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The purpose of the present study was to determine whether age, sex, or angiotensin I-converting enzyme (ACE) genotype influences the effects of strength training (ST) on glucose homeostasis. Nineteen sedentary young (age = 20-30 yr) men (n = 10) and women (n = 9) were studied and compared with 21 sedentary older (age = 65-75 yr) men (n = 12) and women (n = 9) before and after a 6-mo total body ST program. Fasting insulin concentrations were reduced in young men and in older men with ST (P < 0.05 in both). In addition, total insulin area under the curve decreased by 21% in young men (P < 0.05), and there was a trend for a decrease (11%) in older men (P = 0.06). No improvements in insulin responses were observed in young or older women. The ACE deletion/deletion genotype group had the lowest fasting insulin and insulin areas under the oral glucose tolerance test (OGTT) curve before training (all P < 0.05), but those with at least one insertion allele had a trend for a greater reduction in total insulin area than deletion homozygotes (P = 0.07). These results indicate that ST has a more favorable effect on insulin response to an OGTT in men than in women and offer some support for the hypothesis that ACE genotype may influence insulin responses to ST.

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PURPOSE: The purpose of this study was to compare age and gender effects of strength training (ST) on resting metabolic rate (RMR), energy expenditure of physical activity (EEPA), and body composition. METHODS: RMR and EEPA were measured before and after 24 wk of ST in 10 young men (20-30 yr), 9 young women (20-30 yr), 11 older men (65-75 yr), and 10 older women (65-75 yr). RESULTS: When all subjects were pooled together, absolute RMR significantly increased by 7% (5928 +/- 1225 vs 6328 +/- 1336 kJ.d-1, P < 0.001). Furthermore, ST increased absolute RMR by 7% in both young (6302 +/- 1458 vs 6719 +/- 1617 kJ x d(-1), P < 0.01) and older (5614 +/- 916 vs 5999 +/- 973 kJ x d(-1), P < 0.05) subjects, with no significant interaction between the two age groups. In contrast, there was a significant gender x time interaction (P < 0.05) for absolute RMR with men increasing RMR by 9% (6645 +/- 1073 vs 7237 +/- 1150 kJ x d(-1), P < 0.001), whereas women showed no significant increase (5170 +/- 884 vs 5366 +/- 692 kJ x d(-1), P = 0.108). When RMR was adjusted for fat-free mass (FFM) using ANCOVA, with all subjects pooled together, there was still a significant increase in RMR with ST. Additionally, there was still a gender effect (P < 0.05) and no significant age effect (P = NS), with only the men still showing a significant elevation in RMR. Moreover, EEPA and TEE estimated with a Tritrac accelerometer and TEE estimated by the Stanford Seven-Day Physical Activity Recall Questionnaire did not change in response to ST for any group. CONCLUSIONS: In conclusion, changes in absolute and relative RMR in response to ST are influenced by gender but not age. In contrast to what has been suggested previously, changes in body composition in response to ST are not due to changes in physical activity outside of training.

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OBJECTIVES: To determine the effects of resistive training (RT) on insulin action and assess the determinants of the changes in insulin action. DESIGN: Longitudinal study. SETTING: Outpatient setting. PARTICIPANTS: Eighteen older men and older postmenopausal women (65-74 years) with normal (6 men and 5 women) or impaired glucose tolerance (4 men and 3 women). INTERVENTION: Six months of progressive whole-body RT. MEASUREMENTS: Upper and lower body strength was assessed by the one repetition maximum test. Total body fat and fat-free mass (FFM) were determined by dual-energy x-ray absorptiometry before and after 6 months of RT. Insulin sensitivity was estimated from the relationship of glucose utilization (M) to the concentration of insulin (I) during the last 30 minutes of 3-hour hyperinsulinemic-euglycenic clamps (240 pmol x min(-2) x min(-1)) (M/I) before and after RT. RESULTS: RT significantly improved upper- and lower-body muscular strength (P < .005). FFM increased after RT in the entire group (P < .01) with no significant change in body fat. Although the change in M was larger in men (13%) than women (3%), the difference was not significant. The change in M was a function of initial M (r = -0.53, P < .05). There was a trend (0.060+/-0.006 vs 0.066+/-0.006 micromol x kg(-1) x min(-1)/pmol/l, n = 18) for M/I to increase after RT in the combined group of men and women (P = .06). There were no significant relationships between changes in M or M/I with changes in body composition or strength. CONCLUSION: A 6-month RT program tends to improve insulin action in insulin-resistant older adults. These results suggest that RT may be useful in ameliorating insulin resistance that often occurs with physical inactivity, obesity, and loss of muscular strength in older insulin resistant men and women.

