Thermogenic effect of adrenaline: interaction with insulin

Summary The contribution of insulin (3.6 pmol sd kg body mass^–1·min^–1 to adrenaline-induced (0.164 nmol · kg fat free mass^–1·min^–1) thermogenesis was studied in ten postabsorptive healthy volunteers using two sequential protocols. Variables considered were oxygen consumption as well as carbon dioxide production, heart rate, blood pressure, plasma concentrations of glucose, insulin, glycerol, free fatty acids,-HO-butyrate and lactate. Adrenaline increased plasma concentrations of glucose, glycerol, free fatty acids, and-HO-butyrate, and heart rate and metabolic rate during normo-insulinaemia [61.3 (SEM 6.6) pmol·^–1]. Similar effects were observed during hyperinsulinaemia [167.9 (SEM 18.7) pmol·^–1], but the effect of adrenaline on oxygen consumption was reduced. On average, metabolic rate increased by 12.9% during normo-insulinaemia and by 8.9% during hyperinsulinaemia. We concluded that relative hyperinsulinaemia resulted in decreased adrenaline-induced thermogenesis and therefore increased whole body anabolism.     

The effects of buffer ingestion on metabolic factors related to distance running performance

We examined the effects of sodium bicarbonate (BIC) and sodium citrate (CIT) ingestion on distance running performance. Seven male runners [mean = 61.7 (SEM 1.7) ml · kg^–1 · min^–1] performed three 30-min treadmill runs at the lactate threshold (LT) each followed by a run to exhaustion at 110% of LT. The runs were double-blind and randomly assigned from BIC (0.3 g · kg body mass^–1), CIT (0.5 g · kg body mass^–1) and placebo (PLC, wheat flour, 0.5 g · kg body mass^–1). Venous blood samples were collected at 5, 15 and 25 min during the run and immediately post-exhaustion (POST-EX) and analysed for pH, and the concentrations of lactate ([1a^–]_b) and bicarbonate ([HCO₃ ^– ]). Performance was measured as running time to exhaustion at 110% of LT (TIME-EX). The pH was significantly higher (P 0.05) for the BIC and CIT trials during exercise, but not POST-EX compared to PLC. The [1a^–]_b was significantly higher (P 0.05) for the CIT trial compared to PLC during exercise, and for both CIT and BIC compared to PLC at POST-EX. Blood [HCO₃ ^–] was significantly higher (P 0.05) during exercise for BIC compared to PLC. TIME-EX was not significantly different among treatments: BIC 287 (SEM 47.4) s; CIT 172.8 (SEM 29.7) s; and PLC 222.3 (SEM 39.7) s. Despite the fact that buffer ingestion produced favourable metabolic conditions during 30 min of high intensity steady-state exercise, a significant improvement in the subsequent maximal exercise run to exhaustion did not occur.     

Hormonal regulation of potassium shifts during graded exhausting exercise

Summary Serum potassium, aldosterone and insulin, and plasma adrenaline, noradrenaline and cyclic adenosine 3:5-monophosphate (cAMP) concentrations were measured during graded exhausting exercise and during the following 30 min recovery period in six untrained young men. During exercise there was an increase in concentration of serum potassium (4.74 mmol·1^–1, SEM 0.12 at the end of exercise vs 3.80 mmol·1^–1, SEM 0.05 basal,P<0.001), plasma adrenaline (2.14 nmol·1^–1, SEM 0.05 at the end of exercise vs 0.30 nmol·1^–1, SEM 0.02 basal,P<0.001), plasma noradrenaline (1.10 nmol·1^–1, SEM 0.64 at the end of exercise vs 1.50 nmol·1^–1, SEM 0.05 basal,P< 0.001), serum aldosterone (0.92 nmol·1^–1, SEM 0.14 at the end of exercise vs 0.36 nmol·1^–1, SEM 0.05 basal,P<0.01), and plasma cAMP (35.4 nmol·1^–1, SEM 2.3 at the end of exercise vs 21.4 nmol·1^–1, SEM 4.5 basal,P<0.05). While concentrations of serum potassium, plasma adrenaline and cAMP returned to their basal levels immediately after exercise, those of plasma noradrenaline and serum aldosterone remained elevated 30 min later (1.90 nmol·1^–1, SEM 0.01,P<0.01; and 0.85 nmol·1^–1, SEM 0.12,P<0.01, respectively). Serum insulin concentration did not change during exercise (6.47 mlU·1^–1, SEM 0.58 at the end of exercise vs 5.47 mlU·1^–1, SEM 0.41 basal, NS) but increased significantly (P<0.02) at the end of the recovery period (7.12 mlU·1^–1, SEM 0.65). Serum potassium increases with exhausting exercise appeared to be caused not only by its release from contracting muscles but also by an -adrenergic stimulation produced by adrenaline and noradrenaline. On the other hand, the increased levels of plasma noradrenaline maintained during the recovery period may have served to avoid excessive hypokalaemia through the stimulation of muscle -receptors. Thus, catecholamines may play an important role in the regulation of serum potassium concentrations during and after exercise. Any disturbance of these adrenergic effects may lead either to an excessive increase or to a decrease of kalaemia, with the consequent risk of arrhythmias linked to exercise.     

