resting level by 36% and 30%, respectively. The Pi/PCr ratio was increased from 0.30+/-0.04 at rest to 0.63+/-0.13 during exercise while the adenosine triphosphate (ATP)/Pi ratio was decreased. The pH decreased from 7.02+/-0.03 to 6.93+/-0.04 during exercise and returned to control level (7.09+/-0.08) only during the second recovery period. These results suggest that the masseter muscle is characterized by high ATP turnover and, therefore, high oxidative phosphorylative activity in agreement with its constitution of predominantly fatigue resistant type I fibers.     

Physiological correlates of 3-kilometer running performance in male children

The purpose of this study was to examine the influence of body fatness, aerobic and anaerobic ability on 3-km running performance in 19 physically active boys (mean +/- SD, age = 10.4 +/- 0.9 yrs). The sum of six skinfolds, VO2 at 8.04 and 9.65 km.hr-1, and VO2max were measured in the laboratory. Run time for 3 km was assessed twice on separate days on a 200-meter indoor track. Prior to each run, every child performed two 55-meter sprints and two vertical jumps. Mean +/- SD values for the sum of skinfolds, %VO2max at each running speed, VO2max and 3-km run time were: 33.9 +/- 14.9 mm; 70.6 +/- 6.6% and 81.0 +/- 7.9%; 54.6 +/- 5.0 ml.kg-1.min-1; 16.41 +/- 2.58 min, respectively. Significant (p < 0.05) correlations were observed between the following variables and run time: sum of skinfolds (r = 0.72); vertical jump (r = 0.67); sprint time (r = 0.59); VO2max (r = 0.61); and, %VO2max at each treadmill speed (r = 0.79 and r = 0.75, respectively). Stepwise multiple regression analysis indicated that the combination of the %VO2max at 8.04 km.hr-1 and vertical jump accounted for 83% (adjusted R2) of the variance in running time (SEE = 1.06 min, p < 0.05). This study suggests that 3-km run time in physically active boys is influenced by aerobic and anaerobic indices as well as body fatness, supporting the notion that children, compared to adults, are not metabolic specialists.     

A new reliable laboratory test of endurance performance for road cyclists

PURPOSE: The purpose of this study was to devise and evaluate a laboratory test of cycling performance that simulates the variable power demands of competitive road racing. The test is a 100-km time trial interspersed with four 1-km and four 4-km sprints. METHODS: On three occasions separated by 5-7 d, eight endurance-trained cyclists (peak oxygen uptake 5.0 +/- 0.7 L.min-1, peak power output 411 +/- 43 W, mean +/- SD) performed the test on their own bikes mounted on an air-braked Kingcycle ergometer. Subjects were free to regulate their power output but were asked to complete each sprint and the full distance as quickly as possible. The only feedback given to the cyclists during each test was elapsed distance. RESULTS: In the first test, time for the 100 km and mean times for the 1-km and 4-km sprints were 151:42 +/- 10:36, 1:16 +/- 0:06, and 5:31 +/- 0:16 min:s, respectively; these times improved by 1.6-2.2% in the second test, but there was little further improvement in the third test (0.7 to -0.5%). The between-test correlation for 100-km time was 0.93 (95% CI 0.79 to 0.98), and the within-cyclist coefficient of variation was 1.7% (95% CI 1.1 to 2.5%). Mean sprint performance showed similar good reliability (within-subject variation and correlations for the 1-km and 4-km sprint times of 1.9%, 2.0%, 0.93, and 0.81, respectively). CONCLUSIONS: The high reliability of this laboratory test will make the test useful for research on performance of competitive road cyclists.     

