Rise In Growth Hormone Concentration Research Articles

The Role Of Lactate In The Exercise-induced Growth Hormone Response

PURPOSE During the last thirty years the contention that lactate is the major stimulus for the exercise induced hGH response (EIGR) has undergone a cycle of popularity and rejection. Currently, there is a growing body of evidence of the ubiquity of roles for lactate and in this regard the EIGR is no exception. McArdles disease is a type V inherited glycogen storage disease in which moyphorylase is absent. Accordingly these individuals do not produce lactate during exercise and hence represent an ideal model to explore the role of lactate in the EIGR. The present study examined the acute hGH response to a standardised graded exercise stimulus in McArdles patients. METHODS Eleven patients entered the study. All have McArdles disease as confirmed by both DNA and muscle biopsy analysis. Participants completed an incremental exercise test on a motorised treadmill. This comprised walking, beginning at 1.5 kph and increasing by 0.5 kph with each 3-minute stage. A 60s rest interval was given between successive stages for blood sampling. The test was terminated either after completion of 3 minutes at 6.5 kph or when a CR10 pain scale rating of “4” was achieved. Capillary (earlobe) blood samples for lactate and hGH determination were taken before the test and after each stage. HR was measured continuously throughout exercise. RESULTS Six individuals demonstrated no EIGR whilst five individuals demonstrated a modest rise in growth hormone concentration during exercise with peak values ranging from 0.73 to 8.40 μg.1−1. The two groups which arose from this demonstrated a significantly higher (p<0.05) peak heart rate in those who had an EIGR (169.25 ± 10.34 bpm vs 131.83 ± 24.00, mean ± SD). Although peak heart rate as a percentage of age-predicted maximal heart rate demonstrated a non-significant difference between the two groups, calculation of effect size revealed a meaningful difference (1.36) suggesting that those who produce hGH in response to exercise have a higher relative heart rate than those who do not. CONCLUSION The dichotomous response observed in McArdles patients in the present study suggests that lactate is not the primary stimulus for the EIGR. However, by virtue of a modest response in half the participants, lactate may be a co-stimulus of the EIGR along with other factors that have yet to be fully identified.

Growth hormone responses to varying doses of oral arginine

Intravenous (IV) arginine invokes an increase in growth hormone (GH) concentrations, however, little is known about the impact of oral arginine ingestion on the GH response. Objective The purpose of this study was to determine the dose of oral arginine that elicits an optimal GH response and to determine the time course of the response. Design Eight healthy males (18–33 years – 24.8 ± 1.2 years) were studied on 4 separate occasions. Following an overnight fast at 0700 h, a catheter was placed in a forearm vein. Blood samples were taken every 10 min for 5 h. Thirty minutes after sampling was initiated, the subject ingested a dose of arginine (5, 9 or 13 g) or placebo (randomly assigned). Results Mean resting GH values for the placebo, 5, 9 and 13 g day were 0.76, 0.67, 2.0 and 0.79 μg/L ( n = 6), respectively. Integrated area under the curve was not different with 13 g (197.8 ± 65.7 min μg/L), yet it increased with 5 and 9 g compared with the placebo (301.5 ± 74.6, 524.28 ± 82.9 and 186.04 ± 47.8 min μg/L, respectively, P < 0.05). Mean peak GH levels were 2.9 ± 0.69, 3.9 ± 0.85, 6.4 ± 1.3 and 4.73 ± 1.27 μg/L on each day for the placebo, 5, 9 and 13 g days. Conclusion In conclusion, 5 and 9 g of oral arginine caused a significant GH response. A 13 g dose of arginine resulted in considerable gastrointestinal distress in most subjects without augmentation in the GH response. The rise in GH concentration started ∼30 min after ingestion and peaked ∼60 min post ingestion.

Role of increased insulin demand in the adaptation of the endocrine pancreas to pregnancy.