Effects of glucose ingestion or glucose infusion on fuel substrate kinetics during prolonged exercise

To determine if bypassing both intestinal absorption and hepatic glucose uptake by intravenous glucose infusion might increase the rate of muscle glucose oxidation above 1 g · min^–1, ten endurance-trained subjects were studied during 125 min of cycling at 70% of peak oxygen uptake (VO_{2 peak}). During exercise the subjects ingested either a 15 g · 100 ml^–1 U-¹⁴C labelled glucose solution or H₂O labelled with a U-¹⁴C glucose tracer for the determination of the rates of plasma glucose oxidation (Rox) and exogenous carbohydrate (CHO) oxidation from plasma¹⁴C glucose and¹⁴CO₂ specific activities, and respiratory gas exchange. Simultaneously, 2-³H glucose was infused at a constant rate to measure glucose turnover, while unlabelled glucose (25% dextrose) was infused into those subjects not ingesting glucose to maintain plasma glucose concentration at 5 mmol · l^–1. Despite similar plasma glucose concentrations [ingestion 5.3 (SEM 0.13) mmol · l^–1; infusion 5.0 (0.09) mmol · l^–1], compared to glucose infusion, CHO ingestion significantly increased plasma insulin concentrations [12.9 (1.0) vs 4.8 (0.5) mU · l^–1;P<0.05], raised total Rox values [9.5 (1.2) vs 6.2 (0.7) mmol · 125 min^–1 kg fat free mass^–1 (FFM);P<0.05] and rates of CHO oxidation [37.2 (2.8)vs 24.1 (3.9) mmol · 125 min^–1 kg FFM^–1;P<0.05]. An increased reliance on CHO metabolism with CHO ingestion was associated with a decrease in fat oxidation. Whereas the contribution from fat oxidation to energy production increased to 51 (10)% with glucose infusion, it only reached 18 (4)% with glucose ingestion (P<0.05). Despite these differences in plasma insulin concentration and rates of fat oxidation, the rates of glucose oxidation by muscle were similar after 125 min of exercise for both trials [ingestion 93 (8); infusion 85 (5) mol · min^–1 kg FFM^–1], suggesting that peak rates of muscle glucose oxidation were primarily dependent on blood glucose concentration which, in turn, regulated the hepatic appearance of ingested CHO.     

Caffeine increases maximal anaerobic power and blood lactate concentration

Summary The aim of this study was to specify the effects of caffeine on maximal anaerobic power (W _max). A group of 14 subjects ingested caffeine (250 mg) or placebo in random double-blind order. TheW _max was determined using a force-velocity exercise test. In addition, we measured blood lactate concentration for each load at the end of pedalling and after 5 min of recovery. We observed that caffeine increasedW _max [964 (SEM 65.77) W with caffeine vs 903.7 (SEM 52.62) W with placebo;P<0.02] and blood lactate concentration both at the end of pedalling [8.36 (SEM 0.95) mmol · l^–1 with caffeine vs 7.17 (SEM 0.53) mmol · l^–1 with placebo;P<0.011 and after 5 min of recovery [10.23 (SEM 0.97) mmol · l^–1 with caffeine vs 8.35 (SEM 0.66) mmol · l^–1 with placebo;P<0.04]. The quotient lactate concentration/power (mmol · l^–1 · W^–1) also increased with caffeine at the end of pedalling [7.6 · 10^–3 (SEM 3.82 · 10^–5) vs 6.85 · 10^–3 (SEM 3.01 · 10^–5);P<0.01] and after 5 min of recovery [9.82·10^–3 (SEM 4.28 · 10^–5) vs 8.84 · 10^–3 (SEM 3.58 · 10^–5);P<0.02]. We concluded that caffeine increased bothW _max and blood lactate concentration.     