An orphan nuclear receptor activated by pregnanes defines a novel steroid signaling pathway

PURPOSE: To determine the effects of 28 d of creatine supplementation during training on body composition, strength, sprint performance, and hematological profiles. METHODS: In a double-blind and randomized manner, 25 NCAA division IA football players were matched-paired and assigned to supplement their diet for 28 d during resistance/agility training (8 h x wk[-1]) with a Phosphagen HP (Experimental and Applied Sciences, Golden, CO) placebo (P) containing 99 g x d(-1) of glucose, 3 g x d(-1) of taurine, 1.1 g x d(-1) of disodium phosphate, and 1.2 g x d(-1) of potassium phosphate (P) or Phosphagen HP containing the P with 15.75 g x d(-1) of HPCE pure creatine monohydrate (HP). Before and after supplementation, fasting blood samples were obtained; total body weight, total body water, and body composition were determined; subjects performed a maximal repetition test on the isotonic bench press, squat, and power clean; and subjects performed a cycle ergometer sprint test (12 x 6-s sprints with 30-s rest recovery). RESULTS: Hematological parameters remained within normal clinical limits for active individuals with no side effects reported. Total body weight significantly increased (P < 0.05) in the HP group (P 0.85 +/- 2.2; HP 2.42 +/- 1.4 kg) while no differences were observed in the percentage of total body water. DEXA scanned body mass (P 0.77 +/- 1.8; HP 2.22 +/- 1.5 kg) and fat/bone-free mass (P 1.33 +/- 1.1; HP 2.43 +/- 1.4 kg) were significantly increased in the HP group. Gains in bench press lifting volume (P -5 +/- 134; HP 225 +/- 246 kg), the sum of bench press, squat, and power clean lifting volume (P 1,105 +/- 429; HP 1,558 +/- 645 kg), and total work performed during the first five 6-s sprints was significantly greater in the HP group. CONCLUSION: The addition of creatine to the glucose/taurine/electrolyte supplement promoted greater gains in fat/bone-free mass, isotonic lifting volume, and sprint performance during intense resistance/agility training.     

The effect of propionyl L-carnitine on skeletal muscle metabolism in renal failure

The effect of propionyl L-carnitine on skeletal muscle metabolism in chronic renal failure. Carnitine deficiency, resulting in defective oxidative ATP synthesis, has been implicated in the myopathy of chronic renal failure. Using 31P magnetic resonance spectroscopy we examined calf muscle metabolism in 10 dialysed patients before and after 8 weeks of propionyl L-carnitine (PLC) 2 g.p.o. daily. Resting phosphocreatine/ATP (4.41 +/- 0.20 [SEM]) decreased to normal control levels on PLC (3.98 +/- 0.14; controls 4.00 +/- 0.06). In contrast, there was no effect of PLC on aerobic and anaerobic metabolism of muscle during or following 2-10 min exercise. The maximal calculated oxidative capacity (Qmax) remained below normal (28 +/- 3 mM/min before and 24 +/- 3 mM/min after PLC; controls 49 +/- 3 mM/min). Qmax correlated positively with hemoglobin concentration ([Hb]) after PLC (p < 0.03). Oxidative capacity assessed by phosphocreatine recovery T significantly improved with PLC administration (0.93 +/- 0.1 to 0.74 +/- 0.08 min) in those patients (n = 6) with [Hb] > 10 g/dl. [Hb] was rate limiting to oxidative metabolism in recovery from exercise but only following treatment with PLC. Patients with anemia or those subjects who use relatively more non-oxidatively synthesized ATP during exercise, do not respond to PLC. Oxidative metabolism did not normalize on PLC suggesting that anemia and carnitine deficiency are not the only causes of mitochondrial dysfunction in renal failure.     

Creatine supplementation and age influence muscle metabolism during exercise

Young [n = 5, 30 +/- 5 (SD) yr] and middle-aged (n = 4, 58 +/- 4 yr) men and women performed single-leg knee-extension exercise inside a whole body magnetic resonance system. Two trials were performed 7 days apart and consisted of two 2-min bouts and a third bout continued to exhaustion, all separated by 3 min of recovery. 31P spectra were used to determine pH and relative concentrations of Pi, phosphocreatine (PCr), and beta-ATP every 10 s. The subjects consumed 0.3 g . kg-1 . day-1 of a placebo (trial 1) or creatine (trial 2) for 5 days before each trial. During the placebo trial, the middle-aged group had a lower resting PCr compared with the young group (35.0 +/- 5.2 vs. 39.5 +/- 5.1 mmol/kg, P < 0.05) and a lower mean initial PCr resynthesis rate (18.1 +/- 3.5 vs. 23.2 +/- 6.0 mmol . kg-1 . min-1, P < 0.05). After creatine supplementation, resting PCr increased 15% (P < 0.05) in the young group and 30% (P < 0.05) in the middle-aged group to 45.7 +/- 7.5 vs. 45.7 +/- 5.5 mmol/kg, respectively. Mean initial PCr resynthesis rate also increased in the middle-aged group (P < 0.05) to a level not different from the young group (24.3 +/- 3.8 vs. 24.2 +/- 3.2 mmol . kg-1 . min-1). Time to exhaustion was increased in both groups combined after creatine supplementation (118 +/- 34 vs. 154 +/- 70 s, P < 0.05). In conclusion, creatine supplementation has a greater effect on PCr availability and resynthesis rate in middle-aged compared with younger persons.     

