Weight loss and wrestling training: effects on nutrition, growth, maturation, body composition, and strength

Roemmich, James N., and Wayne E. Sinning. Weight lossand wrestling training: effects on nutrition, growth, maturation, bodycomposition, and strength. J. Appl.Physiol. 82(6): 1751-1759, 1997.Adolescentwrestlers (n = 9, 15.4 yr) andrecreationally active control adolescent males(n = 7, 15.7 yr) were measured before,at the end (late season), and 3.5-4 mo after a wrestling season toassess the influence of dietary restriction on growth, maturation, bodycomposition, protein nutrition, and muscular strength. Controlsconsumed adequate amounts of energy, carbohydrate (CHO), protein, andfat, and demonstrated normal gains in weight, fat mass (FM) andfat-free mass (FFM). Wrestlers consumed a high-CHO (61 ± 2% kcal),low-fat (24 ± 2% kcal) diet during the season but did not consumeadequate energy (24.7 ± 3.5 kcal · kg¹ · day¹)or protein (0.9 g · kg¹ · day¹).Deficient dietary intake reduced prealbumin levels (26.0 ± 1.9 vs.20.2 ± 0.9 mg/dl) and slowed the accrual of lean arm and thigh cross-sectional muscle areas(A_XSECT,T_XSECT, respectively). Forwrestlers, dietary deficiency also decreased weight (60.3 ± 3.5 to58.0 ± 3.3 kg), relative fat (9.9 ± 0.5 to 8.0 ± 0.7%), and FM (6.0 ± 0.5 to 4.7 ± 0.6 kg). Postseason,wrestlers and controls consumed similar diets, and wrestlers hadsignificant increases in prealbumin,A_XSECT, andT_XSECT. Wrestlers also increased their weight (6.1 ± 0.6 kg), FFM (3.0 ± 0.6 kg), and FM (3.2 ± 0.5 kg) postseason. Rates of bone maturation and segmental growth were not different between the groups. The wrestlers hadreductions in elbow and knee strength from preseason to late season butincreases postseason. Lean tissue changes were associated with thechanges in strength and power (r = 0.72-0.91, P < 0.001). Aftercovariance for FFM or limb-specific cross section, few significantchanges remained. In conclusion, dietary restriction reduced proteinnutrition and muscular performance but produced little effect on linear growth and maturation. Prealbumin levels and the rate of lean tissueaccrual were positively related (r = 0.43, P  0.05).

     

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

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 cyclingexercise on circulating growth hormone (GH), insulin-like growthfactors I and II (IGF-I and -II), and insulin-like growth factorbinding 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 thefollicular 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. GHincreased significantly in response to exercise under bothE₂ conditions. 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 increasein IGF BP-3 30 min after exercise for the periovulatory study. Thesefindings indicate that the modulation of GH secretion associated withmenstrual cycle variations in circulatingE₂ affects GH measured afterexercise, at least in part, by an increase in baseline levels. Theacute increase in IGF-I induced by exercise appears to be independentof the GH response and is not affected by menstrual cycle timing.

     

Human growth hormone response to repeated bouts of aerobic exercise

Kanaley, J. A., J. Y. Weltman, J. D. Veldhuis, A. D. Rogol,M. L. Hartman, and A. Weltman. Human growth hormone response torepeated bouts of aerobic exercise. J. Appl.Physiol. 83(5): 1756-1761, 1997.We examinedwhether repeated bouts of exercise could override growth hormone (GH)auto-negative feedback. Seven moderately trained men were studied onthree occasions: a control day (C), a sequential exercise day (SEB; at1000, 1130, and 1300), and a delayed exercise day (DEB; at 1000, 1400, and 1800). The duration of each exercise bout was 30 min at 70%maximal O₂ consumption (O_{2 max}) on a cycleergometer. Standard meals were provided at 0600 and 2200. GH wasmeasured every 5-10 min for 24 h (0800-0800). Daytime(0800-2200) integrated GH concentrations were ~150-160% greater during SEB and DEB than during C: 1,282 ± 345, 3,192 ± 669, and 3,389 ± 991 min · µg · l¹for C, SEB, and DEB, respectively [SEB > C(P < 0.06), DEB > C(P < 0.03)]. There were nodifferences in GH release during sleep (2300-0700). Deconvolutionanalysis revealed that the increase in 14-h integrated GH concentrationon DEB was accounted for by an increase in the mass of GH secreted perpulse (per liter of distribution volume,l_v): 7.0 ± 2.9 and 15.9 ± 2.6 µg/l_v for C and DEB,respectively (P < 0.01). Comparisonof 1.5-h integrated GH concentrations on the SEB and DEB days (30 minexercise + 60 min recovery) revealed that, with each subsequentexercise bout, GH release apparently increased progressively, with aslightly greater increase on the DEB day [SEB vs. DEB: 497 ± 162 vs. 407 ± 166 (bout 1), 566 ± 152 vs. 854 ± 184 (bout2), and 633 ± 149 vs. 1,030 ± 352 min · µg · l¹(bout 3),P < 0.05]. We conclude thatthe GH response to acute aerobic exercise is augmented with repeatedbouts of exercise.

