Effects of testosterone propionate or dihydrotestosterone propionate on plasma FSH and LH levels in neonatal rats and on sexual differentiation of the brain.

The present study tests the hypothesis that the effects of perinatal androgen administration on the development of the brain are brought about indirectly by a suppression of plasma gonadotropin (GTH) titers. Both castrated male and intact female rats were treated neonatally with 5 alpha-dihydrotestosterone propionate (DHTP) or testosterone propionate (TP) throughout the first ten postnatal days of life and the corresponding effects on neonatal plasma FSH and LH levels and the subsequent ability of the adult to exhibit cyclic GTH release and female sex behavior (lordosis) were determined. In males castrated within 24 h of birth, subcutaneous injections of DHTP (60 or 180 mug per 100 g average body weight) or TP (60 mug/100 g) given on day 2, 4, 6, 8 and 10 reduced plasma levels of FSH and LH as determined by radioimmunoassay 48 h following the first and last injections. However, TP but not DHTP masculinized the development of the regulation of GTH release as mesured by luteinization of subcutaneous ovarian grafts, and also suppressed the ability of adult neonatally castrated male primed with estradiol benzoate and progesterone to display lordosis behavior. In intact females, the same neonatal DHTP and TP injection regime lowered FSH and LH plasma levels following the last injection (day 12), while DHTP lowered LH, but not FSH, following the first injection (day 4). All TP treated females had ovaries devoid of CL by 45 days of age and showed prolonged vaginal cornification. However, DHTP failed to masculinize the pattern of GTH release in females since DHTP-treated females, like oil-treated females, possessed CL(days 45 and 100) and exhibited vaginal cycles (days 80-100). Lordosis quotients of females treated neonatally with DHTP were as high as those of oil-treated females and significantly higher than those of TP-treated females. These results demonstrate that the ability of TP to induce maculine differentiation of the neural regulation of GTH release and female sex behavior does not depend on its ability to depress circulating LH and FSH levels in the neonatal male, or LH levels in the neonatal female rat.

Effects of aerobic exercise on low back pain patients in treatment.

BACKGROUND CONTEXT: Aerobic exercise (AE) has been prescribed to improve fitness and well-being in apparently healthy individuals and cardiac, orthopedic, and other patient populations. AE has not previously been studied as a sole treatment for low back pain patients (LBPP). PURPOSE: This study evaluated the effects of low to moderate aerobic exercise as an adjunct treatment for LBPP, 30 to 60 years of age, in a neurosurgical practice during a 2.5-year follow-up to an initial 10-week exercise program. The purpose of this study was to determine the effects of short- and long-term AE on LBPP. The initial 10-week phase compared AE and nonexercising controls on mood states and pain/symptoms. STUDY DESIGN/SETTING: A matched stratified design was used to input LBPP with similar previous clinical treatments as well as age and sex into AE or control groups. PATIENT SAMPLE: After screening 68 LBPP from a New England private neurosurgical practice, 40 patients met qualification criteria, and 35 volunteered for this AE research study. The LBPP in this study were 30 to 60 years old and had the following medical diagnoses: herniated nucleus pulposus at one or more lumbar levels, degenerative discopathy, lumbosacral strain, and spinal canal and/or foraminal stenosis. OUTCOME MEASURES: The measure of mood states was the Profile of Mood States, and the measure of pain was the Brief Pain Inventory. The 2.5-year follow-up phase compared AE and nonexercise patients on the following treatment variables: medical office visits for pain/symptoms, physical therapy referrals, epidural steroid injections for pain/symptoms, prescription of pain medications, and work status. METHODS: Thirty-five LBPP were matched stratified into an AE or nonexercise control group for a 10-week exercise program. After the 10-week exercise program, all subjects were given the opportunity to cross over to the opposite group. Those patients choosing to exercise were advised to follow a low to moderate aerobic exercise prescription (walking or cycling, 60% age-predicted maximal heart rate, 4 days per week for 45 minutes per day). None of the original AE group crossed over to the nonexercise group because of symptoms relating to their previous exercise participation. All participants were contacted at 6-month intervals, and the number of medical office visits for pain/symptoms, physical therapy referrals, number of epidural steroid injections, and number of prescriptions for pain was charted for 2.5 years. Work status was evaluated by comparing the change in number of patients not working, working part time, working full time, or number changing from full time to part time or not working from randomization to the end of follow-up. Patients following the exercise prescription at least 50% of the time were compared with those exercising less than 50% of the time during the 2.5-year follow-up. Significance was determined at the.05 level using Fisher's exact test or the Kruskal-Wallis test. RESULTS: The initial 10-week AE phase of the study indicated that low to moderate AE significantly improved mood profile (AE X=-9.58; control X=19.11; p<.01) but did not alter pain levels. AE patients in the 2.5-year follow-up phase received significantly fewer pain medication prescriptions (AE X=2.76; control X=13.35; p<.02) and were given fewer physical therapy referrals (AE X=0.17; control X=1.64; p<.002). There was no significant difference in the number of medical office visits for pain or epidural blocks administered to either group. Work status was improved only in exercising patients (AE X=+0.24; control X=-0.35; p<.04). CONCLUSIONS: Low to moderate aerobic exercise appears to improve mood states and work status and reduce the need for physical therapy referrals and pain medication prescriptions for LBPP in the care of a neurosurgeon.