Transgenic A1 adenosine receptor overexpression markedly improves myocardial energy state during ischemia-reperfusion

A1 adenosine (A1AR) activation may reduce ischemia-reperfusion injury. Metabolic and functional responses to 30 min global normothermic ischemia and 20 min reperfusion were compared in wild-type and transgenic mouse hearts with approximately 100-fold overexpression of coupled cardiac A1ARs. 31P-NMR spectroscopy revealed that ATP was better preserved in transgenic v wild-type hearts: 53 +/- 11% of preischemic ATP remained after ischemia in transgenic hearts v only 4 +/- 4% in wild-type hearts. However, recovery of ATP after reperfusion was similar in transgenic (46 +/- 5%) and wild-type hearts (37 +/- 12%). Reductions in phosphocreatine (PCr) and cytosolic pH during ischemia were similar in both groups. However, recovery of PCR on reperfusion was higher in transgenic (67 +/- 8%) v wild-type hearts (36 +/- 8%), and recovery of pH was greater in transgenic (pH = 7.11 +/- 0.05) v wild-type hearts (pH = 6.90 +/- 0.02). Bioenergetic state ([ATP]/[ADP].[Pi]) was higher in transgenic v wild-type hearts during ischemia-reperfusion. Time to ischemic contracture was prolonged in transgenic (13.6 +/- 0.8 min) v wild-type hearts (10.4 +/- 0.3 min). Degree of contracture was lower and recovery of function in reperfusion higher in transgenic v wild-type hearts. In conclusion, A1AR overexpression reduces ATP loss and improves bioenergetic state during severe ischemic insult and reperfusion. These changes may contribute to improved functional tolerance.     

Screening a peptidyl database for potential ligands to proteins with side-chain flexibility

OBJECTIVE: Microdialysis and 31P-NMR spectroscopy were used to test opposing hypotheses that ischemic preconditioning inhibits adenine nucleotide degradation and purine efflux, or that preconditioning activates cardiovascular adenosine formation to provide enhanced cardioprotection. METHODS: 31P-NMR spectra and matching interstitial fluid (ISF) or venous effluent samples were obtained from Langendorff perfused rat hearts. Control hearts (n = 9) underwent 30 min of global normothermic ischemia and 30 min reperfusion. Preconditioned hearts (n = 6) were subjected to a 5 min ischemic episode and 10 min reflow prior to 30 min ischemia and 30 min reperfusion. Effects of repetitive ischemia-reperfusion (3 x 5 min ischemic episodes) on adenosine levels and energy metabolism were also assessed (n = 8). RESULTS: Preconditioning improved post-ischemic recovery of heart rate x left ventricular developed pressure (71 +/- 5 vs 43 +/- 8%, P < 0.05) and end-diastolic pressure (14 +/- 3 vs 29 +/- 4 mmHg, P < 0.05) compared with control hearts, respectively. Preconditioning did not alter intracellular ATP, phosphocreatine (PCr), inorganic phosphate (Pi), H+ or free Mg2+ during global ischemia, but improved recoveries of PCr, Pi, and delta GATP on reperfusion. ISF adenosine increased more than 20-fold during 30 min ischemia. The 5 min preconditioning episode increased ISF adenosine 3-fold, and reduced ISF adenosine and inosine during subsequent prolonged ischemia by up to 75%. Venous purine levels during reperfusion were also reduced by preconditioning. Accumulation of adenosine in ISF and venous effluent during repetitive ischemia was progressively reduced despite comparable changes in substrate for adenosine formation via 5'-nucleotidase, (5'-AMP), and in allosteric modulators of this enzyme (Mg2+, H+, Pi, ADP, ATP). CONCLUSIONS: (i) Ischemic preconditioning reduces interstitial and vascular adenosine levels during ischemia-reperfusion, (ii) reduced ISF adenosine during ischemia is not due to reduced ischemic depletion of adenine nucleotides in preconditioned rat hearts, (iii) preconditioning may inhibit adenosine formation via 5'-nucleotidase in ischemic rat hearts, and (iv) improved functional recovery with preconditioning is unrelated to metabolic/bioenergetic changes during the ischemic insult, but may be related to improved post-ischemic recovery of [Pi] and delta GATP in this model.     

