The effects of short-term resistance training on endocrine function in men and women

This investigation examined hormonal adaptations to acute resistance exercise and determined whether training adaptations are observed within an 8-week period in untrained men and women. The protocol consisted of a 1-week pre-conditioning orientation phase followed by 8 weeks of heavy resistance training. Three lower-limb exercises for the quadriceps femoris muscle group (squat, leg press, knee extension) were performed twice a week (Monday and Friday) with every other Wednesday used for maximal dynamic 1 RM strength testing. Blood samples were obtained pre-exercise (Pre-Ex), immediately post-exercise (IP), and 5?min post-exercise (5-P) during the first week of training (T-1), after 6 weeks (T-2) and 8 weeks (T-3) of training to determine blood concentrations of whole-blood lactate (LAC), serum total testosterone (TT), sex-hormone binding globulin (SHBG), cortisol (CORT) and growth hormone (GH). Serum TT concentrations were significantly (P?≤?0.05) higher for men at all time points measured. Men did not demonstrate an increase due to exercise until T-2. An increase in pre-exercise concentrations of TT were observed both for men and women at T-2 and T-3. No differences were observed for CORT between men and women; increases in CORT above pre-exercise values were observed for men at all training phases and at T-2 and T-3 for women. A reduction in CORT concentrations at rest was observed both in men and women at T-3. Women demonstrated higher pre-exercise GH values than men at all training phases; no changes with training were observed for GH concentrations. Exercise-induced increases in GH above pre-exercise values were observed at all phases of training. Women demonstrated higher serum concentrations of SHBG at all time points. No exercise-induced increases were observed in men over the training period but women increased SHBG with exercise at T-3. SHBG concentrations in women were also significantly higher at T-2 and T-3 when compared to T-1 values. Increases in LAC concentrations due to exercise were observed both for men and women for all training phases but no significant differences were observed with training. These data illustrate that untrained individuals may exhibit early-phase endocrine adaptations during a resistance training program. These hormonal adaptations may influence and help to mediate other adaptations in the nervous system and muscle fibers, which have been shown to be very responsive in the early phase of strength adaptations with resistance training.     

Acute hormonal and neuromuscular responses to hypertrophy,strength and power type resistance exercise

The purpose of the current study was to determine the acute neuroendocrine response to hypertrophy (H), strength (S), and power (P) type resistance exercise (RE) equated for total volume. Ten male subjects completed three RE protocols and a rest day (R) using a randomized cross-over design. The protocols included (1) H: 4 sets of 10 repetitions in the squat at 75% of 1RM (90 s rest periods); (2) S: 11 sets of three repetitions at 90% of 1RM (5 min rest periods); and (3) P: 8 sets of 6 repetitions of jump squats at 0% of 1RM (3 min rest periods). Total testosterone (T), cortisol (C), and sex hormone binding globulin (SHBG) were determined prior to (PRE), immediately post (IP), 60 min post, 24 h post, and 48 h post exercise bout. Peak force, rate of force development, and muscle activity from the vastus medialis (VM) and biceps femoris (BF) were determined during a maximal isometric squat test. A unique pattern of response was observed in T, C, and SHBG for each RE protocol. The percent change in T, C, and SHBG from PRE to IP was significantly (p ≤ 0.05) greater in comparison to the R condition only after the H protocol. The percent of baseline muscle activity of the VM at IP was significantly greater following the H compared to the S protocol. These data indicate that significant acute increases in hormone concentrations are limited to H type protocols independent of the volume of work competed. In addition, it appears the H protocol also elicits a unique pattern of muscle activity as well. RE protocols of varying intensity and rest periods elicit strikingly different acute neuroendocrine responses which indicate a unique physiological stimulus.     

