Rigorous running increases growth hormone and insulin-like growth factor-I without altering ghrelin.

It has been suggested that ghrelin may play a role in growth hormone (GH) responses to exercise. The present study was designed to determine whether ghrelin, GH, insulin-like growth factor-I (IGF-I), and IGF-binding protein-3 (IGFBP-3) were altered by a progressively intense running protocol. Six well-trained male volunteers completed a progressively intense intermittent exercise trial on a treadmill that included four exercise intensities: 60%, 75%, 90%, and 100% of Vo2max. Blood samples were collected before exercise, after each exercise intensity, and at 15 and 30 mins following the exercise protocol. Subjects also completed a separate control trial at the same time of day that excluded exercise. GH changed significantly over time, and GH area under the curve (AUC) was significantly higher in the exercise trial than the control trial. Area under the curve IGF-I levels for the exercise trial were significantly higher than the control trial. There was no difference in the ghrelin and IGFBP-3 responses to the exercise and control trials. Pearson correlation coefficients revealed significant relationships between ghrelin and both IGF-I and IGFBP-3; however, no relationship between ghrelin and GH was found. In conclusion, intense running produces increases in total IGF-I concentrations, which differs from findings in previous studies using less rigorous running protocols and less frequent blood sampling regimens. Moreover, running exercise that produces substantial increases in GH does not affect peripheral ghrelin levels; however, significant relationships between ghrelin and both IGF-I and IGFBP-3 exist during intense intermittent running and recovery, which warrants further investigation.

Effect of estrogen on serum DHEA in younger and older women and the relationship of DHEA to adiposity and gender.

This case-controlled study consisted of 2 parts. The objective of part 1 was to determine the relationship between DHEA, body mass index (BMI), and age in young males, young females, and postmenopausal (PM) females. Part 2 examined the effects of estrogen on DHEA by analyzing the relationship between DHEA and age in young females on and off oral contraceptives (OCs) and PM females on and off estrogen or hormone replacement therapy (ERT/HRT). The study was performed at the Obstetrics and Gynecology Clinic, Texas Tech Health Sciences Center-Amarillo, Exercise Physiology Laboratory at Southeastern Louisiana University, and Woman's Health Research Institute, Woman's Hospital, Baton Rouge, LA. Part 1 groups consisted of: (1) young males between the ages of 18 to 40 years; (2) normally cycling females off OCs, ages 18 to 40 years; and (3) PM females older than 40 years not receiving ERT/HRT. Part 2 groups consisted of: (1) normally cycling females on OCs, ages 18 to 40 years;, (2) normally cycling females off OCs, ages 18 to 40 years; (3) PM females 50 years or older not receiving ERT/HRT; and (4) PM females 50 years or older receiving ERT/HRT. The main outcome measure was serum DHEA concentrations. For part 1, there were significant (P <.05) inverse relationships between DHEA and age for young males; young females, off OCs; PM females, no ERT/HRT r = -.44, -.26, and -.25, respectively. There were no significant relationships between DHEA and BMI for any of the groups. DHEA concentrations were significantly higher in young males than young females even after accounting for age. For part 2, DHEA concentrations were significantly higher in young females off OCs compared with young females on OCs, and significantly higher in PM women off ERT/HRT than those on ERT\HRT. There were significant inverse relationships between DHEA and age for young females and PM females on and off ERT/HRT. From these findings, we conclude that there is an inverse relationship between DHEA and age for young males, young females off OCs, and PM females, no ERT/HRT. No relationship between BMI and DHEA was observed in these same 3 groups. These results agree with previous findings in young men, but differ from previous findings in obese young females. The data also suggest that estrogen treatment (OCs and ERT/HRT) suppresses DHEA concentrations in premenopausal and PM females, and that DHEA declines with age in PM females regardless of estrogen treatment.

Effects of aerobic exercise on serum leptin levels in obese women.

It has been demonstrated that leptin concentrations in obese patients may be altered by weight loss. We examined the effects of a 9-week aerobic exercise program on serum leptin concentrations in overweight women (20-50% above ideal body mass) under conditions of weight stability. Sixteen overweight women, mean (SE) age 42.75 (1.64) years, comprised the exercise group which adhered to a supervised aerobic exercise program. A graded exercise treadmill test was conducted before and after the exercise program to determine maximal oxygen uptake (VO2max) using open-circuit spirometry. The women demonstrated improved aerobic fitness (VO2max increased 12.29%), however, body fat and the body mass index did not change significantly [42.27 (1.35)-41.87 (1.33)%]. Fourteen women, age 40.57 (2.80) years, did not exercise over the same time period and served as a control group. Serum leptin levels were not significantly altered for either the exercise [28.00 (2.13)-31.04 (2.71) ng x ml(-1)] or the control group [33.24 (3.78)-34.69 (3.14) ng x mg(-1)]. The data indicate that 9 weeks of aerobic exercise improves aerobic fitness, but does not affect leptin concentrations in overweight women.

