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1 Department of Neurobiology, 2 Department of Physiological Science, and 3 Brain Research Institute, University of California, Los Angeles 90095; and 4 National Aeronautics and Space Administration-Ames Research Center, Moffett Field, California 94035
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ABSTRACT |
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 TOP
 ABSTRACT
 INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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Plasma growth hormone (GH) measured by immunoassay [immunoassayable GH (IGH)] and by tibial bioassay [bioassayable GH (BGH)] increases in humans in response to exercise. In rats, however, IGH does not change in response to exercise. The objective of this study was to determine the BGH response to an acute exercise bout in rats. The rats ran on a treadmill at a rate of 27 m/min for 15 min, after which plasma and pituitary hormones, including IGH and BGH, and plasma metabolites were measured. Plasma and pituitary IGH were unchanged from control groups after the acute exercise bout, whereas plasma BGH was increased by 300% and pituitary BGH was decreased by 50%. Plasma thyroxine and corticosterone levels were significantly increased after a single exercise bout, but plasma testosterone, 3,5,3'-triiodothyronine, glucose, lactate, and triglyceride concentrations were unchanged. Given previous results from in situ nerve stimulation studies (Gosselink KL, Grindeland RE, Roy RR, Zhong H, Bigbee AJ, Grossman EJ, and Edgerton VR. J Appl Physiol 84: 1425-1430, 1998), these in vivo results are consistent with the rapid BGH response during exercise being induced by the activation of muscle afferents.
proprioception; immunoassay; bioassay; plasma hormones; pituitary
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INTRODUCTION |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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MULTIPLE VARIANTS OF GROWTH hormone (GH) are known to exist, many of which are not measured by the commonly used immunoassay techniques (29, 31). For example, Ellis and Grindeland (5) showed that the injection of monkey anti-rat GH (the same polyclonal antibody used in our GH immunoassay) and rat plasma into hypophysectomized rats did not inhibit body weight gain. These variants also respond differently to a range of stimuli. When rats are subjected to metabolic challenges such as fasting or cold exposure, GH measured by immunoassay (IGH) is unchanged, whereas pituitary GH measured by tibial bioassay (BGH) decreases (6). Previous experiments in our and other laboratories have shown that BGH is a pituitary-derived, biologically active peptide, which exists in humans (10, 18, 19, 20, unpublished observations), rats (5, 6, 12, 13), cattle (7), and cats (unpublished observations).
Whereas BGH is known to respond to metabolic perturbations (6), recent data indicate that stimulation of proprioceptive neuromuscular afferents may be an additional pathway through which BGH is regulated. Gosselink et al. (12, 13) recently showed rapid BGH release from the rat pituitary in response to a short bout of electrical stimulation (15 min or less) of low-threshold axons of the promixal ends of severed tibial and peroneal nerves, which innervate predominantly fast muscles. Neither muscle-derived nor other metabolic factors appeared to be involved in facilitating BGH release under these conditions, because stimulating the distal ends of these cut nerves for the same amount of time had no effect on plasma or pituitary BGH concentrations (13). On the basis of these data, we hypothesized that an acute bout of exercise in rats, similar in activation patterns to the in situ stimulation of muscle nerve afferents (12, 13), would elicit a substantial increase in plasma BGH and a concomitant decrease in pituitary BGH.
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METHODS |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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Nine-week-old male albino rats (Harlan Sprague Dawley, Indianapolis, IN; body weight 350 ± 3 g), were housed two per cage in a 12:12 light-dark cycle at 24 ± 1°C and given Purina rat chow and tap water ad libitum. After 7 days of adaptation to the laboratory environment, the rats were divided into three groups: 1) nonexercised controls (Con; n = 8), 2) rats acclimatized to treadmill exercise but not run on the experiment day (Acc; n = 8), and 3) rats that were acclimatized to treadmill exercise and run on the experiment day (Ex; n = 8).
Training regimen and sample collection. Acc and Ex rats were exercised daily during the light cycle (5-15 min at 27-40 m/min; 0° incline) on a rodent treadmill (Columbus Instruments) for 15 consecutive days before the experiment day. An air-puff stimulus was used sparingly during the early stages of acclimatization but not at all on the day of the experiment. The acclimatization process was used to acquaint the animals to the treadmill and to ensure that the Ex rats would run on the experiment day. Animals were used in accordance with National Institutes of Health guidelines and with the approval of the Institutional Animal Care and Use Committee.