     

IGF-I and/or growth hormone preserve diaphragm fiber size with moderate malnutrition

Resistance to theanabolic effects of growth hormone (GH) occurs with severe caloricdeficit. This study examined whether moderate caloric deficit (50% ofdaily intake for 7 days) in the adolescent rat exceeds a criticalthreshold for GH action and whether a combination of GH andinsulin-like growth factor I (IGF-I) would have enhanced anaboliceffects on the diaphragm (Dia). Five groups of rats (4 wk old) werestudied: 1) control (Ctl),2) nutritionally deprived (ND),3) ND + GH,4) ND + IGF-I, and5) ND + GH + IGF-I. IGF-I was givenby continuous infusion (200 µg/day). GH was injected subcutaneously(250 µg every 12 h). Contractile and fatigue properties of the Diawere determined in vitro. Quantitative histochemical methods were usedto determine Dia fiber type proportions, cross-sectional areas, andsuccinate dehydrogenase activities. The body weight of Ctl ratsincreased 46% compared with 7% in ND animals, whereas that of ND ratsreceiving growth factors was intermediate. Serum IGF-I levels werereduced 54% in ND animals and maintained with the provision of growthfactors. Dia fatigue resistance was improved in ND animals receivinggrowth factors. There were no differences in Dia contractileproperties, fiber type proportions, or succinate dehydrogenaseactivities across groups. ND resulted in atrophy/growth arrest of allDia fibers (20-32%) compared with Ctl. Administration of IGF-Iand/or GH completely prevented atrophy/growth arrest of all Diafibers. No additive or synergistic effects were noted. We propose thatthese growth factors may provide useful short-term adjunctivenutritional support in circumstances in which the provision of optimalnutrition may be delayed or inadequate.

     

Insulin-like growth factor I (IGF-I) in a growth-enhanced transgenic (GH-overexpressing) bony fish,the tilapia (<Emphasis Type="Italic">Oreochromis niloticus</Emphasis>): indication for a higher impact of autocrine/paracrine than of endocrine IGF-I

Several lines of growth hormone (GH)-overexpressing fish have been produced and analysed for growth and fertility parameters. However, only few data are available on the growth-promoting hormone insulin-like growth factor I (IGF-I) that mediates most effects of GH, and these are contradictory. Using quantitative real-time RT-PCR, radioimmunoassay, in situ hybridization, immunohistochemistry, and radiochromatography we investigated IGF-I and IGF binding proteins (IGFBPs) in an adult (17 months old) transgenic (GH-overexpressing) tilapia (Oreochromis niloticus). The transgenics showed an around 1.5-fold increase in length and an approximately 2.3-fold higher weight than the non-transgenics. Using radioimmunoassay, the serum IGF-I levels were lower (6.22 ± 0.75 ng/ml) in transgenic than in wild-type (15.01 ± 1.49 ng/ml) individuals (P = 0.0012). Radioimmunoassayable IGF-I in transgenic liver was 4.2-times higher than in wild-type (16.0 ± 2.21 vs. 3.83 ± 0.71 ng/g, P = 0.0017). No hepatocytes in wild-type but numerous hepatocytes in transgenic liver contained IGF-I-immunoreactivity. RT-PCR revealed a 1.4-times higher IGF-I mRNA expression in the liver of the transgenics (10.51 ± 0.82 vs. 7.3 ± 0.49 pg/μg total RNA, P = 0.0032). In correspondence, in situ hybridization showed more IGF-I mRNA containing hepatocytes in the transgenics. A twofold elevated IGF-I mRNA expression was determined in the skeletal muscle of transgenics (0.33 ± 0.02 vs. 0.16 ± 0.01 pg/μg total RNA, P < 0.0001). Both liver and serum of transgenics showed increased IGF-I binding. The increased IGFBP content in the liver may lead to retention of IGF-I, and/or the release of IGF-I into the circulation may be slower resulting in accumulation of IGF-I in the hepatocytes. Our results indicate that the enhanced growth of the transgenics likely is due to enhanced autocrine/paracrine action of IGF-I in extrahepatic sites, as shown here for skeletal muscle.     

