The effects of swimming and lactate on the release of testosterone were examined in male rats. During in vivo experiments, male rats were catheterized via the right jugular vein and blood was collected at 0, 10, 15, 30, and 60 min following the exercise, or they were catheterized via the right jugular vein and the left femoral vein and blood was collected at 0, 2, 5, 10, 15, 30, 60, and 120 min after a 10-min infusion at lactate (13 mg.kg-1.min-1). Trunk blood and blood from the testicular vein were also collected after 10 min of swimming or water immersion. In an in vitro experiment, testicular fragments were challenged with lactate (0.01-10 mM) and/or human chorionic gonadotropin (hCG; 0.5 IU.mL-1), and the mediobasal hypothalamus (MBH) was challenged with lactate (8 mM). The post-exercise levels of plasma lactate and testosterone at 10, 15, and 30 min were higher than resting levels. Plasma luteinizing hormone (LH) was increased following 30 min of swimming. Administration of lactate or hCG increased in a dose dependent manner testicular cyclic adenosine 3':5' monophosphate (cAMP) and testosterone release. Plasma testosterone increased after swimming and lactate infusion. Incubation of MBH with lactate increased the gonadotropin-releasing hormone (GnRH) level in the medium. These results suggest that the increased plasma testosterone levels in male rats during exercise is at least partially a result of a direct and LH-independent stimulatory effect of lactate on the secretion of testosterone by increasing testicular cAMP production. Swim-elevated plasma LH may be a result of a rise of GnRH caused by lactate.

Effects of calcitonin peptides, including human calcitonin (hCT), salmon calcitonin (sCT), and calcitonin gene-related peptide (CGRP), on the secretion of testosterone and luteinizing hormone (LH) in male rats were studied. Male rats were injected intravenously with human chorionic gonadotropin (hCG), calcitonin peptides, or hCG plus calcitonin peptides. Blood samples were collected at several intervals following hormone challenge. In an in vitro experiment, testis blocks were incubated with hCG (0, 0.05, 0.5, or 5 IU/ml) or hCG (0.5 IU/ml) plus calcitonin peptides (0-10(-9) or 10(-6) M) at 34 degrees C for 30 minutes. Both medium and plasma samples were extracted by ether and analyzed for testosterone by radioimmunoassay (RIA). The concentration of calcium in each plasma sample was measured by an automatic calcium analyzer. The anterior pituitary gland (AP) was incubated with or without calcitonin peptides (0-10 nM) at 37 degrees C for 30 minutes. They were then incubated with gonadotropin releasing hormone (GnRH, 10 nM) for a further 30 minutes. The concentration of LH in AP medium was measured by RIA. The accumulation of cyclic adenosine monophosphate (cAMP) and cyclic guanosine monophosphate (cGMP) in both testicular tissues and APs were measured by RIA. A single intravenous injection of calcitonin peptides decreased the basal and hCG-stimulated levels of plasma testosterone gradually from 60 to 180 or 360 minutes after challenge. The plasma calcium was not altered by the injection of calcitonin peptides and/or hCG. Administration of calcitonin peptides in vitro resulted in a dose-dependent inhibition of both basal and hCG-stimulated release of testosterone.(ABSTRACT TRUNCATED AT 250 WORDS)