Research Abstracts

Physical Activity and Risk for Breast Cancer
A.T. Bentz, S.D. Carter, C.M. Schneider, FACSM. Rocky Mountain Cancer Rehabilitation Institute, University of Northern Colorado, Greeley, CO

Ninety % of breast cancer cases have no genetic link, which suggests that a relationship exists between modifiable lifestyle behaviors and the risk for breast cancer. Physical activity has been identified as a modifiable behavior that may contribute to decreased risk for the development of breast cancer. PURPOSE: To identify the relationship between physical activity and the risk for breast cancer. METHODS: This study included women diagnosed with breast cancer (n=905) and women free from breast cancer (n=2016). Participants completed a five-page comprehensive questionnaire identifying risks for breast cancer including past physical activity. Activity was categorized: below average, average, above average, and highly competitive during ages 10-15 years and 15-30 years. Statistical analysis was performed using logistic regression. RESULTS: Below average physical activity during ages 10-15 years contributed significantly to the risk for breast cancer (OR=1.557, CI 1.061-2.285). The results remained significant when controlling for age and family history. (OR=1.954, CI 1.175-3.247). Postmenopausal women (n=1417) showed a significant increase in risk for breast cancer with below average physical activity during ages 10-15 years (OR=1.847, CI 1.077-3.170), whereas no significance was found for premenopausal women (n=1504). Interestingly, family history was significant for premenopausal (OR=1.806, CI 1.217-2.682), not postmenopausal women. CONCLUSION: Any level of physical activity during pubertal years may exert a protective effect from the risk for postmenopausal breast cancer. This protection may be related to menstrual cycle alterations resulting in fewer years of cumulative estrogen exposure. The results from this study support the hypothesis that the cause of pre and postmenopausal breast cancers may be different. Postmenopausal breast cancer may be strongly related to years of estrogen exposure, which may be decreased with physical activity, whereas premenopausal breast cancer may have a strong familial genetic link.

The Exercise Response is Patient Specific, Not Cancer Specific
D.S. Hydock, S.D. Carter, S.N. Drum, M.A. Roozeboom, J.R. Schaffer, R. Hayward, C.M. Schneider, FACSM. Rocky Mountain Cancer Rehabilitation Institute, University of Northern Colorado, Greeley, CO

Evidence is mounting that suggests exercise training has a positive effect on cancer recovery. However, questions remain regarding the influence of cancer type on the response to exercise training. PURPOSE: The purpose of this investigation was to compare the response of breast cancer patients to patients with other forms of cancer following exercise training. METHODS: Seventy-five cancer patients participated in fitness assessments which examined pulmonary function (PF), cardiorespiratory fitness (CF), muscular strength (MS), muscular endurance (ME), and range of motion (ROM). In addition, subjects completed inventories that assessed fatigue (Fa) and depression (De). Subjects were assigned to either the breast cancer group (BC, n = 43) or the cancer group (C, n = 32) which included individuals with other commonly diagnosed cancers (i.e., ovarian, cervical, prostate). Groups participated in an exercise intervention program 2 to 3 days per week for 6 months. The exercise intervention consisted of cardiorespiratory training, resistance training, and flexibility training. Following the 6-month intervention, all subjects were reassessed. RESULTS: Both BC and C groups demonstrated significant increases in CF, ME, and ROM with concomitant decreases in Fa and De (p < 0.05). No significant differences were found between the BC and C groups. CONCLUSION: Cancer survivors show improvements in functional capacity and mood state with the implementation of individually prescribed exercise. This suggests that individualizing exercise is patient specific and not cancer specific.

Exercise Intervention and the Effect on Cancer Patients
S.N. Drum, S.D. Carter, M.A. Roozeboom, D.S. Hydock, J.R. Schaffer, G.T. Knofczynski, R. Hayward, C.M. Schneider, FACSM. Rocky Mountain Cancer Rehabilitation Institute, University of Northern Colorado, Greeley, CO

Patients with cancer are at risk for muscular weakness and reduced functional capacity which contributes to debilitating fatigue and depression. The benefits of exercise for cancer patients have not been extensively investigated. PURPOSE: To assess the effects of individualized exercise therapy on selected physiological and psychological variables in cancer patients. METHODS: One hundred-three cancer patients were studied (75 exercise and 28 usual care). All subjects completed an exercise assessment at baseline and again after 6 months. Subjects were assessed on body fat (%F), pulmonary function (PF), time on treadmill (TOT), predicted VO2max (PV02), range of motion (ROM), muscular strength (MS), muscular endurance (ME), flexibility (FLEX), fatigue (F), and depression (D). Subjects in the exercise group participated in a personalized exercise intervention that included cardiovascular, muscular strength, muscular endurance, and flexibility activities. Each subject was trained by a cancer rehabilitation exercise specialist 2-3 times per week while the non-exercise group received usual care. RESULTS: Significant (p < .05) exercise improvements were found following the 6-month intervention in PVO2, TOT, ME, and ROM. Significant (p < .05) decreases were found for F and D. Additionally, after the 6-month personalized exercise program, significant (p < .05) improvements were observed for TOT, PVO2, and D when compared to the usual care group. CONCLUSION: The results suggest that individualized exercise intervention improves cardiovascular function and reduces depression and fatigue in cancer patients. Thus it appears that personalized exercise prescription is a valid means to enhance the quality of life of cancer patients.