Effect of carbohydrate ingestion on sprint performance following continuous and intermittent exercise

PURPOSE: This investigation was conducted to study the effects on sprint performance of glucose and fructose ingestion during a 15-min rest period half way through 90 min of continuous and intermittent exercise. On three occasions, eight subjects cycled at 76 +/- 2% VO2max for 90 min (continuous trials: CON trials) with a 15-min half-time break. METHODS: On another three occasions, they cycled for 90 min between moderate (65% VO2max) and high (100% VO2max) intensity (intermittent trials: INT trials) with the same half-time. In both trials, 90-min exercise was followed by a 40-s Wingate test to evaluate remaining sprint capacity. During half-time, they consumed either 20% glucose polymer (G), 20% fructose (F) or sweet placebo (P). Ingestion of G maintained plasma glucose levels, carbohydrate oxidation rate and lower value of ratings of perceived exertion (RPE) in both trials and indicated higher sprint performance compared with P (mean power of CON trials: 614.3 +/- 23.3 W vs 574.0 +/- 22.7 W, P < 0.001, INT trials: 629.5 +/- 27.6 W vs 596.3 +/- 25.5 W, P < 0.01). RESULTS: Ingestion of F showed similar effect in CON trials (603.8 +/- 26.1 W vs 574.0 +/- 22.7 W, P < 0.01) but had no positive effect in INT trials. Additionally, mean power of G was higher than F (629.5 +/- 27.6 W vs 598.4 +/- 34.2 W, P < 0.01) in INT trials. CONCLUSIONS: These results indicated that ingestion of G during half-time of 90-min exercise could maintain carbohydrate utilization and improve sprint performance in both CON and INT trials.     

Antiemetics in oncology]

OBJECTIVE: To assess the effects of 50 micrograms of inhaled salmeterol on pulmonary function, selected physical capacities, and fine motor control in 16 nonasthmatic male cyclists and triathletes, mean age of 23.2 (SD = 3.5) years. DESIGN: Randomized double-blind placebo-controlled crossover trial. SETTING: Human Physical Performance Laboratory, the University of Western Australia. SUBJECTS: Sixteen healthy male high-performance nonasthmatic athletes with a mean age of 23.2 years participated in the study. INTERVENTION: Subjects attended three experimental testing sessions at which salmeterol (50 micrograms), a placebo, or "no treatment" was administered in random order in a double-blind fashion, on separate occasions, prior to exercise. MAIN OUTCOME MEASURES: During each testing, session lung function was measured before and 10 min after the treatment. Tests of reaction time and hand steadiness and then two anaerobic cycle tests followed. The first, a 10-s all-out sprint was followed, after a 3-min rest, by a 30-s all-out sprint performed on a front access bicycle ergometer. After 10 min recovery, leg flexion-extension peak torque was measured on a Biodex isokinetic dynamometer at speeds of 120 and 180 degrees s-1. MAIN RESULTS: Lung function variables, reaction time, movement time, alactic anaerobic power, lactacid anaerobic power, and leg-flexion and leg-extension muscular strength were similar among the three treatment groups. CONCLUSIONS: The preexercise administration of 50 micrograms of inhaled salmeterol has no performance-enhancing effects in nonasthmatic athletes. We believe that athletes with asthma should be permitted to use salmeterol before competition.     