Effect of insulin-like growth factor I and/or growth hormone on diaphragm of malnourished adolescent rats

Lewis, Michael I., Thomas J. LoRusso, and Mario Fournier.Effect of insulin-like growth factor I and/or growthhormone on diaphragm of malnourished adolescent rats.J. Appl. Physiol. 82(4):1064-1070, 1997.Young growing animals appear to havesignificantly reduced "nutritional reserve" to short periods ofunstressed starvation compared with adults, with resultant growtharrest and/or atrophy of diaphragm (Dia) muscle fibers. The aimof this study was to assess in an adolescent rat model of acutenutritional deprivation (ND; 72 h) the impact of insulin-like growthfactor I (IGF-I), with or without added growth hormone (GH), on thecross-sectional areas (CSA) of individual Dia muscle fibers. Fivegroups were studied: 1) control(Ctr); 2) ND;3) ND given IGF-I (ND/IGF-I); 4) ND given GH (ND/GH); and5) ND given a combination of IGF-I and GH (ND/IGF-I/GH). IGF-I was given by a subcutaneously implanted osmotic minipump (200 µg/day), whereas GH was administered twice daily by a subcutaneous injection (250 µg every 12 h). Isometric contractile and fatigue properties of the Dia were determined in vitro.Forces were normalized for muscle CSA (i.e., specific force). Dia fibertype proportions were determined histochemically, and fiber CSA wasquantified by using a computer-based image-processing system. Totalserum IGF-I concentrations were significantly reduced in ND and ND/GHanimals, compared with Ctr, and elevated in the groups receiving IGF-I.The provision of growth factors did not alter the contractile orfatigue properties of ND animals. Dia fiber type proportions weresimilar among the groups. In ND animals, there was a significantreduction in the CSA of types I, IIa, IIx, and IIc Dia fibers comparedwith Ctr. The administration of IGF-I alone or in combination with GHto ND animals significantly diminished the reduction in Dia fiber size.GH alone had no effect on Dia fiber size in ND animals. We concludethat with acute ND the peripheral resistance to the action of GHappears to be bypassed by the administration of IGF-I alone or incombination with GH.

     

Maintenance of myonuclear domain size in rat soleus after overload and growth hormone/IGF-I treatment

The purpose ofthis study was to determine the effects of functional overload (FO)combined with growth hormone/insulin-like growth factor I (GH/IGF-I)administration on myonuclear number and domain size in rat soleusmuscle fibers. Adult female rats underwent bilateral ablation of theplantaris and gastrocnemius muscles and, after 7 days of recovery, wereinjected three times daily for 14 days with GH/IGF-I (1 mg/kg each; FO + GH/IGF-I group) or saline vehicle (FO group). Intact rats receivingsaline vehicle served as controls (Con group). Muscle wet weight was32% greater in the FO than in the Con group: 162 ± 8 vs. 123 ± 16 mg. Muscle weight in the FO + GH/IGF-I group (196 ± 14 mg) was59 and 21% larger than in the Con and FO groups, respectively. Meansoleus fiber cross-sectional area of the FO + GH/IGF-I group (2,826 ± 445 µm²) was increasedcompared with the Con (2,044 ± 108 µm²) and FO (2,267 ± 301 µm²) groups. The difference infiber size between the FO and Con groups was not significant. Meanmyonuclear number increased in FO (187 ± 15 myonuclei/mm) and FO + GH/IGF-I (217 ± 23 myonuclei/mm) rats compared with Con (155 ± 12 myonuclei/mm) rats, although the difference between FO and FO + GH/IGF-I animals was not significant. The mean cytoplasmic volume permyonucleus (myonuclear domain) was similar across groups. These resultsdemonstrate that the larger mean muscle weight and fibercross-sectional area occurred when FO was combined with GH/IGF-Iadministration and that myonuclear number increased concomitantly withfiber volume. Thus there appears to be some mechanism(s) that maintainsthe myonuclear domain when a fiber hypertrophies.

     

