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The SARS-CoV-2 pandemic is not only a threat to physical health but is also having severe impacts on mental health. Although increases in stress-related symptomatology and other adverse psycho-social outcomes, as well as their most important risk factors have been described, hardly anything is known about potential protective factors. Resilience refers to the maintenance of mental health despite adversity. To gain mechanistic insights about the relationship between described psycho-social resilience factors and resilience specifically in the current crisis, we assessed resilience factors, exposure to Corona crisis-specific and general stressors, as well as internalizing symptoms in a cross-sectional online survey conducted in 24 languages during the most intense phase of the lockdown in Europe (22 March to 19 April) in a convenience sample of N = 15,970 adults. Resilience, as an outcome, was conceptualized as good mental health despite stressor exposure and measured as the inverse residual between actual and predicted symptom total score. Preregistered hypotheses (osf.io/r6btn) were tested with multiple regression models and mediation analyses. Results confirmed our primary hypothesis that positive appraisal style (PAS) is positively associated with resilience (p < 0.0001). The resilience factor PAS also partly mediated the positive association between perceived social support and resilience, and its association with resilience was in turn partly mediated by the ability to easily recover from stress (both p < 0.0001). In comparison with other resilience factors, good stress response recovery and positive appraisal specifically of the consequences of the Corona crisis were the strongest factors. Preregistered exploratory subgroup analyses (osf.io/thka9) showed that all tested resilience factors generalize across major socio-demographic categories. This research identifies modifiable protective factors that can be targeted by public mental health efforts in this and in future pandemics. © 2021, The Author(s).

The aim of the study was to investigate the palmitic acid incorporation into intramuscular acylglycerols in perfused hind-limb skeletal muscles of different fibre types in rats either fasted for 48 h or exposed to cold (6 °C) for 12 h. Hind-limb preparations of fasted and cold exposed rats were perfused with buffers containing tritium labelled and cold palmitic acid. Palmitic acid incorporation into intracellular lipid pools in the soleus, plantaris, red and white gastrocnemius and red and white quadriceps was measured. It was found that fasting increased approximately 2-fold palmitic acid incorporation in all muscles examined regardless of the fibre type composition of the muscle. On the other hand, exposure to cold had no effect on the palmitic acid incorporation into intramuscular acylglycerols regardless the muscle fibre type. The increased incorporation of palmitic acid into acylglycerols in fasted animals is in line with data showing that 48 h fasting stimulates the expression of plasma membrane proteins putatively facilitating fatty acid uptake. It appears that although 12 h cold exposure increases the use of fatty acids as energy substrates it does not alter the incorporation of palmitic acid into intramuscular acylglycerols in the perfused rat hind-limb.

The aim of this study was to establish whether the rate of fatty acid (FA) incorporation and its utilization by the isolated soleus muscle is modified under conditions of thyroid hormone deficit or excess. The rate of palmitic acid (PA) uptake, oxidation and incorporation into intramuscular lipids with increasing PA concentration (0.5-1.5 mM) in the incubation medium were determined. In hypothyroid rats intramuscular triacylglycerol (TG) synthesis was increased, while the rate of PA oxidation to CO2 and incorporation into mono- and diacylglycerols (MG/DG) and phospholipids (PL) remained unchanged. In rats with triiodothyronine (T3) excess the rate of all processes studied was enhanced, although the percentage incorporation of PA into different classes of intramuscular lipids was fairly constant and, independently of thyroid state and FA concentration in the medium, was 56-66% for TG, 9-14% for MG/DG and 24-32% for PL. Our results thus indicate that even short-term T3 excess accelerates the rate of FA uptake and metabolism in the oxidative soleus muscle, whereas in hypothyroid rats only intramuscular TG synthesis is affected.

Tympanic temperature (Tty), mean skin temperature (Tsk) and dynamics of sweating were measured in male subjects, performing prolonged, bicycle-exercise. The exercise was performed under thermoneutral environment after the normal-mixed (C) and low-carbohydrate (LCHO) diet. No difference in changes of Tty was observed after the C and LCHO diets. Sweating was triggered much faster after the LCHO diet. The delay in onset and inertia time of sweating was shorter after the LCHO diet. It is concluded that LCHO diet affects the thermoregulatory responses to exercise by acceleration of sweating, without noticeable differences in body temperature.