ORG 9487 neuromuscular block at the adductor pollicis and the laryngeal adductor muscles in humans

BACKGROUND: ORG 9487 is a new steroidal nondepolarizing muscle relaxant with a rapid onset of action. This study was designed to determine the neuromuscular blocking profile of ORG 9487 at the adductor muscles of the larynx and the adductor pollicis. METHODS: In 30 adults, anesthesia was induced with propofol (2-5 mg/kg) and fentanyl (2-3 microg/kg). After train-of-four stimulation, the block of the laryngeal adductor muscles was evaluated by measuring the pressure changes in the cuff of the tracheal tube placed between the vocal cords, and the force of the contraction of the adductor pollicis was measured with a force transducer. Patients were randomly allocated to receive ORG 9487 at intravenous bolus doses of 0.75, 1.5 or 2 mg/kg (n = 10 in each group). RESULTS: Time to peak effect was significantly shorter at the vocal cords than at the adductor pollicis muscle (P < 0.001). Onset time at the vocal cords was 62 +/- 16 s, 62 +/- 13 s, and 52 +/- 14 s (mean +/- SD) after doses of 0.75, 1.5, and 2 mg/kg, respectively (not significant). Onset time at the adductor pollicis muscle was 126 +/- 33 s, 96 +/- 20 s, and 82 +/- 21 s after 0.75, 1.5, and 2 mg/kg doses, respectively (P < 0.001). Maximum block was significantly less intense at the vocal cords than at the adductor pollicis muscle (69 +/- 15% vs. 94 +/- 4% after 0.75 mg/kg; 86 +/- 7% vs. 97 +/- 4% after 1.5 mg/kg; and 91 +/- 5% vs. 99 +/- 1% after 2 mg/kg). After 1.5 mg/kg duration to 25%, recovery was 3.7 +/- 2.2 min versus 10.2 +/- 2.5 min at the vocal cords and the adductor pollicis muscle, respectively, and 75% recovery occurred at 9.7 +/- 3.7 min at the vocal cords and at 18.3 +/- 5.2 min at the adductor pollicis muscle. CONCLUSIONS: ORG 9487 has a rapid onset of action at the laryngeal adductor and the adductor pollicis muscles. Onset and duration of action are faster at the vocal cords than at the adductor pollicis muscle. However, the maximum block obtained at the laryngeal muscles was less than at the adductor pollicis, regardless of the dose of ORG 9487.     

Metabolic response to halothane in piglets susceptible to malignant hyperthermia: an in vivo 31P-NMR study

Using in vivo 31P-nuclear magnetic resonance spectroscopy, we studied the skeletal muscle metabolism of 17 anesthetized malignant hyperthermia-susceptible piglets and 25 control piglets during and after a halothane stress test. At rest, the phosphocreatine- (PCr) to-ATP ratio was 12% higher in the anesthetized piglets than in the control piglets, which may reflect a higher proportion of fast glycolytic fibers in the former. About 15 min of halothane administration sufficed to provoke onset of a reaction, which was characterized by a reciprocal drop in PCr and an increase in Pi with commencing intracellular acidosis. Halothane was withdrawn after a 20% drop in PCr. Within the next few minutes, intracellular pH dropped sharply and phosphomonoesters (PME) accumulated excessively. ATP was observed to decrease in 8 of the 17 animals. Halothane inhalation provoked a switch of metabolism toward glycolysis. Accumulation of PME suggests a mismatch between glycogenolysis and glycolysis. Despite severe acidification, glycolysis was not completely halted. Recovery of PCr and Pi started approximately 5 min after halothane withdrawal, with a longer time constant for recovery of the former. PME and intracellular pH aberrations lingered and started to recover later. Lost ATP was never restored within the observed recovery period of approximately 20 min.     

