The effects of adaptation to a high-fat diet on endurance performance are equivocal, and there is little data regarding the effects on high-intensity exercise performance. This study examined the effects of a high-fat/moderate protein diet on submaximal, maximal, and supramaximal performance. Twenty non-highly trained men were assigned to either a high-fat/moderate protein (HFMP; 61% fat diet) (n = 12) or a control (C; 25% fat) group (n = 8). A maximal oxygen consumption test, two 30-s Wingate anaerobic tests, and a 45-min timed ride were performed before and after 6 weeks of diet and training. Body mass decreased significantly (-2.2 kg; p < or = .05) in HFMP subjects. Maximal oxygen consumption significantly decreased in the HFMP group (3.5 +/- 0.14 to 3.27 +/- 0.09 L x min(-1)) but was unaffected when corrected for body mass. Perceived exertion was significantly higher during this test in the HFMP group. Main time effects indicated that peak and mean power decreased significantly during bout 1 of the Wingate sprints in the HFMP (-10 and -20%, respectively) group but not the C (-8 and -16%, respectively) group. Only peak power was lower during bout 1 in the HFMP group when corrected for body mass. Despite significantly reduced RER values in the HFMP group during the 45-min cycling bout, work output was significantly decreased (-18%). Adaptation to a 6-week HFMP diet in non-highly trained men resulted in increased fat oxidation during exercise and small decrements in peak power output and endurance performance. These deleterious effects on exercise performance may be accounted for in part by a reduction in body mass and/or increased ratings of perceived exertion.
The high rate of continuation of hormone treatment indicates that, despite the recent adverse publicity, these women feel well informed and were not willing to discontinue with their hormone therapy if they felt well. A regular discussion of the risks and benefits of HRT remains mandatory.
Our lab has previously demonstrated that estrogen (E2) downregulates the expression and function of voltage‐gated, L‐type Ca2+ channels (CaL) in coronary arteries in vitro. In this study we hypothesized that the in vivo depletion of E2 would generate an increase in Ca2+‐dependent arterial tone. Mice (C57BL/6) underwent an ovariectomy (OVX) or sham surgery at 8‐wks of age. Biotelemetry measured a drop in heart rate (p=0.002) and blood pressure (p=0.09) in OVX mice within 2‐wks post‐surgery suggesting a baroreceptor reflex compensation. Mice were sacrificed 4‐wks post‐surgery and the mesenteric arteries isolated. The OVX mice demonstrated atrophied uteri and low E2 plasma levels. In the mesenteric arteries, Western blots demonstrated a slight (p=0.12) increase in CaL expression from OVX mice. Mesenteric arterial reactivity experiments indicated no difference between groups in their spontaneous tone and response to the CaL agonist, FPL64176 (3×10−7 to 1×10−6). This suggests that, while E2 depletion alone does not promote hypertension, other underlying pathologies in conjunction with E2 depletion may lead to hypertension and other cardiovascular diseases. Support: NIGMM of the NIH, Grant #P20 GM103429–11
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