Melatonin and gonadotropin secretion after acute exercise in physically active males

Summary Serum concentrations of luteinizing hormone (LH), follicle stimulating hormone, testosterone (T) and melatonin were measured in seven physically active male volunteers after exercise on a treadmill using the Bruce protocol. Measurements were made on blood samples obtained before exercise, within 30 s after exercise, at 15 min after exercise, and subsequently at 30-min intervals after exercise for a total duration of 180 min. Serum LH concentration fell from a peak post-exercise level of 15.7 (4.7) IU·l^–1 [mean (SD)] to a nadir of 10.3 (2.4) IU·l^–1 (P<0.004). Nadir values in individual volunteers were seen between 60 and 150 min after exercise. This fall in serum LH was paralleled by a similar fall in the concentration of serum T. Serum melaonin concentrations did not change significantly after exercise. It is concluded that melatonin, despite is reported anti-gonadotropic properties, does not play a role in the depression of serum LH after acute strenuous exercise in physically active males     

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.     

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

Summary Nine well-trained subjects performed 15-, 30-and 45-s bouts of sprint exercise using a cycle ergometer. There was a significant difference in the mean power between a 15-s sprint (706.0 W, SD 32.5) and a 30-s sprint (627.0 W, SD 27.8;P<0.01). The mean power of the 30-s sprint was higher than that of the 45-s sprint (554.7 W, SD 29.8;P<0.01). Blood ammonia and lactate were measured at rest, immediately after warming-up, and 2.5, 5, 7.5, 10, 12.5 min after each sprint. The peak blood ammonia content was 133.8 mol·1^–1, SD 33.5,- for the 15-s sprint, 130.2 ol·1^–1, SD 44.9, for the 30-s sprint, and 120.8 mol ·1^–1, SD 24.6, for the 45-s sprint. Peak blood lactates after the 15-, 30- and 45-s sprints were 8.1 mmol · 1^–1, SD 1.7, 11.2 mmol · 1^–1, SD 2.4, and 14.7 mmol ·1^–1, SD 2.1, respectively. There was a significant linear relationship between peak blood ammonia and lactate in the 15-s (r, 0.709;P< 0.05), 30-s (r, 0.797;P<0.05) and 45-s (r, 0.696;P<0.05) sprints. Though the peak blood lactate content increased significantly with increasing duration of the sprints (P<0.01), no significant difference was found in peak blood ammonia content among the 15-, 30- and 45-s sprints. These results suggest that the peak value of ammonia in the blood appears in sprints within 15-s and that the blood ammonia level is linked to the lactate in the blood.     

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.     

Plasma metabolites, volume and electrolytes following 30-s high-intensity exercise in boys and men

It has been shown that boys recover faster than men following brief, high-intensity exercise. Better to understand this difference, plasma metabolite concenration, volume, electrolyte concentration [electrolyte], and hydrogen ion concentration [H⁺] changes were compared in five prepubescent boys [mean age 9.6 (SD 0.9) years] and 5 men [mean age 24.9 (SD 4.3) years] following 30-s, all-out cycling. Blood was collected prior to, at the end, and at the 1st, 3rd and 10th min following exercise. At the 10th min of recovery, the men's lactate concentration was 14.2 (SD 1.8) mmol · l^–1 and [H⁺] was 66.1 (SD 5.9) nmol · l^–1, compared with 5.7 (SD 0.7) mmol · l^–1 and 47.5 (SD 1.2) nmol · l^–1 respectively, in the boys (P < 0.01 for both). The glycerol concentration was higher in the boys at the end of exercise and until the 3rd min of recovery. Plasma volume (PV) decreased more in the men [16.9 (SD 3.0)%] than in the boys [9.4 (SD 2.8)%]. In both groups, [electrolyte] increased after exercise, tending to be higher in the men. Recovery of plasma [electrolyte] and PV started earlier in the boys (1st min) than in the men (3rd min). These findings would support the notion of a lesser reliance on glycolytic energy pathways in children and may explain the faster recovery of muscle power in boys compared to men.     

