Impact of Exercise and Activity on Weight Regain and Musculoskeletal Health Post-Ovariectomy.

The purpose of this study was to determine whether obesity and/or exercise training alters weight regain and musculoskeletal health after ovariectomy (OVX). Female rats were fed high-fat diet (HFD) to reveal obesity-prone (OP) and obesity-resistant (OR) phenotypes. The OP and OR exercising (EX) and sedentary (SED) rats were calorically restricted to lose 15% of body weight using medium-fat diet. Rats were then maintained in energy balance for 8 wk before OVX. After OVX and a brief calorically limited phase, rats were allowed to eat ad libitum until body weight plateaued. Starting at weight loss, EX ran 1 h·d, 6 d·wk, 15 m·min. Energy intake, spontaneous physical activity (SPA), and total energy expenditure were evaluated at the end of weight maintenance pre-OVX, and at three time points post-OVX: before weight regain, during early regain, and after regain. Data are presented as mean ± SE. Exercise attenuated weight regain after OVX in OP only (OP-EX, 123 ± 10 g; OP-SED, 165 ± 12 g; OR-EX, 121 ± 6 g; OR-SED, 116 ± 6 g), which was primarily an attenuation of fat gain. The early post-OVX increase in energy intake explained much of the weight regain, and was similar across groups. Exercising improved bone strength, as did maintaining SPA. Group differences in muscle mitochondrial respiration were not significant. The large decrease in SPA due to OVX was persistent, but early weight regain was dependent on decreased SPA. In conclusion, leanness and exercise do not necessarily protect from OVX-induced weight gain. Exercise prevented weight gain in obese rats, but loss of SPA was the greatest contributor to post-OVX weight gain. Thus, understanding the mechanisms resulting in reduction in SPA after ovarian hormone loss is critical in the prevention of menopause-associated metabolic dysfunction.

Ibuprofen before Exercise Does Not Prevent Cortical Bone Adaptations to Training.

Using a nonsteroidal anti-inflammatory drug (NSAID) before a single bout of mechanical loading can reduce bone formation response. It is unknown whether this translates to an attenuation of bone strength and structural adaptations to exercise training. PURPOSE: This study aimed to determine whether nonsteroidal anti-inflammatory drug use before exercise prevents increases in bone structure and strength in response to weight-bearing exercise. METHODS: Adult female Wistar rats (n = 43) were randomized to ibuprofen (IBU) or vehicle (VEH) and exercise (EX) or sedentary (SED) groups in a 2 × 2 (drug and activity) ANCOVA design with body weight as the covariate, and data are reported as mean ± SE. IBU drops (30 mg·kg BW) or VEH (volume equivalent) were administered orally 1 h before the bout of exercise. Treadmill running occurred 5 d·wk for 60 min·d at 20 m·min with a 5° incline for 12 wk. Micro-CT, mechanical testing, and finite element modeling were used to quantify bone characteristics. RESULTS: Drug-activity interactions were not significant. Exercise increased tibia cortical cross-sectional area (EX = 5.67 ± 0.10, SED = 5.37 ± 0.10 mm, P < 0.01) and structural estimates of bone strength (Imax: EX = 5.16 ± 0.18, SED = 4.70 ± 0.18 mm, P < 0.01; SecModPolar: EX = 4.01 ± 0.11, SED = 3.74 ± 0.10 mm, P < 0.01). EX had increased failure load (EX = 243 ± 9, SED = 202 ± 7 N, P < 0.05) and decreased distortion in response to a 200-N load (von Mises stress at tibia-fibula junction: EX = 48.2 ± 1.3, SED = 51.7 ± 1.2 MPa, P = 0.01). There was no effect of ibuprofen on any measurement tested. Femur results revealed similar patterns. CONCLUSION: Ibuprofen before exercise did not prevent the skeletal benefits of exercise in female rats. However, exercise that engenders higher bone strains may be required to detect an effect of ibuprofen.

Developmental windows of breast cancer risk provide opportunities for targeted chemoprevention.

The magnitude of the breast cancer problem implores researchers to aggressively investigate prevention strategies. However, several barriers currently reduce the feasibility of breast cancer prevention. These barriers include the inability to accurately predict future breast cancer diagnosis at the individual level, the need for improved understanding of when to implement interventions, uncertainty with respect to optimal duration of treatment, and negative side effects associated with currently approved chemoprevention therapies. None-the-less, the unique biology of the mammary gland, with its postnatal development and conditional terminal differentiation, may permit the resolution of many of these barriers. Specifically, lifecycle-specific windows of breast cancer risk have been identified that may be amenable to risk-reducing strategies. Here, we argue for prevention research focused on two of these lifecycle windows of risk: postpartum mammary gland involution and peri-menopause. We provide evidence that these windows are highly amenable to targeted, limited duration treatments. Such approaches could result in the prevention of postpartum and postmenopausal breast cancers, correspondingly.