Brain natriuretic peptide inhibits hypoxic pulmonary hypertension in rats

Brainnatriuretic peptide (BNP) is a pulmonary vasodilator that is elevatedin the right heart and plasma of hypoxia-adapted rats. To test thehypothesis that BNP protects against hypoxic pulmonary hypertension, wemeasured right ventricular systolic pressure (RVSP), right ventricle(RV) weight-to-body weight (BW) ratio (RV/BW), and percentmuscularization of peripheral pulmonary vessels (%MPPV) in rats givenan intravenous infusion of BNP, atrial natriuretic peptide (ANP), orsaline alone after 2 wk of normoxia or hypobaric hypoxia (0.5 atm).Hypoxia-adapted rats had higher hematocrits, RVSP, RV/BW, and %MPPVthan did normoxic controls. Under normoxic conditions, BNP infusion(0.2 and 1.4 µg/h) increased plasma BNP but had no effect on RVSP,RV/BW, or %MPPV. Under hypoxic conditions, low-rate BNP infusion (0.2 µg/h) had no effect on plasma BNP or on severity of pulmonaryhypertension. However, high-rate BNP infusion (1.4 µg/h) increasedplasma BNP (69 ± 8 vs. 35 ± 4 pg/ml, P < 0.05),lowered RV/BW (0.87 ± 0.05 vs. 1.02 ± 0.04, P < 0.05), and decreased %MPPV (60 vs. 74%,P < 0.05). There was also a trend towardlower RVSP (55 ± 3 vs. 64 ± 2, P = not significant).Infusion of ANP at 1.4 µg/h increased plasma ANP in hypoxic rats (759 ± 153 vs. 393 ± 54 pg/ml, P < 0.05) but had noeffect on RVSP, RV/BW, or %MPPV. We conclude that BNP may regulatepulmonary vascular responses to hypoxia and, at the doses used in thisstudy, is more effective than ANP at blunting pulmonary hypertensionduring the first 2 wk of hypoxia.

     

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

Kraemer, R. R., L. G. Johnson, R. Haltom, G. R. Kraemer, H. Gaines, M. Drapcho, T. Gimple, and V. Daniel Castracane. Effects of hormone replacement on growth hormone and prolactin exercise responses in postmenopausal women. J. Appl.Physiol. 84(2): 703-708, 1998.Exercise elevatesgrowth hormone (GH) and prolactin (PRL) blood concentrations inpremenopausal women. Postmenopausal women taking hormone replacementtherapy (HRT) maintain higher estrogen levels that could affect GH andPRL. The purpose of the study was to determine the effects of HRT on GHand PRL responses to treadmill exercise. Seventeen healthy women whowere postmenopausal (naturally or surgically) [8 on HRT; 9 not onHRT (NHRT)], completed 30 min of treadmill exercise at 79.16 ± 1.2% maximal O₂ consumption (HRT group) and 80.19 ± 0.91% maximalO₂ consumption (NHRT group). Bloodsamples were collected from an intravenous catheter during an exercisesession and during a control session without exercise. GH and PRLconcentrations were significantly higher in the exercise trial than inthe nonexercise trial, whereas resting concentrations were similar forboth 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 inthe exercise trial were significantly higher for HRT than for NHRTsubjects. This is the first study to demonstrate that HRT enhancestreadmill-exercise-induced GH release and that similar PRL responses totreadmill exercise occur in postmenopausal women regardless of HRTstatus.

     

Anabolic influences of insulin-like growth factor I and/or growth hormone on the diaphragm of young rats

Lewis, Michael I., Thomas J. LoRusso, and Mario Fournier.Anabolic influences of insulin-like growth factor I and/or growth hormone on the diaphragm of young rats. J. Appl. Physiol. 82(6): 1972-1978, 1997.It iscontroversial whether insulin-like growth factor I (IGF-I), growthhormone (GH), or their combination might enhance body growthand/or tissue anabolism in the well-fed animal with an intactsomatotrophic axis. To assess this further, we studied four groups ofadolescent rats: 1) control (Ctr),2) GH,3) IGF-I, and4) GH/IGF-I. IGF-I was given via anosmotic minipump, whereas GH was injected subcutaneously for a period of 72 h. Diaphragm (Dia) contractile and fatigue properties were determined in vitro. Quantitative histochemical and morphometric analyses were performed on Dia fibers. Total serum IGF-I levels weresignificantly increased in the groups receiving growth factors. Although body weight increased to a greater extent in the animals receiving growth factors, a further synergistic effect was noted in theGH/IGF-I animals compared with either GH or IGF-I groups. Costal Diamass was greater in the groups receiving growth factors. The Dia ofGH/IGF-I animals was more fatigue resistant than the Dia in Ctr. Thecross-sectional area of types IIa and IIx fibers were increased to asimilar extent in all groups receiving growth factors compared withCtr. Succinate dehydrogenase activity of type IIa fibers wassignificantly greater in the GH/IGF-I animals compared with the othergroups. We conclude that the short-term provision of growth factors towell-nourished, normally growing adolescent rats can accelerate bodygrowth and promote selective hypertrophy of predominantly type II Diafibers.

