Plasma vasopressin,renin activity,and aldosterone responses to maximal exercise in active college females

Summary The effect of maximal treadmill exercise on plasma concentrations of vasopressin (AVP); renin activity (PRA); and aldosterone (ALDO) was studied in nine female college basketball players before and after a 5-month basketball season. Pre-season plasma AVP increased (p<0.05) from a pre-exercise concentration of 3.8±0.5 to 15.8±4.8 pg · ml⁻¹ following exercise. Post-season, the pre-exercise plasma AVP level averaged 1.5±0.5 pg · ml⁻¹ and increased to 16.7±5.9 pg · ml⁻¹ after the exercise test. PRA increased (p<0.05) from a pre-exercise value of 1.6±0.6 to 6.8±1.7 ngAI · ml⁻¹ · hr⁻¹ 5 min after the end of exercise during the pre-season test. In the post-season, the pre-exercise PRA was comparable (2.4±0.6 ngAI · ml⁻¹ · hr⁻¹), as was the elevation found after maximal exercise (8.3±1.9 ngAI · ml⁻¹ · hr⁻¹). Pre-season plasma ALDO increased (p<0.05) from 102.9±30.8 pg · ml⁻¹ in the pre-exercise period to 453.8±54.8 pg · ml⁻¹ after the exercise test. In the post-season the values were 108.9±19.4 and 365.9±64.4 pg · ml⁻¹, respectively. Thus, maximal exercise in females produced significant increases in plasma AVP, renin activity, and ALDO that are comparable to those reported previously for male subjects. Moreover, this response is remarkably reproducible as demonstrated by the results of the two tests performed 5 months apart.     

Effects of inducing physiological hyperglucagonemia on metabolic responses to exercise

The purpose of the present study was to assess the effects of exogenously increasing the circulating levels of glucagon on the metabolic responses to exercise in rats. A total of six groups of rats were infused (iv) either with glucagon (20 or 50 ng·kg⁻¹·min⁻¹) or saline (0.9% NaCl), either in the resting state or during a bout of running exercise (45 min, 26 m·min⁻¹, 0% grade). Blood samples were taken at the end of the 45-min experiment. Animals infused with glucagon at 50 ng·kg⁻¹·min⁻¹ showed significantly (P<0.01) higher mean plasma glucagon concentrations than animals infused with saline or glucagon at 20 ng·kg⁻¹·min⁻¹. In addition, exercise resulted in significantly (P<0.05) higher mean plasma glucagon concentrations, compared to rest, in all groups. In spite of these differences in glucagon concentrations, there were no significant (P>0.05) effects of exercise and glucagon infusion on mean hepatic glycogen, plasma glucose, insulin, C-peptide, β-hydroxybutyrate, or catecholamine concentrations. Although exercise resulted in a significant (P<0.01) increase in plasma glycerol and free fatty acid concentrations and a significant (P<0.05) decrease in glycogen in the soleus muscle, these responses were not affected by the glucagon infusion. These results suggest that the liver is non-responsive to physiological hyperglucagonemia in a short-term (45 min) exercise situation. Electronic Publication     

The influence of free fatty acids on glycogen recovery in rat heart after exercise

Summary Glycogen supercompensation is the term used to denote the abnormally high levels of glycogen found in the heart shortly after an exercise-induced reduction of the substrate. Using rats, we tested whether this condition was linked to the use of plasma free fatty acids (FFA), which normally rise with exercise. Before a 1-h swim, animals received an injection of either saline (S) or nicotinic acid (NA). The nicotinic acid treatment dramatically suppressed the rise in plasma FFA observed in the S-group. Exercise caused a significant but similar reduction (35–38%) of the myocardial glycogen content in both groups. After 1 h of recovery in the S-group, myocardial glycogen reached a value of 30.3±1.7 Μmol·g⁻¹ or 113% of that measured before the exercise began. In contrast, the value for hearts from the NA-group with reduced FFA levels was 24.0±1.9 Μmol·g⁻¹ or only 91% of that measured before exercise. After 2 h the values were 33.8±1.4 and 29.0±1.9 Μmol·g⁻¹ respectively. These data indicate that glycogen repletion in rat heart after exercise is related to the amount of FFA present in the plasma. We suggest that carbohydrate metabolism is diverted towards synthesis and storage as a result of the glycolytic inhibition exerted by the increased use of fat as an energy source as previously observed in hearts from fasted or diabetic animals. This work was supported by a grant from the Utah Heart Association and the Deseret Gym Corporation     

