Effects of hydration state on plasma testosterone,cortisol and catecholamine concentrations before and during mild exercise at elevated temperature

This investigation examined the influence of pre-exercise hydration status, and water intake during low intensity exercise (5.6 km · h^–1 at 5% gradient) in the heat (33° C), on plasma testosterone (TEST), cortisol (CORT), adrenaline (A), and noradrenaline (NA) concentrations at baseline (BL), pre-exercise (PRE), and immediately (IP), 24 h (24 P), and 48 h postexercise (48 P). Ten active men participated in four experimental treatments. These treatments differed in preexercise hydration status [euhydrated or hypohydrated (HY, –3.8 (SD 0.7)% body mass)] and water intake during exercise (water ad libitum or no water intake during exercise, NW). There were no significant changes in TEST, CORT, or A concentrations with time (BL, PRE, IP, 24 P, and 48 P), or among treatments. However, significant increases from BL and PRE plasma NA concentrations were observed at IP during all four treatment conditions. In addition, HY + NW resulted in significantly higher plasma NA concentrations at IP compared to all other treatments. These results suggest that moderate levels of hypohydration during prolonged, low intensity exercise in the heat do not influence plasma TEST, CORT, or A concentrations. However, plasma NA appears to respond in a sensitive manner to these hydration and exercise stresses.     

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.     

Ultradian rhythmicity and induced changes in salivary testosterone

Testosterone and cortisol respond to exercise stimuli and modulate adaptation. Episodic basal secretion of these hormones may modify the responsiveness of these hormones. We sought to identify episodic steroid secretion via frequent salivary sampling and investigate any interaction between ultradian rhythmicity and induced changes in testosterone. Salivary testosterone and cortisol concentrations of seven males (age 20–40 years) were measured every 10 min between 0800 and1600 h on three consecutive days. On either the second or third day, three interventions designed to elicit a hormonal response were randomly assigned: sprint exercise (two 30-s maximal efforts on a cycle ergometer); boxing (two 30-s maximal punching efforts); and a violent video game (10 min of player vs. player combat). On the other days subjects were inactive. Testosterone data on non-intervention days suggested pulsatile secretion with a pulse interval of 47 ± 9 min (mean ± SD). The sprint intervention substantially affected hormones: it elicited a small transient elevation in testosterone (by a factor of 1.21; factor 90% confidence limits ×/÷1.21) 10 min after exercise, and a moderate elevation in cortisol peaking 50 min post-exercise (factor 2.3; ×/÷2.6). The testosterone response correlated with the change in testosterone concentration in the 10 min prior to the sprint (r = 0.78; 90% CL 0.22–0.95) and with a measure of randomness in testosterone fluctuations (r = 0.83; 0.35–0.96). Thus, the salivary testosterone response to exercise may be dependent on the underlying ultradian rhythm and aspects of its regulation. This interaction may have important implications for adaptation to exercise.     

Relationship between stress hormones and testosterone with prolonged endurance exercise

Previous pharmacological and pathological studies have reported negative relationships between circulating testosterone and certain stress hormones (i.e., cortisol and prolactin) in humans. These relationships have subsequently been used in hypotheses explaining the subclinical resting testosterone levels often found in some endurance-trained males, but as of yet no one has specifically examined these relationships as they relate to exercise. Thus, we examined the relationship between total and free testosterone levels and cortisol, and between total and free testosterone and prolactin following prolonged endurance exercise in trained males. Twenty-two endurance-trained males volunteered to run at 100% of their ventilatory threshold (VT) on a treadmill until volitional fatigue. Blood samples were taken at pre-exercise baseline (B0); volitional fatigue (F0); 30 min (F30), 60 min (F60), and 90 min (F90) into recovery; and at 24 h post-baseline (P24 h). At F0 [mean running time = 84.8 (3.8) min], exercise induced significant changes (P<0.05) from B0 in total testosterone, cortisol and prolactin. All three of these hormones were still significantly elevated at F30; but at F60 only cortisol and prolactin were greater than their respective B0 values. Free testosterone displayed no significant changes from B0 at F0, F30, or the F60 time point. At F90, neither cortisol nor prolactin was significantly different from their B0 values, but total and free testosterone were reduced significantly from B0. Cortisol, total testosterone and free testosterone at P24 h were significantly lower than their respective B0 levels. Negative relationships existed between peak cortisol response (at time F30) versus total testosterone (at F90, r=–0.53, P<0.05; and at P24 h, r=–0.60, P<0.01). There were no significant relationships between prolactin and total or free testosterone. In conclusion, the present findings give credence to the hypothesis suggesting a linkage between the low resting testosterone found in endurance-trained runners and stress hormones, with respect to cortisol.     

