scholarly journals Exercise-induced changes in circulating growth factors with cyclic variation in plasma estradiol in women

1997 ◽  
Vol 82 (6) ◽  
pp. 1946-1951 ◽  
Author(s):  
Mette Hornum ◽  
Dan M. Cooper ◽  
Jo Anne Brasel ◽  
Alina Bueno ◽  
Kathy E. Sietsema

Hornum, Mette, Dan M. Cooper, Jo Anne Brasel, Alina Bueno, and Kathy E. Sietsema. Exercise-induced changes in circulating growth factors and cyclic variation in plasma estradiol in women. J. Appl. Physiol. 82(6): 1946–1951, 1997.—The effect of 10 min of high-intensity cycling exercise on circulating growth hormone (GH), insulin-like growth factors I and II (IGF-I and -II), and insulin-like growth factor binding protein 3 (IGF BP-3) was studied in nine eumenorrheic women (age 19–48 yr) at two different phases of the menstrual cycle. Tests were performed on separate mornings corresponding to the follicular phase and to the periovulatory phase of the menstrual cycle, during which plasma levels of endogenous estradiol (E2) were relatively low (272 ± 59 pmol/l) and high (1,112 ± 407 pmol/l), respectively. GH increased significantly in response to exercise under both E2conditions. Plasma GH before exercise (2.73 ± 2.48 vs. 1.71 ± 2.09 μg/l) and total GH over 10 min of exercise and 1-h recovery (324 ± 199 vs. 197 ± 163 ng) were both significantly greater for periovulatory phase than for follicular phase studies. IGF-I, but not IGF-II, increased acutely after exercise. IGF BP-3, assayed by radioimmunoassay, was not significantly different at preexercise, end exercise, or at 30-min recovery time points and was not different between the two study days. When assayed by Western blot, however, there was a significant increase in IGF BP-3 30 min after exercise for the periovulatory study. These findings indicate that the modulation of GH secretion associated with menstrual cycle variations in circulating E2affects GH measured after exercise, at least in part, by an increase in baseline levels. The acute increase in IGF-I induced by exercise appears to be independent of the GH response and is not affected by menstrual cycle timing.

2021 ◽  
Author(s):  
Sarah Ahmad ◽  
Rodney Hansen ◽  
Matthew Schmolesky

AbstractResearch suggests strong inter-relationships between physical exercise, levels of brain-derived neurotrophic factor (BDNF), levels of estrogen, and the menstrual cycle, and yet no single study has examined these factors collectively in humans. The current study assessed the effect of an acute bout of vigorous aerobic exercise (20 minutes of stationary cycling at 80% of heart rate reserve) on serum BDNF and estradiol in healthy, eumenorrheic women, ages 18-28. In addition, this study determined whether basal BDNF or the exercise-induced increase in BDNF varies throughout the menstrual cycle. Thirty-four subjects were assigned to an experimental (n = 27) or control condition (n = 7). Exercise transiently increased both estradiol (51.2%) and BDNF (23.6%), and basal levels of BDNF and estradiol predicted the magnitude of the exercise-induced increases. Basal BDNF did not vary significantly throughout the menstrual cycle. Exercise-induced changes in BDNF did not correlate with menstrual cycle day or basal estradiol. Basal estradiol and basal BDNF showed a marginally significant positive correlation. Taken together, these results indicate that brief, vigorous aerobic exercise is sufficient to elevate both BDNF and estradiol in healthy women and that the menstrual cycle dramatically influences the magnitude of exercise-induced changes in estradiol, but not BDNF


1995 ◽  
Vol 144 (1) ◽  
pp. 83-90 ◽  
Author(s):  
E Magnan ◽  
L Mazzocchi ◽  
M Cataldi ◽  
V Guillaume ◽  
A Dutour ◽  
...  