Previous investigations from this laboratory have demonstrated that during graded exercise with exercise intensities increasing every 3 min until exhaustion the multiple choice reaction time (RT) decreased until the intensity exceeded the lactate threshold (LT) by approximately 25%, and then rapidly increased. The aim of this study was to follow up changes in RT during prolonged exercise at constant intensities above and below LT and to relate these changes to changes in venous blood lactate [La−]b, and plasma catecholamine [CA]pl concentration responses to the exercise. For this purpose eight young soccer players exercised for 20-min on a cycle ergometer at 10% above LT, and nine exercised for 60 min at an intensity 30% below LT. During both tests RT, heart rate (HR), as well as [La−]b, and [CA]pl were measured. Above LT, RT decreased from the 5th min until the end of exercise, whilst HR, [La−]b, and [CA]pl increased progressively. Significant inverse correlations were ascertained between RT and plasma adrenaline (r = − 0.651) and noradrenaline concentrations (r = − 0.678). During exercise below LT, RT decreased up to approximately 40 min, then it reached a nadir, and stabilized at this level. This was accompanied by only small changes in [La−]b and [CA]pl. The present findings would indicate that young athletes are able to maintain for a relatively long time, or even increase, their psychomotor performance during endurance exercise both below and above the LT.

Plasma membranes from skeletal muscles were prepared and a binding assay was performed using [ 125 I]iodoinsulin. The kinetic parameters of the hormone–receptor interaction were analyzed by the Scatchard method. Muscle insulin sensitivity was expressed as the concentration of insulin required to produce the half-maximum stimulation of lactate production and glycogen formation, the latter measured as incorporation of [U- 14 C]glucose. 2-Deoxy-[2,6- 3 H]glucose was used for assessing, in vitro, the rate of glucose transport to the soleus muscle. It was found that hypothermia decreases the rate of glucose transport into skeletal muscle. The in vitro sensitivity of the soleus to insulin, measured either as lactate production or glycogen synthesis, was significantly increased in the group of hypothermic rats. We have also shown that, under hypothermic conditions, the number of insulin receptors is significantly increased in hind-limb skeletal muscles but these changes mainly involve the low affinity receptor class. It is possible that hypothermia primarily decreases the rate of glucose transport due to the lowering of body temperature. The increase in the number of insulin receptors plus increased sensitivity to insulin in the skeletal muscle of hypothermic rats may be part of a compensatory mechanism stabilizing muscle glycogen stores despite hypoinsulinemia.

The effect of prolonged elevation of blood adrenaline concentration (sustained up to 60 h) on exercise performance and lactate threshold (TLA) was investigated in 24 rats on the basis of a incremental, multistage treadmill exercise test, performed before and after subcutaneous implantation of retard adrenaline tablets (15 mg), which release adrenaline at a constant rate of approx. 1.6 micrograms min-1. Blood samples for lactate (LA) determinations were taken from the rats' tails after each exercise stage. The results obtained indicate that hyperadrenalinemia within the physiologic range, sustained for 6 or 12 h, decreases exercise performance, measured as the maximal speed of running, increases blood LA concentration during submaximal and maximal exercise, and shifts TLA toward lower exercise intensities than in control or sham-operated rats. When adrenaline excess was maintained for 60 h the maximal running speed was still reduced, and exercise blood LA was even higher than during earlier stages of hyperadrenalinemia, but TLA returned to control values. In the rat, a moderate excess of circulating adrenaline, sustained up to 60 h, reduces maximal exercise performance, and causes marked elevations in submaximal and maximal blood lactate concentration. However, this is accompanied by lowering of TLA only in the early stages of hyperadrenalinemia (6 and 12 h), which suggests that shifts of TLA may occur independently of absolute levels of blood lactate during graded exercise.