Exhausting handgrip exercise reduces the blood flow in the active calf muscle exercising at low intensity

The calf and forearm blood flows (Q _calf and Q _forearm respectively), blood pressure, heart rate and oxygen uptake of six men and women were studied during combined leg and handgrip exercise to determine whether a reduction of exercise-induced hyperaemia would occur in the active leg when exhausting rhythmic handgrip exercise at 50% maximal voluntary contraction (MVC) was superimposed upon rhythmic plantar flexion lasting for 10 min at 10% MVC (P₁₀) prior to this combined exercise. The Q _calf and Q _forearm were measured by venous occlusion plethysmography during 5-s rests interposed during every minute of P₁₀ exercise and immediately after combined exercise. The muscle sympathetic nerve activity (MSNA) changes were also recorded during leg exercise alone and combined exercise. During plantar flexion performed 60 times · min^–1 with a load equal to 10% MVC (P₁₀), Q _calf was maintained at a constant level, which was significantly higher than the resting value (P < 0.001). When rhythmic handgrip contraction at 50% MVC (H₅₀) and P₁₀ were performed simultaneously, the combined exercise was concluded due to forearm exhaustion after a mean of 51.2 (SEM 5.5) s. At exhaustion, Q _calf had decreased significantly from 20.6 (SEM 3.0) ml · 100 ml^–1 · min^–1 (10th min during P₁₀ exercise) to 15.3 (SEM) ml · 100 ml^–1 · min^–1 (P = 0.001), whereas Q _forearm had increased significantly (0.001 < P < 0.01) from 8.6 (SEM 1.9) ml · 100 ml^–1 · min^–1 (10th min of P₁₀ exercise) to 26.2 (SEM 3.2) ml · 100 ml^–1 · min^–1. The mean blood pressure remained at an almost constant level during the 3rd to 10th min of P₁₀ exercise and increased markedly when H₅₀ was added. The calf vascular conductance during combined exercise decreased significantly (0.001 < P < 0.01) compared with that at the 10th min of P₁₀ alone. Although the MSNA (expressed as burst rate) remained unchanged during P₁₀ exercise for 10 min, it increased markedly when exhausting H₅₀ and P₁₀ exercise were performed simultaneously. These findings indicated that superimposition of exhausting handgrip exercise at 50% MVC caused a vasoconstriction in the exercising calf due to increased MSNA, which counteracted the vasodilatation in this active muscle.     

Dietary intervention and training in swimmers

Summary To ascertain if muscle damage occurred in swimmers as a result of high-intensity training and to find if fluid and dietary manipulation could affect muscle damage, we studied 40 members of the University of Florida swimming team using creatine kinase (CK) and lactic dehydrogenase (LDH) as markers of muscle damage during a 6-month period of intensive training. During this time, training intensity, fluid intake during exercise and dietary supplementation were all modified one by one to examine their individual effects. During a control period of 4 weeks, all swimmers drank water before and during (120 min) workouts. CK in men at the end of this period averaged 315, SD 122 (normal < 170 IU · l^–1). Half of the swimmers were then given 500 ml of a glucose-electrolyte solution (GES) (Na 21 mmol · l^–1, Cl 13 mmol · l^–1, K 2.5 mmol · l^–1, PO₄ 5 mmol · l^–1 and glucose 6%) before workouts and twice at intervals during the workout, while half continued to drink the same volume of water. One week after division into fluid groups, the workout intensity was increased by about 10%. Another week later CK had increased to 500, SD 180 IU · l^–1 in swimmers drinking water, but fell to 280, SD 105 IU · l^–1 in those drinking GES (P < 0.05). The second phase of the study began after a 4-week control period during which all athletes drank water before and during workouts. The swimmers were divided into four matched groups. Group I drank water before and during workouts and 250 ml of a 16% sucrose solution after; group II drank water before and during exercise and 250 ml of a milk protein supplement (MPS) containing 15 g lactalbumin and 16% sugar afterwards; group III drank GES before and during and the sucrose drink after exercise; group IV drank GES before and during and the MPS drink after exercise. Then during a 6-week period, the intensity of exercise was progressively increased by 25%. CK increased 61% (P < 0.01) in group I men, while it fell 12% (P < 0.05) in groups II and III, and 41% (P < 0.01) in group IV. In women, CK in group I increased 18% (P < 0.05); in group II it decreased 3.5%, in group III was unchanged, and in group IV declined 12.6% (P < 0.05). The final phase of the study was performed on 8 olympic swimmers who performed identical workouts each Saturday for 4 weeks. The 1st week they ingested water before and during exercise and the 16% sucrose solution afterwards. The 2nd week the GES solution was consumed before and during exercise and the sucrose solution afterwards. The 3rd week water was consumed before and during and MPS afterward and the 4th week GES before and during and MPS afterwards. Determination of CK and LDH before, immediately after, and at intervals afterwards showed that CK and LDH increased less when GES was the test fluid during exercise than when water was consumed. Recovery, as judged by return of CK and LDH to control values was more rapid when MPS was the post-exercise fluid than when the sucrose solution was given.     