Lactate disposal in resting trained and untrained forearm skeletal muscle during high intensity leg exercise

Summary At a given oxygen uptake ( O₂) and exercise intensity blood lactate concentrations are lower following endurance training. While decreased production of lactate by trained skeletal muscle is the commonly accepted cause, the contribution from increased lactate removal, comprising both uptake and metabolic disposal, has been less frequently examined. In the present study the role of resting skeletal muscle in the removal of an arterial lactate load (approximately 11 mmol·-l^–1) generated during high intensity supine leg exercise (20 min at approximately 83% maximal oxygen uptake) was compared in the untrained (UT) and trained (T) forearms of five male squash players. Forearm blood flow and the venoarterial lactate concentration gradient were measured and a modified form of the Fick equation used to determine the relative contributions to lactate removal of passive uptake and metabolic disposal. Significant lactate uptake and disposal were observed in both forearms without any change in forearm O₂. Neither the quantity of lactate taken up [UT, 344.2 (SEM 118.8) mol·100 ml^–1; T, 330.3 (SEM 85.3) mol·100 ml^–1] nor the quantity disposed of [UT, 284.0 (SEM 123.3) mol·100 ml^–1, approximately 83% of lactate uptake; T, 300.8 (SEM 77.7) mol·100 ml^–1, approximately 91% of lactate uptake] differed between the two forearms. It is concluded that while significant lactate disposal occurs in resting skeletal muscle during high intensity exercise the lower blood lactate concentrations following endurance training are unlikely to result from an increase in lactate removal by resting trained skeletal muscle.     

Breakdown of high-energy phosphate compounds and lactate accumulation during short supramaximal exercise

Summary Muscle ATP, creatine phosphate and lactate, and blood pH and lactate were measured in 7 male sprinters before and after running 40, 60, 80 and 100 m at maximal speed. The sprinters were divided into two groups, group 1 being sprinters who achieved a higher maximal speed (10.07±0.13 m ·s^–1) than group 2 (9.75±0.10 m ·s^–1), and who also maintained the speed for a longer time. The breakdown of high-energy phosphate stores was significantly greater for group 1 than for group 2 for all distances other than 100 m; the breakdown of creatine phosphate for group 1 was almost the same for 40 m as for 100 m. Muscle and blood lactate began to accumulate during the 40 m exercise. The accumulation of blood lactate was linear (0.55±0.02 mmol · s^–1 ·1^–1) for all distances, and there were no differences between the groups. With 100 m sprints the end-levels of blood and muscle lactate were not high enough and the change in blood pH was not great enough for one to accept that lactate accumulation is responsible for the decrease in running speed over this distance.We concluded that 1) in short-term maximal exercise, performance depends on the capacity for using high-energy phosphates at the beginning of the exercise, and 2) the decrease in running speed begins when the high-energy phosphate stores are depleted and most of the energy must then be produced by glycolysis.     

Effect of endurance training on excessive CO2 expiration due to lactate production in exercise

Summary We attempted to determine the change in total excess volume of CO₂ Output (CO₂ excess) due to bicarbonate buffering of lactic acid produced in exercise due to endurance training for approximately 2 months and to assess the relationship between the changes of CO₂ excess and distance-running performance. Six male endurance runners, aged 19–22 years, were subjects. Maximal oxygen uptake (VO_2max), oxygen uptake (VO₂) at anaerobic threshold (AT), CO₂ excess and blood lactate concentration were measured during incremental exercise on a cycle ergometer and 12-min exhausting running performance (12-min ERP) was also measured on the track before and after endurance training. The absolute magnitudes in the improvement due to training for C02 excess per unit of body mass per unit of blood lactate accumulation (Ala^–) in exercise (CO₂ excess·mass^–1·la^–), 12-min ERP, VO₂ at AT (AT-VO₂) and VO_2max on average were 0.8 ml·kg^–1·l^–1·mmol^–1, 97.8m, 4.4 ml·kg^–1· min^–1 and 7.3 ml·kg^–1·min^–1, respectively. The percentage change in CO₂ excess·mass^–1·la^– (15.7%) was almost same as those of VO_2max (13.7%) and AT-VO₂ (13.2%). It was found to be a high correlation between the absolute amount of change in CO₂ excess·mass^–1·la^– and the absolute amount of change in AT-VO₂ (r=0.94, P<0.01). Furthermore, the absolute amount of change in C02 excess·mass^–1·la^–, as well as that in AT-VO₂ (r=0.92, P<0.01), was significantly related to the absolute amount of change in 12-min ERP (r=0.81, P<0.05). It was concluded that a large CO₂ excess·mass^–1·la^–1 of endurance runners could be an important factor for success in performance related to comparatively intense endurance exercise such as 3000–4000 m races.     