Plasma human growth hormone ([HGH]), adrenaline ([A]), noradrenaline ([NA]) and blood lactate ([La-](b)) concentrations were measured during progressive, multistage exercise on a cycle ergometer in 12 endurance-trained athletes [aged 32.0 (SEM 2.0) years]. Exercise intensities (3 min each) were increased by 50 W until the subjects felt exhausted. Venous blood samples were taken after each intensity. The [HGH] and catecholamine concentrations increased negligibly during exercise of low to moderate intensities revealing an abrupt rise at the load corresponding to the lactate threshold ([La-]-T). Close correlations (P0.001) were found between [La-]b and plasma [HGH] (r = 0.64), [A] (r = 0.71) and [NA] (r = 0.81). The mean threshold exercise intensities for [HGH], [A] and [NA], detected by log-log transformation, [154 (SEM 19) W, 162 (SEM 15) W and 160 (SEM 17) W, respectively] were not significantly different from the [La-]-T [161 (SEM 12) W]. The results indicated that the threshold rise in plasma [HGH] followed the patterns of plasma catecholamine and blood lactate accumulation during progressive exercise in the endurance-trained athletes.

Both intensive training and bed confinement impair orthostatic tolerance, however, moderate training may exert beneficial effect on cardiovascular adjustment to gravitational stimuli. It was hypothesized that moderate training attenuates effects of bed rest. To test this assumption 24 healthy male volunteers aged 20.8+/-0.9 yrs were subjected to 6 degrees head down bed rest (HDBR) for 3 days before and after 6 weeks of moderate endurance training. Before and after HDBR graded LBNP tests (-15, -30, -50 mmHg) were performed. During these tests heart rate (HR), stroke volume (SV), blood pressure (BP), plasma catecholamines, ACTH, adrenomedullin, atrial natriuretic peptide, plasma renin activity (PRA) and hematocrit were determined. HDBR did not systematically influence LBNP tolerance up to -50 mmHg, but it enhanced rates of reduction of SV, cardiac output and systolic BP and increased elevations of HR and PRA. Training did not alter significantly effects of HDBR on LBNP-induced changes in HR, SV, CO and TPR but it attenuated decrease in systolic BP and diminished increases in plasma noradrenaline and PRA. In conclusion, training has negligible effect on the HDBR-induced changes in central hemodynamics during LBNP but may increase vascular sensitivity to some vasoconstricting factors.

Endurance training is considered as a factor impairing orthostatic tolerance although an improvement and lack of effect have been also reported. The mechanisms of the changes and their relation to initial tolerance of orthostasis are not clear. In the present study, effect of moderate running training on hemodynamic and neurohormonal changes during LBNP, a laboratory test simulating orthostasis, was investigated in subjects with high (HT) and low (LT) tolerance of LBNP. Twenty four male, healthy subjects were submitted to graded LBNP (-15, -30 and -50 mmHg) before and after training. During each test heart rate (HR), stroke volume (SV) and blood pressure, plasma catecholamines, ACTH, adrenomedullin, atrial natriuretic peptide, and renin activity were determined. Basing on initial test, 13 subjects who withstood LBNP at -50 mmHg for 10 min were allocated into HT group and 11 subjects who earlier showed presyncopal symptoms to LT group. Training improved LBNP tolerance in six LT subjects. This was associated with attenuated rate of HR increase and SV decline (before training, at -30 mmHg deltaHR was 21 +/- 4 beats/min and deltaSV - -36+/- 8 ml while after training the respective values were 8 +/- 4 beats/min and -11+/- 6 ml). No differences in hemodynamic response were found in HT subjects and those from LT group whose LBNP tolerance was unchanged. In neither group training affected neurohormonal changes except inhibition of plasma ACTH rise in subjects with improvement of LBNP tolerance. It is concluded that some subjects with low orthostatic tolerance may benefit from moderate training due to improvement of cardiac function regulation.

