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Hormonal Responses to Endurance and Resistance Exercise in Females Aged 19–69 Years

^a Department of Biology, University of New Brunswick, Fredericton, Canada
^b Faculty of Kinesiology, University of New Brunswick, Fredericton, Canada
^c College of Kinesiology, University of Saskatchewan, Saskatoon, Canada

Jennifer L. Copeland, College of Kinesiology, University of Saskatchewan, 105 Gymnasium Place, Saskatoon, SK, Canada S7N 5C2 E-mail: jec324{at}duke.usask.ca.

Decision Editor: John A. Faulkner, PhD

	Abstract

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Thirty cross-trained, female subjects (19–69 years) completed an endurance exercise session (ES), a resistance exercise session (RS), and a control session (CS) in a randomized, balanced design. The ES consisted of 40 minutes of cycling at 75% maximum heart rate, and the RS consisted of 3 sets of 10 repetitions of eight exercises. During the CS, subjects performed no exercise. Before and after exercise, and after 30 minutes of recovery, blood samples were analyzed for plasma lactate and serum growth hormone, insulin-like growth factor 1, testosterone, estradiol, dehydroepiandrosterone, and cortisol. Samples were taken during the CS at the same intervals as during the exercise sessions. There were no age-related differences in intensity measures during exercise. Absolute change from baseline in testosterone (p < .001), estradiol (p < .05), and growth hormone (p < .01) was significantly greater in the ES and RS compared with that in the CS. Absolute change in dehydroepiandrosterone was significantly greater in the RS only (p < .05). Results indicate that an acute bout of exercise can increase concentrations of anabolic hormones in females across a wide age range.

THE mechanisms responsible for biological aging have not been clearly delineated, as aging is a complex, multifactorial process with a high degree of individual variability. It is believed that a major portion of age-related changes are a result of lifestyle and environmental influences, which may explain why some individuals age more successfully than others ⁽¹⁾. It has been well documented that there are significant changes in endocrine function with increasing age. Levels of anabolic hormones such as testosterone, growth hormone, dehydroepiandrosterone (DHEA), and estrogen have been shown to decrease with age ^(2)(3)(4)(5). Reduced levels of anabolic hormones may be responsible for many of the changes in body composition and loss of function that are associated with aging. In men, age-related changes in insulin-like growth factor 1 (IGF-I) and testosterone have been shown to be significantly related to muscle mass ⁽⁶⁾, and many of the changes in body composition that occur with aging are similar to changes observed in subjects with growth hormone deficiency ⁽⁴⁾. Females experience a similar decline in anabolic hormones ⁽³⁾⁽⁷⁾, and it has been shown that quadriceps muscle function is significantly correlated to serum IGF-I and the sulfate conjugate of DHEA in elderly women ⁽⁸⁾. There is also some evidence that loss of estrogen after menopause accelerates the loss of muscle mass and bone mineral density in female subjects ⁽⁹⁾, and low levels of testosterone have been shown to be a limiting factor in strength and muscle development in older female subjects ⁽⁷⁾.

Pharmacological replacement of many of these hormones could be beneficial to aging adults; however, in some cases the potential risks of replacement therapy may outweigh the benefits. Coinciding with these changes in endocrine function is a decrease in physical activity participation as we age ⁽¹⁰⁾, and it is unclear how much of the decrease in hormone levels may actually be related to decreases in physical activity ⁽¹¹⁾. It is well known that an acute bout of exercise can stimulate an increase in anabolic hormones, and this has been demonstrated in response to endurance exercise ^(12)(13) and also to resistance exercise ⁽¹⁴⁾.

Although females experience greater disturbances of the endocrine system with aging and are at an even greater risk of losing lean mass and functional capacity, there has been relatively little research looking at the endocrine response of older female subjects to exercise. To our knowledge there have been no studies comparing the hormonal response to different types of exercise (resistance and endurance) in the same group of female subjects. The exercise protocols used in endocrine studies are often not indicative of the types of exercise regimes typically prescribed to the general population. If maintaining optimal levels of anabolic hormones is to become an important part of exercise prescription for aging female subjects, more research is clearly needed. Therefore, the purpose of this study was to determine the hormonal response to a typical resistance and endurance exercise session in adult females of varying age.