Muscle glycogen resynthesis rate in humans after supplementation of drinks containing carbohydrates with low and high molecular masses

The rate of muscle glycogen synthesis during 2 and 4 h of recovery after depletion by exercise was studied using two energy equivalent carbohydrate drinks, one containing a polyglucoside with a mean molecular mass of 500 000–700 000 (C drink), and one containing monomers and oligomers of glucose with a mean molecular mass of approximately 500 (G drink). The osmolality was 84 and 350 mosmol · l⁻¹, respectively. A group of 13 healthy well-trained men ingested the drinks after glycogen depleting exercise, one drink at each test occasion. The total amount of carbohydrates consumed was 300 g (4.2 g · kg⁻¹) body mass given as 75 g in 500 ml water immediately after exercise and again 30, 60 ad 90-min post exercise. Blood glucose and insulin concentrations were recorded at rest and every 30 min throughout the 4-h recovery period. Muscle biopsies were obtained at the end of exercise and after 2 and 4 h of recovery. Mean muscle glycogen contents after exercise were 52.9 (SD 27.4) mmol glycosyl units · kg⁻¹ (dry mass) in the C group and 58.3 (SD 35.4) mmol glycosyl units · kg⁻¹ (dry mass) in the G group. Mean glycogen synthesis rate was significantly higher during the initial 2 h for the C drink compared to the G drink: 50.2 (SD 13.7) mmol · kg⁻¹ (dry mass) · h⁻¹ in the C group and 29.9 (SD 12.5) mmol · kg⁻¹ (dry mass) · h⁻¹ in the G group. During the last 2 h the mean synthesis rate was 18.8 (SD 33.3) and 23.3 (SD 22.4) mmol · kg⁻¹ (dry mass) · h⁻¹ in the C and G group, respectively (n.s.). Mean blood glucose and insulin concentrations did not differ between the two drinks. Our data indicted that the osmolality of the carbohydrate drink may influence the rate of resynthesis of glycogen in muscle after its depletion by exercise. Accepted: 9 September 1999     

Tricarboxylic acid cycle intermediates accumulate at the onset of intense exercise in man but are not essential for the increase in muscle oxygen uptake

It was proposed that a contraction-induced increase in tricarboxylic acid cycle intermediates (TCAI) is obligatory for the increase in muscle oxygen uptake at the start of exercise. To test this hypothesis, we measured changes in muscle TCAI during the initial seconds of intense exercise and used dichloroacetate (DCA) in an attempt to alter the level of TCAI. Five men performed strenuous leg kicking exercise (64±8 W) under noninfused control (CON) and DCA-supplemented conditions; biopsies (vastus lateralis) were obtained at rest and after 5, 15, and 180 s of exercise. In CON, the total concentration of three measured TCAI (ΣTCAI: citrate, malate, and fumarate) increased (p<0.05) by 71% during the first 15 s of exercise. The ΣTCAI was lower (p<0.05) in DCA than in CON at rest [0.18±0.02 vs 0.64±0.09 mmol kg⁻¹ dry weight (d.w.)], after 5 s (0.30±0.07 vs 0.85±0.14 mmol kg⁻¹ d.w.), and 15 s of exercise (0.60±0.07 vs 1.09±0.16 mmol kg⁻¹ d.w.), but not different after 3 min (3.12±0.53 vs 3.23±0.55 mmol kg⁻¹ d.w.). Despite differences in the level of muscle TCAI, muscle phosphocreatine degradation was similar in DCA and CON during the first 15 s of exercise (17.5±3.3 vs 25.6±4.1 mmol kg⁻¹ d.w.). Taken together with our previous observation that DCA does not alter muscle oxygen uptake during the initial phase of intense leg kicking exercise (Bangsbo et al. Am J Physiol 282:R273–R280, 2002), the present data suggest that muscle TCAI accumulate during the initial seconds of exercise; however, this increase is not essential for the contraction-induced increase in mitochondrial respiration.     