Abstract The physiological role of endogenous circulating GHreleasing hormone (GHRH) and somatostatin (SRIH) on spontaneous pulsatile and neostigmine-induced secretion of GH was investigated in adult rams actively immunized against each neuropeptide. All animals developed antibodies at concentrations sufficient for immunoneutralization of GHRH and SRIH levels in hypophysial portal blood. In the anti GHRH group, plasma GH levels were very low; the amplitude of GH pulses was strikingly reduced, although their number was unchanged. No stimulation of GH release was observed after neostigmine administration. The reduction of GH secretion was associated with a decreased body weight and a significant reduction in plasma IGF-I concentration. In the antiSRIH group, no changes in basal and pulsatile GH secretion or the GH response to neostigmine were observed as compared to controls. Body weight was not significantly altered and plasma IGF-I levels were reduced in these animals. These results suggest that in sheep, circulating SRIH (in the systemic and hypophysial portal vasculature) does not play a significant role in pulsatile and neostigmine-induced secretion of GH. The mechanisms of its influence on body weight and production of IGF-I remain to be determined. Journal of Endocrinology (1995) 144, 83–90


1984 ◽  
Vol 107 (3) ◽  
pp. 295-301 ◽  
Author(s):  
Stig Engkjær Christensen ◽  
Otto Lunde Jørgensen ◽  
Niels Møller ◽  
Hans Ørskov

Abstract. The effects of increases in body temperature on growth hormone (GH)-release were studied in 10 young normal males in the fasting state as well as postprandially. The temperature increase of one degree centigrade was attained by external heating using thermostatically controlled water blankets covered by heat-reflecting aluminium foil. The increase in plasma GH after heating was partially suppressed in the non-fasting state reaching a mean of 7.9 ± 3.5 (sem), ng/ml, range 1.0–36 ng/ml. In contrast all subjects exhibited higher increases, mean 18.3 ± 4.0 ng/ml, range 7–44 ng/ml, in response to heating when fasting. The results were compared in the same subjects to the plasma GH-responses obtained during exercise (450 kpm/min for 40 min) inducing a similar increase in body temperature of about one degree centrigrade. Nevertheless the response in plasma GH (8.4 ± 3.3 ng/ml, range 0.4–34 ng/ml) was smaller than obtained by the heat test despite a rate of temperature increase on exercise which was about twice as high. Furthermore, the same exercise performed in a cold room under circumstances which precluded any major rises in core temperature resulted in complete inhibition of GH-release. The results indicate that exercise per se does not stimulate GH-secretion, indeed it may inhibit the response expected to be evoked by the exercise-induced rise in temperature. Evidence is also presented that it is core and not cutaneous temperature which modulated GH release. The procedure used for inducing the rise in temperature and plasma GH may be used as a simple, acceptable and safe clinical test for GH-insufficiency.


1996 ◽  
Vol 270 (4) ◽  
pp. R838-R845 ◽  
Author(s):  
J. A. Smith ◽  
A. B. Gray ◽  
D. B. Pyne ◽  
M. S. Baker ◽  
R. D. Telford ◽  
...  

We investigated how moderate exercise affects neutrophil microbicidal activity and whether exercise-induced responses are associated with changes in growth hormone (GH) secretion. Biological fluctuations were controlled for and GH secretion was manipulated by glucose ingestion. In eight men, 1 h of moderate exercise increased intracellular H2O2 generation in response to phorbol 12-myristate 13-acetate stimulation by threefold (P = 0.025) and complement receptor expression by 20% (P = 0.045). These responses were accompanied by a twofold increase in the plasma concentration of elastase, a marker of neutrophil activation in vivo. The plasma concentration of GH increased 10-fold after exercise, but this was reduced to 3-fold by glucose ingestion (P < 0.001), which also blunted elastase release (P < 0.001). Although the magnitude of H2O2 generation increased in proportion to the increase in plasma GH concentration, it declined progressively once this exceeded 20 ng/ml. The net response of neutrophils to exercise may represent a balance between the individual responses of subpopulations that are unaffected, primed, or fully activated by circulating mediators that respond to exercise and to dietary glucose intake.