	Methods

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Subjects
Thirty healthy females were recruited to participate in this study. The age range of subjects was 19–69 years with six subjects grouped in each of five age quintiles. (Mean ages and age ranges, in years: quintile 1, 25.0, 19–31; quintile 2, 34.5, 31–37; quintile 3, 43.8, 40–49; quintile 4, 52.8, 50–55; and quintile 5, 62.3, 57–69). All subjects were recreationally trained individuals who had been regularly participating in both resistance and endurance exercise for at least the past 4 months. For the purposes of this study, "regular" exercise was defined as a minimum of three, 1-hour exercise sessions per week. All subjects were nonsmokers and free from use of hormonal contraceptives or any hormone therapy. Quintile divisions were based strictly on chronological age; however, all subjects in quintiles 1, 2, and 3 were eumenorrheic (based on self-reported regular menstrual cycles for the previous year) and all subjects in quintile 5 were postmenopausal (based on an absence of menses for a minimum of 1 year). The majority of subjects in quintile 4 had experienced oligomenorrhea within the previous year. Before participating in the study, subjects over the age of 50 were cleared for unrestricted physical activity by a physician. The experimental protocol was approved by the Institutional Review Board and subjects gave written informed consent.

Experimental Protocol
Following the screening and information session, subjects were required to attend five sessions. The first session consisted of a general fitness appraisal using the Canadian Physical Activity, Fitness, and Lifestyle Appraisal (CPAFLA) ⁽¹⁵⁾. The CPAFLA measured health-related fitness components including aerobic fitness, body composition, and musculoskeletal fitness. Percent body fat was determined by using the three-site (tricep, suprailiac, and abdomen) Jackson and Pollock equation ⁽¹⁶⁾, and the Siri equation ⁽¹⁷⁾. The second session was a familiarization session in which subjects were introduced to the experimental protocols. Subjects were shown the eight exercises to be used in the resistance exercise session (supine chest press, latissimus pulldown, seated leg press, biceps curl, triceps pushdown, leg extension, leg curl, and shoulder press). At this time each subject's 10 repetition maximum (10 RM) was determined for each of the eight exercises, and each subject gave a rating of perceived exertion (RPE) using the Borg scale ⁽¹⁸⁾. The procedure for determining a 10 RM is described by Wathen ⁽¹⁹⁾. Subjects then completed a graded, progressive, maximal exercise test on a Monark cycle ergometer (Monark, Varberg, Sweden) in order to determine individual maximum heart rates. Each heart rate was recorded by using a Polar Vantage XL heart rate monitor (Polar Electro, Kempele, Finland).

Subjects completed the next three testing sessions within a 7-day period. The three sessions consisted of an endurance exercise session, a resistance exercise session, and a control session in which no exercise was performed. Sessions were performed by using a balanced, randomized design and were all performed at the same time of day, with at least 1 day between each session. All sessions were performed in the morning (7 AM to 10 AM) and during days 14–21 of the menstrual cycle of all premenopausal subjects. Subjects were given strict pretesting guidelines to follow before each session. They were instructed to avoid physical activity for the previous 24 hours, to avoid caffeine for 2 hours before the sessions, to eat a standardized presession meal on each of the 3 days, and to keep a dietary record for the 24 hours prior to each session.

The endurance exercise session consisted of 40 minutes of cycling on a Monark cycle ergometer at 75% of each subject's previously determined maximum heart rate. Heart rate was monitored continuously by using a Polar Vantage XL heart rate monitor and subjects gave an RPE by using the Borg scale every 5 minutes. The resistance exercise session was 30–40 minutes in length and consisted of 3 sets of 10 repetitions of the eight exercises listed previously. The intensity was set at each subject's 10 RM and 1 minute of rest was given between sets. Heart rate was monitored continuously during the session and subjects gave an RPE after the third set of each exercise. During the control session, subjects sat quietly for 35 minutes.