Substrate utilisation during exercise and shivering

It is generally assumed that exercise and shivering are analogous processes with regard to substrate utilisation and that, as a consequence, exercise can be used as a model for shivering. In the present study, substrate utilisation during exercise and shivering at the same oxygen consumption (V˙O₂) were compared. Following an overnight fast, eight male subjects undertook a 2-h immersion in cold water, designed to evoke three different intensities of shivering. At least 1 week later they undertook a 2-h period of bicycle ergometry during which the exercise intensity was varied to match the V˙O₂ recorded during shivering. During both activities hepatic glucose output (HGO), the rate of glucose utilisation (Rd), blood glucose, plasma insulin, free fatty acid (FFA) and beta-hydroxybutyrate (B-HBA) concentrations were measured. The V˙O₂ measured during the different levels of shivering averaged 0.49 l · min⁻¹ (level 1: low), 0.6 l · min⁻¹ (level 2: low-moderate), and 0.9 l · min⁻¹ (level 3: moderate), and corresponded closely to the levels measured during exercise. HGO and Rd were greater (P < 0.05) during exercise than during shivering at the same V˙O₂ (9.5% and 14.7%, respectively). The average (SD) HGO during level 3 exercise was 3.0 (0.91) mg · kg⁻¹ . min⁻¹ compared to 2.76 (1.0) mg · kg⁻¹ . min⁻¹ during shivering. The values for Rd were 3.06 (0.98) mg · kg⁻¹ · min⁻¹ during level 3 exercise and 2.68 (0.82) mg · kg⁻¹ · min⁻¹ during shivering. Blood glucose levels did not differ between conditions, averaging 5.4 (0.3) mmol . l⁻¹ over all levels of shivering and 5.2 (0.3) mmol · l⁻¹ during exercise. Plasma FFA and B-HBA were higher (P < 0.01) during shivering than during corresponding exercise (12.3% and 33.3%, respectively). FFA averaged 0.61 (0.2) mmol · l⁻¹ over all levels of shivering and 0.47 (0.16) mmol · l⁻¹ during exercise. The figures for B-HBA were 0.44 (0.13) mmol · l⁻¹ during all levels of shivering and 0.32 (0.1) mmol · l⁻¹ during exercise. Plasma insulin was higher (P < 0.05) during level 2 and 3 shivering compared to corresponding exercise; at these levels the average value for plasma insulin was 95.9 (21.9) pmol · l⁻¹ during shivering and 80.6 (16.1) pmol · l⁻¹ during exercise. On the basis of the present findings it is concluded that, with regard to substrate utilisation, shivering and exercise of up to 2 h duration should not be regarded as analogous processes. Accepted: 12 February 1997     

Beta-endorphin immunoreactivity during high-intensity exercise with and without opiate blockade

Nine highly fit men [mean (SE) maximum oxygen uptake, : 63.9 (1.7) ml·kg^–1·min^–1; age 27.6 (1.6) years] were studied during two treadmill exercise trials to determine plasma β-endorphin immunoreactivity during intense exercise (80% ). A double-blind experimental design was used, and subjects performed the two exercise trials in counterbalanced order. Exercise trials were 30 min in duration and were conducted 7 days apart. One exercise trial was undertaken following administration of naloxone (1.2 mg; 3 cm³) and the other after receiving a placebo (0.9% NaCl saline; 3 cm³). Prior to each experimental trial, a flexible catheter was placed into an antecubital vein and baseline blood samples were collected. Thereafter, each subject received either a naloxone or placebo bolus injection. Blood samples were also collected after 10, 20 and 30 min of continuous exercise. β-Endorphin was higher (P<0.05) during exercise when compared to pre-exercise in both trials. However, no statistically significant difference was found (P>0.05) between exercise time points within either experimental trial. β-endorphin immunoreactivity was greater (P<0.05) in the naloxone than in the placebo trial during each exercise sampling time point [10 min: 63.7 (3.9) pg·ml^–1 vs 78.7 (3.8) pg·ml^–1; 20 min: 68.7 (4.1) pg·ml^–1 vs 83.8 (4.3) pg·ml^–1; 30 min: 71.0 (4.3) pg·ml^–1 vs 82.5 (3.2) pg·ml^–1]. These data suggest that intense exercise induces significant increases in β-endorphin that are maintained over time during steady-rate exercise. Exercise and naloxone had an interactive effect on β-endorphin release that warrants further investigation. Electronic Publication     