Twelve male, sedentary volunteers (22.0 +/-) were submitted to three weeks of a bicycle ergometer training, consisting of 45 min exercise (at 70% VO2max), 4 times in the first week and 3 times in the next 2 weeks. They performed four incremental exercise tests with the power output increased by 50 W every 3 min until volitional exhaustion: two before training (C1 and C2), and after one (T1) and three (T3) weeks of training. Before and after each load the plasma noradrenaline (NA), adrenaline (A) and blood lactate (LA) concentrations were determined in venous blood samples as well as plasma growth hormone (HGH) and cortisol concentrations before and at the end of exercise. A decrease in NA concentration was found already after 1 week of training at power output of 100 W (p0.01) and 200 W (p0.05). Similar decline was maintained after 3 weeks of training. No significant training-induced differences in plasma A concentration were found, however, the thresholds for both catecholamines were significantly shifted towards higher values after 3 weeks of training. One week of training caused a decrease in the pre-exercise (p0.01), as well as post-exercise (p0.05) plasma cortisol and HGH concentrations. It was concluded that endurance training induced a decrease in HGH, cortisol and NA concentration already after one week of training. A decline of pre-exercise plasma HGH and cortisol levels with time of experiment may, in part, indicate familiarization to exercise protocol.

The study was designed to find out (1) whether the effect of 3-day bed rest on blood glucose (BG) and plasma insulin (IRI) responses to glucose ingestion depends on preceding physical activity and (2) whether plasma adrenaline (A), noradrenaline (NA) and cardiovascular changes following a glucose load are modified by bed rest. Eleven sedentary students (22.5+/-0.3 yrs), 8 long distance runners (18.6+/-0.3 yrs) and 10 strength trained athletes (21.2+/-2.1 yrs) were examined before and after bed rest. Plasma IRI, BG, NA, A, heart rate (HR), and blood pressure (BP) were measured during 2 hrs following glucose (75 g) ingestion. The responses of BG and IRI to glucose load were calculated as incremental areas under the curves (auc). Both in athletes and untrained subjects bed rest markedly increased IRIauc, while BGauc was elevated only in sedentary subjects (p0.05). The greatest increases in IRIauc and IRI/BG ratios were found in the endurance athletes. The data from all subjects (n = 29) revealed that the initial plasma NA and glucose-induced increases in NA and A were lowered after bed rest (p0.01). These effects were most pronounced in the endurance athletes. Bed rest did not influence HR or BP in any group. It is concluded that (1) the athletes have more adequate compensation for the bed-rest-induced decrement in insulin sensitivity than sedentary men; (2) three-day bed rest diminishes basal sympathetic activity and attenuates sympathoadrenal response to oral glucose; (3) endurance athletes have greater sympathetic inhibition than strength athletes or sedentary men.

The aim of this study was to find out whether creatine (Cr) feeding affects total creatine (TCr), phosphocreatine (PCr), adenine nucleotide contents and beta-hydroxy-acyl-CoA-dehydrogenase (HAD) activity in myocardium as compared to red skeletal muscle. Ten adult Wistar rats received Cr (2.5% of diet weight) for 7 days. In Cr fed rats, PCr was increased (by approx. 20%) in cardiac and in soleus muscles with ATP elevated in myocardium and TCr and free Cr in soleus. In both muscles, Cr feeding enhanced HAD activity. It is concluded, that dietary Cr does increase cardiac muscle high energy phosphate reserves and its oxidative potential.

The aim of this study was to follow up the electromyographic activity (EMG) of dynamically working muscles with simultaneous determinations of blood lactate and plasma catecholamine concentrations during progressive exercise. Twenty eight male soccer players aged 20.6 +/- 0.8 yrs performed incremental bicycle ergometer exercise test. The test consisted of 3-min stages exercise separated by 1-min rest intervals. Work load at each stage increased by 50 W until volitional exhaustion. The root mean square (rms)-EMG activity of the rectus femoris and soleus muscles were recorded continuously during exercise. Venous blood samples were taken after each exercise stage for determination of blood lactate (LA). Additionally in seven subjects adrenaline (A) and noradrenaline (NA) concentrations were determined. The EMG activity increased negligibly during exercise of low to moderate intensities revealing an abrupt rise at the load corresponding to thresholds of blood lactate and plasma catecholamine accumulation (LA-T, A-T, NA-T). Close correlations (P0.001) were found between blood LA concentration and EMG derived from rectus f. (r = 0.72) and soleus (r = 0.68) muscles. The mean threshold exercise intensities for m. rectus f. and m. soleus EMG (176 +/- 9 W and 172 +/- 9 W, respectively) did not differ significantly from lactate (164 +/- 7 W), noradrenaline (178 +/- 6 W) and adrenaline (180 +/- 5 W) thresholds, all of them detected by log-log transformation. The results indicate that threshold character of EMG changes in dynamically working muscles reflects to some extend the patterns of blood lactate and plasma catecholamine changes during incremental exercise.