Influence of moderate cold exposure on blood lactate during incremental exercise

Summary This study examined the effect of exposure of the whole body to moderate cold on blood lactate produced during incremental exercise. Nine subjects were tested in a climatic chamber, the room temperature being controlled either at 30°C or at 10°C. The protocol consisted of exercise increasing in intensity in 35 W increments every 3 min until exhaustion. Oxygen consumption (VO₂) was measured during the last minute of each exercise intensity. Blood samples were collected at rest and at exhaustion for the measurement of blood glucose, free fatty acid (FFA), noradrenaline (NA) and adrenaline (A) concentrations and, during the last 15 s of each exercise intensity, for the determination of blood lactate concentration [la^–]_b. TheVO₂ was identical under both environments. At 10°C, as compared to 30°C, the lactate anaerobic threshold (Th_{an, la} ^–) occurred at an exercise intensity 15 W higher and [Th_{an, la} ^–]_b was lower for submaximal intensities above the Th_{an, la} ^– Regardless of ambient temperature, glycaemia, A and NA concentrations were higher at exhaustion while FFA was unchanged. At exhaustion the NA concentration was greater at 10°C [15.60 (SEM 3.15) nmol·l^–1] than at 30°C [8.64 (SEM 2.37) nmol·l^–1]. We concluded that exposure to moderate cold influences the blood lactate produced during incremental exercise. These results suggested that vasoconstriction was partly responsible for the lower [la^–]_b observed for submaximal high intensities during severe cold exposure.     

Effect of heat stress on muscle blood flow during dynamic handgrip exercise

Summary During exercise in a hot environment, blood flow in the exercising muscles may be reduced in favour of the cutaneous circulation. The aim of our study was to examine whether an acute heat exposure (65–70°C) in sauna conditions reduces the blood flow in forearm muscles during handgrip exercise in comparison to tests at thermoneutrality (25° C). Nine healthy men performed dynamic handgrip exercise of the right hand by rhythmically squeezing a water-filled rubber tube at 13% (light), and at 34% (moderate) of maximal voluntary contraction. The left arm served as a control. The muscle blood flow was estimated as the difference in plethysmographic blood flow between the exercising and the control forearm. Skin blood flow was estimated by laser Doppler flowmetry in both forearms. Oesophageal temperature averaged 36.92 (SEM 0.08) ° C at thermo-neutrality, and 37.74 (SEM 0.07) ° C (P<0.01) at the end of the heat stress. The corresponding values for heart rate were 58 (SEM 2) and 99 (SEM 5) beats -min^–1 (P<0.01), respectively. At 25° C, handgrip exercise increased blood flow in the exercising forearm above the control forarm by 6.0 (SEM 0.8) ml · 100 ml^–1 · min^–1 during light exercise, and by 17.9 (SEM 2.5) ml · 100 ml^–1 · min^–1 during moderate exercise. In the heat, the increases were significantly higher: 12.5 (SEM 2:2) ml · 100 ml^–1 · min^–1 at the light exercise level (P<0.01), and 32.2 (SEM 5.9) ml · 100 ml^–1·min^–1 (P<0.05) at the moderate exercise level. Skin blood flow was not significantly different in any of the test conditions between the two forearms. These results suggested that hyperthermia of the observed magnitude did not reduce blood flow in active muscles during light or moderate levels of dynamic handgrip exercise.     

