Influence of beta-alanine supplementation on skeletal muscle carnosine concentrations and high intensity cycling capacity.

Muscle carnosine synthesis is limited by the availability of beta-alanine. Thirteen male subjects were supplemented with beta-alanine (CarnoSyn) for 4 wks, 8 of these for 10 wks. A biopsy of the vastus lateralis was obtained from 6 of the 8 at 0, 4 and 10 wks. Subjects undertook a cycle capacity test to determine total work done (TWD) at 110% (CCT(110%)) of their maximum power (Wmax). Twelve matched subjects received a placebo. Eleven of these completed the CCT(110%) at 0 and 4 wks, and 8, 10 wks. Muscle biopsies were obtained from 5 of the 8 and one additional subject. Muscle carnosine was significantly increased by +58.8% and +80.1% after 4 and 10 wks beta-alanine supplementation. Carnosine, initially 1.71 times higher in type IIa fibres, increased equally in both type I and IIa fibres. No increase was seen in control subjects. Taurine was unchanged by 10 wks of supplementation. 4 wks beta-alanine supplementation resulted in a significant increase in TWD (+13.0%); with a further +3.2% increase at 10 wks. TWD was unchanged at 4 and 10 wks in the control subjects. The increase in TWD with supplementation followed the increase in muscle carnosine.

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.

Moderate exercise, postprandial lipemia, and skeletal muscle lipoprotein lipase activity.

One mechanism by which prior exercise decreases the plasma triacylglycerol (TG) response to dietary fat may involve enhanced clearance of TG-rich lipoproteins. The purpose of the present study was to examine the influence of moderate intensity exercise on postprandial lipemia and muscle lipoprotein lipase (LPL) activity. Eight physically active, normolipidemic men aged 27.0 years (SD 4.2), body mass index 24.5 kg. m(-2) (SD 1.3), participated in 2 oral fat-tolerance tests with different preceding conditions. The afternoon before one test ( approximately 16 hours), subjects cycled for 90 minutes at 62.3% (SD 1.7%) of maximal oxygen uptake. Before the other test, subjects refrained from exercise. Samples of muscle, venous blood, and expired air were obtained in the fasted state. Subjects then consumed a high-fat meal (1.4 g fat, 1.2 g carbohydrate, 0.2 g protein, 73 kJ energy per kg body mass) before further blood and expired air samples were collected until 6 hours. The 6-hour areas under the TG concentration v time curves for plasma and for the chylomicron-rich fraction were lower (P <.05) after exercise (plasma, 7.91 [SE 1.09] v 5.72 [SE 0.47] mmol. L(-1). h; chylomicron-rich fraction, 1.98 [SE 0.51] v 0.92 [SE 0.16] mmol. L(-1). h). Muscle LPL activity was not significantly influenced by prior exercise, but the 4 subjects who had higher muscle LPL activity after exercise also had the most noticeable decreases in postprandial lipemia. The difference in lipemia between trials was inversely related to the difference in LPL activity (rho = -.79, P <.05). In the fasted state and postprandially, carbohydrate oxidation was lower after exercise (P <.05). Thus moderate exercise attenuates postprandial lipemia, possibly by altering muscle LPL activity.

Glutamine supplementation promotes anaplerosis but not oxidative energy delivery in human skeletal muscle.

The aims of the present study were twofold: first to investigate whether TCA cycle intermediate (TCAI) pool expansion at the onset of moderate-intensity exercise in human skeletal muscle could be enhanced independently of pyruvate availability by ingestion of glutamine or ornithine alpha-ketoglutarate, and second, if it was, whether this modification of TCAI pool expansion had any effect on oxidative energy status during subsequent exercise. Seven males cycled for 10 min at approximately 70% maximal O2) uptake 1 h after consuming either an artificially sweetened placebo (5 ml/kg body wt solution, CON), 0.125 g/kg body wt L-(+)-ornithine alpha-ketoglutarate dissolved in 5 ml/kg body wt solution (OKG), or 0.125 g/kg body wt L-glutamine dissolved in 5 ml/kg body wt solution (GLN). Vastus lateralis muscle was biopsied 1 h postsupplement and after 10 min of exercise. The sum of four measured TCAI (SigmaTCAI; citrate, malate, fumarate, and succinate, approximately 85% of total TCAI pool) was not different between conditions 1 h postsupplement. However, after 10 min of exercise, SigmaTCAI (mmol/kg dry muscle) was greater in the GLN condition (4.90 +/- 0.61) than in the CON condition (3.74 +/- 0.38, P < 0.05) and the OKG condition (3.85 +/- 0.28). After 10 min of exercise, muscle phosphocreatine (PCr) content was significantly reduced (P < 0.05) in all conditions, but there was no significant difference between conditions. We conclude that the ingestion of glutamine increased TCAI pool size after 10 min of exercise most probably because of the entry of glutamine carbon at the level of alpha-ketoglutarate. However, this increased expansion in the TCAI pool did not appear to increase oxidative energy production, because there was no sparing of PCr during exercise.

The effect of 13 weeks of running training followed by 9 d of detraining on postprandial lipaemia.