Caffeine, performance, and metabolism during repeated Wingate exercise tests

Investigations examining the ergogenic and metabolic influence of caffeine during short-term high-intensity exercise are few in number and have produced inconsistent results. This study examined the effects of caffeine on repeated bouts of high-intensity exercise in recreationally active men. Subjects (n = 9) completed four 30-s Wingate (WG) sprints with 4 min of rest between each exercise bout on two separate occasions. One hour before exercise, either placebo (P1; dextrose) or caffeine (Caf; 6 mg/kg) capsules were ingested. Caf ingestion did not have any effect on power output (peak or average) in the first two WG tests and had a negative effect in the latter two exercise bouts. Plasma epinephrine concentration was significantly increased 60 min after Caf ingestion compared with P1; however, this treatment effect disappeared once exercise began. Caf ingestion had no significant effect on blood lactate, O2 consumption, or aerobic contribution at any time during the protocol. After the second Wingate test, plasma NH3 concentration increased significantly from the previous WG test and was significantly higher in the Caf trial compared with P1. These data demonstrate no ergogenic effect of caffeine on power output during repeated bouts of short-term, intense exercise. Furthermore, there was no indication of increased anaerobic metabolism after Caf ingestion with the exception of an increase in NH3 concentration.     

Muscle function during brief maximal exercise: accurate measurements on a friction-loaded cycle ergometer

A friction loaded cycle ergometer was instrumented with a strain gauge and an incremental encoder to obtain accurate measurement of human mechanical work output during the acceleration phase of a cycling sprint. This device was used to characterise muscle function in a group of 15 well-trained male subjects, asked to perform six short maximal sprints on the cycle against a constant friction load. Friction loads were successively set at 0.25, 0.35, 0.45, 0.55, 0.65 and 0.75 N.kg-1 body mass. Since the sprints were performed from a standing start, and since the acceleration was not restricted, the greatest attention was paid to the measurement of the acceleration balancing load due to flywheel inertia. Instantaneous pedalling velocity (v) and power output (P) were calculated each 5 ms and then averaged over each downstroke period so that each pedal downstroke provided a combination of v, force and P. Since an 8-s acceleration phase was composed of about 21 to 34 pedal downstrokes, this many v-P combinations were obtained amounting to 137-180 v-P combinations for all six friction loads in one individual, over the widest functional range of pedalling velocities (17-214 rpm). Thus, the individual's muscle function was characterised by the v-P relationships obtained during the six acceleration phases of the six sprints. An important finding of the present study was a strong linear relationship between individual optimal velocity (vopt) and individual maximal power output (Pmax) (n = 15, r = 0.95, P < 0.001) which has never been observed before. Since vopt has been demonstrated to be related to human fibre type composition both vopt, Pmax and their inter-relationship could represent a major feature in characterising muscle function in maximal unrestricted exercise. It is suggested that the present method is well suited to such analyses.     

Pulsatile tinnitus. A 15-year experience

BACKGROUND: We have previously demonstrated by 31P nuclear magnetic resonance (NMR) that succinylcholine (SCh) induces metabolic changes in denervated muscle. To specify those changes, we attempted to inhibit them using two different kinds of drugs, dantrolene and vecuronium. METHODS: Three weeks after unilateral sciatic nerve section, 75 male Wistar rats were randomly assigned to one of the following 5 groups: (1) non-pretreated normal muscle group; (2) non-pretreated denervated muscle group; (3) denervated muscle group pretreated with a low dose of vecuronium (0.02 mg.kg(-1)); (4) denervated muscle group pretreated with a high dose of vecuronium (0.2 mg.kg(-1)); (5) denervated muscle group pretreated with dantrolene (2 mg.kg(-1)). The change of the inorganic phosphate/phosphocreatine (Pi/PCr) ratio of each muscle was measured by 31P-NMR before and after SCh (1 mg.kg(-1)) administration and the corresponding peak amplitude of the electromyograms (EMG) was determined. RESULTS: The high dose of vecuronium totally inhibited SCh-induced fasciculation on EMG (100%-->2%). In this group, though the Pi/PCr ratio significantly increased 10 min after SCh, the peak after 5 min disappeared. The inhibition with dantrolene was about the same order of magnitude as with the low dose of vecuronium (35%:21%). However, the increase in the Pi/PCr only lasted about 10 min, in contrast to the other drugs. CONCLUSION: Our findings indicate that the Pi/PCr increases 5 and 10 min after SCh, respectively, as a result of two different processes. The first peak is caused by an excessive energy consumption in response to excessive muscle contraction. This in turn triggers the second peak, caused by breakdown of glycogen, initiated by an increased Ca2+ concentration.