Effects of pre-exercise ingestion of carbohydrate on glycaemic and insulinaemic responses during subsequent exercise at differing intensities

The development of rebound hypoglycaemia has been reported after pre-exercise carbohydrate (CHO) ingestion in some studies but not in others. Differences in the experimental design and factors such as the exercise intensity are likely to be responsible for the discrepancies between these studies. Exercise intensity might be a crucial factor since it affects both insulinaemia and glucose uptake. Therefore the aim of the present study was to compare the glycaemic and insulinaemic responses to exercise at different intensities after ingestion of a standardized pre-exercise CHO load. Eight moderately trained subjects consumed 75 g of glucose 45 min prior to 20 min of exercise at 40%, 65% or 80% maximal power output. Blood samples were collected before glucose ingestion, at 15 min intervals at rest and 5 min intervals during exercise. During exercise, measurements of heart rate and breath-by-breath analysis of expired gas were performed continuously. The trials were performed at [mean (SEM)] 55 (1), 77 (1) and 90 (1) percentages maximal oxygen uptake . At the onset of exercise, plasma glucose concentration returned to pre-ingestion levels, while the insulin concentration was more than three times higher than at rest [on average 57 (7) compared to 16 (1) μU·ml^–1). During exercise, plasma glucose concentrations decreased during the first 5 min of exercise and then stabilized in all trials at concentrations that would not be considered to be hypoglycaemic. There were no significant differences in glucose or insulin concentrations between the three trials during exercise. These data suggest that the glycaemic response to ingestion of 75 g of CHO 45 min pre-exercise is similar during exercise of different intensities. Electronic Publication     

Endocrine responses during exercise-heat stress: effects of prior isotonic and hypotonic intravenous rehydration

Exercise following exercise-induced dehydration (EID) has been shown to elevate concentrations of plasma norepinephrine (NE) and hypothalamic-pituitary-adrenal axis hormones. However, it is not known how intravenous (i.v.) rehydration (Rh) with isotonic (ISO) or hypotonic (HYPO) saline affects these hormone concentrations. It was hypothesized that HYPO, versus ISO, would lead to lower plasma NE and cortisol concentrations ([CORT]) during subsequent exercise following EID due to a decrease in plasma sodium concentration [Na⁺]. Eight non-heat acclimated men completed three experimental treatments (counterbalanced design) immediately following EID (33°C) to ?4% body mass loss. The Rh treatments were i.v. 0.9% NaCl (ISO, 25 ml?·?kg^?1), i.v. 0.45% NaCl (HYPO, 25 ml?·?kg^?1), and no fluid (NF). After Rh and rest (2?h total), the subjects walked at 53–54 percent of maximal O₂ uptake for 45?min at 36°C. After Rh, the following observations were made before/during exercise: percentage change in plasma volume (PV) was lower in NF compared to ISO and HYPO but similar between ISO and HYPO; Δ[Na⁺] was similar between ISO and NF and higher in ISO compared to HYPO; Δ plasma NE was higher in NF compared to ISO and HYPO, but similar between ISO and HYPO; Δ plasma [CORT] was higher in NF compared to ISO and HYPO and higher in ISO compared to HYPO; rectal temperature was higher in NF compared to ISO and HYPO. These data would suggest that sympathetic nervous activity and [CORT] during exercise, subsequent to EID and Rh, was affected by lower PV (probably through cardiopulmonary baroreflexes) as well as core temperature. Furthermore, [CORT] was affected by Δ[Na⁺] after Rh through an unknown mechanism.     

Changes in serum concentration of antioxidants following treadmill exercise testing in patients with suspected ischaemic heart disease

Twenty-four subjects with suspected ischaemic heart disease underwent a treadmill exercise stress test (TEST). Nine individuals developed ischaemia as defined by standard criteria. Total plasma antioxidant status (TPAS), and serum concentrations of vitamin E were measured pre-TEST, and 0, 1, 2, 4, 8 and 24 h following the treadmill test. Mean serum vitamin E concentrations fell by 33% in the group as a whole (from 9.53 +/- 0.92 mg/L pre-TEST to 6.39 +/- 1.06 mg/L immediately post stress test, P < 0.02) and rose to baseline over the subsequent 24 h. The levels of serum vitamin E fell by 34% in the group of patients who had a positive TEST, and 32% in those who did not develop ischaemia during the TEST. Serum cholesterol concentrations also fell significantly during the TEST. In the total group serum cholesterol fell by 6.5% (P = 0.0052), and in the subgroup who were positive for ischaemia the fall in serum cholesterol was 10.3% (P = 0.004). The reduction in serum cholesterol was 4.1% in the subgroup who did not develop ischaemia (P > 0.05). Mean total plasma antioxidant status showed no significant temporal change for the group as a whole, although there was a nonsignificant decrease immediately post-TEST in the ischaemic group and a slight rise at 8 h in the group negative for ischaemia.     