Enhanced endurance in trained cyclists during moderate intensity exercise following 2 weeks adaptation to a high fat diet

These studies investigated the effects of 2 weeks of either a high-fat (HIGH-FAT: 70% fat, 7% CHO) or a high-carbohydrate (HIGH-CHO: 74% CHO, 12% fat) diet on exercise performance in trained cyclists (n = 5) during consecutive periods of cycle exercise including a Wingate test of muscle power, cycle exercise to exhaustion at 85% of peak power output [90% maximal oxygen uptake ( O_2max), high-intensity exercise (HIE)] and 50% of peak power output [60% O_2max, moderate intensity exercise (MIE)]. Exercise time to exhaustion during HIE was not significantly different between trials: nor were the rates of muscle glycogen utilization during HIE different between trials, although starting muscle glycogen content was lower [68.1 (SEM 3.9) vs 120.6 (SEM 3.8) mmol · kg ^–1 wet mass, P < 0.01] after the HIGH-FAT diet. Despite a lower muscle glycogen content at the onset of MIE [32 (SEM 7) vs 73 (SEM 6) mmol · kg ^–1 wet mass, HIGH-FAT vs HIGH-CHO, P < 0.01], exercise time to exhaustion during subsequent MIE was significantly longer after the HIGH-FAT diet [79.7 (SEM 7.6) vs 42.5 (SEM 6.8) min, HIGH-FAT vs HIGH-CHO, P<0.01]. Enhanced endurance during MIE after the HIGH-FAT diet was associated with a lower respiratory exchange ratio [0.87 (SEM 0.03) vs 0.92 (SEM 0.02), P<0.05], and a decreased rate of carbohydrate oxidation [1.41 (SEM 0.70) vs 2.23 (SEM 0.40) g CHO · min^–1, P<0.05]. These results would suggest that 2 weeks of adaptation to a high-fat diet would result in an enhanced resistance to fatigue and a significant sparing of endogenous carbohydrate during low to moderate intensity exercise in a relatively glycogen-depleted state and unimpaired performance during high intensity exercise.     

Fuel kinetics during intense running and cycling when fed carbohydrate

On two occasions, six well-trained, male competitive triathletes performed, in random order, two experimental trials consisting of either a timed ride to exhaustion on a cycle ergometer or a run to exhaustion on a motor-driven treadmill at 80% of their respective peak cycling and peak running oxygen (VO_2max) uptakes. At the start of exercise, subjects drank 250 ml of a 15 g·100 ml^–1 w/v [U-¹⁴C]glucose solution and, thereafter, 150 ml of the same solution every 15 min. Despite identical metabolic rates [VO₂ 3.51 (0.06) vs 3.51 (0.10) 1·min^–1; values are mean (SEM) for the cycling and running trials, respectively], exercise times to exhaustion were significantly longer during cycling than running [96 (14) vs 63 (11) min; P < 0.05]. The superior cycling than running endurance was not associated with any differences in either the rate of blood glucose oxidation [3.8 (0.1) vs 3.9 (0.4) mmol· min^–1], or the rate of ingested glucose oxidation [2.0 (0.1) vs 1.7 (0.2) mmol· min^–1] at the last common time point (40 min) before exhaustion, despite higher blood glucose concentrations at exhaustion during running than cycling [7.0 (0.9) vs 5.8 (0.5) mmol·1^–1; P < 0.05]. However, the final rate of total carbohydrate (CHO) oxidation was significantly greater during cycling than running [24.0 (0.8) vs 21.7 (1.4) mmol C₆·min^–1; P < 0.01]. At exhaustion, the estimated contribution to energy production from muscle glycogen had declined to similar extents in both cycling and running [68 (3) vs 65 (5)%]. These differences between the rates of total CHO oxidation and blood glucose oxidation suggest that the direct and/or indirect (via lactate) oxidation of muscle glycogen was greater in cycling than running.     

Glycogen and triglyceride utilization in relation to muscle metabolic characteristics in men performing heavy-resistance exercise