Changes in carotid blood flow and electrocardiogram in humans during and after walking on a treadmill

Blood flow velocity in the common carotid artery and the electrocardiogram were measured simultaneously by telemetry in seven male subjects during 20-min walking on a treadmill at an exercise intensity corresponding to a mean oxygen uptake of 26.0 (SD 2.9) ml · kg ^–1 · min ^–1. The mean cardiac cycle was shortened from 0.814 (SD 0.103) s to 0.452 (SD 0.054) s during this exercise. Of this shortening, 73% was due to shortening of the diastolic period and 27% to shortening of the systolic period. In the relatively small shortening of the mean systolic period [from 0.377 (SD 0.043) s to 0.268 (SD 0.029) s], the isovolumetric contraction time was shortened by 56%. During exercise, the heart rate (f _c) increased by 79.4% [from 74.3 (SD 9.3) beats · min ^–1 to 133.3 (SD 14.8) beats · min ^–1], and the peak blood velocity (S₁) in the common carotid artery increased by 56.1% [from 0.82 (SD 0.10) m · s^–1 to 1.28 (SD 0.11) m · s^–1]. After exercise, the S₁ decreased rapidly to the resting level. The f _c decreased more slowly, still being higher than the initial resting level 5 min after exercise. The diastolic velocity wave and the end-diastolic foot decreased during exercise. The blood flow rate in the carotid artery increased transiently by 13.5% at the beginning of exercise [from 5.62 (SD 0.63) ml · s^–1 to 6.38 (SD 0.85) ml · s^–1] and by 26.5% at the end of the exercise period [from 5.62 (SD 0.63) ml · s^–1 to 7.11 (SD 1.34) ml · s^–1]. The increase of blood flow in the carotid artery at the onset of exercise may have been mainly related to cerebral activation, and partly to an increase of blood flow to the skin of the head. The physiological significance for cerebral function of the increase of blood flow in the artery after the end of exercise is unknown.     

Sodium citrate and anaerobic performance: implications of dosage

Summary The use of sodium bicarbonate to improve anaerobic performance is well known but other buffering agents have been used with some success. Sodium citrate is one such substance which has been used but without the normal gastro-intestinal discomfort usually associated with sodium bicarbonate ingestion. The effects of five doses of sodium citrate (0.1 g·kg^–1 body mass, 0.2 g·kg^–1 body mass, 0.3 g·kg^–1 body mass, 0.4 g·kg^–1 body mass and 0.5 g·kg^–1 body mass) on anaerobic performance were studied in order to determine the minimal and most productive dose required for performance enhancement. A maximal test was performed for 1^–1, min on a cycle ergometer. Total work and peak power were measured at the end of the exercise period. Blood was drawn 1.5 h prior to the test session and measured for pH, partial pressure of carbon dioxide and concentrations of bicarbonate, base excess and lactate. In all but the control and placebo trials subjects then ingested one of five doses of sodium citrate which was contained in 400 ml of flavoured drink. Blood was again taken 90 min later and this was repeated after the completion of the exercise test. The greatest amount of work was completed in the trial with citrate given at 0.5 g·kg^–1 body mass (44.63 kJ, SD 1.5) and this was also true for peak power (1306 W, SD 75). The post-exercise blood lactate concentration was also highest during this trial 15.9 mmol·1^–1, SD 1.1. Post-exercise pH decreased significantly in all trials (P<0.0001) while the administration of the sodium citrate in all doses above 0.1 g·kg^–1 body mass significantly increased resting pH values. Blood bicarbonate concentrations also increased with dose in an almost linear fashion with the administration of sodium citrate. Bicarbonate increases were all significant, P<0.05 (citrate 0.1 g·kg^–1 body mass), P<0.01 (citrate 0.2 g·kg^–1 body mass, 0.3 g·kg^–1 body mass and 0.4 g·kg^–1 body mass) and P<0.005 (citrate 0.5 g·kg^–1 body mass). The administration of sodium citrate also significantly increased base excess values (citrate 0.1 g·kg^–1 body mass,P<0.01; 0.2 g·kg^–1body mass, P<0.001; 0.3 g·kg^–1 body mass, P<0.001; 0.4 g·kg^–1 body mass, P<0.001; 0.5 g·kg^–1 body mass, P<0.0001) above control and placebo values. All post-exercise base excess values were significantly lower than basal or pre-exercise values (P<0.0001). It was concluded that sodium citrate was an effective ergogenic aid for anaerobic performance of approximately 60-s duration, with the most effective of those dosages tested being 0.5 g·kg^–1 body mass.     