Serum leptin concentrations in response to acute exercise in postmenopausal women with and without hormone replacement therapy.

The purpose of the study was to examine the effects of acute exercise and hormone replacement therapy on serum leptin concentrations in postmenopausal women. Subjects were 15 healthy, postmenopausal women, 8 on hormone replacement therapy (HRT) and 7 not on hormone replacement therapy (NHRT). Group comparisons indicated no significant differences between HRT and NHRT groups with respect to age, height, weight, BMI, sum of skinfolds, or VO2max, and verified significant differences in estradiol and FSH concentrations. After an overnight fast, each subject completed 30 min of treadmill exercise at approximately 80% VO2max. Over 2 hr and 10 min, baseline, exercise, and recovery blood samples were collected from an intravenous catheter. A control session conducted a month later consisted of the same blood sampling protocol without exercise. Leptin concentrations declined significantly over the course of both the exercise and control sessions, gradually decreasing from baseline levels to -1.54 +/- 0.49 ng. ml-1 postexercise, and continuing to decline to a low of -2.89 +/- 0.59 ng. ml-1 at the end of the session. There was no significant difference between groups with respect to this decline. This is the first study to document that diurnal changes in leptin concentrations in postmenopausal women are not altered by acute treadmill exercise or HRT status. The study underscores the need to account for a diurnal reduction in leptin over the course of an exercise trial.

Serum leptin concentration in women: effect of age, obesity, and estrogen administration.

OBJECTIVE: To compare serum leptin levels in normally cycling reproductive females (20-35 years old) with those in age-matched males, in women who were receiving oral contraceptives, and in older (postmenopausal) women (50-65 years old) who were or who were not receiving hormone replacement therapy. DESIGN: Case-control study. SETTING: Obstetrics and Gynecology Clinic, Texas Tech University Health Sciences Center-Amarillo, or the Exercise Physiology Laboratory at Southeastern Louisiana University. PATIENT(S): Normally cycling women between the ages of 20-35 years and age-matched controls who were receiving oral contraceptives. Postmenopausal women between the ages of 50-65 years who were or who were not receiving hormone replacement therapy. MAIN OUTCOME MEASURE(S): Serum leptin concentration. RESULT(S): In all groups, serum leptin concentrations were correlated significantly with body mass index. Leptin levels were significantly higher in young women than young men (P <.001), but no other statistically significant differences were found for the other three comparisons. CONCLUSION(S): Serum leptin concentrations expressed as a measure of adiposity (body mass index) are greater in young normally cycling females (20-35 years old) than in age-matched males. There is no difference in levels of serum leptin between young and postmenopausal (50-65 years old) women. Estrogen administration, either in young women who are receiving estrogen-progestin oral contraceptives or in postmenopausal women who are receiving hormone replacement therapy, does not effect serum leptin concentrations.

Premenstrual syndrome: diagnosis and treatment experiences.

We sought to examine the diagnosis and treatment experiences of women in the United States who reported having been diagnosed with premenstrual syndrome (PMS) by a physician. A survey of 220 women, randomly selected, ages 26-56, who subscribed to a woman's health newsletter and reported being given a diagnosis of PMS by a physician was conducted. Subjects reported (1) they sought medical help for 5.33 +/- 6.23 years before receiving a diagnosis, (2) they sought help from 3.75 +/- 3.22 physicians for PMS symptoms, (3) they thought the majority (71%) of physicians they used were not adequately informed to diagnose and treat them, (4) only a minority (23%) of physicians used a symptom chart, currently the only way to confirm a PMS diagnosis, when determining their diagnosis, and (5) only approximately 1 in 4 (26%) physicians provided them with a helpful treatment. Seventy-six percent of subjects reported that a PMS diagnosis resulted from their own suggestion, with an agreement by the physician. Eighty-one percent reported that the initial suggestion of PMS came from a non-medical source. The most commonly recommended and used treatments were vitamins, exercise, and diet modification. Current treatment satisfaction was 15.6% not very satisfied, 48.8% somewhat satisfied, and 35% very satisfied. Satisfaction was higher if natural progesterone or hysterectomy with oophorectomy was included as a treatment, although a high percentage of satisfaction was seen with several treatments. Data indicate that physicians from whom most of the women sought care between 1974 and 1994 failed to recognize, diagnose, or treat their PMS using the standards and protocols published in the medical literature.

