Soy-based diets reportedly protect against the development of atherosclerosis; however, the underlying mechanism(s) for this protection remains unknown. In this report, the mechanism(s) contributing to the atheroprotective effects of a soy-based diet was addressed using the apolipoprotein E knockout (apoE-/-) mice fed soy protein isolate (SPI) associated with or without phytochemicals (SPI+ and SPI-, respectively) or casein (CAS). Reduced atherosclerotic lesions were observed in aortic sinus and enface analyses of the descending aorta in SPI+- or SPI(-)-fed apoE-/- mice compared with CAS-fed mice. SPI+-fed mice showed 20% fewer lesions compared with SPI(-)-fed mice. Plasma lipid profiles did not differ among the 3 groups, suggesting alternative mechanism(s) could have contributed to the atheroprotective effect of soy-based diets. Real-time quantitative PCR analyses of proximal aorta showed reduced expression of monocyte chemoattractant protein-1 (MCP-1), a monocyte chemokine, in mice fed both soy-based diets compared with the CAS-fed mice. These findings paralleled the reduced number of macrophages observed in the lesion site in the aorta of SPI+- or SPI(-)-fed mice compared with CAS-fed mice. In an in vitro LPS-induced inflammation model, soy isoflavones (genistein, daidzein, and equol alone or in combination) dose dependently inhibited LPS-induced MCP-1 secretion by macrophages, suggesting a role for soy isoflavones for the protective in vivo effects. Collectively, these findings suggest that the reduction in atherosclerotic lesions observed in mice fed the soy-based diet is mediated in part by inhibition of MCP-1 that could result in reduced monocyte migration, an early event during atherogenesis.

Adrenal-sympathico function, blood carbohydrates and lipids, and water and electrolyte balance were studied in six highly trained male marathon runners prior to and after running a marathon (26.2 miles; 42.2 km) and on control days corresponding to the above times. Fluid intake was not sufficient to maintain body weight, the runners losing approximately 2.8 kg. Estimated plasma volume losses (161 ml, 4.4%) indicated that most of the fluid loss was extravascular. Tre rose an average 2.4 degrees C and a significant negative correlation between running time and rise in Tre was observed. Glucose, fatty acids, glycerol, hemoglobin, and plasma proteins were significantly elevated after the race. Small but statistically significant increments in lactate and pyruvate were also observed. Alterations in adrenal-sympathico function were indicated by increased levels of cortisol, epinephrine, and norepinephrine.

The metabolic, thermal, and cardiovascular responses of two male Caucasians to 1 2 h exposure to ambient temperature ranging between 28 degrees C and 5 degrees C were studied and related to the respective ambient temperatures. The metabolic heat production increased linearly with decreasing ambient temperature, where heat production (kcal times m- minus 2 times h- minus 1) = minus 2.79 Ta degrees C + 103.4, r = -0.97, P smaller than 0.001. During all exposures below 28 degrees C, the rate of decrease in mean skin temperature (Tsk) was found to be an exponential function dependent upon the ambient temperature (Ta) and the time of exposure. Reestablishment of Tsk steady state occurred at 90-120 min of exposure, and the time needed to attain steady state was linearly related to decreasing Ta. The net result was that a constant ratio of 1.5 of the external thermal gradient to the internal thermal gradient was obtained, and at all experimental temperatures, the whole body heat transfer coefficient remained constant. Cardiac output was inversely related to decreasing Ta, where cardiac output (Q) = minus 0.25 Ta degrees C + 14.0, r = minus 0.92, P smaller than 0.01. However, the primary reason for the increased Q, the stroke output, was also described as a third-order polynomial, although the increasing stroke volume throughout the Ta range (28-5 degrees C) was linearly related to decreasing ambients. The non-linear response of this parameter which occurred at 20 degrees C larger than or equal to Ta larger than or equal to 10 degrees C suggested that the organism's cardiac output response was an integration of the depressed heart rate response and the increasing stroke output at these temperatures.

Five male volunteers performed 20 min of steady-state submaximal exercise on a motor-driven treadmill at five intensities (30, 45, 60, 75, and 90% VO2 max) as well as several maximal aerobic capacity tests. Peripheral venous plasma testosterone concentrations increased above resting values in proportion to exercise intensity. However, this increase in plasma testosterone concentration was virtually equal in magnitude to the decrease in plasma volume observed consequent to the exercise bouts, resulting in no change in total testosterone contents. There was an unexpected anticipatory elevation in resting preexercise control testosterone concentration and content with increasing work intensity. The possibility that testosterone has a direct role in the organism's response to whole-body exercise is questioned.

Six endurance-trained and heat-acclimatized adult males ran for 1 h (or until exhaustion) at room temperature (23.8 degrees C) on three occasions. The work loads approximated 37, 56, and 74% of the subjects' aerobic capacities. Venous blood samples were drawn, and urine was collected before and immediately after each exercise bout. Metabolic cost was partitioned by energy substrate, and metabolic water production was quantified from urinary nitrogen, oxygen, and carbon dioxide production. Total body water loss was recorded as the decrease in body weight during the exercise. All subjects completed 1 h of exercise at the two lower exercise intensities but, due to exhaustion, averaged only 35.5 min at the highest work intensity. There were no significant changes in plasma volume after the exercise bouts. Metabolic water production increased with increasing work intensity as did the fraction of total caloric expenditure derived from carbohydrate metabolism. Plasma protein content significantly increased at all levels of exercise intensity. Metabolic water production alone would be of minimal help in plasma volume maintenance and thermoregulation during endurance exercise.

Oxygen uptakes and running speeds of two marathon runners as well as average slopes of the running terrain were measured approximately every 3 miles of a competitive marathon. The runners had energy expenditures requiring from 68 to 100% of their Vo2 max, confirming previous estimates. As the race progressed, both runners exhibited decreases in V92 while running at similar rates and slopes. At 23.4 miles, one runner was found to be utilizing 4.54 l/min, a value equivalent to his Vo2 max.

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