Different responses of selected hormones to three types of exercise in young men

Exercise is a potent stimulus for release of growth hormone (GH), cortisol, testosterone and prolactin, and prolonged exercise inhibits insulin secretion. These responses seem to be specific to the type of exercise but this has been poorly characterised primarily because they have not been compared during exercise performed by the same individuals. We investigated hormone responses to resistance, sprint and endurance exercise in young men using a repeated measures design in which each subject served as their own control. Eight healthy non-obese young adults (18–25 years) were studied on four occasions in random order: 30-s cycle ergometer sprint (Sprint), 30-min resistance exercise bout (Resistance), 30-min cycle at 70 % VO_2max (Endurance), and seated rest in the laboratory (Rest). Cortisol, GH, testosterone, prolactin, insulin and glucose concentrations were measured for 60 min after the four different interventions. Endurance and sprint exercise significantly increased GH, cortisol, prolactin and testosterone. Sprint exercise also increased insulin concentrations, whereas this decreased in response to endurance exercise. Resistance exercise significantly increased only testosterone and glucose. Sprint exercise elicited the largest response per unit of work, but the smallest response relative to mean work rate in all hormones. In conclusion, the nature and magnitude of the hormone response were influenced by exercise type, perhaps reflecting the roles of these hormones in regulating metabolism during and after resistance, sprint and endurance exercise.     

Cortisol and testosterone concentrations in wheelchair athletes during submaximal wheelchair ergometry

It is yet unknown how upper body exercise combined with high ambient temperatures affects plasma testosterone and cortisol concentrations and furthermore, how these hormones respond to exercise in people suffering spinal cord injuries. The purpose of this study was to characterize plasma testosterone and cortisol responses to upper body exercise in wheelchair athletes (WA) compared to able-bodied individuals (AB) at two ambient temperatures. Four WA [mean age 36 (SEM 13) years, mean body mass 66.9 (SEM 11.8) kg, injury level T₇–T₁₁], matched with five AB [mean age 33.4 (SEM 8.9) years, mean body mass 72.5 (SEM 13.1) kg] exercised (cross-over design) for 20 min on a wheelchair ergometer (0.03 kg resistance · kg⁻¹ body mass) at 25 °C and 32 °C. Blood samples were obtained before (PRE), at min 10 (MID), and min 20 (END) of exercise. No differences were found between results obtained at 25 °C and 32 °C for any physiological variable studied and therefore these data were combined. Pre-exercise testosterone concentration was lower (P < 0.05) in WA [18.3 (SEM 0.9) nmol · l⁻¹] compared to AB [21.9 (SEM 3.6) nmol · l⁻¹], and increased PRE to END only in WA. Cortisol concentrations were similar between groups before and during exercise, despite higher rectal temperatures in WA compared to AB, at MID [37.21 (SEM  0.14) and 37.02 (SEM  0.08)°C, respectively] and END [37.36 (SEM 0.16) and 37.19 (SEM 0.10)°C, respectively]. Plasma norepinephrine responses were similar between groups. In conclusion, there were no differences in plasma cortisol concentrations, which may have been due to the low relative exercise intensities employed. The greater exercise response in WA for plasma testosterone should be confirmed on a larger population. It could have been the result of the lower plasma testosterone concentrations at rest in our group. Accepted: 4 September 2000     