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OBJECTIVES: To examine the possible influences of age and gender on muscle volume responses to strength training (ST). DESIGN: Prospective intervention study. SETTING: University of Maryland Exercise Science and Wellness Research Laboratories. PARTICIPANTS: Eight young men (age 20-30 years), six young women (age 20-30 years), nine older men (age 65-75 years), and ten older women (age 65-75 years). INTERVENTION: A 6-month whole-body ST program that exercised all major muscle groups of the upper and lower body 3 days/week. MEASUREMENTS: Thigh and quadriceps muscle volumes and mid-thigh muscle cross-sectional area (CSA) were assessed by magnetic resonance imaging before and after the ST program. RESULTS: Thigh and quadriceps muscle volume increased significantly in all age and gender groups as a result of ST (P < .001), with no significant differences between the groups. Modest correlations were observed between both the change in quadriceps versus the change in total thigh muscle volume (r = 0.65; P < .001) and the change in thigh muscle volume versus the change in mid-thigh CSA (r = 0.76, P < .001). CONCLUSIONS: The results indicate that neither age nor gender affects muscle volume response to whole-body ST. Muscle volume, rather than muscle CSA, is recommended for studying muscle mass responses to ST.

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BACKGROUND: Because of the scarcity of data available from direct comparisons of age and gender groups using the same relative training stimulus, it is unknown whether older individuals can increase their muscle mass as much as young individuals and whether women can increase as much as men in response to strength training (ST). In addition, little is known about whether the hypertrophic response to ST is affected by myostatin genotype, a candidate gene for muscle hypertrophy. METHODS: Eleven young men (25 +/- 3 years, range 21-29 years), 11 young women (26 +/- 2 years, range 23-28 years), 12 older men (69 +/- 3 years, range 65-75 years), and 11 older women (68 +/- 2 years, range 65-73 years) had bilateral quadriceps muscle volume measurements performed using magnetic resonance imaging (MRI) before and after ST and detraining. Training consisted of knee extension exercises of the dominant leg three times per week for 9 weeks. The contralateral limb was left untrained throughout the ST program. Following the unilateral training period, the subjects underwent 31 weeks of detraining during which no regular exercise was performed. Myostatin genotype was determined in a subgroup of 32 subjects, of which five female subjects were carriers of a myostatin gene variant. RESULTS: A significantly greater absolute increase in muscle volume was observed in men than in women (204 +/- 20 vs 101 +/- 13 cm3, p < .01), but there was no significant difference in muscle volume response to ST between young and older individuals. The gender effect remained after adjusting for baseline muscle volume. In addition, there was a significantly greater loss of absolute muscle volume after 31 weeks of detraining in men than in women (151 +/- 13 vs 88 +/- 7 cm3, p < .05), but no significant difference between young and older individuals. Myostatin genotype did not explain the hypertrophic response to ST when all 32 subjects were assessed. However, when only women were analyzed, those with the less common myostatin allele exhibited a 68% larger increase in muscle volume in response to ST (p = .056). CONCLUSIONS: Aging does not affect the muscle mass response to either ST or detraining, whereas gender does, as men increased their muscle volume about twice as much in response to ST as did women and experienced larger losses in response to detraining than women. Young men were the only group that maintained muscle volume adaptation after 31 weeks of detraining. Although myostatin genotype may not explain the observed gender difference in the hypertrophic response to ST, a role for myostatin genotype may be indicated in this regard for women, but future studies are needed with larger subject numbers in each genotype group to confirm this observation.

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PURPOSE: The purpose of this study was to examine the effects of age and gender on the strength response to strength training (ST) and detraining. METHODS: Eighteen young (20-30 yr) and 23 older (65-75 yr) men and women had their one-repetition maximum (1 RM) and isokinetic strength measured before and after 9 wk of unilateral knee extension ST (3 d x wk(-1)) and 31 wk of detraining. RESULTS: The young subjects demonstrated a significantly greater (P < 0.05) increase in 1 RM strength (34+/-3%; 73+/-5 vs 97+/-6 kg; P < 0.01) than the older subjects (28+/-3%; 60+/-4 vs 76+/-5 kg, P < 0.01). There were no significant differences in strength gains between men and women in either age group with 9 wk of ST or in strength losses with 31 wk of detraining. Young men and women experienced an 8+/-2% decline in 1 RM strength after 31 wk of detraining (97+/-6 vs 89+/-6 kg, P < 0.05). This decline was significantly less than the 14+/-2% decline in the older men and women (76+/-5 vs 65+/-4 kg, P < 0.05). This strength loss occurred primarily between 12 and 31 wk of detraining with a 6+/-2% and 13+/-2% decrease in the young and older subjects, respectively, during this period. DISCUSSION: These results demonstrate that changes in 1 RM strength in response to both ST and detraining are affected by age. However, ST-induced increases in muscular strength appear to be maintained equally well in young and older men and women during 12 wk of detraining and are maintained above baseline levels even after 31 wk of detraining in young men, young women, and older men.

