Weight loss from exercise is often less than expected. Putative compensatory mechanisms may limit exercise-induced reductions in body fat and might be proportional to exercise energy expenditure (ExEE). This study was conducted to determine compensation for (the difference between accumulated exercise energy expenditure and changes in body tissue energy stores) and compensatory responses to 1,500 or 3,000 kcal/wk of ExEE. Overweight-to-obese ( n = 36) sedentary men and women were randomized to groups expending 300 or 600 kcal/exercise session, 5 days/wk, for 12 wk. Fourteen participants in the 300-kcal group and 15 in the 600-kcal group completed the study. The primary outcome was energy compensation assessed through changes in body tissue energy stores. Secondary outcomes were putative compensatory responses of resting metabolic rate, food reinforcement, dietary intake, and serum acylated ghrelin and glucagon-like peptide-1. All measures were determined pre- and posttraining. The 3,000 kcal/wk group decreased ( P < 0.01) percentage and kilograms of body fat, while the 1,500 kcal/wk group did not. The 1,500 and 3,000 kcal/wk groups compensated for 943 (-164 to 2,050) and 1,007 (32 to 1,982) kcal/wk (mean, 95% CI, P ≥ 0.93), or 62.9% and 33.6% of ExEE, respectively. Resting metabolic rate and energy intake did not change. Food reinforcement and glucagon-like peptide-1 decreased ( P < 0.02), whereas acylated ghrelin increased ( P ≤ 0.02). Compensation is not proportional to ExEE. Similar energy compensation occurred in response to1,500 and 3,000 kcal/wk of ExEE. ExEE of 3,000 kcal/wk is sufficient to exceed compensatory responses and reduce fat mass.
Background: More than 80% of patients entering cardiac rehabilitation (CR) are overweight, and >50% have metabolic syndrome. Current CR exercise protocols result in little weight loss and minimal changes in cardiac risk factors. We sought to design an exercise protocol that would lead to greater weight loss and risk factor change.
Objective: To assess the correlation of erectile function (EF) and physical activity (PhA) by using standardized, validated instruments in healthy men.
Methods: A urologist examined 674 men aged 45-60 yr at their place of work. That included a urological physical examination, medical history, and assessment of testosterone (T) and sex hormone-binding globulin; all men completed the 5-item International Index of Erectile Function (IIEF-5) as well as the Paffenbarger score.
Background And Purpose: Physiologically, it appears plausible for physical activity to decrease stroke risk; however, epidemiological studies have produced mixed findings. Furthermore, few studies have examined specific kinds and intensities of activities. The purpose of this study was to examine the association between physical activity, including its various components (walking, climbing stairs, participation in sports and recreational activities), and stroke risk.
We conducted a prospective study to assess the association between cardiorespiratory fitness and prostate cancer. The subjects were men, aged 20-80 yr, who received a preventive medical exam at the Cooper Clinic in Dallas, TX, during 1970-1989 and provided information on cardiorespiratory fitness and prostate cancer (N = 12,975). Cardiorespiratory fitness was assessed at a baseline examination between 1971 and 1989 using a maximal exercise treadmill test.
