Mark S. Sothmann

Adiposity, Fat Distribution, and Cardiovascular Risk

STUDY OBJECTIVE To determine the relative importance of adiposity and fat distribution to cardiovascular risk profile. DESIGN A cross-sectional study. SETTING Clinical research center funded by the National Institutes of Health. PATIENTS Convenience sample of 33 healthy premenopausal women with a wide range of body weight who did not have diabetes mellitus, hirsutism and virilism, gynecologic disorder, cardiac disease, or hypertension. Women participating in exercise or dietary programs or taking medication were excluded. All subjects completed the study. INTERVENTIONS Total body fat mass was determined by hydrostatic weighting, and fat distribution was assessed by subscapular skinfold thickness, subscapular-to-triceps skinfold ratio, the waist-to-hip ratio, and computed tomography. Cardiovascular risk was assessed by the serum insulin response during oral glucose stimulation; levels of triglycerides and total cholesterol; high-density lipoprotein cholesterol to total cholesterol concentrations; and systolic and diastolic blood pressures. MEASUREMENTS AND MAIN RESULTS The anthropometric parameters chosen were significantly associated with the cardiovascular risk profile (P less than 0.001). Visceral fat distribution assessed by computed tomography accounted for a significantly greater degree of variance in the cardiovascular risk factors than the total body fat mass (P less than 0.05). The cumulative insulin response was the primary metabolic variable relating the anthropometric indices to cardiovascular risk. CONCLUSIONS Intra-abdominal fat deposition constitutes a greater cardiovascular risk than obesity alone. Hyperinsulinemia may constitute an important component of the increased cardiovascular risk of abdominal obesity.

Heart rate response of firefighters to actual emergencies : implications for cardiorespiratory fitness

Heart rate (HR) and oxygen consumption (VO2) responses during actual fire-suppression emergencies were monitored in 10 male firefighters. These firefighters worked at 157 +/- 8 beats per minute (bpm) for 15 +/- 7 minutes. This was 88 +/- 6% of their previously determined HR max. Based on treadmill testing, the HR x VO2 relationship was established for each firefighter. The predicted VO2 derived from HR monitoring in actual emergencies was 25.6 +/- 8.7 mL.kg-1.min-1 or 63 +/- 14% of VO2 max (40.0 +/- 6.5 mL.kg-1.min-1). These values on the cardiorespiratory response to actual emergencies are very similar to results derived from studies employing fire-suppression simulations. Recommendations for the VO2 max of firefighters ranging from 33.5 to 42.0 mL.kg-1.min-1 that have been generated from simulation testing appear appropriate given the cardiorespiratory responses to actual emergencies.

Plasma catecholamine response to acute psychological stress in humans : relation to aerobic fitness and exercise training

Existing cross-sectional studies on plasma catecholamine activity provide no support for the concept that a markedly high level of aerobic fitness modifies sympathoadrenal response to an acute psychological challenge in humans. In contrast, compromised sympathetic nervous system activity has been observed in individuals with low aerobic fitness and the relationship probably reflects a global deconditioning syndrome involving both psychological and physiological processes. The relationship between low levels of fitness and plasma norepinephrine may appear as a blunted or augmented response depending upon the nature of the task. Short-term (3-4 months) exercise training studies conducted with humans have not indicated a substantial adaptation in the relative plasma catecholamine change from a preexisting baseline during exposure to acute psychological stress. Exercise training can lower basal circulating plasma norepinephrine, resulting in lower absolute concentrations during an acute challenge, but the studies in this area lack consistency and the absolute change tends to be modest. There is no evidence that fitness or exercise training is significantly associated with plasma epinephrine activity during short-term psychological stress.

Simulated weightlessness to induce chronic hypoactivity of brain norepinephrine for exercise and stress studies.

Although research on the relationship between exercise training and physiological stress reactivity is increasing, we know little about the involvement of brain neurochemistry. Moreover, the few studies that have been performed have concentrated on animals with normally functioning neurochemistry exposed to an acute stressor. Biomedical research is drawing an association between hypoactivation of the physiological stress response and certain medical conditions. As such, there is a need for an animal model that manifests a chronic hypoactivity of the stress system. In this report we describe the results from studies on norepinephrine changes with actual and simulated weightlessness in animals and humans. There is consistent evidence with rats that 14 d of simulated weightlessness produces reduced norepinephrine turnover in selected brainstem nuclei and peripheral tissue mediating the physiological stress response. Little is known about other brain regions, particularly the hypothlamus. These preliminary data suggest that simulated weightlessness is one method by which a chronic hypoactivity of norepinephrine biosynthesis or release might be induced to study exercise training as an intervention.

Selected psychophysiological stress responses in men with high and low body fatness.

Previous research on catecholamine (CA) response to exercise has linked heightened adiposity to a hypostress syndrome. In the present study a cognitive/psychomotor stressor was employed to determine whether this association exists during less metabolically challenging tasks. Moreover, because stress is manifested in a multidimensional manner, measures of behavior and perceived distress were analyzed in addition to the physiological response. Men were selectively recruited for two body fatness groups (low, 12 +/- 4%, N = 9; high, 27 +/- 2%, N = 10) while being matched on age, lean weight, and peak absolute oxygen consumption. All men performed a modified Stroop task for 12 min to induce a psychophysiological stress response. Physiological changes included significant increases in heart rate, venous plasma norepinephrine, and epinephrine. Cognitive/psychomotor responses indicated no change in reaction time during the task but significant cognitive fatigue as indicated by post-task anagram performance. Perceived distress was suggested by elevated state anxiety. The high and low adiposity groups were similar on all measures of the psychophysiological stress response. These findings suggest that elevated adiposity is not characterized by a hypostress state during the relatively low metabolic challenge of a cognitive/psychomotor stressor.