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OBJECTIVE: To determine the effects of heavy resistance strength training (ST) on resting blood pressure (BP) in older men and women. DESIGN: Prospective intervention study. SETTING: University of Maryland Exercise Science Laboratory. PARTICIPANTS: Twenty-one sedentary, healthy older men (69 +/- 1 year, n = 11) and women (68 +/- 1 year, n = 10) served as subjects for the study. INTERVENTION: Six months of progressive whole body ST performed 3 days per week using Keiser K-300 air-powered resistance machines. MEASUREMENTS: One-repetition maximum (1 RM) strength was measured for seven different exercises before and after the ST program. Resting BP was measured on six separate occasions before and after ST for each subject. RESULTS: Substantial increases in 1 RM strength were observed for upper body (UB) and lower body (LB) muscle groups for men (UB: 215 vs 265 kg; LB: 694 vs 838 kg; P < .001) and women (UB: 128 vs 154 kg; LB: 441 vs 563 kg; P < .001). The ST program led to reductions in both systolic (131 +/- 2 vs 126 +/- 2 mm Hg, P < .010) and diastolic (79 +/- 2 vs 75 +/- 1 mm Hg, P < .010) BP. Systolic BP was reduced significantly in men (134 +/- 3 vs 127 +/- 2 mm Hg, P < .01) but not in women (128 +/- 3 vs 125 +/- 3 mm Hg, P < .01), whereas diastolic BP was reduced following training in both men (81 +/- 3 vs 77 +/- 1, mm Hg, P = .054) and women (78 +/- 2 vs 74 +/- 2 mm Hg, P = .055). CONCLUSIONS: Six months of heavy resistance ST may reduce resting BP in older persons. According to the latest guidelines from the Joint National Committee for the Detection, Evaluation, and Treatment of Hypertension, the changes in resting BP noted in the present study represent a shift from the high normal to the normal category.

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This study assessed ultrastructural muscle damage in young (20-30 yr old) vs. older (65-75 yr old) men after heavy-resistance strength training (HRST). Seven young and eight older subjects completed 9 wk of unilateral leg extension HRST. Five sets of 5-20 repetitions were performed 3 days/wk with variable resistance designed to subject the muscle to near-maximal loads during every repetition. Biopsies were taken from the vastus lateralis of both legs, and muscle damage was quantified via electron microscopy. Training resulted in a 27% strength increase in both groups (P < 0.05). In biopsies before training in the trained leg and in all biopsies from untrained leg, 0-3% of muscle fibers exhibited muscle damage in both groups (P = not significant). After HRST, 7 and 6% of fibers in the trained leg exhibited damage in the young and older men, respectively (P < 0.05, no significant group differences). Myofibrillar damage was primarily focal, confined to one to two sarcomeres. Young and older men appear to exhibit similar levels of muscle damage at baseline and after chronic HRST.

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The effect of MK-801 on morphine-induced analgesia, tolerance and opioid binding sites was examined in mice. In analgesia studies, mice received either naloxone or MK-801. Controls were injected with saline. Mice were then injected with morphine 10 or 30 min following naloxone or MK-801, respectively, and tested for analgesia (tail flick assay) 45 min later. Pretreatment with naloxone or MK-801 blocked morphine-induced analgesia. In tolerance studies, mice were pretreated with either saline or MK-801. Thirty minutes later, mice were injected with either saline or morphine (acutely or chronically) and tested for analgesia 24 h later. Pretreatment with MK-801 partially or completely blocked the development of acute and chronic tolerance, respectively. In binding studies, MK-801 displaced [3H]naloxone poorly compared to naloxone or morphine. Together, these data suggest a role for NMDA receptors in morphine-induced analgesia and tolerance. The poor inhibition of the [3H]naloxone binding sites by MK-801 supports the possibility that MK-801 might not act directly on the opioid receptors, but rather, inhibits morphine-induced analgesia and tolerance by some other mechanisms.