A preexercise, postexercise, and 30-minute recovery blood sample was drawn during each of the exercise sessions. During the control session, three samples were drawn at times similar to the sample times in the exercise sessions. The samples were drawn from an indwelling venous catheter inserted in an arm vein, with the first sample drawn immediately upon insertion. The catheter was maintained with a saline lock. Samples were centrifuged and the serum or plasma was stored at -20°C until assayed.

Analytic Methods
Blood samples were analyzed in duplicate for hematocrit by using a Readacrit centrifuge (Becton Dickinson, Franklin Lakes, NJ). Plasma samples from before and after exercise were analyzed for lactate by using spectrophotometric quantitative enzymatic determination (Sigma Diagnostics, St. Louis, MO). Serum samples were analyzed for five anabolic hormones (testosterone, growth hormone, estradiol, IGF-I, and DHEA), as well as the main catabolic hormone, cortisol. Testosterone and cortisol were analyzed by using an automated chemiluminescence system (ACS 180; Chiron Diagnostics, East Walpole, MA). The sensitivity of the assays was 0.35 nmol/L for testosterone and 5.5 nmol/L for cortisol. Serum concentrations of DHEA and estradiol were analyzed by using ¹²⁵I-radioimmunoassay techniques (Diagnostics Systems, Webster, TX) with sensitivities of 0.069 nmol/L and 8.14 pmol/L, respectively. Growth hormone and IGF-I were assayed by using ¹²⁵I-immunoradiometric techniques (Diagnostics Systems) with sensitivities of 0.01 ng/ml and 2.06 ng/ml, respectively. All hormone and lactate analyses were done in duplicate. Average intra-assay variation was 2% for cortisol, 11% for testosterone, 6% for estradiol, 7% for growth hormone, 6% for DHEA, and 3% for IGF-I. For interassay variation to be avoided, all samples from each subject were analyzed in the same assay.

Data Analysis
All hormone data were expressed as absolute change from the baseline sample (postexercise minus preexercise) because we were interested in exercise-induced hormone changes, regardless of the different resting levels in subjects of different ages. Descriptive data are presented as means ± standard deviation. Statistical significance was set at p < .05 and all statistical analyses were performed by using the Minitab v.13 software package (Minitab, State College, PA).

A 3 (session) x 2 (sample differences: postexercise minus preexercise, recovery minus preexercise) x 5 (age quintiles) analysis of variance was performed in order to determine if there was a significant difference in hormone changes between age groups or between exercise sessions. Subject identification was included in the model as a random effect nested in age group. An analysis of variance was also used to determine if there were differences in any intensity measures (RPE, average heart rate, lactate levels) across age or session. Where statistical significance was established, a Tukey post hoc analysis was performed to determine where the significant effects existed. Pearson r correlations were used to analyze the relationship between exercise intensity measurements and hormone changes, as well as between different hormones.

	Results

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Health-Related Fitness Measurements
Table 1 shows the mean results of selected fitness variables, by quintile. Ratings are from normative data from the Canadian population of the same age and gender and can range from "needs improvement" to "excellent" on a five-point scale. Ratings for body composition data are either "healthy" or "unhealthy." All ratings in Table 1 are based on the mean age of the quintile. Although the expected age-related decline in fitness was evident, the ratings account for age and gender and are similar for all quintiles. These descriptive data demonstrate that subjects in each quintile were fit and active for their age.

View larger version (20K): [in this window] [in a new window]   Figure 1. Absolute change in testosterone (T), estradiol (E2), and growth hormone (GH), after endurance and resistance exercises and a control session, for all subjects combined (means ± standard error). Asterisks indicate significant differences from control session: *p < .001, p < .05, p < .01.

View larger version (20K): [in this window] [in a new window]   Figure 2. Absolute change in dehydroepiandrosterone (DHEA), insulin-like growth factor 1 (IGF-I), and cortisol (C), after endurance and resistance exercises and a control session, for all subjects combined (means ± standard error). Asterisk indicates significant difference from control session: *p < .05.