During gestation the demand for insulin increases due to a decrease in insulin sensitivity of the maternal tissues. Simultaneously, pancreatic islet-cell proliferation, as well as insulin production and secretion increase. Both phenomena appear to be caused by the actions of pregnancy hormones. We studied the relationship between the two phenomena by investigating whether the supply of exogenous insulin affects the secretion of pregnancy hormones and islet function during gestation. For that purpose rats were treated with high doses of insulin (4.8 IU day-1 by sub-cutaneous osmotic mini pumps) so that the endogenous demand for insulin was fully satisfied from day 8-14 of gestation. Euglycaemia (5.0 mM) was maintained by intra venous infusion of glucose. The treatment suppressed insulin synthesis, as measured by in situ hybridization, in both pregnant and cyclic rats. In addition, in pregnant rats the increments in insulin secretion and in islet-cell proliferation were partly prevented. Furthermore, the data also suggest that in pregnant rats the treatment partly prevented the decrease in insulin sensitivity. Finally, the treatment did not affect the plasma concentrations of progesterone, prolactin and placental lactogen, but prevented the rise in growth hormone concentrations in pregnant rats. The present data suggest that, next to direct effects of pregnancy hormones and growth hormone on the pancreatic islets, a decreased insulin sensitivity in the maternal tissues, induced by actions of the same hormones, is involved in the regulation of islet function during gestation.

Test of growth hormone secretion in adults: poor reproducibility of the insulin tolerance test.

The insulin tolerance test (ITT) is regarded as the most reliable provocative test in the diagnosis of growth hormone (GH) deficiency in adults. In the present study the test was evaluated by investigating the range of GH responses in normal adult males and females and the intra-individual reproducibility of the test. Sixteen healthy non-obese adults, eight males (median age 31.5 years) and eight females (median age 31.8 years) were tested twice with the ITT, with a minimum of 72 h between each test. The females were tested between day 3 and day 10 of their menstrual cycles. Adequate hypoglycemia was achieved in all cases with a median nadir blood glucose of 1.3 mmol/l (range 0.8-2.0). Growth hormone in serum was measured by immunoradiometric assay and low values were confirmed by a different assay. Median peak GH concentration responses to the ITT were: in males 27.9 micrograms/l, range 5.0-71.1 (test 1) and 30.5 micrograms/l, range 7.9-69.5 (test 2); and in females 9.0 micrograms/l, range 4.1-17.9 (test 1) and 8.4 micrograms/l, range 0.09-42.4 (test 2). The rise in GH concentration during the ITT was higher in males than in females. In the males, all stimulated GH values were > or = 5.0 micrograms/l. In the females, four out of 16 tests gave values below 5.0 micrograms/l and in one test the GH value was around the detection limit of the assays. There was poor reproducibility during repeated testing, with no correlation between the results of the two tests. The results did not correlate to the magnitude of the hypoglycemia.(ABSTRACT TRUNCATED AT 250 WORDS)

Oral glucose inhibits growth hormone secretion induced by human pancreatic growth hormone releasing factor 1-44 in normal man.

The interaction between the inhibitory effect on growth hormone secretion of a 75 g oral glucose load and the stimulatory effect of human pancreatic growth hormone releasing factor 1-44 (hpGRF 1-44, 10 micrograms i.v.) has been studied in six normal subjects. hpGRF 1-44 alone induced a rise in growth hormone concentrations (maximum mean +/- SEM, 16.5 +/- 1.7 mU/l 15 min after injection) while growth hormone levels were suppressed by oral glucose alone (less than 1.5 mU/l from 45 to 135 min after glucose ingestion). When hpGRF 1-44 was injected 60 min after oral glucose, the growth hormone response was attenuated (maximum, 6.7 +/- 1.4 mU/l at 15 min, P less than 0.05). Increments of blood glucose within the physiological range diminish the growth hormone response to hpGRF 1-44 in normal man.

Effect of growth hormone on acute glucagon and insulin release.

The aim was to clarify whether or not sudden spike concentrations of plasma growth hormone (GH) can affect the endocrine pancreas in vivo. The peaking of GH was reproduced by an injection (10 mg/kg iv) of bovine GH to anesthetized normal, pancreatectomized, and alloxan-diabetic dogs. In portal but not in peripheral blood, immunoreactive plasma glucagon (IRG), glucagon-like activity (GLI), and immunoreactive insulin (IRI), were significantly elevated within 10 min in normal and alloxan-diabetic dogs. In pancreatectomized dogs, GH did not affect either IRG or GLI. When a physiological dose of GH (6 microgram/kg) calculated to produce ambient peak plasma concentrations of 40 ng/ml was given to four conscious, normal dogs with indwelling portal catheters, a rise of IRG from 108 +/- 19 to 170 +/- 17 pg/ml and of IRI from 20 +/- 12 to 67 +/- 19 muU/ml (mean +/- SE) occurred within 2 min. GLI was not affected. Thus a sudden rise in GH concentration can stimulate the release of a) GLI in the presence but not in the absence of the pancreas, and b) pancreatic IRG and IRI but not extrapancreatic IRG.