Effect of varying initial drink volume on rehydration of horses

Body mass (BM), water intake (WI), and plasma osmolality (P(osm)) and electrolyte concentrations were measured in six 2-year-old Arabian horses provided either 4 l, 8 l, or an unlimited amount of water (UW) for drinking during the initial 5 min of recovery from 45-km of treadmill exercise. After weighing, horses were placed in a stall and further WI between 20 and 60 min of recovery was measured. During exercise, horses lost 3.3+/-0.3%, 3.2+/-0.1%, and 3.3+/-0.2% (P>.05) of BM and P(osm) increased by 7.2+/-0.5, 7.9+/-0.8, and 7.7+/-0.5 mOsm/kg (P>.05) for 4 l, 8 l, and UW, respectively. WI during the first 5 min of recovery was 4.0+/-0.0, 8.0+/-0.0, and 9.0+/-1.3 l and was accompanied by 2.4+/-0.4, 5.8+/-0.9, and 6.1+/-0.7 mOsm/kg decreases (P<.05) in P(osm) for 4 l, 8 l, and UW, respectively. Between 20 and 60 min of recovery, WI was 6.2+/-1.5, 1.2+/-0.6, and 1.0+/-0.7 l (P<.05) for 4 l, 8 l, and UW, respectively. Thus, total WI was 10.2+/-1.5, 9.2+/-0.6, and 10.0+/-1.1 l (P>.05) for 4 l, 8 l, and UW, respectively. After 60 min of recovery, persisting BM loss was 1.3+/-0.5%, 1.1+/-0.2%, and 1.0+/-0.2% (P>.05) for 4 l, 8 l, and UW, respectively and P(osm) had returned to pre-exercise values for all treatments. In conclusion, limiting the volume of water initially provided to horses dehydrated by endurance exercise had no significant effect on total WI during the initial 60 min of recovery; however, persisting BM loss was observed with all treatments. Further, following exercise-induced dehydration, the primary stimulus of thirst was an increase in plasma tonicity rather than hypovolemia.     

Effects of pre-exercise ingestion of differing amounts of carbohydrate on subsequent metabolism and cycling performance

Studies on the effect of the pre-exercise ingestion of carbohydrate on metabolism and performance have produced conflicting results, perhaps because of differences in the designs of the studies. The purpose of the present study was to examine the effects of ingesting differing amounts of glucose pre-exercise on the glucose and insulin responses during exercise and on time-trial (TT) performance. Nine well-trained male cyclists completed four exercise trials separated by at least 3 days. At 45 min before the start of exercise subjects consumed 500 ml of a beverage containing either 0 g (PLAC), 25 g (LOW), 75 g (MED) or 200 g (HIGH) of glucose. The exercise trials consisted of 20 min of submaximal steady-state exercise (SS) at 65% of maximal power output immediately followed by a [mean (SEM)] 691 (12) kJ TT. Plasma insulin concentrations at the onset of exercise were significantly higher (P<0.05) in MED and HIGH compared with LOW and PLAC. Plasma glucose concentration fell rapidly (P<0.05) during SS exercise in all glucose trials, but remained steady in PLAC. No difference in plasma glucose concentration was observed between the glucose trials at any time. Hypoglycaemia (less than 3.5 mmol·l^–1) was observed in six subjects during SS but only after ingesting glucose pre-exercise. However, there was no difference in TT performance between the four trials. The ingestion of 0, 25, 75 or 200 g of glucose 45 min before a 20 min submaximal exercise bout did not affect subsequent TT performance. In addition, mild rebound hypoglycaemia following pre-exercise glucose ingestion did not negatively affect performance. Electronic Publication     

Effect of prolonged exercise and pre-exercise dietary manipulation on hepatic triglycerides in trained men