On the experiment day, Ex rats were exercised for 15 min at 27 m/min. After the exercise session, the rats were immediately anesthetized with methoxyflurane, bled via cardiac puncture, and decapitated. The order of euthanasia was such that one rat from each group was killed in sequence, and then this order was repeated until all rats were killed. This protocol was followed to account for any discrepancy in hormone and/or metabolite levels among groups with respect to the time of day. Blood was collected in heparinized syringes, placed in 15-ml plastic conical tubes, and chilled immediately on ice to preserve glucose. Samples were centrifuged at 1,000 g for 30 min at 5°C. A 1-ml aliquot of plasma from each rat was placed in a cryovial containing sodium fluoride as a preservative to prevent glucose degradation and was stored at
70°C for in vitro metabolite and
hormone analyses. The remaining plasma was pooled by group for
bioassay; i.e., one pooled plasma sample contained eight individual
plasma samples from a given group. Anterior pituitaries were removed
from all animals, placed in cryovials by group (n = 8),
and stored at 70°C. The pituitaries were then weighed and homogenized by group in handheld glass homogenizers in 5 ml of 0.01 M
sodium carbonate and was further diluted with 0.85% sodium chloride
for immunoassay and bioassay.
Hormone and metabolite analyses.
IGH was measured by the double-antibody RIA method of Schalch and
Reichlin (23) using rat GH (VII-38-C, 3 IU/mg) that was purified and radioiodinated in house. Monkey anti-rat GH was used as
the primary antibody (1:65,000 working dilution), with goat anti-monkey
gamma globulin (1:20) as the secondary antibody (Antibodies, Davis,
CA). Inter- and intra-assay variations for the GH immunoassay were 6 and 4%, respectively. BGH was quantified using the tibial bioassay
method of Greenspan et al. (14), with bovine pituitary GH
(XIV-44-C5, 1.5 IU/mg) used for the standard curve at total dose levels
of 5, 15, and 45 µg/rat. The intra-assay coefficient of variation for
the bioassay was ~3%. Briefly, bioassay rats were injected
intraperitoneally with saline (baseline control), standards, or pooled
plasma or pituitary samples (5 rats/group; 0.5 ml
sample · rat
1 · day1 × 4 days). On the fifth day, the rats were overdosed with
CO2. The left tibia was removed, split longitudinally and
prepared for staining in 2.5% AgNO3 (12).
Once stained, 10 width measurements were taken along the epiphyseal
tibial plate and averaged for each rat. Each average tibial width was
then converted into a BGH value from the standard curve. The mean BGH
value (± SE) was then calculated for each group. The standard curve
for this assay is shown in Fig. 1.
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Statistics. For all hormone and metabolite analyses except BGH, the number of animals per group was eight; overall differences in hormones and metabolites were measured using one-way ANOVA, and a Tukey-Kramer post hoc test was used to identify differences between individual groups, with P < 0.05 considered significant. For BGH, variance and statistical significance of difference were determined for five rats per group; that is, five bioassay rats were injected with pooled plasma or pituitary samples from the eight rats in each experimental group (Con, Acc, and Ex). Thus the hypothesis being tested is whether the bioassay rats respond differently to a given plasma or pituitary sample from Con, Acc, or Ex rats. Two total dose levels of pituitary BGH (0.67 and 0.22 mg tissue) were assayed using a four-point assay procedure, and one dose level of plasma BGH was assayed using a bracketed three-point assay method (25). Power was >80% for all measures, except for Con vs. Ex T4, which had a power of 69%.
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RESULTS |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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After the rats ran for 15 min at 27 m/min, the plasma
concentrations of BGH were 300% higher and pituitary BGH 50% lower in Ex than Con rats (Fig. 2). No changes
were observed in the plasma or pituitary BGH levels of the Acc rats
compared with Con. In the Ex rats, neither plasma nor pituitary IGH was
significantly different from Con (Fig.
3). The Acc rats showed significantly higher plasma IGH levels than Ex rats, but the levels did not differ
from Con. The increase in plasma IGH observed in Acc rats (Fig. 3) may
have been due to the extensive handling during treadmill acclimatization during the previous weeks (26). If so,
this effect would be expected in Ex rats as well. However, IGH levels in the Ex rats were not different from Con. It is possible that resting
IGH levels were elevated in the Ex rats before exercise and then
decreased postexercise. Pituitary IGH levels were similar in all
groups.