The present study examined the influence of training, followed by a short period of detraining, on postprandial lipaemia. Fourteen normolipidaemic, recreationally active young adults aged 18-31 years participated, in two self-selected groups: three men and five women (BMI 21.7-27.6 kg/m2) completed 13 weeks of running training, after which they refrained from exercise for 9 d; three men and three women (BMI 21.5-25.6 kg/m2) maintained their usual lifestyle. Oral fat tolerance tests were conducted at baseline and again 15 h, 60 h and 9 d after the runners' last training session. Blood samples were drawn after an overnight fast and at intervals for 6 h after consumption of a high-fat meal (1.2 g fat, 1.4 g carbohydrate, 70.6 kJ energy/kg body mass). Heparin was then administered (100 IU/kg) and a further blood sample was drawn for measurement of plasma lipoprotein lipase (EC 3.1.1.34; LPL) activity. Endurance fitness improved in runners, relative to controls (maximal O2 uptake +3.2 (SE 1.1) ml/kg per min v. -1.3 (SE 1.2) ml/kg per min; P < 0.05). In the absence of the acute effect of exercise, i.e. 60 h after the last training session, there was no effect of training on either postprandial lipaemia or on post-heparin LPL activity. However, changes during 9 d of detraining in both these variables differed significantly between groups; after 2d without exercise (60 h test), the runners' lipaemic response was 37% higher than it was the morning after their last training session (15 h test; runners v. controls P < 0.05), with a reciprocal decrease in post-heparin LPL activity (P < 0.01). These findings suggest that improved fitness does not necessarily confer an effect on postprandial lipaemia above that attributable to a single session of exercise.

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.

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.

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.

Acceptance and perception of percutaneous endoscopic gastrostomy by patients with upper aerodigestive tract cancer.

Surgeons have identified a role for percutaneous endoscopic gastrostomy (PEG) in selected patients with upper aerodigestive tract cancer, but little is known about the patient's acceptance and perception of PEG. Nineteen patients with upper aerodigestive tract cancer had placement of a PEG and were asked about their perceptions via a series of descriptors and associated questions. The 13 patients who had PEG placement under local anaesthesia and intravenous midazolam were questioned 12-16 h later and reported that the procedure was comfortable and not as bad as expected. These patients together with a further 6 patients who had placement under general anaesthesia were questioned about their acceptance of the PEG tube after 10 days. Comfort, ease of use and maintenance, and coverage by clothing confirms that PEG is an acceptable delivery system for enteral nutrition in patients with upper aerodigestive tract cancer.

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.

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.

Human muscle metabolism during intermittent maximal exercise.

Eight male subjects volunteered to take part in this study. The exercise protocol consisted of ten 6-s maximal sprints with 30 s of recovery between each sprint on a cycle ergometer. Needle biopsy samples were taken from the vastus lateralis muscle before and after the first sprint and 10 s before and immediately after the tenth sprint. The energy required to sustain the high mean power output (MPO) that was generated over the first 6-s sprint (870.0 +/- 159.2 W) was provided by an equal contribution from phosphocreatine (PCr) degradation and anaerobic glycolysis. Indeed, within the first 6-s bout of maximal exercise PCr concentration had fallen by 57% and muscle lactate concentration had increased to 28.6 mmol/kg dry wt, confirming significant glycolytic activity. However, in the tenth sprint there was no change in muscle lactate concentration even though MPO was reduced only to 73% of that generated in the first sprint. This reduced glycogenolysis occurred despite the high plasma epinephrine concentration of 5.1 +/- 1.5 nmol/l after sprint 9. In face of a considerable reduction in the contribution of anaerobic glycogenolysis to ATP production, it was suggested that, during the last sprint, power output was supported by energy that was mainly derived from PCr degradation and an increased aerobic metabolism.

Effect of training on muscle metabolism during treadmill sprinting.

Sixteen subjects volunteered for the study and were divided into a control (4 males and 4 females) and experimental group (4 males and 4 females, who undertook 8 wk of sprint training). All subjects completed a maximal 30-s sprint on a nonmotorized treadmill and a 2-min run on a motorized treadmill at a speed designed to elicit 110% of maximum oxygen uptake (110% run) before and after the period of training. Muscle biopsies were taken from vastus lateralis at rest and immediately after exercise. The metabolic responses to the 110% run were unchanged over the 8-wk period. However, sprint training resulted in a 12% (P less than 0.05) and 6% (NS) improvement in peak and mean power output, respectively, during the 30-s sprint test. This improvement in sprint performance was accompanied by an increase in the postexercise muscle lactate (86.0 +/- 26.4 vs. 103.6 +/- 24.6 mmol/kg dry wt, P less than 0.05) and plasma norepinephrine concentrations (10.4 +/- 5.4 vs. 12.1 +/- 5.3 nmol/l, P less than 0.05) and by a decrease in the postexercise blood pH (7.17 +/- 0.11 vs. 7.09 +/- 0.11, P less than 0.05). There was, however, no change in skeletal muscle buffering capacity as measured by the homogenate technique (67.6 +/- 6.5 vs. 71.2 +/- 4.5 Slykes, NS).