Effects of pre-exercise carbohydrate feedings on muscle glycogen use during exercise in well-trained runners

Summary The purpose of this study was to examine the effects of pre-exercise glucose and fructose feedings on muscle glycogen utilization during exercise in six well-trained runners ( =68.2±3.4 ml·kg^–1·min^–1). On three separate occasions, the runners performed a 30 min treadmill run at 70% . Thirty minutes prior to exercise each runner ingested 75 g of glucose (trial G), 75 g of fructose (trial F) or 150 ml of a sweetened placebo (trial C). During exercise, no differences were observed between any of the trials for oxygen uptake, heart rate or perceived exertion. Serum glucose levels were elevated as a result of the glucose feeding (P<0.05) reaching peak levels at 30 min post-feeding (7.90±0.24 mmol·l^–1). With the onset of exercise, glucose levels dropped to a low of 5.89±0.85 mmol·l^–1 at 15 min of exercise in trial G. Serum glucose levels in trials F and C averaged 6.21±0.31 mmol·l^–1 and 5.95±0.23 mmol·l^–1 respectively, and were not significantly different (P<0.05). There were also no differences in serum glucose levels between any of the trials at 15 and 30 min of exercise. Muscle glycogen utilization in the first 15 min of exercise was similar in trial C (18.8±8.3 mmol·kg^–1), trial F (16.3±3.8 mmol·kg^–1) and trial G (17.0±1.8 mmol·kg^–1), and total glycogen use was also similar in trial C (25.6±7.9 mmol·kg^–1), trial F (35.4±5.7 mmol·kg^–1) and trial G (24.6±3.2 mmol·kg^–1). In contrast to previous research, these results suggest that pre-exercise feedings of fructose or glucose do not affect the rate of muscle glycogen utilization during 30 min of treadmill running in trained runners.     

Effects of moderate endurance exercise and training on in vitro lymphocyte proliferation,interleukin-2 (IL-2) production,and IL-2 receptor expression

This study was designed to examine immunological responses to an acute bout of cycle ergometry exercise before and after moderate endurance training. Previously sedentary males were randomly assigned to matched training (n=9) or control (n=6) groups. Training comprised 12 weeks during which supervised cycle ergometer exercise took place [30 min at 65–70% of maximal oxygen intake , 4–5 days · week^–1]. An acute bout of exercise (60 min; 60% was performed initially and after the 12-week interval. Samples of peripheral venous blood were taken at rest, after 30 and 60 min of exercise, and at 30 and 120 min post-exercise. Training improved by an average of 20% (40.6 to 49.2 ml · kg^–1 · min^–1). Relative to baseline and control measures, the resting concentration of (CD3-CD16⁺/CD56⁺) natural killer (NK) cells increased by 22% (P<0.05). The resting count of total CD25⁺ [interleukin-2 receptor (IL-2R) chain] lymphocytes did not change following training, but dual staining analysis showed a 100% increase in the fraction of CD16⁺ CD25⁺ NK cells (P < 0.05). Likewise the resting CD122⁺ (IL-2R chain) lymphocyte count increased 35% after training, the greatest increases (44%) being in CD16⁺ CD122⁺ NK cells (P<0.05). Soluble IL-2R levels also increased 33% (P< 0.05) after training. Following acute exercise at the same relative intensity; trained individuals exhibited a larger increase in the NK cell count, reduced lymphocytopenia, and attenuation of exercise-induced suppression of lymphocyte proliferation and IL-2 production (P<0.05). In addition, smaller increases in CD4 and CD8 counts during exercise were noted, but with faster recovery post-exercise (P<0.05). Addition of recombinant IL-2 (rIL-2) to phytohemagglutinin-stimulated peripheral blood mononuclear cell cultures did not reverse exercise-induced suppression of cell proliferation, either before or after training. However, rIL-2 did augment the spontaneous blastogenesis of exercise and post-training samples relative to baseline (P < 0.05). We conclude that moderate endurance training is associated with sustained alterations in immune function, both at rest and when exercising. Further investigations are necessary to determine the impact on overall health and susceptibility to disease.     