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Recent studies have demonstrated that opioid receptors may be functional at early stages of ontogeny, and may modulate specific developmental functions. It is presently unknown, however, which particular opioid receptor subtype(s) may be involved. In the pre-ent study, we have used selective radioligand binding conditions in combination with quantitative autoradiography to examine the ontogeny of mu-, kappa- and delta-opioid receptors in the developing rat brain. Membrane binding data indicate that the affinities of mu-, kappa- and delta-sites for radiolabeled drugs are similar in neonatal and adult rats. mu- And kappa-receptors are present in significant densities during early neonatal periods, while delta-receptors appear much later. Autoradiographic data indicate that mu- and kappa-receptors appear early in the development of several brain regions, including the neostriatum, olfactory tubercle and rostral midbrain, and later in other regions such as the thalamus and hypothalamus. Whereas the densities of kappa-binding sites remain relatively constant throughout development, there is a transient appearance and/or redistribution of mu-receptors in several brain areas. delta-Receptors are present in low densities in the basal forebrain at birth. The level of delta-receptor binding increases markedly during the third postnatal week in all brain areas examined. The early appearance of mu- and kappa-receptors during the ontogeny of the brain suggests that these receptors, at least in part, mediate the developmental actions of exogenous and endogenous opioids.

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BAM 18 is a derivative of the opioid precursor proenkephalin A. Although it exists in rat and guinea-pig brain in relatively high concentrations, its physiological function is presently unknown. In the present study we have determined the opioid receptor selectivity of this peptide using radioligand binding and peripheral tissue bioassay. When selective binding conditions were used, BAM 18 bound to the mu opioid receptor with an affinity three times that of the kappa opioid receptor and over 10 times that of the delta opioid receptors (Ki = 0.29, 0.75, and 3.2 nM respectively). BAM 18 also displayed mixed receptor selectivity in in vitro bioassay. Ke values for naloxone antagonism of BAM 18 agonist activity in the electrically stimulated guinea-pig ileum and the mouse vas deferens were 4.3 and 9.9 nM, respectively. These data indicate that BAM 18 binds to all three opioid receptor subtypes with a selectivity profile of mu greater than kappa greater than delta.

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The opioid receptor selectivity of BAM 18 was determined by radioligand binding and peripheral tissue bioassay. Using selective radioligand binding conditions, BAM 18 bound to the mu opioid receptor with an affinity twice that of the K receptor and over 10 times that of the delta opioid receptor (Ki = 0.29, 0.84 and 3.9 nM, respectively). Ke values for naloxone antagonism of BAM 18 activity in the electrically stimulated guinea pig ileum and the mouse vas deferens were 4.3 and 9.9 nM respectively. The pharmacological profile of BAM 18 was similar to that of metorphamide.

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The effects of N,N'-bis-(O-methoxybenzylaminohexyl)-cystamine tetrahydrochloride (BHC), 2-brom-d-lysergic acid diethylamide (BOL) and prazosin on 5-hydroxytryptamine (5-HT) dose-response curves in rabbit ear artery and thoracic aorta were determined. BHC, an irreversible alpha-adrenoceptor antagonist, and prazosin had no substantial effect while BOL shifted the 5-HT dose-response curve to the right in aorta. BHC shifted the curve to the right and reduced maximal response to 5-HT in ear artery. BOL shifted the curve to the right only above 10(-6) M 5-HT in control, but at all concentrations studied in BHC-pretreated ear arteries. In vitro denervation of the ear artery with 6-hydroxydopamine did not significantly alter the 5-HT dose-response curve, nor the effect of BHC on that curve. On the other hand, desipramine decreased the contractile response to high concentrations of 5-HT in non-denervated ear arteries. Prazosin increased the 5-HT threshold and slope of the curve in the ED50 region, but had no inhibitory effect on contractile responses above 3 x 10(-7) M 5-HT or on maximal response. It is concluded that 5-HT acts exclusively on 5-HT receptors in aorta, but on both alpha-adrenergic and 5-HT receptors in ear artery. 5-HT also possesses a small indirect sympathomimetic action at high concentrations in the ear artery. Prazosin has no effect on 5-HT receptors in either vessel and blocks the alpha-adrenoceptor stimulation by 5-HT in ear artery.

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The contractile effect of propranolol in isolated rabbit ear artery was assessed in reserpinized and in surgically and chemically denervated blood vessels. Reserpinization and surgical denervation either had no effect on or enhanced the ear artery contractile response to 10(-6) to 10(-4) M propranolol. In contrast, the contractile response to propranolol was nearly abolished after denervation of the ear artery in vitro with 6-hydroxydopamine (6-OHDA). Dose-response curves to norepinephrine were shifted to the left by factors of 4.9 in 6-OHDA denervated ear arteries and 15.6 in untreated arteries in the presence of 10(-7) M desipramine. The diluent for 6-OHDA shifted both the norepinephrine and propranolol dose-response curves to the right. It is proposed that propranolol caused a contractile response in ear artery by an action on the postsynaptic tissues of this vessel. 6-OHDA denervation caused nonspecific desensitization in rabbit ear artery leading to the loss of response of this vessel to propranolol.

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