Interstitial emphysema of the stomach due to perforated appendicitis.

There are three recognised variations of gas within the wall of the stomach (interstitial emphysema, cystic pneumatosis and emphysematous gastritis). Only 26 cases of interstitial emphysema have been described, with an overall mortality of 42%, and we report the first known case of this rare phenomenon associated with acute appendicitis. A description of the clinical and radiological features of these three types of intramural stomach gas is presented and the literature pertinent to interstitial emphysema is reviewed.

Influence of single-leg training on muscle metabolism and endurance during exercise with the trained limb and the untrained limb.

We have previously shown that single-leg training results in improved endurance for exercise with the untrained leg (UTL) as well as for exercise with the trained leg (TL). The purpose of this study was to see whether the improved endurance of the untrained leg could be explained on the basis of changes in muscle metabolism. Exercise time to exhaustion at 80% of maximum oxygen uptake (VO2 max) was determined for each leg separately, pre- and post-training. Muscle metabolite concentrations were measured pre- and post-training in biopsy samples obtained immediately before this endurance test and at the pre-training point of exhaustion (END1). After six weeks of single-leg training endurance time was increased for both the UTL and the TL (UTL 34.0 +/- 16.4 min vs 97.9 +/- 26.3 min, P less than 0.01; TL 28.3 +/- 10.1 min vs 169.0 +/- 32.6 min, P less than 0.01). No changes in muscle metabolite concentrations were found in resting muscle. Training increased muscle ATP (P less than 0.05) and glycogen (P less than 0.01) concentrations and decreased muscle lactate concentration (P less than 0.05) in the TL at END1. No significant changes in muscle metabolite concentrations were found for the UTL. The improved endurance of the contralateral limb after single-leg training could not be explained on the basis of changes in muscle metabolism.

Human muscle metabolism during sprint running.

Biopsy samples were obtained from vastus lateralis of eight female subjects before and after a maximal 30-s sprint on a nonmotorized treadmill and were analyzed for glycogen, phosphagens, and glycolytic intermediates. Peak power output averaged 534.4 +/- 85.0 W and was decreased by 50 +/- 10% at the end of the sprint. Glycogen, phosphocreatine, and ATP were decreased by 25, 64, and 37%, respectively. The glycolytic intermediates above phosphofructokinase increased approximately 13-fold, whereas fructose 1,6-diphosphate and triose phosphates only increased 4- and 2-fold. Muscle pyruvate and lactate were increased 19 and 29 times. After 3 min recovery, blood pH was decreased by 0.24 units and plasma epinephrine and norepinephrine increased from 0.3 +/- 0.2 nmol/l and 2.7 +/- 0.8 nmol/l at rest to 1.3 +/- 0.8 nmol/l and 11.7 +/- 6.6 nmol/l. A significant correlation was found between the changes in plasma catecholamines and estimated ATP production from glycolysis (norepinephrine, glycolysis r = 0.78, P less than 0.05; epinephrine, glycolysis r = 0.75, P less than 0.05) and between postexercise capillary lactate and muscle lactate concentrations (r = 0.82, P less than 0.05). The study demonstrated that a significant reduction in ATP occurs during maximal dynamic exercise in humans. The marked metabolic changes caused by the treadmill sprint and its close simulation of free running makes it a valuable test for examining the factors that limit performance and the etiology of fatigue during brief maximal exercise.

A simple one-step enzymatic fluorometric method for the determination of glycerol in 20 microliters of plasma.

An assay for the determination of glycerol concentration in blood or other biological materials is described. The method is based on the conversion of glycerol to dihydroxyacetone in the presence of NAD, the reaction being catalysed by the enzyme glycerol dehydrogenase. The NADH which is formed in stoichiometric quantities during the reaction is estimated fluorometrically. In the presence of the ketone-trapping agent hydrazine the reaction can be made to go to completion above above pH 9.0. Using the method described, glycerol can be measured routinely in a 20-microliters sample of serum or plasma. Although the enzyme is known to react with sorbitol and ethanol, the addition of these substances to the reaction mixture had no significant effect on the determination of glycerol.

Can drugs help patients with lower limb ischaemia?

The prevalence of symptomatic arterial disease of the lower limbs is 2 per cent of the population aged 45-60, but it has a relatively benign course, with 70 per cent of patients requiring no therapy. Of the numerous drugs used in the treatment of the disease, there is no evidence to suggest that antilipaemic drugs, anticoagulants, vasodilators or rheological agents confer any benefit to the patient. The initial use of antiplatelet drugs and prostaglandins has been disappointing despite the undoubted importance of the platelet/endothelial interaction in the aetiology of atherosclerosis. As it is unlikely that we can reverse advanced disease, this is hardly surprising. Long term use of these drugs may prevent deterioration in those patients with progressive disease, and controlled trials on this aspect of treatment are now required. Symptomatic relief in the claudicant may perhaps be obtained with naftidrofuryl and suloctodil and with the former in more severe ischaemia, but their use should not replace the beneficial effects of exercise and cessation of smoking.