Effects of Exercise on Endothelial Function in an MNU-Induced Rat Mammary Tumor Model
R. Ruangthai1, R. Hayward1, C.M. Schneider1, H. McCarty2 and K. Westerlind2. 1Department of Kinesiology, University of Northern Colorado, Greeley, CO; 2AMC Cancer Research Center, Denver, CO.

The purpose of this study was to assess endothelial function in N-methyl-N-nitrosourea (MNU)-treated rats following eight weeks of moderate exercise training. A secondary purpose was to determine if exercise training altered vascular responsiveness to the chemotherapeutic agent 5-fluorouracil (5-FU). Virgin female Sprague Dawley rats were injected with MNU (50 mg/kg, i.p.) at 21 days of age, and at 28 days assigned to one of four groups: 1) non MNU + no exercise (NM+NE), 2) non MNU + exercise (NM+E), 3) MNU + no exercise (M+NE), 4) MNU + exercise (M+E). The exercise regimen consisted of treadmill running at 20-25 m/min, 15%grad, 30 min/d, 5 d/wk for 8 weeks. Vascular reactivity was evaluated in isolated aortic rings following 0, 4, and 8 weeks of exercise training. No significant differences in vascular responsiveness were noted between M+E and NM+E, or between M+NE and NM+NE animals at 0, 4, or 8 weeks. IN addition, four weeks of exercise training resulted in no significant changes in vasoactivity for any group. However, 8 weeks of exercise training resulted in increased maximal endothelium-dependent vasorelaxation to acetycholine (ACh, 1x10-5 M) (M+NE, 56+7%; M+E, 69+8%; p<0.05) following norepinephrine-induced (1x10-7 M) vasoconstriction. Exposure of aortic rings from each group to 5-FU (7x10-3 M) resulted in vasorelaxation. Rings obtained from exercise trained animals demonstrated enhanced vasorelaxation to ACh (1x10-5 M) following 5-FU-induced vasoconstriction compared to rings obtained from untrained animals (p<0.05). The results demonstrate that exercise training can enhance endothelium-dependent vasodilation in an MNU-induced rat mammary tumor model and that these changes may serve to counteract the vasoconstrictive properties of 5-FU.

Attenuation of Chemotherapy-Induced Vascular Dysfunction by Exercise Training: Possible Role of Nitric Oxide Syhthase
R. Ruangthai1, R. Hayward1, C.M. Schneider, FACSM1, H. McCarty2, K. Westerlind, FACSM2 Department of Kinesiology, University of Northern Colorado, Greeley, CO,, Rocky Mountain Cancer Rehabilitation Institute, University of Northern Colorado, Greeley, CO1, AMC Cancer Research Center, Denver CO 2

We have previously shown that exercise training enhances endothelium-dependent vasodilation in a rat mammary tumor model, and that these changes resulted in an attenuation of vasoconstriction caused by the chemotherapeutic agent 5-fluororuacil (5-FU). We hypothesized that this was the result of increased nitric oxide (NO) production by the vasculature. In order to investigate possible mechanisms involved with the exercise-induced attenuation of vascular dysfunction, we determined endothelial nitric oxide synthase (eNOS) protein content in the aorta of N-methyl-N-nitrosourea (MNU)-treated rats following eight weeks of moderate exercise training. Virgin female Sprague Dawley rats were injected with MNU (25 mg/kg, i.p.) at 21 days of age, and at 28 days assigned to either sedentary or exercise groups. The exercise regimen consisted of treadmill running at 20-23 m/min, +15% grade, 30 min/d, 5 d/wk for 8 weeks. Our results show no significant differences in aortic eNOS protein content between sedentary and exercise groups following 2 or 4 weeks of exercise training. However, after 6 weeks of exercise training, significant (p<0.05) increases in aortic eNOS protein content were observed in exercise trained rats when compared to sedentary animals. Following 8 weeks of exercise training, increases in eNOS protein content were sustained, however differences between sedentary and exercise trained animals were not statistically significant. These data demonstrate that moderate exercise training increases aortic eNOS protein content in a rat mammary tumor model. This suggests that the attenuation of 5-FU-induced vasoconstriction may be due, at least in part, to an increase in aortic eNOS protein content