Summary Nine bodybuilders performed heavy-resistance exercise activating the quadriceps femoris muscle. Intermittent 30-s exhaustive exercise bouts comprising 6–12 repetitions were interspersed with 60-s periods for 30 min. Venous blood samples were taken repeatedly during and after exercise for analyses of plasma free fatty acid (FFA) and glycerol concentration. Muscle biopsies were obtained from the vastus lateralis muscle before and after exercise and assayed for glycogen, glycerol-3-phosphate, lactate and triglyceride (TG) content. The activities of citrate synthase (CS), lactate dehydrogenase, hexokinase (HK), myokinase, creatine kinase and 3-hydroxyacyl-CoA dehydrogenase (HAD), were analysed. Histochemical staining procedures were used to assess fibre type composition, fibre area and capillary density. TG content before and after exercise averaged (SD) 23.9 (13.3) and 16.7 (6.4) mmol kg^–1 dry wt. The basal triglyceride content varied sixfold among individuals and the higher the levels the greater was the change during exercise. The glycogen content decreased (P<0.001) from 690 (82) to 495 (95) mmol kg^–1 dry wt. and lactate and glycerol-3-phosphate increased (P<0.001) to 79.5 (5.5) and 14.5 (7.3) mmol kg^–1 dry wt., respectively, after exercise. The HK and HAD/CS content respectively correlated with glycogen or TG content at rest and with changes in these metabolites during exercise. FFA and glycerol concentrations increased slightly (P<0.001) during exercise. Lipolysis may, therefore, provide energy during heavy-resistance exercise of relatively short duration. Also, storage and utilization of intramuscular substrates appear to be influenced by the metabolic profile of muscle.     

Effect of acute mild hypoxia during exercise on plasma free and sulphoconjugated catecholamines

Catecholamine (CA) response to hypoxic exercise has been investigated during severe hypoxia. However, altitude training is commonly performed during mild hypoxia at submaximal exercise intensities. In the present study we tested whether submaximal exercise during mild hypoxia compared to normoxia leads to a greater increase of plasma concentrations of CA and whether plasma concentration of catecholamine sulphates change in parallel with the CA response. A group of 14 subjects [maximal oxygen uptake, 62.6 (SD 5.2) ml · min^–1 · kg^–1 body mass] performed two cycle ergometer tests of 1-h duration at the same absolute exercise intensities [191 (SD 6) W] during normoxia (NORM) and mild hypoxia (HYP) followed by 30 min of recovery during normoxia. Mean plasma concentrations of noradrenaline ([NA]), adrenaline ([A]), and noradrenaline sulphate ([NA-S]) were elevated (P < 0.01) after HYP and NORM compared with mean resting values and were higher after HYP [20.9 (SEM 3.1), 2.2 (SEM 0.24), 8.12 (SEM 1.5) nmol · 1^–1, respectively] than after NORM [(13.7 (SEM 0.9), 1.5 (SEM 0.14), 6.8 (SEM 0.7) nmol · 1^–1, respectively P < 0.01]. The higher plasma [NA-S] after HYP (P < 0.05) were still measurable after 30 min of recovery. From our study it was concluded that exercise at the same absolute submaximal exercise intensity during mild hypoxia increased plasma CA to a higher extent than during normoxia. Plasma [NA-S] response paralleled the plasma [NA] response at the end of exercise but, in contrast to plasma [NA], remained elevated until 30 min after exercise.     

The influence of a respiratory acidosis on the exercise blood lactate response

Summary The purpose of the present study was to examine the influence of a respiratory acidosis on the blood lactate (La) threshold and specific blood La concentrations measured during a progressive incremental exercise test. Seven males performed three step-incremental exercise tests (20 W · min^–1) breathing the following gas mixtures; 21% O₂ balance-nitrogen, and 21% O₂, 4% CO₂ balance-nitrogen or balance-helium. The log-log transformation of La oxygen consumption (VO₂) relationship and a 1 mmol ·1^–1 increase above resting values were used to determine a La threshold. Also, theVO₂ corresponding to a La value of 2 (La2) and 4 (La4) mmol · 1^–1 was determined. Breathing the hypercapnic gas mixtures significantly increased the resting partial pressure of carbon dioxide (PCO₂) from 5.6 kPa (42 mm Hg) to 6.1 kPa (46 mm Hg) and decreased pH from 7.395 to 7.366. During the incremental exercise test,PCO₂ increased significantly to 7.2 kPa (54 mm Hg) and 6.8 kPa (51 mm Hg) for the hypercapnic gas mixtures with nitrogen and helium, respectively, and pH decreased to 7.194 and 7.208. In contrast, bloodPCO₂ decreased to 4.9 kPa (37 mm Hg) at the end of the normocapnic exercise test and pH decreased to 7.291. A blood La threshold determined from a log-log transformation [1.20 (0.28) 1·min^–1] or as an increase of 1 mmol·1^–1[1.84 (0.46) 1·min^–1] was unaffected by the acid-base alterations. Similarly, theVO₂ corresponding to La2 and La4 was not affected by breathing the hypercapnic gas mixtures [2.12 (0.46) 1·min^–1 and 2.81 (0.52) 1·min^–1, respectively]. Blood La values were reduced significantly at maximal exercise while breathing the hypercapnic gas mixtures (5.72±1.34 mmol ·1^–1) compared with the normocapnic test (6.96±1.14 mmol·1^–1). It is concluded that respiratory-induced acid-base manipulations due to the inspiration of 4% CO₂ have a negligible influence on the blood La response during a progressive exercise test at low and moderate power outputs. Lower blood La values are observed at maximal exercise with an induced respiratory acidosis but this negative influence is less than what has been reported for an induced metabolic acidosis.     