Formation of acetylcarnitine in muscle of horse during high intensity exercise

Summary To study the changes in carnitine in muscle with sprint exercise, two Thoroughbred horses performed two treadmill exercise tests. Biopsies of the middle gluteal were taken before, after exercise and after 12 min recovery. Resting mean muscle total carnitine content was 29.5 mmol · kg⁻¹ dry muscle (d. m.). Approximately 88% was free carnitine, 7% acetylcarnitine and acylcarnitine was estimated at 5%. Exercise did not affect total carnitine, but resulted in a marked fall in free carnitine and almost equivalent rise in acetylcarnitine. The results are consistent with a role for carnitine in the regulation of the acetyl-CoA/CoA ratio during sprint exercise in the Thoroughbred horse by buffering excess production of acetyl units.     

Circulating reverse triiodothyronine in humans during exercise

Summary Circulating thyroxine (T₄), triiodothyronine (T₃) and reverse triiodothyronine (rT₃) as well as blood lactate and glucose concentrations were measured in a group of 12 trained volunteer subjects prior to and after swimming 0.18 or 0.9 km, to determine if increase in metabolic activity was accompanied by diversion of T₄ monodeiodination from the active (T₄ to T₃) to the inactive (T₄ to rT₃) pathway. The resting T₄, T₃, and rT₃ levels were 8.5 Μg·100 ml⁻¹, 108 ng·100 ml⁻¹, and 57 ng·100 ml⁻¹, respectively, whereas after 0.18 km of swimming the corresponding levels were 9.5 Μg·100 ml⁻¹, 135 ng. 100 ml⁻¹ and 70 ng·100 ml⁻¹. After 0.9 km of swimming, T₄, T₃, and rT₃ levels were 9.0 Μg·100 ml⁻¹, 126 ng·100 ml⁻¹, and 66 ng·100 ml⁻¹, respectively. The swimming was accompanied by hemoconcentration and increase in blood lactate but not in glucose concentrations. In two other investigations thyroid hormones were measured prior to and after 60 or 90 min of moderate exercise on a bicycle ergometer. This exercise had no effect on circulating thyroid hormone levels. Free thyroxine (FT₄) concentration and thyroxine binding globulin (TBG) capacity were unaltered after exercise. In conclusion, brief strenuous swimming or moderate bicycle exercise had minor or no effect on thyroid hormone concentrations when consideration was given to the attendant hemoconcentration. Even when exercise induced small T₃ and rT₃ changes were noted, they were in the same direction (increase) thus demonstrating a lack of diversion of peripheral T₄ monodeiodination. Investigations partially supported by NIH grant AG-01613 and the Narveen Medical Research Foundation, St. Louis, Missouri, USA     

Effect of short-term endurance training on exercise capacity,haemodynamics and atrial natriuretic peptide secretion in heart transplant recipients