Thirty overweight women participated in 8 week slimming program consisting of a self-controlled low-energy diet (4.2 MJ/day) supplemented with highly viscous fibres and mineral tablets containing calcium, potassium and sodium phosphates (Redusan Combi, Biokraft Pharma AB, Sweden). Half of the patients received in double blind manner mineral tablets during first 4 weeks and placebo (without phosphates) during next 4 weeks (group 1) while the remaining patients were treated (cross-over) with placebo first and mineral tablets in the final period (group 2). The rate of weight loss was similar in groups 1 and 2 (4.7 vs 5.2 kg during the first 4 weeks and 2.7 vs 3.0 kg in the further 4 weeks). During periods of phosphate supplementation, the resting metabolic rate (RMR) increased by approx. 12% (p0.05) in group 1 and 19% (p0.05) in group 2. Phosphate supplementation ameliorated also a decrease in plasma triiodothyronine level and a decrease in thyroxine to triiodothyronine ratio. There were no differences between groups in the plasma insulin, catecholamine, growth hormone, cortisol and testosterone levels. Phosphate supplementation did not affect plasma lipids or blood glucose concentration. It is concluded that phosphate supplementation in obese patients on a low-energy diet enhances RMR irrespectively of the rate of weight loss. This effect seems to be, at least partly, due to an influence of phosphates on peripheral metabolism of thyroid hormones.

Maximal oxygen uptake (VO2 max) and lactate threshold (LT) were measured during graded, incremental exercise in 8 healthy, untrained volunteers (aged 22 +/- 0.9 yrs) following 3 days on a control, mixed diet, or a ketogenic (50% fat, 45% protein and 5% carbohydrates) diet of equal energy content. Before and after exercise tests acid base balance, plasma beta-hydroxybutyrate (beta-HB), free fatty acid (FFA), and some hormone concentrations were determined. In comparison with the normal diet, the ketogenic diet resulted in: an increased VO2 max, decreased respiratory exchange ratio an a shift of LT towards higher exercise loads. Blood LA concentrations were lower before, during and after exercise. Post exercise blood pH, as well as pre-and post exercise base excess and bicarbonates were reduced. Resting beta-HB concentration was elevated to approx. 2.0 mM, and FFA to approx. 1.0 mM. During a 1 h recovery period beta-HB decreased to 0.85 mM (p0.01) after the ketogenic diet, while plasma FFA did not change after exercise under either conditions. Both the pre-and post-exercise levels of adrenaline, noradrenaline, and cortisol were enhanced, whilst plasma insulin concentration was decreased on the ketogenic diet. It is concluded that the short-term ketogenic diet does not impair aerobic exercise capacity, as indicated by elevated VO2 max and LT. This may be due to increased utilization of beta-HB and FFA when carbohydrate stores are diminished. Stimulation of the sympatho-adrenal system, and cortisol secretion with reduced plasma insulin concentration seem to be of importance for preservation of working capacity.