Effects of hormone replacement on growth hormone and prolactin exercise responses in postmenopausal women.

Exercise elevates growth hormone (GH) and prolactin (PRL) blood concentrations in premenopausal women. Postmenopausal women taking hormone replacement therapy (HRT) maintain higher estrogen levels that could affect GH and PRL. The purpose of the study was to determine the effects of HRT on GH and PRL responses to treadmill exercise. Seventeen healthy women who were postmenopausal (naturally or surgically) [8 on HRT; 9 not on HRT (NHRT)], completed 30 min of treadmill exercise at 79.16 +/- 1.2% maximal O2 consumption (HRT group) and 80.19 +/- 0.91% maximal O2 consumption (NHRT) group). Blood samples were collected from an intravenous catheter during an exercise session and during a control session without exercise. GH and PRL concentrations were significantly higher in the exercise trial than in the nonexercise trial, whereas resting concentrations were similar for both trials. GH and PRL peaked at 10.8 +/- 1.60 and 12.67 +/- 2.58 ng/ml, respectively, for HRT subjects and at 4.90 +/- 1.18 and 9.04 +/- 2.17 ng/ml, respectively, for NHRT subjects. GH concentrations in the exercise trial were significantly higher for HRT than for NHRT subjects. This is the first study to demonstrate that HRT enhances treadmill-exercise-induced GH release and that similar PRL responses to treadmill exercise occur in postmenopausal women regardless of HRT status.

Effects of estrogen replacement therapy on dehydroepiandrosterone, dehydroepiandrosterone sulfate, and cortisol responses to exercise in postmenopausal women.

OBJECTIVE: To determine the effects of hormone replacement therapy (HRT) on dehydroepiandrosterone (DHEA), DHEA sulfate (DHEAS), and cortisol (F) responses to treadmill exercise. DESIGN: Controlled clinical study. SETTING: Female volunteers in an academic research environment. PATIENT(S): Sixteen healthy, postmenopausal women (7 were receiving HRT, 9 were not). INTERVENTION(S): Blood samples were taken from an intravenous catheter before, during, and after 30 minutes of treadmill exercise following an overnight fast. A second session was conducted one month later for the same subjects using the same blood sampling protocol without exercise. MAIN OUTCOME MEASURE(S): Serum DHEA, DHEAS, and F concentrations. RESULT(S): The HRT and untreated DHEA area under the curve (AUC) for the exercise trials was significantly greater than that for the control trials. The untreated, but not the HRT, DHEAS AUC for the exercise trials was significantly greater than that for the control trials. The HRT and untreated F AUC for the exercise trials was significantly greater than that for the control trials. The AUC for the HRT exercise trials was significantly higher than the untreated exercise trials for DHEA and F, but not DHEAS. CONCLUSION(S): Data suggest that treadmill exercise elevates DHEA, DHEAS, and F levels in postmenopausal women and that HRT enhances the DHEA and F responses.

Effects of low-volume resistive exercise on beta-endorphin and cortisol concentrations.

It has been recently suggested that high and sustained lactate levels may elicit increases in peripheral B-EN concentrations (16). We have observed elevated and sustained lactate concentrations in response to a low-volume resistive exercise protocol (14) that were similar to those from other exercise protocols that produced elevated beta-endorphin (B-EN) concentrations. Thus, the purpose of the study was to determine the effects of a low-volume (21,700 J) resistive exercise repetition maximum (RM) protocol using weight machines on peripheral lactate, B-EN and cortisol concentrations. Subjects completed 3 sets of bench press, lat-pull, leg extension, and leg curl exercise at a 10-RM load. Blood samples were collected and rating of perceived exertion (RPE, 15-point Borg scale) was assessed before exercise (-40 and -10 min), after each exercise, and after the exercise session (+ 35 min); blood samples were collected at 7 additional post-exercise times. RPE increased significantly throughout the exercise. Lactate concentrations rose significantly to peak at 8.54 mM at LE. B-EN and cortisol concentrations (-10) of 4.63 +/- 0.54 pmol.l-1 and 12.09 +/- 1.44 micrograms.dl-1, respectively, were not significantly elevated over time. The data suggest that a low-volume resistive exercise protocol using weight machines elevates lactate concentrations without altering B-EN and cortisol concentrations.

Follicular and luteal phase hormonal responses to low-volume resistive exercise.