The purpose of this study was to examine the effect of exercise and pre-exercise dietary manipulation on hepatic triglyceride concentration (HTGC). HTGC was measured by proton magnetic resonance spectroscopy (¹H-MRS) before and after 90 min of moderate intensity cycling in six endurance trained males following 67 h of mixed diet (M) and an isocaloric minimal carbohydrate (2%) high fat (83%) diet (HF). Diets were administered by balanced crossover design. Whole-body fat oxidation, plasma-free fatty acid (FFA), glycerol and triglyceride concentrations were significantly elevated during exercise in HF versus M (P < 0.05 for all). There was no significant treatment × time interaction for HTGC (P = 0.368). However, there was a significant net increase in HTGC (time effect) during the combined 6 h exercise and post-exercise period (P = 0.037). In conclusion, we observed no measurable net change in the hepatic triglyceride pool across a period involving a prolonged exercise bout. Furthermore, manipulation of pre-exercise dietary intake did not influence the interaction between the hepatic triglyceride concentration and exercise in lean trained men. This supports the contention that hepatic triglycerides do not meaningfully contribute to the high rate of fat oxidation observed during acute exercise, or the enhancement of this with regular exercise training and/or pre-exercise dietary manipulation.     

Fluid replacement beverages and maintenance of plasma volume during exercise: role of aldosterone and vasopressin

Summary Previous experiments have demonstrated that consumption of a glucose polymer-electrolyte (GP-E) beverage is superior to water in minimizing exercise-induced decreases in plasma volume (PV). We tested the hypothesis that elevated plasma concentrations of vasopressin and/or aldosterone above that seen with water ingestion may explain this observation. Six trained cyclists performed 115 min of constant-load exercise (approximately 65% of maximal oxygen consumption) on a cycle ergometer on two occasions with 7 days separating experiments. Ambient conditions were maintained relatively constant for both exercise tests (29–30° C; 58–66% relative humidity). During each experiment, subjects consumed 400 ml of one of the following beverages 20 min prior to exercise and 275 ml immediately prior to and every 15 min during exercise: (1) distilled water or (2) GP-E drink contents = 7% carbohydrate (glucose polymers and fructose; 9 mmol·1^–1 sodium; 5 mmol·^1–1 potassium; osmolality 250 mosmol·1^–1). No significant difference (P>0.05) existed in mean skin temperature, rectal temperature, oxygen consumption, carbon dioxide production or the respiratory exchange ratio between treatments. Further, no significant differences existed in plasma osmolality and plasma concentrations of sodium, potassium, chloride or magnesium between treatments. Plasma volume was better maintained (P<0.05) in the GP-E trial at 90 and 120 min of exercise when compared to the water treatment. No differences existed in plasma levels of vasopressin or aldosterone between treatments at any measurement period. Further, the correlation coefficients between plasma concentrations of vasopressin and aldosterone and change in PV during exercise were 0.42 (P<0.05) and 0.16 (P>0.05), respectively. Therefore, although these experiments support the notion that a GP-E beverage is superior to water in minimizing exercise-induced disturbances in PV during prolonged exercise, the mechanism to explain this observation is not due to differences in plasma concentrations of vasopressin or aldosterone alone.     

Immobilization and cold stress affect sympatho-adrenomedullary system and pituitary-adrenocortical axis of rats exposed to long-term isolation and crowding

Changes in plasma levels of noradrenaline (NA), adrenaline (A), adrenocorticotropic hormone (ACTH) and corticosterone (CORT), as well as in cytosol glucocorticoid receptor (GR) and heat shock protein 70 (Hsp 70) in hippocampus of adult rat males exposed to two long-term types of psychosocial stress, both under basal conditions and in response to immobilization and cold as heterotypic additional stressor were studied. Long-term isolation produced a significant elevation of basal plasma ACTH and CORT levels, but did not affect that of NA and A, while long-term crowding conditions did not elevate the basal plasma levels of these hormones. Long-term isolation of rats exposed to 2 h of immobilization or cold led to a significant elevation of plasma NA, A and CORT in comparison with the controls. Long-term crowding conditions and exposure of animals to immobilization or cold also resulted in an increased plasma NA, A and CORT levels, but to a lesser extent in comparison with the long-term isolation. At the same time, plasma ACTH was significantly more elevated in long-term crowded than in long-term isolated rats. Both kinds of long-term psychosocial stresses (isolation and crowding) had similar but less pronounced effects on cytosol GR and Hsp 70 concentrations in hippocampus comparing to acute immobilization and cold stress. It seems that long-term psychosocial stresses attenuate the effects of an additional stress on hippocampal GR and Hsp 70 concentrations. These data suggest that individual housing of rats appear to act as a stronger stressor than crowding conditions. When the animals suffering a long-term isolation were exposed to either acute immobilization or cold, a stronger activation of the sympatho-adrenomedullary system (SAS) was recorded in comparison with that found in the long-term crowded group subjected to short-term immobilization or cold. No significant differences in the activity of hypotalamo-pituitary-adrenal (HPA) axis were observed between long-term isolated and long-term crowded rats.     