View larger version (22K): [in this window] [in a new window]   Figure 3. Postexercise change in testosterone (T), estradiol (E2), and growth hormone (GH), by age quintile following endurance and resistance exercises and a control session (means ± standard error). Numbers 1–5 represent age quintiles 1–5; n = 6 in each quintile.

View larger version (21K): [in this window] [in a new window]   Figure 4. Postexercise change in dehydroepiandrosterone (DHEA), insulin-like growth factor 1 (IGF-I), and cortisol (C), by age quintile following endurance and resistance exercises and a control session (means ± standard error). Numbers 1–5 represent age quintiles 1–5; n = 6 in each quintile.

	Discussion

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The results of this study indicate that an acute bout of physical exercise can increase levels of estradiol, testosterone, DHEA, and growth hormone in female subjects between the ages of 19 and 69 years. Although we did find a significant age effect for baseline levels of testosterone, estradiol, IGF-I, and DHEA, we were unable to detect any significant differences in exercise-induced hormone changes between age quintiles, although this could be due to the small sample size. With the exception of DHEA, there were also no differences in the hormone response to the two different types of exercise (endurance and resistance).

The study of growth hormone and testosterone responses to exercise in older subjects has increased as a result of the potential impact of these hormones on age-related changes in body composition. The similar increases in growth hormone and testosterone in both young and older subjects found in this study are not consistent with previous research. Craig and colleagues ⁽²⁰⁾ found that, in males, testosterone and growth hormone both increased in response to resistance exercise, but that the increases were much smaller in older males when compared with those in young males. Hakkinen and Pakarinen ⁽²¹⁾ showed no change in growth hormone in elderly men or women in response to resistance exercise, despite observing increases in young men and women. They also found no increase in testosterone in females of any age. Hakkinen and colleagues ⁽⁷⁾ reported no change in testosterone in middle-aged or elderly women in response to resistance exercise, and they found that growth hormone only increased after exercise in middle-aged women, not in elderly women. Similarly, Pyka and colleagues ⁽²²⁾ reported that the growth hormone response to resistance exercise was greatly diminished in older subjects. In the present study, our inability to detect differences related to age may be due to a small sample size. However, the different findings in the present study may be also explained by differences in exercise intensity. Craig and colleagues ⁽²⁰⁾ acknowledged that the differences in hormonal response they found between the two age groups may have been more related to intensity than age, and they did not take measurements of exercise intensity such as lactate level or heart rate. Hakkinen and colleagues ⁽⁷⁾ measured preexercise and postexercise lactate levels and found that the middle-aged women had significantly greater increases in lactate than the elderly women, which could explain the lack of growth hormone response in the elderly women. Previous research has shown that the release of growth hormone is related to exercise intensity ⁽²²⁾. In the present study there were no significant differences across age in any intensity measurements (heart rate, RPE, or lactate). Pearson correlation coefficients from this study indicated that change in testosterone and change in growth hormone were significantly correlated to average exercise heart rate and RPE.

Training status also plays an important role in mediating the hormone response to exercise. Hakkinen and colleagues ⁽⁷⁾ noted that significant exercise-induced changes in free testosterone only occurred in women after a 6-month resistance training program. Similarly, Kraemer and colleagues ⁽²³⁾ reported that acute testosterone responses in older male subjects were significantly greater following a 10-week resistance training program. This is supported by our results, because our female subjects had been regularly training for at least 4 months and they experienced a significant acute increase in testosterone after exercise.

Finding methods of maintaining or increasing endogenous levels of DHEA or its sulfate conjugate, DHEAS, is particularly appealing because of the potential effect of DHEA on lean body mass, bone density, and quality of life ⁽²⁴⁾. DHEA was the only hormone measured in this study that responded specifically to only one type of exercise. DHEA increased significantly in response to the resistance exercise, but not to the endurance exercise. This is in contrast to previous work that found increases in DHEA(S) in female subjects in response to endurance exercise ⁽¹²⁾. Cortisol, another adrenal hormone, was also measured. During the endurance session and the control session, cortisol decreased significantly over time, which is somewhat surprising because cortisol typically increases in response to exercise ⁽¹²⁾. The decrease in cortisol found here may reflect a combination of the typical diurnal variation of this hormone and a preexercise increase in cortisol in response to the catheter insertion. However, during the resistance session the cortisol response was significantly different from that of the other sessions. It appears that during the resistance session this decline of cortisol was blunted. Secretion of both cortisol and DHEA is stimulated by adrenocorticotropic hormone, so levels of these two hormones typically follow a similar pattern. Exercise-induced changes in adrenal hormones such as DHEA and cortisol may be more intensity dependent, and in this study RPE and postexercise lactate levels were both significantly higher in the resistance exercise session.