Hormone responses to a continuous bout of rock climbing in men

Rock climbing is rapidly increasing in popularity as a recreational activity and as a competitive sport. Few studies have tested acute physiological responses to climbing, and no studies to date have tested hormone responses to a climbing-based workout. This study aimed to measure testosterone (T), growth hormone (GH), and cortisol (C) responses to continuous vertical climbing in young male rock climbers. Ten male rock climbers, aged between 21 and 30 years, climbed laps on a submaximal 55' climbing route for 30 min, or until exhaustion, whichever came first. Heart rate (HR) was recorded after every lap. Blood samples were collected by venipuncture before (Pre), immediately post (IP), and 15 min after the climbing exercise (P15) to assess blood lactate and plasma GH, T, and C. Subjects climbed 24.9 ± 1.9 min and 507.5 ± 82.5 feet. Peak HR was 182.1 ± 2.3 bpm, and lactate (Pre: 2.9 ± 0.6 mmol/dL, IP: 11.1 ± 1.0 mmol/dL) significantly (P < 0.05) increased from Pre to IP. T concentrations significantly (P < 0.05) increased from Pre (6.04 ± 0.31 ng/mL) to IP (7.39 ± 0.40 ng/mL) and returned to baseline at P15 (6.23 ± 0.33 ng/mL). Cortisol levels did not significantly change during the protocol. GH significantly (P < 0.01) increased from Pre (0.63 ± 0.17 ng/mL) to IP (19.89 ± 4.53 ng/mL) and remained elevated at P15 (15.03 ± 3.89 ng/mL). An acute, short-term bout of high-intensity continuous climbing was an effective exercise stimulus for elevating plasma testosterone and growth hormone levels in young males.     

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.     

The Impact of heat exposure and repeated exercise on circulating stress hormones

To determine if heat exposure alters the hormonal responses to moderate, repeated exercise, 11 healthy male subjects [age?=?27.1 (3.0) years; maximal oxygen consumption, V˙O_2max?=?47.6 (6.2) ml?·?kg?· min^?1; mean (SD)] were assigned to four different experimental conditions according to a randomized-block design. While in a thermoneutral (23°C) or heated (40°C, 30% relative humidity) climatic chamber, subjects performed either cycle ergometer exercise (two 30-min bouts at ≈50% V˙O_2max, separated by a 45-min recovery interval, CEx and HEx conditions), or remained seated for 3?h (CS and HS conditions). Blood samples were analyzed for various exercise stress hormones [epinephrine (E), norepinephrine (NE), dopamine, cortisol and human growth hormone (hGH)]. Passive heating did not alter the concentrations of any of these hormones significantly. During both environmental conditions, exercise induced significant (P < 0.001) elevations in plasma E, NE and hGH levels. At 23°C during bout 1: E?=?393 (199) pmol?·?l^?1 (CEx) vs 174 (85) pmol?·?l^?1 (CS), NE?=?4593 (2640) pmol?·?l^?1 (CEx) vs 1548 (505) pmol?·?l^?1 (CS), and hGH?=?274 (340) pmol?·?l^?1 (CEx)vs 64 (112) pmol?·?l^?1 (CS). At 40°C, bout 1: E?=?596 (346) pmol?·?l^?1 (HEx) vs 323 (181) pmol?·?l^?1 (HS), NE?=?7789 (5129) pmol?·?l^?1 (HEx) vs 1527 (605) pmol?·?l^?1 (HS), and hGH?=?453 (494) pmol?·?l^?1 (HEx) vs 172 (355) pmol?·?l^?1 (HS). However, concentrations of plasma cortisol were increased only in response to exercise in the heat [HEx?=?364 (168) nmol?·?l^?1 vs HS?=?295 (114) nmol?·?l^?1). Compared to exercise at room temperature, plasma levels of E, NE and cortisol were all higher during exercise in the heat (P < 0.001 in all cases). The repetition of exercise did not significantly alter the pattern of change in cortisol or hGH levels in either environmental condition. However, repetition of exercise in the heat increased circulatory and psychological stress, with significantly (P < 0.001) higher plasma concentrations of E and NE. These results indicate a differential response of the various stress hormones to heat exposure and repeated moderate exercise.     

Response of testosterone to prolonged aerobic exercise during different phases of the menstrual cycle

Purpose

To examine the androgen response to exercise in women under conditions of high (H) and low (L) estrogen (E₂) levels.