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.     

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.     

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.     

Exercise induces pentane production and neutrophil activation in humans. Effect of propranolol

Summary The effect of -adrenergic receptor blockade on exercise-induced lipid peroxidation in man has been examined by measuring the production of pentane in expired air. For this purpose, five healthy male subjects were subjected to dynamic exercise of graded intensity on a cycle ergometer (10 min at 45%, 5 min at 60% and 75% maximal oxygen uptake 1 h after ingestion of either a placebo or 40-mg propranolol. At rest, mean pentane concentration ([pent]) with placebo was 4.13 pmol · l^–1, SD 2.14. After exercise, this value significantly increased by 310% (17.1 pmol · l^–1, SD 7.73, P < 0.01). Oral administration of 40-mg propranolol significantly lowered the mean resting [pent] to 1.75 pmol · l^–1, SD 0.77, P < 0.05. After exercise, the increase of [pent] was much smaller (240%) and was less significant (P < 0.2) than with the placebo. The mechanism of this inhibitory effect of propranolol remains to be elucidated. However, as indicated by the measurement of plasma myeloperoxidase concentration, it can be concluded that the antioxidant property of propranolol cannot be attributed to the inhibition of neutrophil activation, a possible source of free radicals during exercise.     

Metabolic and circulatory responses to the ingestion of glucose polymer and glucose/electrolyte solutions during exercise in man

Summary Six men exercised on a cycle ergometer for 60 min on two occasions one week apart, at 68±3% of . On one occasion, a dilute glucose/electrolyte solution (E: osmolality 310 mosmol · kg^–1, glucose content 200 mmol·l^–1) was given orally at a rate of 100 ml every 10 min, beginning immediately prior to exercise. On the other occasion, a glucose polymer solution (P: osmolality 630 mosmol · kg^–1, glucose content equivalent to 916 mmol · l^–1) was given at the same rate. Blood samples were obtained from a superficial forearm vein immediately prior to exercise and at 15-min intervals during exercise; further samples were obtained at 15-min intervals for 60 min at rest following exercise. Heart rate and rectal temperature were measured at 5-min intervals during exercise.Blood glucose concentration was not different between the two tests during exercise, but rose to a peak of 8.7±1.2 mmol · l^–1 (mean±SD) at 30 min post-exercise when P was drunk. Blood glucose remained unchanged during and after exercise when E was drunk. Plasma insulin levels were unchanged during exercise and were the same on both trials, but again a sharp rise in plasma insulin concentration was seen after exercise when P was drunk. The rate of carbohydrate oxidation during exercise, as calculated from and the respiratory exchange ratio, was not different between the two tests. A fall in plasma volume, calculated from changes in haematocrit and haemoglobin concentration, occurred after 15 mins of exercise: the fall was of the same magnitude (9%) at this point on both tests, but thereafter plasma volume was significantly lower with P than with E for the remainder of the exercise period and throughout recovery. Serum osmolality increased during exercise (p<0.05) on the P trial, but was unchanged on the E trial. Heart rate was higher (p<0.05) during the last 20 min of exercise on the P trial.These results suggest that the carbohydrate consumed during the P trial was not available to the working muscles during exercise, and was probably not emptied from the stomach and absorbed to any significant extent until exercise stopped. The differences in plasma volume and osmolality between the two trials are consistent with the net movement of water into the gut which is known to occur at rest when solutions of high osmolality are taken. In more prolonged exercise, this effective dehydration may impair performance.     

Haematological and acute-phase responses associated with delayed-onset muscle soreness in humans