Thirty six obese women (BMI 29.5 to 44.0 kg m-2, aged 27 to 45 yrs) participated in the 4- week weight reducing program. All of them have prescribed low fat diet of approx. 4.2 MJ (1000 kcal per day) with high viscous fibre capsules as a basic supplement. In addition 18 women (group 1) received Redusan mineral tablets containing mainly calcium and potassium phosphates while the remaining subjects (group 2) were given Placebo instead of mineral tablets. Before energy restriction and after 4 weeks on the diet, half of the women from each group performed 30 min--bicycle ergometer exercise (30-50 W; HR approx. 110 beats.min-1). The remaining subjects were submitted to oral glucose (75 g) tolerance test (OGTT). Weight loss during energy restriction was not affected by phosphate supplementation (4.6 +/- 0.4 and 5.2 +/- 0.5 kg in group 1 and 2, respectively). Phosphates caused a significant increase (p0.05) in the resting metabolic rate (RMR). Net energy cost of work, resting and post-exercise blood glucose, lactate, plasma FFA, adrenalin, cortisol, growth hormone, insulin and testosterone did not differ between the groups receiving phosphates and placebo while respiratory exchange ratio was slightly higher (p0.05), and the plasma beta-hydroxybutyrate concentration lower (p0.05) than without phosphate supplementation. Post-exercise plasma noradrenaline was significantly lowered after 4 weeks of energy restriction in group 2 (on Placebo). Neither blood glucose, plasma insulin and noradrenaline responses to oral glucose ingestion nor the glucose induced thermogenesis were significantly affected by phosphate supplementation, whilst blood pressure increases following glucose load were reduced (p0.05). In conclusion, the present study confirmed a potential usefulness of phosphate supplementation during energy restriction in obese patients due to its effect on resting metabolic rate. The results did not, however, reveal any major alterations in the metabolic and hormonal responses to exercise or to glucose ingestion in comparison with placebo treatment.

1. The effects of hypohydration produced by 48 hr water deprivation were examined in dogs during moderate treadmill exercise at an ambient temperature (Ta) of 21 degrees C. 2. Hypohydration caused a significant elevation in plasma levels of adrenaline (A), proteins (pp) and osmolality (pOsm). 3. During 1 hr of running, plasma concentrations of adrenaline (A) and noradrenaline (NA) rose significantly, whilst no change in these hormones occurred in dogs hydrated ad libitum. 4. The results suggest that hypovolemia in the dog may be a sufficient stimulus to intensify the sympatho-adrenal response to moderate exercise performed at a room Ta.

It was shown that 15-min electrical stimulation of the rat sciatic nerve greatly increases the in vitro measured sensitivity of lactate formation, glucose transport, and glycogen synthesis to insulin, impaired by previous tenotomy. The insulin sensitivity of all these processes was, however, still below that found in the stimulated intact soleus muscle. Extending the stimulation up to 30 min did not cause any further changes in insulin sensitivity either in tenotomized or in intact muscles.

Relationships between energy expenditure, body mass index (BMI), blood glucose (BG) responses to glucose ingestion were studied in 35 women aged 22-55 yrs with normal carbohydrate tolerance. In 13 of them plasma insulin (IRI) and catecholamine concentrations were also determined. Thirty seven per cent of patients did not respond to glucose load with an increased energy expenditure. In the remaining women the average thermogenic effect amounted to approx. 10% of their initial metabolic rate. A significant negative correlation (r = -0.415, n = 35, P(0.02) was found between BMI and the overall thermal effect of glucose (sigma TEG) calculated as a sum of the post-glucose energy expenditure measured every 15 min during 2 h minus the baseline value. Neither the fasting nor the post glucose BG concentrations correlated with sigma TEG. Significant correlations were ascertained between sigma TEG and the fasting IRI (r = -0.568), the sigma post-glucose IRI (r = -0.723), the ratio of sigma BG/sigma IRI (r = 0.845) and the post-glucose plasma noradrenaline concentration (r = 0.837).in women with normal carbohydrate tolerance the thermogenic effect of glucose depends to a large extent on insulin sensitivity and the glucose-induced activation of the sympathetic nervous system.