Exercise tolerance of heart transplant patients is often limited. Central and peripheral factors have been proposed to explain such exercise limitation but, to date, the leading factors remain to be determined. We examined how a short-term endurance exercise training programme may improve exercise capacity after heart transplantation, and whether atrial natriuretic peptide (ANP) release may contribute to the beneficial effects of exercise training by minimizing ischaemia and/or cardiac and circulatory congestion through its vasodilatation and haemoconcentration properties. Seven heart transplant recipients performed a square-wave endurance exercise test before and after 6 weeks of supervised training, while monitoring haemodynamic parameters, ANP and catecholamine concentrations. After training, the maximal tolerated power and the total mechanical work load increased from 130.4 (SEM 6.5) to 150.0 (SEM 6.0) W (P < 0.05) and from 2.05 (SEM 0.1) to 3.58 (SEM 0.14) kJ · kg⁻¹ (P < 0.001). Resting heart rate decreased from 100.0 (SEM 3.4) to 92.4 (SEM 3.5) beats · min⁻¹ (P < 0.05) but resting and exercise induced increases in cardiac output, stroke volume, right atrial, pulmonary capillary wedge, systemic and pulmonary artery pressures were not significantly changed by training. Exercise-induced decrease of systemic vascular resistance was similar before and after training. After training arterio-venous differences in oxygen content were similar but maximal lactate concentrations decreased from 6.20 (SEM 0.55) to 4.88 (SEM 0.6) mmol · 1⁻¹ (P < 0.05) during exercise. Similarly, maximal exercise noradrenaline concentration tended to decrease from 2060 (SEM 327) to 1168 (SEM 227) pg · ml⁻¹. A significant correlation was observed between lactate and catecholamines concentrations. The ANP concentration at rest and the exercise-induced ANP concentration did not change throughout the experiment [104.8 (SEM 13.1) pg · ml⁻¹ vs 116.0 (SEM 13.5) pg · ml⁻¹ and 200.0 (SEM 23.0) pg · ml⁻¹ vs 206.5 (SEM 25.9) pg · ml⁻¹ respectively]. The results of this study suggested that the significant improvement in exercise capacity observed after this short-term endurance training period may have arisen mainly through peripheral mechanisms, associated with the possible decrease in plasma catecholamine concentrations and reversal of muscle deconditioning and/or prednisone-induced myopathy.     

Effects of dietary leucine supplementation on exercise performance

Branched chain amino acids (BCAA), particularly leucine, have been suggested to be ergogenic for both endurance and strength/power performance. This study investigated the effects of dietary leucine supplementation on the exercise performance of outrigger canoeists. Thirteen (ten female, three male) competitive outrigger canoeists [aged 31.6 (2.2) year, VO_2max 47.1 (2.0) ml kg⁻¹ min⁻¹] underwent testing before and after 6-week supplementation with either capsulated L-leucine (45 mg kg⁻¹ d⁻¹; n=6) or placebo (cornflour; n=7). Testing included anthropometry, 10 s upper body power and work and a row to exhaustion at 70–75% maximal aerobic power where perceived exertion (RPE), heart rate (HR) and plasma BCAA and tryptophan concentrations were assessed. Leucine supplementation resulted in significant increases in plasma leucine and total BCAA concentrations. Upper body power and work significantly increased in both groups after supplementation but power was significantly greater after leucine supplementation compared to the placebo [6.7 (0.7) v. 6.0 (0.7) W kg⁻¹]. Rowing time significantly increased [77.6 (6.3)–88.3 (7.3) min] and average RPE significantly decreased [14.5 (1.5)–12.9 (1.4)] with leucine supplementation while these variables were unchanged with the placebo. Leucine supplementation had no effect on the plasma tryptophan to BCAA ratio, HR or anthropometric variables. Six weeks’ dietary leucine supplementation significantly improved endurance performance and upper body power in outrigger canoeists without significant change in the plasma ratio of tryptophan to BCAA.Parts of this work have previously been presented in abstract form: Crowe MJ, Weatherson JN (2002) The effects of dietary L-leucine supplementation on exercise performance. Sports Medicine and Science at the Extremes. Australian Conference of Science and Medicine in Sport. 12–16 October, Melbourne, Australia     

The effect of severe eccentric exercise-induced muscle damage on plasma elastase, glutamine and zinc concentrations

The aim of this study was to determine if severe exercise-induced muscle damage alters the plasma concentrations of glutamine and zinc. Changes in plasma concentrations of glutamine, zinc and polymorphonuclear elastase (an index of phagocytic cell activation) were examined for up to 10 days following eccentric exercise of the knee extensors of one leg in eight untrained subjects. The exercise bout consisted of 20 repetitions of electrically stimulated eccentric muscle actions on an isokinetic dynamometer. Subjects experienced severe muscle soreness and large increases in plasma creatine kinase activity indicative of muscle fibre damage. Peak soreness occurred at 2 days post-exercise and peak creatine kinase activity [21714 (6416) U · l⁻¹, mean (SEM)] occurred at 3 days post-exercise (P < 0.01 compared with pre-exercise). Plasma elastase concentration was increased at 3 days post-exercise compared with pre-exercise (P < 0.05), and is presumably indicative of ongoing phagocytic leucocyte infiltration and activation in the damaged muscles. There were no significant changes in plasma zinc and glutamine concentrations in the days following eccentric exercise. We conclude that exercise-induced muscle damage does not produce changes in plasma glutamine or zinc concentrations despite evidence of phagocytic neutrophil activation. Accepted: 3 November 1997     