Nocturnal hormonal responses to resistance exercise

The effects of resistance exercise on the nocturnal responses of cortisol (CO), testosterone (TEST), human growth hormone (hGH), and thyroid hormones (T₃, T₄) were examined in eight trained weight lifters. Each subject completed two trials using a counterbalanced design: a control, no exercise trial (CON) and a heavy resistance exercise session of three sets of six exercises to exhaustion (RE). The exercise session took place between 1900 and 2000 hours. Blood was sampled prior to and at 20-min intervals after RE. For both trials blood was sampled at hourly intervals from 2100 hours until 0700 hours. The hGH and CO concentrations were increased up to 40-min post-exercise (P < 0.05), but returned to resting levels 1 h post-exercise. Nocturnal hGH concentration was not affected by RE (P > 0.26) and peaked at 0200 hours and declined until 0700 hours. Similarly, the CO responses were similar between the trails (P > 0.14). This CO concentrations declined from 2200 hours until 0100 hours, then increased steadily until 0700 hours. The TEST concentrations during both trials rose steadily from 2200 hours until 0700 hours; however, the rise in TEST from 0500–0700 hours during RE was greater than during the CON trails (P = 0.059). The T₃ concentrations were unchanged by exercise and were similar at all times between trails. The T₄ concentrations were elevated for 20 min after RE; however nocturnal T₄ concentrations were lower after RE than during CON. These results would suggest that bGH and CO may have limited nocturnal reactivity to resistance exercise. However, the nocturnal alterations of TEST and T4 after resistance exercise, although small, may have implications for muscle anabolism.     

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

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

The 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     

Plasma neuropeptide Y-like immunoreactivity and catecholamines during various degrees of sympathetic activation in man

Neuropeptide Y-like immunoreactivity (NPY-LI) and catecholamine concentrations in plasma were analysed during and after 60 min of physical exercise at a work load corresponding to 70% of individual maximal oxygen uptake in nine healthy men of average physical fitness. Systemic plasma NPY-LI increased progressively from 18 +/- 3 to 81 +/- 19 pmol X 1(-1) in parallel with a 10-fold increase in noradrenaline (NA) concentration. The increase in plasma NPY-LI during exercise and the decrease after completion of exercise were much slower than the corresponding changes in NA concentration. This difference is probably related to a slower diffusion of NPY into systemic circulation after release, as well as to a longer half-life of NPY than of NA in plasma. Reversed phase HPLC and sephadex G-50 gel-filtration chromatography revealed that the main component of NPY-LI in plasma during exercise eluted in a similar position as synthetic human NPY. During exercise plasma NPY-LI correlated well with the plasma concentration of NA (r = 0.80), but not with that of adrenaline (ADR), suggesting a neuronal origin of NPY. The self-ratings of perceived exertion (RPE) were well correlated with the plasma concentrations of both NPY-LI and NA. No clear-cut veno-arterial concentration difference was observed for NPY-LI. Isometric handgrip and orthostatic test doubled plasma NA concentrations but did not cause any increase in plasma NPY-LI. No change in plasma tachykinin-like immunoreactivity was detected during exercise. The present data suggest that NPY is released together with NA during strong, but probably not during mild, sympathetic activation under physiological conditions in man.     