Methods

Ten exercise trained eumenorrheic women (mean ± SD: 20.0 ± 2.2 years, 58.7 ± 8.3 kg, 22.3 ± 4.9 % body fat, VO_2max = 50.7 ± 9.0 mL/kg/min) completed a 60 min treadmill run at ~70 % of VO_2max during both the mid-follicular (L-E₂, 69.7 ± 7.3 % VO_2max) and mid-luteal (H-E₂, 67.6 ± 7.9 % VO_2max) phases of their menstrual cycle. Blood samples were taken pre-exercise (PRE), immediately post (POST), and 30 min into recovery (30R) from exercise and analyzed for total testosterone using ELISA assays. Results were analyzed using repeated measures ANOVA.

Results

Testosterone responses were (mean ± SD: L-E₂, pre = 1.41 ± 0.21, post = 1.86 ± 0.21, 30R = 1.75 ± 0.32 nmol/L; H-E₂, pre = 1.27 ± 0.23, post = 2.43 ± 0.56, 30R = 1.69 ± 0.34 nmol/L). Statistical analysis indicated no significant interaction existed between high and low estrogen conditions across the blood sampling times (p = 0.138). However, a main effect occurred for exercise (p < 0.004) with the post-testosterone concentration being greater than pre, although pre vs. 30R was not different (p > 0.05). All testosterone hormonal concentrations immediately post-exercise greatly exceeded the level of hemoconcentration observed during the L-E₂ and H-E₂ exercise sessions.

Conclusions

Prolonged aerobic exercise induces short-term elevations in testosterone in trained eumenorrheic women, which appears unrelated to estrogen levels and menstrual cycle phase. These increases may occur due to either increased androgen production and/or decreased degradation rates of the hormone, and are not solely the result of plasma fluid shifts from the exercise.     

Influence of acute submaximal exercise on T-lymphocyte suppressor cell function in healthy young men

A defect in T-lymphocyte suppressor cell function has been reported to occur in a number of autoimmune diseases. The influence of exercise on suppressor cell function has not been determined in individuals with autoimmune diseases, nor has it been determined in healthy individuals. The purpose of this investigation was to determine the effect of an acute bout of submaximal exercise on suppressor cell function in healthy males. Each subject (n=10) completed an exercise trial (E; 1 h of cycle ergometry at 70.6% of maximal oxygen uptake, followed by 2 h of recovery) and a resting trial (R; 3 h of seated rest), separated by at least 1 week. Treatment (E or R) order was counterbalanced. Venous blood samples were obtained pre-exercise (PRE), immediately after exercise (POST), and 2 h post-exercise (2HPOST), and at the same time points in the R trial. Lymphocyte phenotype percentages were determined by flow cytometry, while concanavalin- A-induced suppressor cell function was determined on peripheral blood mononuclear cells. No change was observed in the percentage of T-cytotoxic/suppressor cells. Suppressor cell function was significantly different between treatments, with the POST E value [mean (SD) 56.8 (1.6)%] being higher than the POST R value [41.7 (1.9)%]. No significant difference was observed 2HPOST. In conclusion, acute submaximal exercise resulted in a transient increase in suppressor cell function in healthy males. Accepted: 17 January 2000     

Corticotropin releasing hormone and gonadotropin secretion in physically active males after acute exercise

Summary Plasma concentrations of corticotropin releasing hormone (CRH) and the serum concentrations of luteinizing hormone (LH), follicle stimulating hormone (FSH), testosterone, adrenocorticotropic hormone (ACTH) and cortisol were measured in seven physically active males after acute exercise on a treadmill using the Bruce protocol. Measurements were made in the basal pre-exercise state, immediately after exercise, and at 30-min intervals for 3 h after exercise. Serum LH concentrations declined following exercise reaching nadir values between 60 and 180 min after exercise (90 min post exercise in the group). The nadir values in individual volunteers were significantly lower than both the baseline and post-exercise levels. This fall in serum LH concentration appeared to follow a slight but significant elevation of the plasma concentration of CRH which reached peak levels when measured immediately post exercise. Plasma ACTH concentrations paralleled the rise in CRH, but fell to undetectable levels of below 13.8 nmol · l^–1 (< 5 ng · l^–1) 60 min after exercise. Plasma cortisol concentrations peaked approximately 30 min after the rise in ACTH, after which they gradually declined to baseline levels. Plasma testosterone concentrations paralleled the concentrations of LH. The data suggest that CRH, on the basis of its previously described gonadotropin-depressant property, may be the hormone involved in the exercise-mediated decline in serum LH. Alternatively, some as yet unidentified factor(s), may be involved in producing the altered concentrations of both LH and CRH.     