A survey of badminton injuries.

A Badminton Injury Questionnaire (BIQ) was developed to survey the type and frequency of injuries that are likely to occur from playing competitive badminton. Two hundred and thirty-one players, ranging from club players to international champions, completed the survey which indicated an injury incidence rate of .09 and .14 injuries per person per year for male and female badminton players respectively. Badminton participation resulted in relatively few injuries, most of which were cramps, blisters, strains and sprains of the lower extremities and a surprisingly low incidence of tennis elbow.

Fibrinolytic activity is similar in physically active men with and without a history of myocardial infarction.

The purpose of this study was to evaluate fibrinolytic potential at rest and after a fibrinolytic stressor in men with a history of myocardial infarction (MI) compared with an age- and activity-matched group of men without coronary artery disease (CAD). All men were currently enrolled in exercise programs. Tissue-type plasminogen activator (TPA) and plasminogen activator inhibitor 1 (PAI-1) activity and antigen levels were measured at rest and after a maximal exercise test. A 2 x 2 (group x time) ANOVA with repeated measures was used to evaluate fibrinolytic potential. Bivariate regressions were conducted to evaluate relations between fibrinolytic potential and maximal oxygen uptake (VO2max). Age was similar between groups (CAD, 57.5 +/- 6.6; non-CAD, 58.1 +/- 7.3 years); however, VO2max was higher in non-CAD subjects (36.2 +/- 6.2 vs 27.5 +/- 5.9 mL.kg-1.min-1). Mean +/- SEM resting TPA and PAI-1 activities were similar between CAD and non-CAD subjects (TPA, 2.8 +/- 0.2 vs 2.8 +/- 0.2 IU/mL; PAI-1, 15.9 +/- 3.1 vs 13.1 +/- 4.1 AU/mL). Both groups showed similar significant increases in TPA activity with exercise (P < .05), and postexercise TPA activity was also similar (CAD, 9.1 +/- 2.0 IU/mL; non-CAD, 11.7 +/- 2.6 IU/mL). Both groups also showed similar significant decreases in PAI-1 activity with exercise (P < .05) and no differences in postexercise PAI-1 activity (CAD, 13.2 +/- 2.5 AU/mL; non-CAD, 10.4 +/- 3.6 AU/mL). Significantly higher resting TPA antigen levels were seen in CAD (14.8 ng/mL) than non-CAD (10.2 ng/mL) subjects (P < .05), but neither group showed significant changes with exercise (CAD, 12.9 ng/mL; non-CAD, 11.8 ng/mL). Resting PAI-1 antigen was similar in the two groups (CAD, 71.4 ng/mL; non-CAD, 74.2 ng/mL) and did not significantly change with exercise (CAD, 77.9 ng/mL; non-CAD, 72.3 ng/mL). VO2max was positively correlated with postexercise TPA activity (r = .52, P < .05) and negatively correlated with resting TPA antigen (r = -.43, P < .05). Resting TPA antigen was also directly correlated with body mass index (r = .63, P < .05). The finding that functional fibrinolytic activity was not different in physically active men with and without CAD contrasts with previous reports. This suggests that matching subjects on the bases of age and habitual physical activity status and controlling exercise intensity are important factors to consider when evaluating fibrinolytic potential.

Fibrinolytic activity is not dependent upon exercise mode in post-myocardial infarction patients.

In this study we investigated possible differences in fibrinolytic activity in cardiac patients while they performed treadmill and cycle ergometry. Thirteen post-myocardial infarction patients completed two maximal exercise tests on treadmill and cycle ergometers. Blood was collected before and after each exercise test and was analyzed for the fibrinolytic variables, tissue plasminogen activator (t-PA) and plasminogen activator inhibitor-1 (PAI-1) activity, and lactate. Maximal oxygen uptake, heart rate, and ventilation were greater (P < 0.05) on the treadmill than during cycle ergometry, however, blood lactate was similar between modes. t-PA activity significantly increased with exercise (P < 0.05) and there was a trend toward a reduction in PAI-1 activity with exercise, but this did not reach statistical significance. The fibrinolytic responses to maximal exercise did not differ between the two modes of exercise studied. Therefore, exercise intensity, but not the mode of exercise, appeared to be the primary determinant of the fibrinolytic response to acute exercise in these patients.