     

Left ventricular dysfunction following rewarming from experimental hypothermia

This study was aimed at elucidating whetherventricular hypothermia-induced dysfunction persisting after rewarmingthe unsupported in situ dog heart could be characterized as a systolic,diastolic, or combined disturbance. Core temperature of 8 mongrel dogswas gradually lowered to 25°C and returned to 37°C over aperiod of 328 min. Systolic function was described by maximum rate ofincrease in left ventricular (LV) pressure(dP/dt_max),relative segment shortening (SS%), stroke volume (SV), and theload-independent contractility index, preload recruitable stroke work(PRSW). Diastolic function was described by the isovolumic relaxationconstant () and the LV wall stiffness constant(K_p). Comparedwith prehypothermic control, a significant decrease in LV functionalvariables was measured at 25°C:dP/dt_max 2,180 ± 158 vs. 760 ± 78 mmHg/s, SS% 20.1 ± 1.2 vs.13.3 ± 1.0%, SV 11.7 ± 0.7 vs. 8.5 ± 0.7 ml, PRSW 90.5 ± 7.7 vs. 29.1 ± 5.9 J/m · 10²,K_p 0.78 ± 0.10 vs. 0.28 ± 0.03 mm¹, and  78.5 ± 3.7 vs. 25.8 ± 1.6 ms. After rewarming, the significant depression ofLV systolic variables observed at 25°C persisted: dP/dt_max 1,241 ± 108 mmHg/s, SS% 10.2 ± 0.8 J, SV 7.3 ± 0.4 ml, and PRSW52.1 ± 3.6 m · 10², whereasthe diastolic values ofK_p and  returned to control. Thus hypothermia induced a significant depressionof both systolic and diastolic LV variables. After rewarming, diastolicLV function was restored, in contrast to the persistently depressed LVsystolic function. These observations indicate that cooling inducesmore long-lasting effects on the excitation-contraction coupling and the actin-myosin interaction than on sarcoplasmicreticulum Ca²⁺trapping dysfunction or interstitial fluid content, makingposthypothermic LV dysfunction a systolic perturbation.

     

Effects of a competitive wrestling season on body composition, strength, and power in National Collegiate Athletic Association Division III college wrestlers

The purpose of this study was to investigate the effects of a competitive wrestling season on body composition, muscular strength, and muscular power in National Collegiate Athletic Association (NCAA) Division III college wrestlers. A total of 10 wrestlers were assessed throughout 2 consecutive wrestling seasons in late October, late January (midseason), and late March (postseason). Measurements included body weight, body composition (6-site skinfold), muscular strength (back squats and bench press), and muscular power (e.g., power cleans, vertical jump, seated medicine ball put). A repeated-measures analysis of variance (ANOVA) showed no significant changes in body weight, percentage of body fat, or fat-free mass (FFM) from pre- to mid- to postseason (body weight, 77.9 +/- 12.4, 75.7 +/- 11.0, and 79.9 +/- 12.8 kg; percentage of body fat, 11.6 +/- 3.9, 10.5 +/- 3.0, and 12.0 +/- 3.4; FFM, 68.5 +/- 8.7, 67.5 +/- 8.2, and 70.0 +/- 9.0 kg). A statistically significant main effect of time (p < 0.01) was observed for muscular strength, as both the back squat and bench press measures were lower at midseason (back squat, 150.8 +/- 25.2 kg; bench press, 98.3 +/- 25.4 kg) than at pre- and postseason (back squat, 157.9 +/- 25.5 and 161.4 +/- 25.6; bench press, 103.4 +/- 25.5 and 106.4 +/- 26.0). Muscular power did not change significantly throughout the wrestling season. These data indicate that Division III college wrestlers remain relatively weight stable with little change in body composition during a competitive wrestling season. While muscular power is apparently maintained, muscular strength may decline slightly. Our findings suggest that these wrestlers benefit from a training program that emphasizes in-season strength maintenance.     

Growth hormone/IGF-I and/or resistive exercise maintains myonuclear number in hindlimb unweighted muscles

Allen, David L., Jon K. Linderman, Roland R. Roy, Richard E. Grindeland, Venkat Mukku, and V. Reggie Edgerton. Growth hormone/IGF-I and/or resistive exercise maintains myonuclearnumber in hindlimb unweighted muscles. J. Appl.Physiol. 83(5): 1857-1861, 1997.In the presentstudy of rats, we examined the role, during 2 wk ofhindlimb suspension, of growth hormone/insulin-like growth factor I(GH/IGF-I) administration and/or brief bouts of resistance exercise in ameliorating the loss of myonuclei in fibers of the soleusmuscle that express type I myosin heavy chain. Hindlimb suspensionresulted in a significant decrease in mean soleus wet weight that wasattenuated either by exercise alone or by exercise plus GH/IGF-Itreatment but was not attenuated by hormonal treatment alone. Both meanmyonuclear number and mean fiber cross-sectional area (CSA) of fibersexpressing type I myosin heavy chain decreased after 2 wk of suspensioncompared with control (134 vs. 162 myonuclei/mm and 917 vs. 2,076 µm², respectively). NeitherGH/IGF-I treatment nor exercise alone affected myonuclear number orfiber CSA, but the combination of exercise and growth-factor treatmentattenuated the decrease in both variables. A significant correlationwas found between mean myonuclear number and mean CSA across allgroups. Thus GH/IGF-I administration and brief bouts of muscle loadinghad an interactive effect in attenuating the loss of myonuclei inducedby chronic unloading.