The effects of plasma cortisol elevation on total and differential leukocyte counts in response to heavy-resistance exercise

The purpose of this study was to examine the impact of heavy-resistance exercise-induced elevations of plasma cortisol on circulating leukocyte counts. Nine healthy, recreationally weight-trained men volunteered for this investigation. Two exercise protocols were employed. Protocol 1 (P-1) consisted of eight sets of ten-repetition maximum leg-press exercise with 1-min rest periods between sets. Protocol 2 (P-2) was identical except for 3-min rest periods. A non-exercise protocol was used as a control treatment (C). Venous blood samples, heart rates and ratings of perceived exertion were obtained pre-, mid- and 5 min post-exercise. In order to examine the maximal influence of cortisol on leukocyte counts, we placed the subject's highest magnitude of cortisol change in response to one of the heavy-resistance exercise protocols in what we designated as the response protocol (R) and the other value was placed into what was designated as the non-response protocol (NR) for analysis. Significant increases in cortisol occurred from pre- to post-exercise for P-1 [mean (SD) 241.4 (25.0) to 302.0 (60.0) nmol · 1^–1] and in the R conditions pre- to mid- and pre- to post-exercise [218.0(0.0) to 302.4(37.1) to 326.8 (51.9) nmol · 1^–1]. No significant changes in cortisol occurred for P-2, NR or the control conditions. Significant increases in total leukocyte counts occurred from pre- to mid- and pre- to post-exercise both for R [5.6 (0.4) to 7.4 (0.3) to 7.3 (0.3) cells · 10⁹ · 1^–1] and NR [5.7 (0.3) to 6.9 (0.4) to 7.1 (0.4) cells · 10⁹ · 1^–1]. No significant changes in differential leukocyte counts occurred. In addition, no significant correlations between cortisol and total or differential leukocyte counts were observed. These data indicate that acute increases in total leukocytes along with no changes in differential leukocyte counts can occur in response to heavy-resistance exercise that does not significantly elevate plasma cortisol concentrations.     

The effect of a single-circuit weight-training session on the blood biochemistry of untrained university students

Summary The metabolic and hormonal responses to an intensive single-circuit weight-training session were studied in 15 untrained male students. The training programme consisted of ten exercises, employing all the large groups of muscles. Students performed three circuits using a work-to-rest ratio of 30 s:30 s at 70% of one-repetition maximum. The whole programme lasted 30 min. Blood samples were obtained from the anticubital vein 30 min before exercise, immediately after exercise finished and after 1-h, 6-h, and 24-h periods of recovery.The training session produced significant increases in the plasma adrenocorticotropic hormone, cortisol, aldosterone, testosterone, progesterone and somatotropin concentrations. The plasma level of insulin and C-peptide remained unchanged. The strength exercises caused elevated ratios of cortisol:testosterone and cortisol:insulin, indicating a prevalence of stimulation of catabolic processes as well as of mobilization of energy reserves but during the recovery period the reverse of this was observed. Immediately after exercise the mean lactate concentration was 7.19 mmol · 1^–1, SD 0.56, the glucose concentration increased significantly during exercise and decreased rapidly during recovery. The high density lipoprotein-cholesterol increased in 1-h period of recovery compared with the initial level. The concentration of total cholesterol, low density lipoprotein-cholesterol and triglyceride, did not change. Packed cell volume did not change during exercise or recovery.     