Endogenous opioids may modulate catecholamine secretion during high intensity exercise

To determine the effect of endogenous opioids on catecholamine response during intense exercise [80% maximal oxygen uptake ( O_2max)], nine fit men [mean (SE) ( O_2max, 63.9 (1.7) ml · kg^–1 · min^–1; age 27.6 (1.6) years] were studied during two treadmill exercise trials. A double-blind experimental design was used with subjects undertaking the two exercise trials in counterbalanced order. Exercise trials were 20 min in duration and were conducted 7 days apart. One exercise trial was undertaken following administration of naloxone (N; 1.2 mmol · l^–1; 3 ml) and the other after receiving a placebo (P; 0.9% saline; 3 ml). Prior to each experimental trial a flexible catheter was placed into an antecubital vein and baseline blood samples were collected. Immediately afterwards, each subject received bolus injection of either N or P. Blood samples were also collected after 20 min of continuous exercise while running. Epinephrine and norepinephrine were higher (P < 0.05) in the N than P exercise trial with mean (SE) values of 1679 (196) versus 1196 (155) pmol · l^–1 and 24 (2.2) versus 20 (1.7) nmol · · l^–1 respectively. Glucose and lactate were higher (P < 0.05) in the N than P exercise trial with values of 7 (0.37) versus 5.9 (0.31) mmol · l^–1 and 6.9 (1.1) versus 5.3 (0.9) mmol · l^–1 respectively. These data suggest an opioid inhibition in the release of catecholamines during intense exercise.     

Effect of infusing branched-chain amino acid during incremental exercise with reduced muscle glycogen content

Summary The aim of this study was to investigate whether, when muscle glycogen is reduced, a pre-exercise infusion of branched-chain amino acids (BCAA) modifies exercise performance or the metabolic and respiratory responses to incremental exercise. Six moderately trained volunteers took part in the following protocol on two occasions. On day 1, at 9 a.m. in the postabsorptive state, they performed a graded incremental exercise (increases of 35 W every 4 min) to exhaustion (Ex-1). A meal of 1,000 kcal (4,200 kJ; 60% protein, 40% fat) was consumed at 12 p.m. No food was then allowed until the end of the experiment (20–21 h later). A 90-min period of exercise at alternating high and moderate intensities, designed to deplete muscle glycogen, was performed between 6 p.m. and 7.30 p.m. The morning after (day 2), the subjects randomly received either a mixed solution of BCAA (260 mg × kg^–1 × h^–1 for 70 min), or saline. They then repeated the graded incremental exercise to exhaustion (Ex-2). Metabolic and respiratory measurements suggested a muscle glycogen-depleted state had been achieved. No significant differences were observed in total work performed, maximal oxygen uptake or plasma ammonia, alanine, and blood pyruvate concentrations in the two treatments. After BCAA infusion, higher blood lactate concentrations were observed at maximal power output in comparison with those during saline [BCAA 4.97 (SEM 0.41) mmol × l^–1, Saline 3.88 (SEM 0.47) mmol × l^–1,P < 0.05]. In summary, in conditions of reduced muscle glycogen content, after a short period of fasting, BCAA infusion had no significant effect on the total work that could be performed during a graded incremental exercise.     

