Cardiovascular autonomic modulation during 36 h of total sleep deprivation (SD) was assessed in 18 normal subjects (16 men, 2 women, 26.0 +/- 4.6 yr old). ECG and continuous blood pressure (BP) from radial artery tonometry were obtained at 2100 on the first study night (baseline) and every subsequent 12 h of SD. Each measurement period included resting supine, seated, and seated performing computerized tasks and measured vigilance and executive function. Subjects were not supine in the periods between measurements. Spectral analysis of heart rate variability (HRV) and BP variability (BPV) was computed for cardiac parasympathetic modulation [high-frequency power (HF)], sympathetic modulation [low-frequency power (LF)], sympathovagal balance (LF/HF power of R-R variability), and BPV sympathetic modulation (at LF). All spectral data were expressed in normalized units [(total power of the components/total power-very LF) x 100]. Spontaneous baroreflex sensitivity (BRS), based on systolic BP and pulse interval powers, was also measured. Supine and sitting, BPV LF was significantly increased from baseline at 12, 24, and 36 h of SD. Sitting, HRV LF was increased at 12 and 24 h of SD, HRV HF was decreased at 12 h SD, and HRV LF/HF power of R-R variability was increased at 12 h of SD. BRS was decreased at 24 h of SD supine and seated. During the simple reaction time task (vigilance testing), the significantly increased sympathetic and decreased parasympathetic cardiac modulation and BRS extended through 36 h of SD. In summary, acute SD was associated with increased sympathetic and decreased parasympathetic cardiovascular modulation and decreased BRS, most consistently in the seated position and during simple reaction-time testing.

Aerobic exercise reduces coronary heart disease risk, but the mechanisms of this protection are not fully understood. Atherosclerosis is an inflammatory disease mediated by monocyte-derived macrophages, which accumulate in arterial plaques and become activated to release factors, including cytokines, that cause damage. Here we studied the effects of aerobic training on monocyte production of tumor necrosis factor (TNF) in whole blood ex vivo. Healthy young sedentary adults (n = 61, age 20-45 yr) were randomized to a moderate- (M) or a high- (H) intensity 12-wk training program. Whole blood was extracted before and after training, and then it was stimulated by addition of lipopolysaccharide (LPS); inducible TNF was measured in the plasma. Data were analyzed according to intention to treat principles using a random-effect model to determine the impact of training group on maximal aerobic capacity and LPS-stimulated TNF after correcting for covariates. Analyses revealed improvement in aerobic capacity in both the H (9%) and the M (7%) groups. However, aerobic training led to significant (P < 0.001) decreases in TNF release only in the H group. These data suggest that in healthy young adults, a 12-wk high-intensity aerobic training program downregulates blood monocyte production of stimulated cytokine release.

In sedentary, healthy young adults, aerobic conditioning but not strength training enhances autonomic control of the heart, but post hoc analyses suggested that gender plays a significant role in this exercise-related cardioprotection.

No abstract

To test the hypothesis that endurance training Is associated with a decreased llpemla after a high fat meal, 16 young men [22 to 34 years old, nine of whom were trained (T) and seven of whom were untrained (UT)] were recruited. T ran >30 or blked >100 miles a week, while UT had been sedentary for at least the preceding 3 months. Dally caloric Intake and dally caloric expenditure during exercise were 35% and 704% greater, respectively, In T than In UT. V O i^ was 31% greater, while percent body fat was 36% lower In T than In UT. Dietary composition and body height and weight were similar. After a fasting blood sample was taken, the men ate a high fat meal (approximately 56% of total calories as fat In 1100 kcal adjusted to body weight), and additional blood samples were taken hourly for 8 hours. Fasting llplds were similar. Postprandial peak trtglyceride (TGw), percent TG Increase (%TGI), and total llpemlc response (TLR, the area under the llpemla curve In excess of fasting TG) were 42%, 54%, and 75% greater, respectively, In UT vs. T. Stepwlse regression analysis showed that the same three-variable model (training status, fasting TG, and VOJ™,) described the variation In T G^ (/7'=0.97), %TGI (ft'=0.75), and TLR (ft 2 =0.92). Furthermore, this same analysis showed that after adjustment for fasting TG and VOftn.,, the UT group had a significantly greater postprandial llpemla whether expressed as T G^ (/X0.0001), %TGI (p=0.0002), or TLR (p=0.0002). Thus, endurance training appears to be associated with a diminished llpemla after a high fat meal in young adult men. (Arteriosclerosis 9:217-223, March/April 1989) A therosclerosis is the major underlying cause of death and disability in Western society.1 Most research dealing with the etiology of atherosclerotic vascular disease has linked elevated postabsorptive blood cholesterol and low density lipoproteins with an increased risk of developing the disease. In contrast, little attention has been paid to fat tolerance, which may be defined as the plasma triglyceride (TG) response to a fatty meal.2 However, the magnitude of the triglyceridemic response to a standard fatty meal (postprandial lipemia) differs substantially among apparently healthy individuals who are considered normolipidemic on the basis of fasting blood lipid values.3 Even among apparently normolipidemic individuals, the variability in postprandial lipemia may be pathophysiological, since a significant lipemia may persist throughout most of the day in normal adults consuming fatty foods over three meals. 4 In fact, recent work by Zilversmit 3 suggests that postprandial metabolism of TGrich lipoproteins may constitute an atherogenic process in individuals who chronically eat a diet rich in fat and cholesterol. Furthermore, Engelberg 6 has recently reviewed some older literature, which suggests that tissue hypoxia Received January 4,1988; revision accepted October 24,1988. can also result from this postprandial lipemia and that this hypoxia may also be atherogenic. Thus, if the rate of atherogenesis ...