The purpose of the study was to 1) determine the effects of a low-volume resistive exercise protocol on serum concentrations of estradiol (E2), progesterone (P4), growth hormone (GH), testosterone (T), and androstenedione (AN) and 2) ascertain whether the endocrine responses are affected by the phase of the menstrual cycle. Eleven untrained, healthy women were assigned to either an early follicular or luteal testing group. The subjects completed three sets of bench press, lat-pull, leg extension, and leg curl exercises at a 10 repetition maximum load on fixed machines with 2-min of rest between sets. Blood samples were collected through an indwelling cannula before, during, and after the exercise. Area-under-the-response-curve (AUC) data demonstrated that E2 concentrations were significantly elevated in both follicular and luteal phases with a greater response in the luteal phase. Moreover, data suggest there is a luteal phase-induced increase in GH and AN in response to the low-volume resistive exercise; however, P4 and T concentrations in untrained women are not increased by low-volume resistive exercise with 2-min rest periods, nor does the altered hormonal milieu produced by the phase of the menstrual cycle affect these hormonal responses.

Plasma volume changes in response to resistive exercise.

The present study was designed to determine the cumulative effects of a series of four resistive exercises on intravascular plasma volume throughout one exercise session. Seven healthy males, mean (+/- SE) age 26.7 +/- 1.2 y, participated in the study. In two separate trials the subjects' one-repetition maximum (1-RM) and 10-RM were determined. In a third session, an IV catheter was inserted into a forearm vein at 0800 h and kept patent with a heparin lock. At 0940 h three sets of bench press (BP), lat pull (LP), leg extension (LE), and leg curl (LC) were executed at a 10-RM load for 10 repetitions or until failure. Blood samples were collected before (-30, 0), during (after BP, LP, LE, LC), and after [5 min, 15 min, and 25 min into recovery (R5, R15, R25)] the resistive exercise session. Plasma volume was reduced as much as -13.35% at LE and returned to normal after R15. We conclude that plasma volume is substantially reduced after performing a short session of upper and lower body resistive exercises. The findings demonstrate the magnitude of resistive-exercise-induced plasma volume loss and underscore the importance of accounting for plasma volume change when determining response of a particular blood parameter to resistive exercise.

Growth hormone, IGF-I, and testosterone responses to resistive exercise.

It has been suggested that growth hormone (GH), testosterone (T), and insulin-like growth factor I (IGF-I) play large roles in muscle tissue growth; however, in only two investigations IGF-I responses to resistive exercise have been examined. Eight young males who had not weight trained for a minimum of 5 months participated in the study. Three sets of bench press (BP), lat-pull (LP), leg extension (LE), and leg curl (LC) exercises were performed at a 10-RM load for 10 repetitions or until failure. Blood samples were collected from an IV catheter before exercise (-30 min and -10 min), after each individual exercise (BP, LP, LE, LC), and after the exercise session (+5, +15, +25, +35, +95 min; +5:35, +22:30, and +23:30 h). GH, IGF-I, and T determinations were corrected for plasma volume change. GH significantly increased (P < 0.05), but IGF-I did not change. Correction for plasma volume accounted for significant increases in T, but did not account for GH and IGF-I results. These data suggest that moderate resistive exercise may increase GH concentrations, whereas elevated T levels can be accounted for by exercise-induced alteration of plasma volume.

Effects of treadmill running on plasma beta-endorphin, corticotropin, and cortisol levels in male and female 10K runners.

Reports of plasma beta-endorphin (B-EN) levels in response to submaximal exercise have been highly disparate. Variations in experimental design have complicated interpretation of previous research. The present study was designed to determine whether a sequential change in plasma beta-endorphin (B-EN), corticotropin (ACTH), and cortisol levels occurs in response to a 30-min submaximal run. Twenty-three subjects were divided into four groups: male runners, female runners, sedentary males and sedentary females. Subjects ran on a treadmill at 80% of previously determined maximum heart rate. Five plasma samples were obtained through an indwelling catheter before exercise (-30 and 0 min), at 15 and 30 min of exercise, and after 30 minutes of recovery. The run resulted in no rise in B-EN, ACTH, and cortisol despite an elevated rectal temperature. B-EN values were significantly higher in males than in females (p less than 0.01). No sex or training differences were seen with respect to change of hormone concentrations over the course of the run. Three male runners developed symptoms of vasovagal syncope after the catheter placement and had high initial B-EN, ACTH, and cortisol concentrations which decreased throughout the run. These data indicate that gender and training do not affect ACTH and cortisol concentrations before, during, and after 30 min of treadmill running at 80% of maximum heart rate, whereas B-EN concentrations are higher in males under these conditions.