The effect of citrate loading on exercise performance,acid-base balance and metabolism

Summary Nine subjects ( 65±2 ml·kg⁻¹·min⁻¹, mean±SEM) were studied on two occasions following ingestion of 500 ml solution containing either sodium citrate (C, 0.300 g·kg⁻¹ body mass) or a sodium chloride placebo (P, 0.045 g·kg⁻¹ body mass). Exercise began 60 min later and consisted of cycle ergometer exercise performed continuously for 20 min each at power outputs corresponding to 33% and 66% , followed by exercise to exhaustion at 95% . Pre-exercise arterialized-venous [H⁺] was lower in C (36.2±0.5 nmol·l⁻¹; pH 7.44) than P (39.4±0.4 nmol·l⁻¹; pH 7.40); the plasma [H⁺] remained lower and [HCO ₃ ⁻ ] remained higher in C than P throughout exercise and recovery. Exercise time to exhaustion at 95% was similar in C (310±69 s) and P (313±74 s). Cardiorespiratory variables (ventilation, , , heart rate) measured during exercise were similar in the two conditions. The plasma [citrate] was higher in C at rest (C, 195±19 μmol·l⁻¹; P, 81±7 μmol·l⁻¹) and throughout exercise and recovery. The plasma [lactate] and [free fatty acid] were not affected by citrate loading but the plasma [glycerol] was lower during exercise in C than P. In conclusion, sodium citrate ingestion had an alkalinizing effect in the plasma but did not improve endurance time during exercise at 95% . Furthermore, citrate loading may have prevented the stimulation of lipolysis normally observed with exercise and prevented the stimulation of glycolysis in muscle normally observed in bicarbonate-induced alkalosis.     

High-intensity exercise decreases muscle buffer capacity via a decrease in protein buffering in human skeletal muscle

We have previously reported an acute decrease in muscle buffer capacity (βm_{in vitro}) following high-intensity exercise. The aim of this study was to identify which muscle buffers are affected by acute exercise and the effects of exercise type and a training intervention on these changes. Whole muscle and non-protein βm_{in vitro} were measured in male endurance athletes (VO_2max = 59.8 ± 5.8 mL kg⁻¹ min⁻¹), and before and after training in male, team-sport athletes (VO_2max = 55.6 ± 5.5 mL kg⁻¹ min⁻¹). Biopsies were obtained at rest and immediately after either time-to-fatigue at 120% VO_2max (endurance athletes) or repeated sprints (team-sport athletes). High-intensity exercise was associated with a significant decrease in βm_{in vitro} in endurance-trained males (146 ± 9 to 138 ± 7 mmol H⁺·kg d.w.⁻¹·pH⁻¹), and in male team-sport athletes both before (139 ± 9 to 131 ± 7 mmol H⁺·kg d.w.⁻¹·pH⁻¹) and after training (152 ± 11 to 142 ± 9 mmol H⁺·kg d.w.⁻¹·pH⁻¹). There were no acute changes in non-protein buffering capacity. There was a significant increase in βm_{in vitro} following training, but this did not alter the post-exercise decrease in βm_{in vitro}. In conclusion, high-intensity exercise decreased βm_{in vitro} independent of exercise type or an interval-training intervention; this was largely explained by a decrease in protein buffering. These findings have important implications when examining training-induced changes in βm_{in vitro}. Resting and post-exercise muscle samples cannot be used interchangeably to determine βm_{in vitro}, and researchers must ensure that post-training measurements of βm_{in vitro} are not influenced by an acute decrease caused by the final training bout.     

