Cyclists often complain of genital numbness and even of impotence. The purpose of this study was to determine if perineal compression during cycling causes changes in the penile blood supply, impotence and penile numbness. Forty healthy athletic men with a mean age of 30 +/- 5.3 years took part in the study. Transcutaneous penile oxygen pressure was obtained using a device consisting of a modified Clark pO2 electrode, attached to the glans of the penis. All men were measured in a standing position before, in a seated and standing position during and in a standing position after cycling. Additionally, a detailed interview was carried out with each man. The penile blood supply--which correlates with the transcutaneous PO2 at the glans-- decreased significantly in over 70% of the test subjects during cycling in a seated position. Cycling in a standing position did not show any alteration in the penile blood supply as compared to the values measured before exercising. Numbness of the genital region was reported by 61% of the cyclists. 19% of cyclists who had a weekly training distance of more than 400 km complained of erectile dysfunction. The results of the present study showed that there is a deficiency in penile perfusion due to perineal arterial compression. This could be a reason for penile numbness and impotence in long-distance cyclists. Therefore, we suggest restricting the training distance, and taking sufficient pauses during the course of prolonged and vigorous bicycle riding, in order to avoid penile numbness and impotence.

Anesthesiologists' (ASA) classification, plasma protein level, ect. 1,2 but the effect of hyperventilation has not been established. After approval from the Human Research Committee of our hospital and informed consent from each patient was obtained, 17 adult patients scheduled for thyroid adenoma or breast mass surgery (ASA physical status I-II) were randomly divided into a hyperventilation group (n = 8) and a normoventilation group (n = 9). Patients were premedicated with sodium phenobarbital 100 mg and atropine 0.5 mg intramuscularly 60 min before anesthesia. None of the patients had any cardiovascular, central nervous system, or metabolic disease. Endtidal CO 2 (PETCO 2 ) was monitored during induction. As the propofol was infused at a rate of 33.3 mg·min -1 with a micro-infusion pump via the main saphenous vein and continuously flushed with lactated Ringer's solution, the patient was asked to count in the normoventilation group, and to hyperventilate for 90 sec before beginning to count in the hyperventilation group. The propofol dose required for the patient to cease counting was recorded as the minimum induction dose.Age, weight, gender, ASA classification, preoperative albumin, globulin, total protein, urea, hemoglobin concentration 1,2 and baseline PETCO 2 (37.3 ± 2.4 mmHg vs 38.2 ± 1.5 mmHg) were comparable between groups (P > 0.05). The PETCO 2 decreased to 25.9 ± 2.3 mmHg as the patients hyperventilated. The minimum induction dose of propofol was 1.66 ± 0.24 mg·kg -1 in the hyperventilation group and 1.19 ± 0.42 mg·kg -1 in the normoventilation group (P < 0.01).Hyperventilation results in hypocapnia, which may decrease cerebral blood flow. 3 Correspondingly, a smaller fraction of the infused propofol is transported to the central nervous system. On the other hand, voluntary hyperventilation may increase cardiac output. 4 This decreases the peak arterial and peak brain propofol levels, 5 and more propofol is needed to reach the brain concentration at which the patient loses consciousness. The change of protein binding of propofol resulting from hyperventilation could also be part of the explanation.We conclude that hyperventilation increases the induction dose of propofol.