Delayed-onset muscle soreness following unaccustomed or eccentric exercise is associated with inflammation, tissue necrosis and the release of muscle enzymes (Newham et al. 1983). We have investigated the time course of changes in circulating leucocytes and serum levels of some acute phase reactants, serum creatine kinase activity (CK) and muscle pain after a 40-min bout of bench-stepping exercise in eight healthy untrained subjects. Leg muscle soreness was greatest 2 days after the exercise bout. Peak serum CK values [mean (SD) 540 (502) IU·l^–1] occurred 1–7 days post-exercise. Serum C-reactive protein (CRP) was unchanged from pre-exercise levels [7.8 (3.4) mg·l^–1] immediately post-exercise [7.9 (2.3) mg·l^–1] but rose to a peak of 17.0 (3.9) mg·l^–1 1 day post-exercise, thereafter declining to basal levels. Serum levels of iron and zinc fell below pre-exercise levels for 1–3 days post-exercise. Serum albumin, IgG and IgM fell below pre-exercise levels from 1 day post-exercise, reaching minimal values (about 80% of basal levels) at 7 days post-exercise. The exercise did not appear to significantly affect serum levels of alpha-1-antitrypsin and alpha-1-acid glycoprotein. Two and three days after the exercise bout the circulating numbers of total leucocytes, neutrophils, monocytes and basophils fell 15–20% below pre-exercise levels, whereas lymphocytes, eosinophils and platelets were unchanged. The results indicate that a rapid acute phase inflammatory response is initiated within 1 day of a bout of exercise that induces delayed-onset muscle soreness, and that any later tissue necrosis that may occur is not accompanied by further marked changes in acute-phase reactants such as CRP.     

Effect of short-term strenuous exercise on erythrocyte 2,3-diphosphoglycerate in untrained men: a time-course study

The literature on the response of erythrocyte 2,3-diphosphoglycerate (2,3-DPG) following exercise is replete with inconsistencies, and recent studies have shown that the time of blood sampling during and following exercise, as well as the duration of exercise, are important in evaluating the response of 2,3-DPG. Experiments were designed to measure the response of 2,3-DPG following short-term strenuous exercise in two groups of untrained men. Twelve men, 19–22 years old (study 1), exercised on a bicycle ergometer at 122.5 W for 10 min and red blood cell (RBC) 2,3-DPG was measured at 0 and 50 min following exercise. The level of 2,3-DPG (mol · ml^–1 RBC) increased after exercise (P < 0.05), but this increase was not significant when 2,3-DPG was expressed as mol · mol^–1 hemoglobin (Hb). However, following 50min of rest, 2,3-DPG (mol · mol^–1 Hb) decreased significantly. In a second group (study 2), nine other men, aged 18–19 years, exercised at the same workload for 15 min and 2,3-DPG was measured at 0, 30, 60, 180, and 330 min respectively after exercise, and no significant mean changes in the level of the phosphate were observed. Findings from these studies suggest that 2,3-DPG does not provide a compensatory adjustment to facilitate oxygen delivery in the hypoxia of short-term strenuous exercise in untrained males immediately following exercise and when recovery intervals of up to 330min are also examined. It is suggested that 2,3-DPG be reported as mol · mol^–1 Hb, since the phosphate exists on Hb in an equimolar ratio in normal physiological states.     

The effect of pedaling frequency on glycogen depletion rates in type I and type II quadriceps muscle fibers during submaximal cycling exercise

Summary This study was conducted to determine whether the pedaling frequency of cycling at a constant metabolic cost contributes to the pattern of fiber-type glycogen depletion. On 2 separate days, eight men cycled for 30 min at approximately 85% of individual aerobic capacity at pedaling frequencies of either 50 or 100 rev·min^–1. Muscle biopsy samples (vastus lateralis) were taken immediately prior to and after exercise. Individual fibers were classified as type I (slow twitch), or type II (fast twitch), using a myosin adenosine triphosphatase stain, and their glycogen content immediately prior to and after exercise quantified via microphotometry of periodic acid-Schiff stain. The 30-min exercise bout resulted in a 46% decrease in the mean optical density (D) of type I fibers during the 50 rev·min^–1 condition [0.52 (0.07) to 0.28 (0.04)D units; mean (SEM)] which was not different (P>0.05) from the 35% decrease during the 100 rev · min^–1 condition [0.48 (0.04) to 0.31 (0.05)D units]. In contrast, the meanD in type II fibers decreased 49% during the 50 rev·min^–1 condition [0.53 (0.06) to 0.27 (0.04) units]. This decrease was greater (P<0.05) than the 33% decrease observed in the 100 rev·min –1 condition [0.48 (0.04) to 0.32 (0.06) units). In conclusion, cycling at the same metabolic cost at 50 rather than 100 rev·min^–1 results in greater type II fiber glycogen depletion. This is attributed to the increased muscle force required to meet the higher resistance per cycle at the lower pedal frequency. These data are consistent with the view that force development as opposed to velocity of contraction determines the degree of type II fiber recruitment when the metabolic cost of exercise is held constant.