     

Surgical Reintervention in Acromegaly: is it Still worth trying?

Background and ObjectiveThere has not been a formal evaluation of how frequently and to what extent surgical reintervention in patients with persistently active acromegaly may achieve significant, albeit incomplete, reductions in growth hormone (GH) and insulinlike growth factor-I (IGF-I) levels. Of importance, recent studies suggest that the response to radiotherapy and pharmacotherapy is better with lower degrees of hypersomatotropism. The objective of this study was to evaluate the outcome of surgical reintervention in patients with active acromegaly at our institution between 1995 and 2005.MethodsWe retrospectively evaluated the outcome in 53 patients with active acromegaly (49 with macroadenomas) who underwent a second operation a mean of 24.1 ± 25.2 months after the first intervention. Basal and postglucose GH as well as IGF-I levels were analyzed at diagnosis and after the first and second pituitary procedures.ResultsBasal GH decreased in 38 patients (72%): to < 10 ng/mL in 17 and to < 2.5 ng/mL in 11. The mean IGF- I index and basal GH decreased significantly after surgical reintervention: 1.7 ± 0.4 to 1.4 ± 0.4 (P = .0001) and 13.0 ± 12.8 to 8.3 ± 11.3 ng/mL (P = .0001), respectively. Some decrement in IGF-I was observed after surgical reintervention in 30 patients (57%), being greater than 30% in 9 (17%). Only 5 patients (9%) achieved complete biochemical cure (normal IGF-I and a postglucose GH level of < 1 ng/mL). Reoperation achieved a significant decline in basal and postglucose GH levels as well as in IGF-I index only in patients with noninvasive macroadenomas.ConclusionPituitary surgical reintervention in patients with acromegaly results in a low percentage of biochemical cure. If a remnant of a noninvasive macroadenoma is visible and accessible, however, such a procedure may significantly reduce GH and IGF-I levels. (Endocr Pract. 2009;15:431-437)     

Head-down-tilt bed rest alters forearm vasodilator and vasoconstrictor responses

To test thehypothesis that head-down-tilt bed rest (HDBR) for 14 days altersvascular reactivity to vasodilatory and vasoconstrictor stimuli, thereactive hyperemic forearm blood flow (RHBF, measured by venousocclusion plethysmography) and mean arterial pressure (MAP, measured byFinapres) responses after 10 min of circulatory arrest were measured ina control trial (n = 20) and whensympathetic discharge was increased by a cold pressor test (RHBF + coldpressor test; n = 10). Vascularconductance (VC) was calculated (VC = RHBF/MAP). In the control trial,peak RHBF at 5 s after circulatory arrest (34.1 ± 2.5 vs.48.9 ± 4.3 ml · 100 ml¹ · min¹)and VC (0.34 ± 0.02 vs. 0.53 ± 0.05 ml · 100 ml¹ · min¹ · mmHg¹)were reduced in the post- compared with the pre-HDBR tests(P < 0.05). Total excess RHBF over 3 min was diminished in the post- compared with the pre-HDBR trial (84.8 vs. 117 ml/100 ml, P < 0.002). Theability of the cold pressor test to lower forearm blood flow was lessin the post- than in the pre-HDBR test(P < 0.05), despite similarincreases in MAP. These data suggest that regulation of vasculardilation and the interaction between dilatory and constrictorinfluences were altered with bed rest.

     

Effects of short-term inactivity on glucose tolerance, energy expenditure, and blood flow in trained subjects