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A summary of the other plasma hormone and metabolite concentrations
is shown in Table 1. Testosterone
levels were similar in all three groups, as were plasma glucose,
lactate, and triglyceride concentrations. Plasma T3 was
higher in the Ex than Acc group, but neither was different from Con.
Plasma T4 and corticosterone levels were higher in the Ex
than in the Con and Acc groups. Because none of the hormone data in the
Acc group differed from Con, it appears that acclimatization had no
overall effect on resting hormone levels.
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DISCUSSION |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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Evidence that exercise-induced regulation of BGH may be neurally mediated. A single, short bout of treadmill exercise elicited a rapid and significant decrease in rat pituitary BGH and a concomitant increase in plasma BGH levels in the absence of changes in plasma metabolites (glucose, lactate, triglycerides). These changes in BGH secretion were similar to those observed after a similar bout of in situ electrical nerve stimulation, which activated primarily low-threshold fibers from isolated hindlimb nerves (12). Our laboratory proposed that proprioceptive input from low-threshold afferents, which originate in muscle spindles and Golgi tendon organs, can induce BGH secretion from the pituitary (12, 13). The possibility of such a neural connection is consistent with studies showing the presence of neuronal projections from the lumbar spinal cord to the hypothalamus (2, 3), where growth hormone regulatory factors are synthesized and secreted.
The present in vivo data are in agreement with, and extend the results from, the in situ nerve stimulation experiments. Plasma BGH levels were 250% greater than control levels in response to stimulation of one hindlimb nerve (13), whereas whole body exercise increased plasma BGH by 300% in the present study. Whether exercise induces BGH release through the same mechanism(s) as in situ afferent stimulation cannot be fully determined on the basis of the present data alone. In comparing the nerve stimulation and exercise results, the amount of BGH released from the pituitary does not seem to be tightly linked to the mass of muscle from which the activated afferents originate. On the other hand, we have no way of estimating how many muscle receptors such as spindles and tendon organs were activated while the rats ran at the present speed, nor can we assume that all receptors from all muscles have the same effects in inducing the release of BGH. For example, in situ stimulation of the proximal end of the cut nerve innervating the slow soleus muscle alone resulted in increased pituitary BGH and decreased plasma BGH concentrations; presumably BGH continued to be synthesized in the pituitary but was not released (13). During the exercise used in this study, both fast and slow muscles were active, based on rat hindlimb EMG patterns obtained during varying speeds of treadmill locomotion (21). Thus, if the mechanism of BGH release is similar in situ and in vivo, the BGH inhibition observed with electrical stimulation of afferents from the soleus nerve alone may have been overridden by the simultaneous exercise-induced stimulation of afferents from fast muscles during exercise. It appears that the hypothesis that proprioception plays a role in BGH regulation is not unique to rats. A similar phenomenon has been observed in humans in response to short-duration muscle activity. McCall et al. (18, 19) showed that plasma BGH levels increase rapidly after ~6 min of repetitive isometric plantar flexions of one leg. Similarly, a response has been observed in humans during a 15-min bout of treadmill exercise, in which plasma BGH levels peaked at 5 min into the exercise and returned to basal levels within 1 h after the completion of exercise (unpublished observations). Although we cannot definitively state that only proprioceptive afferents played a role in BGH release in these human studies, a more recent study by McCall et al. (20), using a protocol shown to activate primary and secondary muscle spindle afferents, showed that noninvasive muscle vibration in humans induces BGH release. These data further support the hypothesis that BGH can be regulated by the activation of proprioceptive sensory afferents. Interestingly, the efficacy of this neurally induced BGH release seems to be impaired after chronic periods of unloading of the limbs. McCall et al. (18, 19) showed that the exercise-induced BGH response was abolished after 2 days of simulated (bed rest) or actual spaceflight and continued to be depressed throughout 14 days of bed rest or 17 days of spaceflight. The BGH response was restored within 4 days of recovery in both studies. Because the muscle output during the exercise tests was similar before, during, and after bed rest or spaceflight, the metabolic and neural impact in each case would be expected to be the same in both the preunloaded (control) and the unloaded (bed-rest or spaceflight) paradigms. Thus proprioceptive signals derived from weight-bearing neuromuscular activity may play an important role in maintaining the efficacy of neurally mediated BGH secretion.Did metabolic factors contribute to the regulation of BGH in response to exercise? Although there may be a metabolically or humorally mediated component to BGH regulation during exercise, evidence that metabolic factors were not the predominant regulators for BGH secretion in the present study is provided by the absence of changes in plasma metabolites (glucose, lactate, triglycerides) in response to the exercise bout. An exercise-induced increase in plasma T4 has been observed previously (30). Although T4 could have augmented the BGH response in this study, in situ nerve stimulation (12, 13) induced a similar increase in plasma BGH and decrease in pituitary BGH without a change in T4, suggesting that T4 is not necessary for BGH secretion. Also, as expected, corticosterone levels were doubled in the Ex vs. Con rats, reflecting another metabolically associated exercise response, which may have affected BGH release. Because Acc plasma corticosterone did not differ from Con, acclimatization-induced changes in the basal levels of plasma corticosterone cannot account for the increased BGH observed in response to an acute exercise bout. Furthermore, in situ nerve stimulation studies from our laboratory showed increased plasma BGH in the absence of a change in plasma corticosterone levels (12, 13).