Platelet adhesion and aggregation on polyethylene: effect of exhaustive exercise

The aim of the present study was to evaluate the effect of an exhaustive exercise on platelet adhesion and aggregation on polyethylene (PE) in relation to changes in plasma cortisol concentration in order to ascertain the effect of physical stress response in the blood-contacting properties of polymeric materials. Twelve healthy sedentary subjects, six males and six females, were studied. Each subject performed an exercise test on a bicycle ergometer at intensity corresponding to 70% VO2 max until exhaustion. One month after the exercise session, each subject participated in a control rest session. In both sessions, blood samples were drawn every 5 min for cortisol, lactate, hemoglobin, and hematocrit determinations and every 15 min for evaluation of platelet adhesion and aggregation. Individual comparisons between the rest and exercise cortisol patterns identified three categories of cortisol responders to exercise: positive responders (C +, showing higher concentrations during exercise than during rest), negative responders (C -, showing lower concentrations during exercise than during rest), and nonresponders (NR, showing similar concentrations during exercise and rest). The results revealed that C + had lower platelet adhesion and aggregation scores during exercise than during rest; moreover C - had higher scores than C + and NR during exercise. The results obtained demonstrated no effects of sex or exercise on either cortisol plasma levels or platelet adhesion and aggregation on PE surface. With regard to cardiovascular risk, the results suggest that exercise favorably affects platelet functions when mechanisms of metabolic adaptation to prolonged muscular work, expressed by a cortisol increase, are activated during exercise.     

Effect of restricted blood flow on exercise-induced hormone changes in healthy men

To test the influence of the accumulation of metabolites on exercise-induced hormone responses, plasma concentrations of cortisol, growth hormone (GH), insulin, testosterone, thyrotropin (TSH), free thyroxine (fT₄) and triiodothyronine (T₃) were compared during exercise performed under normal conditions (control) and under conditions of restricted blood flow of exercising leg muscles (ischaemia) in nine healthy young men. Blood supply was reduced by 15%–20% by the application of 50?mmHg external pressure over the exercising leg. During 45-min cycling exercise during ischaemia the increase in GH concentration was twice as large as under normal conditions. Despite the below-threshold exercise intensity for activation of the pituitary-adrenocortical system under normal exercise conditions ischaemic exercise elicited cortisol and T₃ responses (concentration increases of 83% and 9.5%, respectively). Ischaemic exercise attenuated the decrease of plasma insulin concentration found under normal conditions. The concentrations of testosterone, TSH and fT₄ were not changed significantly during exercise performed in either condition. The results support the suggested essential role of muscle metaboreceptors in the control of hormone responses during muscle activity.     

Changes in salivary antimicrobial peptides,immunoglobulin A and cortisol after prolonged strenuous exercise

The aim of the present study was to examine whether amount of oral antimicrobial components, human β-defensin-2 (HBD-2), cathelicidin (LL-37), and immunoglobulin A (IgA), might be affected by prolonged strenuous exercise. Ten young male volunteers either exercised on recumbent ergometer at 75% [(V)\dot]\textO_2max \dot{V}{\text{O}}_{{2\max }} for 60 min (exercise session) or sat quietly (resting session). Saliva samples were obtained at 60-min intervals during sessions for measurements of saliva antimicrobial components (HBD-2, LL-37, and IgA), saliva cortisol and osmolality. Saliva flow rate was decreased and saliva osmolality was increased during the 60-min exercise. Saliva HBD-2 and LL-37 concentrations and secretion rates were increased during and after the exercise, whereas saliva IgA concentration and secretion rates were decreased after the exercise. Saliva cortisol was increased during and after the exercise. The areas under the curve of the time courses of saliva levels of HBD-2 and LL-37 were negatively correlated with those of cortisol levels in saliva. The present findings suggested that a single bout of prolonged strenuous exercise caused a transient increase in the oral HBD-2 and LL-37 levels.     

Prolonged exercise does not cause lymphocyte DNA damage or increased apoptosis in well-trained endurance athletes