The purpose of this investigation was to examinethe effects of 7-10 days of inactivity (IA) on glucose tolerance(GT), resting metabolic rate (RMR), thermic effect of a meal (TEM), andlimb blood flow in endurance-trained men. Eight highly trained (peak O₂ consumption 64 ± 2 ml · kg¹ · min¹)endurance athletes participated in this study involving two identicaltest days, one ~24 h after a normal training bout (Tr) and the secondafter 7-10 days of IA. The following tests were conducted at eachvisit: 75-g oral glucose tolerance test (OGTT), RMR, and TEM andmeasurements of calf and forearm blood flow (BF) by using venousocclusive plethysmography. Body weight remained unchangedduring this short period of IA (Tr, 78.5 ± 1 kg; IA, 78.7 ± 1 kg). The area under the glucose and insulin curves increased 65% (Tr,3,375 ± 877 vs. IA, 5,559.4 ± 621 mg · dl¹ · 180 min¹) and 73% (Tr,2,182.5 ± 270 vs. IA, 3,793.1 ± 739 µU · ml¹ · 180 min¹) after IA,respectively (P < 0.01). RMRdecreased significantly (4%; 1.5 ± 0.02 vs. 1.44 ± 0.02 kcal/min; P < 0.05) and respiratory exchange ratio during the OGTT increased (4%, 0.812 ± 0.011 vs. 0.842 ± 0.009; P < 0.05) afterIA, whereas TEM increased similarly in the Tr and IA states. In the Trstate, mean calf BF increased by 22% (3.17 ± 0.22 vs. 3.87 ± 0.38 ml · 100 ml¹ · min¹;P < 0.05) during the OGTT butremained unchanged after IA, whereas no differences at rest or duringOGTTs existed between the two conditions for forearm BF. Incrementalinsulin area above fasting during the OGTT was correlated with meancalf BF in the Tr (r = 0.76, P < 0.05) and IA(r = 0.72, P < 0.05) states. In conclusion, 7-10 days of IA results in a deterioration in GT and a reduction in RMR. After glucose ingestion, calf BF was elevated compared withresting levels in the Tr state but was unchanged in the IA state;however, limb BF was not related to GT or RMR. Thus our findings raisequestions regarding the relative contribution of BF in modulatingglucose tolerance and energy expenditure in endurance athletes in theirhabitual Tr or IA state.

     

Hemodynamic and norepinephrine responses to pacing-induced heart failure in conscious sinoaortic-denervated dogs

Brändle, Marian, Kaushik P. Patel, Wei Wang, andIrving H. Zucker. Hemodynamic and norepinephrine responses topacing-induced heart failure in conscious sinoaortic-denervated dogs.J. Appl. Physiol. 81(4):1855-1862, 1996.The present study was undertaken to determinethe effects of chronic sinoaortic (baroreceptor) denervation (SAD) on the hemodynamic and sympathetic alterations thatoccur in the pacing-induced model of congestive heart failure. Twogroups of dogs were examined: intact(n = 9) and SAD(n = 9). Both groups of dogs werestudied in the control (prepace) state and each week after theinitiation of ventricular pacing at 250 beats/min. After the pacemakerwas turned off, hemodynamic and plasma norepinephrine levels returnedtoward control levels in the prepaced state and after 1 and 2 wk ofpacing. However, by 3 wk all hemodynamic and norepinephrine levelsremained relatively constant over the 10-min observation period withthe pacemaker off. With the pacemaker off, left ventricularend-diastolic pressure went from 2.7 ± 1.4 (SE) mmHg during theprepace state to 23.2 ± 2.9 mmHg in the heart failure state inintact dogs (P < 0.01). Leftventricular end-diastolic pressure increased to 27.1 ± 2.2 mmHgfrom a control level of 4.2 ± 1.9 mmHg in SAD dogs(P < 0.0003). Mean arterial pressuresignificantly decreased in intact and SAD dogs. Resting heart rate wassignificantly higher in SAD dogs and increased to 135.8 ± 8.9 beats/min in intact dogs and 136.1 ± 6.5 beats/min in SAD dogs.There were no significant differences in the hemodynamic parametersbetween intact and SAD dogs after pacing. Plasma norepinephrine wassignificantly lower in intact than in SAD dogs before pacing (197.7 ± 21.6 vs. 320.6 ± 26.6 pg/ml;P < 0.005). In the heart failurestate, plasma norepinephrine increased significantly in both intact(598.3 ± 44.2 pg/ml) and SAD (644.0 ± 64.6 pg/ml) groups. Therewere no differences in the severity or the magnitude of the developedheart failure state in SAD vs. intact dogs. We conclude from these datathat the arterial baroreflex is not the sole mechanism for the increasein sympathetic drive in heart failure.