The effects of two types of acute exercise (1 h treadmill running at 20 m.min-1, or 6 x 10-s periods at 43 m.min-1, 0 degree inclination), as well as two training regimes (endurance and sprint) on the sensitivity of epitrochlearis muscle [fast twitch (FT) fibres] to insulin were measured in vitro in rats. The hormone concentration in the incubation medium producing the half maximal stimulation of lactate (la) production and glycogen synthesis was determined and used as an index of the muscle insulin sensitivity. A single period of moderate endurance as well as the sprint-type exercise increased the sensitivity of la production to insulin although the rate of la production enhanced markedly only after sprint exercise at 10 and 100 microU.ml-1 of insulin. These effects persisted for up to 2 h after the termination of exercise. Both types of exercise significantly decreased the muscle glycogen content, causing a moderate enhancement in the insulin-stimulated rates of glycogen synthesis in vitro for up to 2 h after exercise. However, a significant increase in the sensitivity of this process to insulin was found only in the muscle removed 0.25 h after the sprint effort. Training of the sprint and endurance types increased insulin-stimulated rates of glycolysis 24 h after the last period of exercise. The sensitivity of this process to insulin was also increased at this instant. Both types of training increased the basal and maximal rates of glycogen synthesis, as well as the sensitivity of this process to insulin at the 24th h following the last training session.(ABSTRACT TRUNCATED AT 250 WORDS)

Changes in body temperature, oxygen uptake (VO2), heart rate (HR), sweating rate and plasma osmolarity were examined in 10 human subjects, performing four successive 30 min exercise-bouts of the same intensity (50% VO2 max) separated by 30 min rest periods. In spite of the rest intervals and replacement of body fluid loss there was a progressive increase in VO2. HR, rectal (Tre) and mean body (Tb) temperatures in consecutive exercise bouts. The thermoregulatory efficiency showed an increasing tendency, and a delay in the sweating response at the beginning of each exercise was shortened. It is concluded that a drift in metabolic and temperature responses to exercise, reported throughout a long-term continuous work, occurs also in the euhydrated subjects performing a prolonged intermittent exercise. It is not caused by an impaired thermoregulation during exercise but rather by insufficient restitution of metabolic processes during rest intervals.

Effects of muscle stimulation were studied in the perfused hindleg of late pregnant and age-matched control rats. Muscle stimulation increased tissue glucose uptake in both groups with a tendency towards higher values in the pregnant rats. The stimulation-induced lactate production was markedly larger in pregnant than in control rats. In the pregnant rats muscle tension output decreased more rapidly and vascular resistance was greater than in non-pregnant group. The decline of tension, accompanied by the enhanced lactate production of contracting muscles, may suggest a reduced muscle oxidative potential in late pregnancy and/or delayed adaptation of the local blood flow. The greater vascular resistance found during muscle stimulation in pregnant animals might have been due to the persistent local action of estrogens. The data obtained indicate that pregnancy modifies skeletal muscle function during stimulation in situ.

1. Duration of exercise until exhaustion is significantly correlated with body weight of dogs. 2. Rectal temperature (Tre) achieved at the end of the effort depends on the resting value of Tre, but the exercise-induced increases in Tre are unrelated to the initial Tre. 3. The magnitude of exercise-induced decrease in blood glucose (BG) level is positively correlated with the resting BG level and negatively correlated with the elevations of the plasma free fatty-acid (FFA) concentration. 4. A significant positive relationship is found between the exercise-induced increases in the plasma FFA levels and noradrenalinaemia.

The purpose of the present work was to further elucidate the role of thyroid hormones in the control of body temperature and metabolism during physical exercise. Changes in rectal temperature (T re), some parameters of exercise-metabolism and in the plasma noradrenaline (NA) levels were examined in eight dogs performing submaximal treadmill exercise to exhaustion before and after thyroidectomy (THY). The metabolic responses to adrenaline (A) infusion were also compared in intact and THY dogs. During the exercise performed by THY dogs T re increases were markedly attenuated, plasma FFA level increases were reduced and the pattern of plasma NA changes was modified in comparison with control runs. The reduced exercise-induced FFA mobilization in THY dogs might be attributed to a lower activation of the adrenergic system in the later stage of exercise and to the weaker lipolytic action of catecholamines. The attenuated T re increases during exercise performed by THY dogs and the exercise-hyperthermia described previously in dogs treated with thyroid hormones suggest that an optimum level of thyroid hormones is necessary to induce typical changes in body temperature during physical exercise.