Recent research has demonstrated that lymphocyte apoptosis sensitivity appears to be related to training status and exercise intensity. This work investigated the effect of prolonged, submaximal treadmill running on percentage (%) apoptosis, % necrosis and DNA strand breaks in lymphocytes and related these to changes in total lymphocyte and blood cortisol concentrations in well-trained runners. Venous blood samples (n = 14) were taken immediately before (PRE), immediately after (IPE) and 3 h after (3PE) 2.5 h of treadmill running at 75% of VO₂ max from eight well-trained male endurance athletes (age 34.2 ± 2.44 years) and analysed for cellular content and serum cortisol concentrations. Lymphocytes were isolated from whole blood and % apoptotic and necrotic cell were detected by flow cytometry using Annexin V-FITC and propidium iodide uptake. DNA strand breaks were measured by single-cell gel electrophoresis. Despite a significant (P < 0.001) exercise-induced increase in mean serum cortisol concentrations and reduction in lymphocyte counts, the mean % Annexin-V positive cells (13.3 ± 6.78 in PRE, 11.3 ± 5.51 in IPE and 12.8 ± 6.75 in 3PE samples) were not significantly different at the three time-points (P > 0.05). Mean DNA strand breaks in the lymphocytes also did not change significantly (P > 0.05) rising from 25.7 ± 2.16 to 26.9 ± 1.89 and 27.1 ± 1.38 μm in IPE and 3PE samples, respectively. The exercise-induced changes in total blood lymphocyte counts and cortisol concentrations did not result in a significant change in % apoptotic lymphocytes or DNA strand breaks in the endurance-trained athletes during this prolonged, submaximal exercise.     

Hormonal responses to high- and moderate-intensity strength exercise

The hormonal responses of nine male, strength athletes to strength exercise were examined. The athletes performed one moderate- and one high-intensity strength exercise workout. In the high-intensity workout, the load was 100% of each subject's three-repetition maximum (3-RM) for squats and front squats, and 100% of each subject's six-repetition maximum (6-RM) for leg extensions. In the moderate-intensity workout, the load was 70% of the high-intensity protocol. Rest periods between sets were 4–6 min for both workouts. Blood samples were taken before, 30 min into, and every 15 min for the 1st h after exercise, and then 3, 7, 11, 22 and 33 h after exercise, thus allowing examination of both the acute and prolonged hormonal responses. Blood samples were analyzed for testosterone, luteinizing hormone (LH), follicle stimulating hormone (FSH), cortisol, adrenocorticotrophic hormone (ACTH), growth hormone (GH), insulin-like growth factor (IGF-1), insulin, sex hormone binding globulin, creatine kinase, total protein, glucose and lactate. The acute responses of testosterone and cortisol were greater during the high-intensity protocol as compared to the moderate-intensity protocol. The cortisol response was associated with an increase in ACTH concentration. LH and FSH showed no response to either protocol. Acute GH responses were not different between protocols. There were great inter-individual differences in acute GH responses to both protocols. There were no significant differences between protocols with regard to prolonged responses for any hormone. In both trials, IGF-1 concentrations were significantly lower at 0800 hours the morning after exercise as compared to concentrations found at 0800 hours the morning before exercise. The mechanisms responsible for reducing IGF-1 concentration in these trials are unclear, and it is not known if this reduction observed 22 hours after exercise is of physiological significance. Accepted: 13 December 1999     

Acute hormonal responses to heavy resistance exercise in younger and older men

The purpose of this investigation was to examine the acute responses of several hormones [total and free testosterone (TT and FT, respectively), adrenocorticotropic hormone (ACTH), cortisol (C), growth hormone (GH), and insulin (INS)] to a single bout of heavy resistance exercise (HRE). Eight younger [30-year (30y) group] and nine older [62-year (62y) group] men matched for general physical characteristics and activity levels performed four sets of ten repetitions maximum (RM) squats with 90?s rest between sets. Blood samples were obtained from each subject via an indwelling cannula with a saline lock pre-exercise, immediately post-exercise (IP), and 5, 15 and 30?min post-exercise. Levels of TT, FT, ACTH, C and lactate significantly increased after HRE for both groups. Pre-HRE pairwise differences between groups were noted only for FT, while post-HRE pairwise differences were found for TT, FT, GH, glucose and lactate. Area under the curve analysis showed that the 30y group had a significantly higher magnitude of increase over the entire recovery period (IP, 5, 15, and 30?min post-exercise) for TT, FT, ACTH and GH. Few changes occurred in the INS response with the only change being that the 62y group demonstrated a decrease IP. Lactate remained elevated at 30?min post-HRE. This investigation demonstrates that age-related differences occur in the endocrine response to HRE, and the most striking changes appear evident in the FT response to HRE in physically active young and older men.