Thermoregulatory responses to exercise at low ambient temperature performed after precooling or preheating procedures

Summary Seven male skiers exercised for 30 min on a cycle ergometer at 50% of maximal oxygen uptake and an ambient temperature of 5° C. The exercise was preceded either by cold exposure (PREC) or active warming-up (PREH). The data were compared with control exercise (CONT) performed immediately after entering the thermal chamber from a thermoneutral environment. Cold exposure resulted in negative heat storage (96.1 kJ·m⁻², SE 5.9) leading to significantly lower rectal, mean body and mean skin temperatures at the onset of exercise in PREC, as compared to PREH and CONT. The PREC-PREH temperature differences were still significant at the end of the exercise period. During exercise in the PREC test, oxygen uptake was higher than in PREH test (32.8 ml·kg⁻¹·min⁻¹, SE 1.5 vs 30.5 ml·kg⁻¹·min⁻¹, SE 1.3, respectively). Heart rate showed only a tendency to be higher in PREC than in PREH and CONT tests. In the PREH test skin and body temperatures as well as sweat rate were already elevated at the beginning of exercise. Exercise-induced changes in these variables were minimal. Heat storage decreased with the duration of the exercise. Exercise at low ambient temperature preceded by a 30-min rest in a cold environment requires more energy than the same exercise performed after PREH. This work was partly supported by the Polish Central Programme of Basic Research 06-02.III.2.1.     

Renal protein excretion after exercise in man

Summary Thirteen men were submitted to graded exhaustive cycle exercise to determine the kinetics of proteinuria in the recovery period. Venous blood samples were analysed for haematocrit, lactate, creatinine, total protein and albumin for 1 h following exercise. Urine samples were collected during a 3-h recovery period. Total protein, albumin, and creatinine levels were determined for these samples. Total protein and albumin urinary excretion increased to 581 and 315 μg min⁻¹, respectively, at the end of the 1st h of recovery as compared to 42 and 15 μg · min⁻¹ for resting values. Plasma volume returned to pre-exercise levels between 30 and 60 min after cessation of exercise, while urinary total protein and albumin content still remained above the resting values for the following 2 h. Both post-exercise urinary total protein and albumin excretion followed a logarithmic decline with the same half-life of 54 min, thus requiring about 4 h to regain resting values. The reduction of plasma volume and the degree of dehydration do not seem to be involved in the process. The present study indicates the delayed recovery of protein handling by the kidney, as compared with other biochemical parameters, and provides accurate information on the kinetics of post-exercise proteinuria.     

Effects of a 24-h carbohydrate-poor diet on metabolic and hormonal responses during prolonged glucose-infused leg exercise

Summary Extant literature dealing with metabolic and hormonal adaptations to exercise following carbohydrate (CHO) reduced diets is not sufficiently precise to allow researchers to partial out the effects of reduced blood glucose levels from other general effects produced by low CHO diets. In order to shed light on this issue, a study was conducted to examine the effects of a 24-h CHO-poor diet on substrate and endocrine responses during prolonged (75 min; 60% ) glucose-infused leg exercise. Eight subjects exercised on a cycle ergometer in the two following conditions: 1) after a normal diet (CHO_N), and 2) after a 24-h low CHO diet (CHO_L). In both conditions, glucose was constantly infused intravenously (2.2 mg · kg⁻¹ · min⁻¹) from the 10th to the 75th min of exercise in relatively small amounts (10.4±0.8 g). No significant differences in blood glucose concentrations were found between the two conditions at rest and during exercise although a significant increase (p<0.01) in glucose level was observed in both conditions after 40 min of exercise. The CHO_L as compared to the CHO_N condition, was associated with significantly (p<0.05) lower resting concentrations of insulin, muscle glycogen (8.7 vs 10.6 g · kg⁻¹), and triacylglycerol, and greater concentrations of Β-hydroxybutyrate (0.5 vs 0.2 mmol · L⁻¹), and free fatty acids. During exercise, the CHO_L condition as compared to the CHO_N condition, was associated with significantly (p<0.05) lower insulin and R values, as well as greater free fatty acid (from min 20 to 60) and epinephrine (min 60 to 75) concentrations. Norepinephrine and glucagon concentrations also showed a net tendency (p<0.06) to be higher in the CHO_L condition. There were no significant differences at rest and during exercise in blood lactate and cortisol concentrations between the two conditions. These results demonstrate that blood glucose is not the sole determinant of the metabolic and hormonal responses during prolonged exercise following a low CHO intake and indicate that other factors may be involved in the regulatory mechanism.     