Estradiol increased significantly in response to both types of exercise in this study. This confirms previous research that reported increases in estradiol after endurance exercise ^(13)(25) and resistance exercise ⁽²⁶⁾. Changes in estrogen are influenced by the intensity and duration of exercise, and by menstrual phase and status ⁽¹³⁾. Fig. 3 shows that in this study there was a clear trend for quintile 5 to have a lower estradiol response to exercise than the other quintiles, which is not surprising because subjects in quintile 5 were all postmenopausal. However, as a result of the large degree of individual variability in estradiol levels, the age effect did not reach statistical significance.

In this study, IGF-I did not change in response to either exercise session. This is in contrast to a study by Kraemer and colleagues ⁽¹⁴⁾ that found an increase in IGF-I in females following a resistance exercise session that was very similar to the one used in this study. However, other work with males found no increase in IGF-I in response to resistance exercise, and no relationship between growth hormone and IGF-I levels ⁽²⁷⁾. Kraemer and colleagues suggested that the increased IGF-I reported in the first study ⁽¹⁴⁾ may have resulted from changes in plasma volume. In the present study we did not correct for changes in plasma volume; however, there were no significant increases in IGF-I that could be explained by hemoconcentration.

It is difficult to determine the mechanisms of increased anabolic hormone levels observed in this study. We did not investigate any changes in metabolic clearance rate that may have occurred with exercise and that may explain the increases in some hormones ⁽²⁸⁾. In addition, we can only speculate on the biological significance of these hormone changes to older adults without knowledge of how age influences hormone receptor density or hormone uptake in the target tissues. However, positive results from studies that used exogenous supplementation of anabolic hormones ⁽²⁹⁾ indicate that the body can still respond to anabolic hormones even though endogenous levels may be declining. Another limitation of this study is the brief sampling time period. Some research has shown delayed increases in testosterone several hours after a resistance exercise session ⁽³⁰⁾. Further research is necessary to document hormone changes during recovery from exercise as well as to determine the significance of transient postexercise hormone changes.

This study is unique in that it compared subjects across a broad age range rather than one "young" group and one "old" group. However, the results must be interpreted cautiously because of the small number of subjects within each age group and the high variability that is inherent in endocrine data. The lack of an age effect in hormone changes may be explained by a lack of age difference in the intensity of the exercise sessions. If there is a threshold of intensity required to stimulate the anabolic hormones measured here, then perhaps both exercise sessions reached this threshold. The exercise protocols used were chosen to be similar to a typical workout that would be prescribed to the average recreational exerciser.

In summary, this study was unable to demonstrate that chronological age had a significant effect on exercise-induced hormone changes. Although our conclusions are limited by the small sample size of each group, these results indicate that increasing age does not necessarily inhibit the hormonal response to a typical bout of exercise in females. Increases in levels of anabolic hormones may be beneficial in preserving lean body mass and subsequently maintaining functional capacity as we age. Although an increase in anabolic hormones must be maintained for muscle anabolism to occur, the potential effect of repeated acute increases over time should not be discounted. Long-term intervention studies are required to further clarify the relationships among exercise, endocrine responses, and successful aging.

	Acknowledgments

 
This study was supported by the Natural Sciences and Engineering Research Council of Canada and the Medical Research Fund of New Brunswick.

We acknowledge Dr. Sam Chu and the Biochemistry Lab staff at the Dr. Everett Chalmers Regional Hospital for their assistance.

Received March 15, 2001

Accepted December 10, 2001

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