The effects of high intensity exercise on muscle and plasma levels of alpha-ketoisocaproic acid

Summary Alpha-ketoisocaproic acid (KIC) is the product of the transamination of the indispensable amino acid leucine, which is the first step in the complete degradation of leucine. To determine the effects of intense exercise on muscle and blood levels of KIC, 7 male volunteers performed cycle exercise to exhaustion. After pedaling at an intensity of 90 W for 3 min, the load was increased by 60 W every 3 min until volitional fatigue. Muscle biopsies were obtained prior to and immediately after exercise and rapidly frozen for later determination of KIC. During exercise, blood lactate levels increased as expected, while plasma KIC levels did not change. Following exercise, plasma KIC levels rose significantly with peak values occurring 15 min after exercise and did not return to pre-exercise values until 60 min after exercise. In contrast, muscle KIC levels increased during exercise from a pre-exercise mean of 49.4±4.1 Μmol · kg⁻¹ wet wt to 78.1±6.5 Μmol · kg⁻¹ after exercise, an average increase of 48% (P<0.05). These data indicate that during intense exercise, leucine transamination in muscle may continue at a faster rate than the decarboxylation of KIC. In addition, plasma levels of KIC did not reflect the intracellular accumulation of KIC during exercise, suggesting a delay in the diffusion of KIC from muscle.     

Hormonal responses during a prolonged military field exercise with variable exercise intensity

The purpose of the present study was to test the hypothesis that the magnitude of hormonal concentration alterations during a prolonged military field exercise with constant energy intake (EI) is influenced by changes in energy deficit (ED) induced by varying the exercise intensity. Basal serum hormone concentrations were measured in a group of healthy young male volunteers (n = 7) during a 20-day field exercise. During the first week of the exercise, the average ED was 4,000 kcal/day (P-I), in the second week only 450 kcal/day (P-II), and in the last week 1,000 kcal/day (P-III). During the first 5 days of the field exercise, significant increases in cortisol (COR, +32%) and growth hormone (GH, +616%) concentrations were observed, while insulin (INS, −70%), total testosterone (TES, −27%), free testosterone (TES_free, −26%) decreased. However, after these initial responses, COR and GH returned to the pre-exercise level by the beginning of P-II. Also TES and TES_free recovered to the pre-exercise level by the beginning of P-III, and INS by the end of P-III. The concentration of TES (+29%) increased above the pre-exercise level by the beginning of P-III. Serum thyroxin (T₄) concentration was significantly lesser (−12%) and urine urea concentration significantly higher (+78%) after the field exercise than before it. Therefore, it can be concluded that the lower levels of ED in the second and third phase (ED <1,000 kcal/day) allowed recovery of hormonal changes observed in the first phase with ED much greater than 1000 kcal/day.     

Pituitary–adrenal responses to arm versus leg exercise in untrained man

The purpose of this study was to examine pituitary–adrenal (PA) hormone responses [beta-endorphin (β-END), adrenocorticotropic hormone (ACTH) and cortisol] to arm exercise (AE) and leg exercise (LE) at 60 and 80% of the muscle-group specific VO₂ peak. Eight healthy untrained men (AE VO₂ peak=32.4±3.0 ml kg⁻¹ min⁻¹, LE VO₂ peak=46.9±5.3 ml kg⁻¹ min⁻¹) performed two sub-maximal AE and LE tests in random order. Plasma β-END, ACTH and cortisol were not different (P>0.05) between AE and LE at either exercise intensity; the 60% testing elicited no changes from pre-exercise (PRE) values. For 80% testing, plasma β-END, ACTH and cortisol were consistently, but not significantly, greater during LE than AE. In general, plasma β-END and ACTH were higher (P<0.05) during 80% exercise, than PRE, for both AE and LE. Plasma cortisol was elevated (P<0.05) above PRE during 80% LE, and following 80% for both AE and LE. Plasma ACTH was higher (P<0.05) during 80% LE and AE versus 60% LE and AE, respectively. Plasma β-END and cortisol were significantly higher during and immediately after 80% LE than 60% LE. Thus, plasma β-END, ACTH and cortisol responses were similar for AE and LE at the two relative exercise intensities, with the intensity threshold occurring somewhere between 60 and 80% of VO₂ peak. It appears that the smaller muscle mass associated with AE was sufficient to stimulate these PA axis hormones in a manner similar to LE, despite the higher metabolic stress (i.e., plasma La^-) associated with LE.     