2012 ◽  
Vol 303 (10) ◽  
pp. R1080-R1089 ◽  
Author(s):  
Bradley C. Nindl ◽  
Maria L. Urso ◽  
Joseph R. Pierce ◽  
Dennis E. Scofield ◽  
Brian R. Barnes ◽  
...  

Insulin-like growth factor-I (IGF-I) resides across different biocompartments [blood, interstitial fluid (ISF), and muscle]. Whether circulating IGF-I responses to exercise reflect local events remains uncertain. We measured the IGF-I response to plyometric exercise across blood, ISF, and muscle biopsy from the vastus lateralis. Twenty volunteers (8 men, 12 women, 22 ± 1 yr) performed 10 sets of 10 plyometric jump repetitions at a 40% 1-repetition maximum. Blood, ISF, and muscle samples were taken pre- and postexercise. Circulating IGF-I increased postexercise: total IGF-I (preexercise = 546 ± 42, midexercise = 585 ± 43, postexercise = 597 ± 45, +30 = 557 ± 42, +60 = 536 ± 40, +120 = 567 ± 42 ng/ml; midexercise, postexercise, and +120 greater than preexercise, P < 0.05); Free IGF-I (preexercise = 0.83 ± 0.09, midexercise = 0.78 ± 0.10, postexercise = 0.79 ± 0.11, +30 = 0.93 ± 0.10, +60 = 0.88 ± 0.10, + 120 = 0.91 ± 0.11 ng/ml; +30 greater than all other preceding time points, P < 0.05). No exercise-induced changes were observed for ISF IGF-I (preexercise = 2.35 ± 0.29, postexercise = 2.46 ± 0.35 ng/ml). No changes were observed for skeletal muscle IGF-I protein, although IGF-I mRNA content increased ∼40% postexercise. The increase in circulating total and free IGF-I was not correlated with increases in ISF IGF-I or muscle IGF-I protein content. Our data indicate that exercise-induced increases in circulating IGF-I are not reflective of local IGF-I signaling.


2011 ◽  
Vol 300 (6) ◽  
pp. R1326-R1332 ◽  
Author(s):  
D. E. Scofield ◽  
H. L. McClung ◽  
J. P. McClung ◽  
W. J. Kraemer ◽  
K. R. Rarick ◽  
...  

This study tested the hypothesis that transdermal fluid (TDF) provides a more sensitive and accurate measure of exercise-induced increases in insulin-like growth factor-I (IGF-I) than serum, and that these increases are detectable proximal, but not distal, to the exercising muscle. A novel, noninvasive methodology was used to collect TDF, followed by sampling of total IGF-I (tIGF-I) and free IGF-I (fIGF-I) in TDF and serum following an acute bout of exercise. Experiment 1: eight men (23 ± 3 yrs, 79 ± 7 kg) underwent two conditions (resting and 60 min of cycling exercise at 60% V̇o2peak) in which serum and forearm TDF were collected for comparison. There were no significant changes in tIGF-I or fIGF-I in TDF obtained from the forearm or from serum following exercise ( P > 0.05); however, the proportion of fIGF-I to tIGF-I in TDF was approximately fourfold greater than that of serum ( P ≤ 0.05). These data suggest that changes in TDF IGF-I are not evident when TDF is sampled distal from the working tissue. To determine whether exercise-induced increases in local IGF-I could be detected when TDF was sampled directly over the active muscle group, we performed a second experiment. Experiment 2: fourteen subjects (22 ± 4 yr, 68 ± 11 kg) underwent an acute plyometric exercise condition consisting of 10 sets of 10 plyometric jumps with 2-min rest between sets. We observed a significant increase in TDF tIGF-I following exercise ( P ≤ 0.05) but no change in serum tIGF-I ( P > 0.05). Overall, these data suggest that TDF may provide a noninvasive means of monitoring acute exercise-induced changes in local IGF-I when sampled in proximity to exercising muscles. Moreover, our finding that the proportion of free to tIGF-I was greater in TDF than in serum suggests that changes in local IGF-I may be captured more readily using this system.


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