     

Enhanced brain natriuretic peptide response to peak exercise in heart transplant recipients

We investigatedthe atrial (ANP) and brain natriuretic peptides (BNP), catecholamines,heart rate, and blood pressure responses to graded upright maximalcycling exercise of eight matched healthy subjects andcardiac-denervated heart transplant recipients (HTR). Baseline heart rate and diastolic blood pressure, together with ANP(15.2 ± 3.7 vs. 4.4 ± 0.8 pmol/l;P < 0.01) and BNP (14.3 ± 2.6 vs. 7.4 ± 0.6 pmol/l; P < 0.01), were elevated in HTR, but catecholamine levels were similarin both groups. Peak exercise O₂uptake and heart rate were lower in HTR. Exercise-inducedmaximal ANP increase was similar in both groups (167 ± 34 vs. 216 ± 47%). Enhanced BNP increase was significant only in HTR (37 ± 8 vs. 16 ± 8%; P < 0.05).Similar norepinephrine but lower peak epinephrine levels were observedin HTR. ANP and heart rate changes from rest to 75% peak exercise werenegatively correlated (r = 0.76, P < 0.05),and BNP increase was correlated with left ventricular mass index(r = 0.83, P < 0.01) after hearttransplantation. Although ANP increase was notexaggerated, these data support the idea that the chronotropiclimitation secondary to sinus node denervation might stimulate ANPrelease during early exercise in HTR. Furthermore, the BNPresponse to maximal exercise, which is related to the left ventricularmass index of HTR, is enhanced after heart transplantation.

     

Effects of the ovarian cycle on sympathetic neural outflow during static exercise

We comparedreflex responses to static handgrip at 30% maximal voluntarycontraction (MVC) in 10 women (mean age 24.1 ± 1.7 yr) during twophases of their ovarian cycle: the menstrual phase (days 1-4) and the follicularphase (days10-12). Changes in muscle sympathetic nerve activity (MSNA; microneurography) in response tostatic exercise were greater during the menstrual compared withfollicular phase (phase effect P = 0.01). Levels of estrogen were less during the menstrual phase(75 ± 5.5 vs. 116 ± 9.6 pg/ml, days 1-4 vs.days 10-12;P = 0.002). Generated tension did not explain differences in MSNA responses (MVC: 29.3 ± 1.3 vs. 28.2 ± 1.5 kg, days 1-4 vs.days 10-12;P = 0.13). In a group of experiments with the use of ³¹P-NMRspectroscopy, no phase effect was observed forH⁺ andH₂PO₄ concentrations(n = 5). During an ischemicrhythmic handgrip paradigm (20% MVC), a phase effect was notobserved for MSNA or H⁺ orH₂PO₄ concentrations,suggesting that blood flow was necessary for the expression of thecycle-related effect. The present studies suggest that, during statichandgrip exercise, MSNA is increased during the menstrual compared withthe follicular phase of the ovarian cycle.

     

Subnormal norepinephrine release relates to presyncope in astronauts after spaceflight

Fritsch-Yelle, Janice M., Peggy A. Whitson, Roberta L. Bondar, and Troy E. Brown. Subnormal norepinephrine release relates to presyncope in astronauts after spaceflight.J. Appl. Physiol. 81(5):2134-2141, 1996.Postflight orthostatic intolerance isexperienced by virtually all astronauts but differs greatly in degreeof severity. We studied cardiovascular responses to upright posture in40 astronauts before and after spaceflights lasting up to 16 days. Weseparated individuals according to their ability to remain standingwithout assistance for 10 min on landing day. Astronauts who could notremain standing on landing day had significantly smaller increases inplasma norepinephrine levels with standing than did those who couldremain standing (105 ± 41 vs. 340 ± 62 pg/ml;P = 0.05). In addition, they hadsignificantly lower standing peripheral vascular resistance (23 ± 3 vs. 34 ± 3 mmHg ^· l^{1 ·} min;P = 0.02) and greater decreases insystolic (28 ± 4 vs. 11 ± 3 mmHg;P = 0.002) and diastolic (14 ± 7 vs. 3 ± 2 mmHg; P = 0.0003) pressures. The presyncopal group also hadsignificantly lower supine (16 ± 1 vs. 21 ± 2 mmHg ^· l^{1 ·} min;P = 0.04) and standing (23 ± 2 vs.32 ± 2 mmHg ^· l^{1 ·} min;P = 0.038) vascular resistance, supine(66 ± 2 vs. 73 ± 2 mmHg; P = 0.008) and standing (69 ± 4 vs. 77 ± 2 mmHg;P = 0.007) diastolic pressure, andsupine (109 ± 3 vs. 114 ± 2 mmHg; P = 0.05) and standing (99 ± 4 vs. 108 ± 3 mmHg; P = 0.006) systolic pressures before flight. This is the first study toclearly document these differences among presyncopal and nonpresyncopalastronauts after spaceflight and also offer the possibility ofpreflight prediction of postflight susceptibility. These resultsclearly point to hypoadrenergic responsiveness, possibly centrallymediated, as a contributing factor in postflight orthostaticintolerance. They may provide insights into autonomic dysfunction inEarthbound patients.