Catecholamines,lymphocyte subsets,and cyclic adenosine monophosphate production in mononuclear cells and CD4+ cells in response to submaximal resistance exercise

We examined the effect of 30 min of submaximal resistance exercise on free and sulphoconjugated plasma catecholamine concentrations determined by high performance (-pressure) liquid chromatography separation, the distribution of circulating lymphocytes quantified by flow cytometry, and isoproterenol induced cyclic adenosine monophosphate (cAMP) production in mononuclear cells (MNL) and CD4⁺ cells. Venous blood samples were taken before, immediately after and 45 min after exercise. Resistance exercise increased free plasma adrenaline (A) and noradrenaline (NA) concentrations, whereas sulphoconjugated catecholamine concentrations remained unchanged. Exercise induced leucocytosis and lymphocytosis was predominantly manifested by an increase in the number of total lymphocytes, monocytes, CD3⁺, CD8⁺ cells and CD3^– CD16/CD56^– cells. Redistribution resulted in a decrease in the CD4^–: CD8⁺ ratio. The total number and distribution of lymphocytes returned to baseline after 45-min rest. An exercise-induced increase in the number of CD3^– CD16/CD56⁺ cells was significantly correlated with the increase in plasma NA (r = 0.66;P = 0.035), indicating a NA dependent process of redistribution. The cAMP-production in MNL was significantly elevated after resistance exercise, when cells were stimulated with 1 mol·1^–1 isoproterenol [pre-exercise 16.5 (SD 3.3); postexercise 21.6 (SD 9.8); 45 min postexercise 10.7 (SD 2.8)]. The cAMP production in CD4⁺ cells was not affected by exercise. Therefore, it is discussed whether redistribution is responsible for the exercise induced increase in cAMP production in MNL.     

The effect of environmental temperature on testosterone and cortisol responses to high Intensity,intermittent exercise in humans

The purpose of this study was to examine the testosterone, cortisol, and the molar ratio of testosterone to cortisol (T:C) blood concentration responses to intermittent, high intensity exercise in the heat. Eight active men [mean age 25 (SD 3) years, mass 71.1 (SD 5.5) kg, height 175.9 (SD 4.4) cm] performed two series of five 15-s Wingate anaerobic power tests in both hot (H, 35°C) and thermoneutral (TN, 22°C) environments. Each period of exercise was separated by 30-s of active recovery. Each series was separated by 60 min of passive recovery. Blood samples were obtained before (PRE), immediately post (IP), and 5(5R), 10(10R), 15(15R), 30(30R), 45(45R), and 60(60R) min following exercise. Peak power was significantly higher, during the first series of exercise, in the H compared to TN. No significant differences were seen in any of the variables between the first and second series of exercise in either environmental condition. Furthermore, no significant differences between these conditions were observed in heart rate, blood lactic acid concentration, or rectal temperature. A significant decrease in cortisol concentration was observed between PRE and IP, during both conditions. However, no significant interactions between TN or H were seen. No change from PRE was observed in testosterone or T:C during either TN or H. It would appear that testosterone and cortisol respond similarly to repeated periods of short duration high intensity exercise, in either thermoneutral or moderately hot environments.     

Effects of catecholamines on water intake in rats

It is known that intraperitoneally (IP) injected adrenaline (A) inhibits food intake in otherwise hungry animals. In a recent work, Hinton et al. (6) showed that IP A also inhibits water intake in thirsty rats, concluding that A's effect is unspecific. We administered A IP or intramuscularly (IM) in different doses in rats made thirsty either by 18-h water deprivation or by subcutaneous injection of hypertonic saline or polyethylene glycol. IP A reduced water intake in all experimental conditions. A dose-related inhibition was observed in water-deprived animals. On the other hand, IM A showed a small effect only at the highest dose (50 micrograms/100 g body weight). When some of these experiments were repeated using noradrenaline (NA) and isoproterenol (IS), IM administration of either substance showed no effect. IP administration reduced water intake significantly only at the highest dose of NA (50 micrograms/100 g). It is concluded that water intake inhibition by catecholamines in rats made thirsty either by osmotic or by volumetric challenges is of porto-hepatic origin and, in contrast with food intake inhibition, has no beta-adrenergic component.