Differential regulation of BGH and IGH. There are clear differences in the BGH and IGH response to exercise. For example, exercise can increase plasma IGH in humans, depending on the intensity and duration of exercise and the fitness level of the individual (1). In addition, IGH levels rise relatively slowly and peak well into or after intensive exercise (1, 16, 17). Although some data suggest that IGH regulatory factors (e.g., GH-releasing factor and somatostatin) in humans are mediated by changes in plasma metabolites (8) or blood acid-base shifts (11) in response to exercise, Schmidt et al. (24) found no correlation between blood lactate concentration and IGH secretion during exercise. Thus the exact mechanism for the exercise-induced increase in human plasma IGH levels is unclear. In adult rats, IGH has been reported to remain constant or decrease in response to exercise (4, 9, 27). On the other hand, a single bout of neuromuscular activity in rats in the present study elicited large and rapid changes in the BGH concentration in the pituitary and plasma. In humans, acute isometric plantar flexion (18, 19) or aerobic treadmill exercise (unpublished observations) also elicited an increase in plasma BGH. Furthermore, our preliminary human treadmill data also indicate a different time course for BGH and IGH release (unpublished observations).
Our data present evidence for differences in the BGH and IGH responses to neuromuscular activity. There are data that further support differences in BGH and IGH regulation at the hypothalamic level. Russell (22) showed that IGH and BGH release from pituitaries in vitro was differentially inhibited by somatostatin. Vodian and Nicoll (28) reported that GH-releasing factor preferentially induced BGH secretion from rat pituitaries. Together, these studies indicate that BGH and IGH are differentially regulated. The observed BGH response to exercise raises a number of issues. 1) Are there different mechanisms of release and/or action of BGH in rats vs. humans? 2) Are there differences in the activation pathways of BGH in response to aerobic vs. resistance exercise? 3) Is there an exercise-intensity threshold for stimulating BGH release? 4) What is the time course (short and long term) for BGH release in response to exercise? The present study is limited in that we did not collect blood samples during or at multiple time points postexercise; thus we cannot provide a time course for the BGH response to exercise in rats. In situ experiments in rats, however, showed that 5 and 10 min of nerve stimulation elicited a BGH response similar to that obtained at 15 min (13), suggesting that BGH release probably occurs, and even peaks very quickly, before the onset of other exercise-induced metabolic factors. The present data suggest that there is a unique, neurally mediated regulatory mechanism for the secretion of BGH in vivo in rats in response to exercise. The long-term effects of BGH release and its physiological consequence with respect to exercise remain to be elucidated.| |
ACKNOWLEDGEMENTS |
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We thank Paul Fung at National Aeronautics and Space Administration (NASA)-Ames Research Center for performing the plasma metabolite analyses.
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FOOTNOTES |
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This study was supported by NASA Grant 199-26-12-09.
A portion of these data has been presented in abstract form (15).
Address for reprint requests and other correspondence: V. R. Edgerton, Univ. of California, Dept. of Physiological Science, 1804 Life Sciences, 405 Hilgard Ave., Los Angeles, CA 90095-1527 (E-mail: vre{at}ucla.edu).
The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
Received 10 December 1999; accepted in final form 17 July 2000.
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REFERENCES |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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Significantly different from Ex,
P < 0.05.