Free testosterone (FT) hormonal responses were compared between high-intensity interval exercise (IE) and steadystate endurance exercise (SSE) in endurance trained males (no.=15). IE session was repeated periods of 90-sec treadmill running at 100-110% maximal oxygen uptake (VO2max) and 90-sec active recovery at 40% VO2max for 42-47 min. The SSE session consisted of a continuous 45-min run at 60-65% VO2max. Total work output was equal for each exercise session. A 45-min supine rest control session (CON) was also performed. All three sessions were on separate days. Pre-session (PRE), immediate post-session (POST), and 12-h post-session (12POST) blood samples were collected and used to determine FT, SHBG, LH, 3- α-androstanediol glucuronide (3-α Diol G) and cortisol. Analysis of variance compared IE and SSE biomarker responses to the reference CON session. IE and SSE each caused an increase (p<0.01) in FT, but IE more so than SSE (p<0.05). The 5α-reductase marker 3-α Diol G response at 12POST IE was elevated while FT was reduced (p<0.05); no such change occurred following SSE. These findings suggest IE might produce a more pronounced turnover of FT by androgen sensitive tissue than the SSE form of exercise.

No abstract

The mechanisms responsible for the gender difference in blood pressure (BP) in humans are not clear. Over the past several years we have studied the spontaneously hypertensive rat (SHR) as a model of sex differences in BP control. In the present study, we tested the hypothesis that renal vascular and microsomal epoxyeicosatrienoic acid (EET) levels are higher in females than males, and increasing vascular EETs by blocking epoxide hydrolase with AUDA will reduce BP more in males than females. Renal vascular and microsomal EETs were higher in female SHR than males. Mean arterial pressure (MAP by telemetry) was higher in males than females during the baseline period of 6 days, and although the epoxide hydrolase inhibitor, AUDA, given for 10 days increased renal microvascular EETs in both groups, AUDA did not affect MAP in either group. These data suggest that EETs do not contribute to the sex differences in hypertension in young SHR.

Polycystic ovary syndrome (PCOS) is the most common hormonal disorder among women of reproductive age. PCOS is strongly linked to increased risk of cardiovascular diseases (CVD). The mechanisms responsible for PCOS hypertension are not clear. We have characterized a rat model of PCOS, the hyperandrogenemic rat (HAF), that exhibits many of the characteristics of PCOS in women. This study aimed to test the hypothesis that PCOS rats exhibit increased T cells in kidney that could potentially play a role in hypertension. Dihydrotestosterone (DHT) (7.5 mg/90 days) or placebo, pellets were implanted subcutaneously in female SD rats (n = 4–5/group) at 4weeks of age and compared to placebo. After 6 weeks of DHT treatment, kidneys were collected and infiltrated CD4+, CD8+, Th17, and CD4+CD28null T cells were measured by flow cytometry. The number of renal infiltrated CD4+ T cells was increased in HAF rats (Placebo: 10 ±1 vs. HAF: 22 ±1 % gated p <0.05). The number of infiltrated Th17 (Placebo: 19 ±1 vs. HAF: 23 ±1 % gated p <0.05) and CD4+CD28nullT cells (Placebo: 6 ±1 vs. HAF: 15 ±2 % gated p <0.05) were significantly increased in HAF rats compared to Placebo. These data show that infiltrated T cells, in particular Th17 and CD4+CD28null subpopulations are increased in the kidney of HAF rats, a model of PCOS. Results from this study suggest a potential role for infiltrated T cells as a link between hypertension and CVD in PCOS patients.

Polycystic ovary syndrome (PCOS) is the most common reproductive disorder in premenopausal women. PCOS is characterized by hyperandrogenemia that does not abate after menopause. Hyperandrogenemic postmenopausal women (HA-PMW) are hypertensive, but the mechanisms responsible have not been elucidated. Hypertension in PMW is less well controlled than in age-matched men. We have developed a model, the hyperandrogenemic postcycling female (PMHAF) rat, aged 13-14 mos, that exhibits many of the characteristics found in HA-PMW. In the present studies we tested the hypothesis that the renin-angiotensin system (RAS) and the sympathetic nervous system (SNS) contribute to hypertension in PMHAF rats. Female Sprague-Dawley rats were implanted with dihydrotestosterone (7.5mg/90d) or placebo pellets beginning at 4 wks of age, and pellets were changed every 85 d. At 12-13 mos of age, PMHAF rats were obese compared to placebo controls, and CT scans showed that both total adipose (TAF) and visceral adipose (VAF) were increased in PMHAF vs placebo controls (n=4/grp) (TAF: 7.9±0.5 vs 5.46±1.00 AU/g BW, p<0.05; VAF, 4.60±0.30 vs 3.45±0.07 AU/g BW, p<0.05). PMHAF rats (n=3/grp) were implanted with radiotelemetry transmitters, and 2 wks later, baseline MAP was measured for 5 d. Then rats were given losartan (40mg/kg/d) or tap water placebo for 5 days, and then tap water was returned. After additional 5 d and return of MAP to baseline, rats were implanted with minipumps containing terazocin and propranolol (10 mg/kg/d for each drug, sc, for 7 d) or saline vehicle. Baseline MAP in PMHAF rats was (128±9 vs 105±9 mmHg, p<0.05). Losartan reduced MAP more in PMHAF than placebo controls (111±9 vs 95±7 mmHg, p<0.05). Intrarenal angiotensinogen and ACE1 mRNA levels were increased by 8 fold and 2 fold, respectively, in PMHAF rats vs placebo controls (p<0.05). α 1 -β 1,2 -Adrenergic blockade reduced MAP by 13% in PMHAF rats, the same level as in placebo controls, and had no effect in placebo controls (110±12 vs 102±5 mmHg, p<0.05 vs baseline MAP). These data suggest that both the RAS and SNS are upregulated in PMHAF rats and contribute to their hypertension. These data also suggest that multiple drug therapy is likely to be necessary to control MAP in PMW with hyperandrogenemia. Supported by PO1HL51971.