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

Summary It was the purpose of this study to determine the effects of respiratory alkalosis before and after high intensity exercise on recovery blood lactate concentration. Five subjects were studied under three different acid-base conditions before and after 45 s of maximal effort exercise: 1) hyperventilating room air before exercise (Respiratory Alkalosis Before=RALB, 2) hyperventilating room air during recovery (Respiratory Alkalosis After=RALA), and 3) breathing room air normally throughout rest and recovery (Control =C). RALB increased blood pH during rest to 7.65±0.03 while RALA increased blood pH to 7.57±0.03 by 40 min of recovery. Neither alkalosis treatment had a significant effect on blood lactate concentration during recovery. The peak lactate values of 12.3±1.2 mmol · L^–1 for C, 11.8±1.2 mmol · L^–1 for RALB, and 10.2±0.9 mmol · L^–1 for RALA were not significantly different, nor were the half-times (t _1/2) for the decline in blood lactate concentration; C=18.2 min, RALB=19.3 min, and RALA=18.2 min. In C, RALB and RALA, the change in base excess from rest to postexercise was greater than the concomitant increase in blood lactate concentration, suggesting the presence of a significant amount of acid in the blood in addition to lactic acid. There was no significant difference in either the total number of cycle revolutions (C=77±2, RALB=77±1) or power output at 5 s intervals between RALB and C during the 45 s. These results suggest that the possible range of respiratory alkalosis changes in intact humans may be insufficient 1) to affect recovery blood lactate concentrations, or 2) to affect intense, short-term exercise performance.     

Carnosine and anserine concentrations in the quadriceps femoris muscle of healthy humans

Summary The content of anserine and carnosine in the lateral portion of the quadriceps femoris muscle of 50 healthy, human subjects has been studied. Anserine was undetectable in all muscle samples examined. Muscle carnosine values for the group conformed to a normal distribution with a mean (SD) value of 20.0 (4.7) mmol · kg^–1 of dry muscle mass. The concentration of carnosine was significantly higher in the muscle of male subjects (21.3, 4.2 mmol · kg^–1 dry mass) than in females of a similar age and training status (17.5, 4.8 mmol · kg^–1 dry mass) (P< 0.005). The test-retest reliability of measures was determined on a subgroup of 17 subjects. No significant difference in mean carnosine concentration was found between the two trials [21.5 (4.0) and 22.0 (5.2) mmol · kg^–1 dry muscle mass; P>0.05]. The importance of carnosine as a physicochemical buffer within human muscle was examined by calculating its buffering ability over the physiological pH range. From the range of carnosine concentrations observed (7.2–30.7 mmol · kg^–1 dry muscle mass), it was estimated that the dipeptide could buffer between 2.4 and 10.1 mmol H⁺ · kg^–1 dry mass over the physiological pH range 7.1–6.5, contributing, on average, approximately 7% to the total muscle buffering. This suggests that in humans, in contrast to many other species, carnosine is of only limited importance in preventing the reduction in pH observed during high intensity exercise.     

Availability of glucose ingested during muscle exercise performed under acipimox-induced lipolysis blockade

This study investigated the percentage of carbohydrate utilization than can be accounted for by glucose ingested during exercise performed after the ingestion of the potent lipolysis inhibitor Acipimox. Six healthy male volunteers exercised for 3 h on a treadmill at about 45% of their maximal oxygen uptake, 75 min after having ingested 250 mg of Acipimox. After 15-min adaptation to exercise, they ingested either glucose dissolved in water, 50 g at time 0 min and 25 g at time 60 and 120 min (glucose, G) or sweetened water (control, C). Naturally labelled [¹³C]glucose was used to follow the conversion of the ingested glucose to expired-air CO₂. Acipimox inhibited lipolysis in a similar manner in both experimental conditions. This was reflected by an almost complete suppression of the exercise-induced increase in plasma free fatty acid and glycerol and by an almost constant rate of lipid oxidation. Total carbohydrate oxidation evaluated by indirect calorimetry, was similar in both experimental conditions [C, 182, (SEM 21); G, 194 (SEM 16) g · 3 h^–1], as was lipid oxidation [C, 57 (SEM 6); G, 61 (SEM 3) g · 3 h^–1]. Exogenous glucose oxidation during exercise G, calculated by the changes in¹³C:¹²C ratio of expired air CO₂, averaged 66 (SEM 5) g · 3 h^–1 (19% of the total energy requirement). Consequently, endogenous carbohydrate utilization was significantly smaller after glucose than after placebo ingestion: 128 (SEM 18) versus 182 (SEM 21) g · 3 h^–1, respectively (P < 0.05). Symptoms of intense fatigue and leg cramps observed with intake of sweet placebo were absent with glucose ingestion.In conclusion, we found glucose ingestion during 3-h exercise with lipolysis blockade could provide metabolic substrate permitting a significant sparing of endogenous carbohydrate and consequently an improvement in performance.