Plasma norepinephrine and heart rate dynamics during recovery from submaximal exercise in man

Summary The time course of heart rate (HR) and venous blood norepinephrine concentration [NE], as an expression of the sympathetic nervous activity (SNA), was studied in six sedentary young men during recovery from three periods of cycle ergometer exercise at 21%±2.8%, 43%±2.1% and 65%±2.3% of respectively (mean±SE). The HR decreased mono-exponentially withτ values of 13.6±1.6 s, 32.7±5.6 s and 55.8±8.1s respectively in the three periods of exercise. At the low exercise level no change in [NE] was found. At medium and high exercise intensity: (a) [NE] increased significantly at the 5th min of exercise (Δ[NE]=207.7±22.5 pg·ml⁻¹ and 521.3±58.3 pg·ml⁻¹ respectively); (b) after a time lag of 1 min [NE] decreased exponentially (τ=87 s and 101 s respectively); (c) in the 1st min HR decreased about 35 beats · min⁻¹; (d) from the 2nd to 5th min of recovery HR and [NE] were linearly related (100 pg·ml⁻¹ Δ[NE]5 beats ·min⁻¹). In the 1st min of recovery, independent of the exercise intensity, the adjustment of HR appears to have been due mainly to the prompt restoration of vagal tone. The further decrease in HR toward the resting value could then be attributed to the return of SNA to the pre-exercise level.     

Sympathetic control of the forearm blood flow in man during brief isometric contractions

Summary Experiments were performed to assess the possible neurally mediated constriction in active skeletal muscle during isometric hand-grip contractions. Forearm blood flow was measured by venous occlusion plethysmography on 5 volunteers who exerted a series of repeated contractions of 4 s duration every 12 s at 60% of their maximum strength of fatigue. The blood flows increased initially, but then remained constant at 20–24 ml·min⁻¹·100 ml⁻¹ throughout the exercise even though mean arterial blood pressure reached 21–23 kPa (160–170 mm Hg). When the same exercise was performed after arterial infusion of phentolamine, forearm blood flow increased steadily to near maximal levels of 38.7±1.4 ml·min⁻¹·100 ml⁻¹. Venous catecholamines, principally norepinephrine, increased throughout exercise, reaching peak values of 983±258 pg·ml⁻¹ at fatigue. Of the vasoactive substances measured, the concentration of K⁺ and osmolarity in venous plasma also increased initially and reached a steady-state during the exercise but ATP increased steadily throughout the exercise. These data indicate a continually increasing α-adrenergic constriction to the vascular beds in active muscles in the human forearm during isometric exercise, that is only partially counteracted by vasoactive metabolites.     

Passive and active wrist joint stiffness following eccentric exercise

The purpose of this study was to investigate the effects of exercise-induced muscle injury on passive and active wrist joint stiffness. Ten male subjects were repeatedly tested over a period of 11 days, once prior to, and four times following a bout of eccentric exercise with the wrist extensor muscles. Static wrist stiffness was measured by applying a 3° ramp and hold displacement of the manipulandum, which stretched the wrist extensor muscles. Wrist extension maximum voluntary contraction (MVC) declined by 24.5% from pre-exercise to 24 h after the exercise bout (P < 0.001). There was a reduced passive range of motion (ROM) from 82.8° pre-exercise to 70.2° on day 1 (P < 0.01), but no change in the passive joint stiffness at the neutral joint position, suggesting mechanical changes in the non-contractile tissues, or swelling that only resisted movement at the extremes of the ROM. Active joint stiffness at 50% pre-exercise MVC declined from 0.299 Nm deg⁻¹ pre-exercise to 0.254 Nm deg⁻¹ on day 1 (P < 0.025). Active joint stiffness at 10% pre-exercise MVC did not change on any of the days of testing compared to pre-exercise. These findings may indicate that large muscle fibers were more affected by the injury than small muscle fibers. Accepted: 7 February 2000