The effects of intense exercise on pain perception, mood, and plasma endocrine levels in man were studied under naloxone and saline conditions. Twelve long-distance runners (mean weekly mileage = 41.5) were evaluated on thermal, ischemic, and cold pressor pain tests and on mood visual analogue scales (VAS). Blood was drawn for determination of plasma levels of beta-endorphin-like immunoreactivity (BEir), growth hormone (GH), adrenocorticotrophic hormone (ACTH), and prolactin (PRL). These procedures were undertaken before and after a 6.3 mile run at 85% of maximal aerobic capacity. Subjects participated on two occasions in a double-blind procedure counterbalanced for drug order: on one day they received 2 i.v. injections of naloxone (0.8 mg in 2 ml vehicle each) at 20 min intervals following the run; on the other day, 2 equal volume injections of normal saline (2 ml). Sensory decision theory analysis of the responses to thermal stimulation showed that discriminability, P(A), was significantly reduced post-run under the saline condition, a hypoalgesic effect; response bias, B, was unaffected. Ischemic pain reports were significantly reduced post-run on the saline day, also a hypoalgesic effect. Naloxone reversed the post-run ischemic but not thermal hypoalgesic effects. Joy, euphoria, cooperation, and conscientiousness VAS ratings were elevated post-run; naloxone attenuated the elevation of joy and euphoria ratings only. Plasma levels of BEir, ACTH, GH, and PRL were significantly increased post-run. The results show that long-distance running produces hypoalgesia and mood elevation in man. The effects of naloxone implicate endogenous opioid neural systems as mechanisms of some but not all of the run-induced alterations in mood and pain perception.

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Four-pi whole body counting for the 1.46 meV photon of 40K has apparent advantages over single-crystal or two-pi counters in efficiency and in subject geometry independence. However, our studies of obese populations have disclosed a systematic undermeasurement of 40K, suggesting that nonhomogeneous K distribution results in systematic undercounting of 40K. In the current study 42K, emitting a 1.52 meV photon, was used in 109 volunteers ranging from 50 to 181 kg, and multiregression covariance analysis was applied to develop correction formulas based on anthropometrics. These corrections quantitatively account for the unappreciated loss of 40K and 42K photons in annular adipose tissue that surrounds the lean body, in which most K+ is concentrated. The correction ranges from 1 to 28% and is a linear (although different) function of weight in both sexes. Thus corrected, body potassium measurements, taken in conjunction with exchangeable sodium and water measurements, provide estimates for whole body osmolality that match measured serum values. Such a quantitative accounting for previously "lost" cation in 58 subjects provides independent evidence for the appropriateness and accuracy of the correction. With this correction, body potassium was recalculated in the 1,492 adult members of a previously reported group of 3,083 subjects.

Thermogenesis after exercise was studied by measuring oxygen consumption in 23 subjects who were classified into three groups according to their routine level of physical activity. VO2 was first measured after a 30-minute rest period 4-hours after breakfast. Then each subject either exercised for 20 minutes at approximately the anaerobic threshold or on a separate non-exercise day remained recumbent. The subject then returned to, or remained, at rest. There was no significant difference in VO2 from the resting level from 40 minutes to 3 hours after exercise, between exercise and non-exercise days in any fitness group. Seven subjects also exercised for a longer period or at a higher intensity. Again, there was no significant difference in the time course of VO2 from 40 minutes to 220 minutes after exercise, between exercise and non-exercise days. Because no sustained effect of moderate or intense exercise on VO2 was demonstrated, we conclude that no appreciable caloric loss beyond that generated by the exercise period itself and the early recovery phase is found in either fit or unfit subjects. These data do not support claims for sustained increases in metabolic rate after exercise in weight-control programs.

The literature suggests that Asians have lower bone mineral density and mass than whites. It has been proposed that these differences may be due to differences in height, weight, and factors other than ethnicity, but no study has made the appropriate direct comparisons. We compared total-body bone mineral density and mass between Asian and white women while controlling for factors known to be associated with bone mineral density and mass. Measurements were made in 129 Asian (primarily of Chinese ancestry) and 274 white women. A subgroup was formed of women who did not have a history of alcoholism, premenopausal amenorrhea, kidney disease, estrogen use, birth control pill use, thyroid disease, steroid use, hysterectomy, or smoking. In both the main group and the subgroups, bone mineral mass was significantly lower in Asian than in white women, but after analysis of covariance with body weight, height, and age (or years since menopause) as covariates, the differences between ethnic groups disappeared, except in the large group of premenopausal women, in whom average bone mineral density in Asians actually exceeded (p < 0.04) that in whites. The data set was also searched for Asian-white pairs who matched on 17 characteristics related to bone mineral density and mass. In the resulting 16 matched pairs, bone mineral density and mass were not different between ethnic groups. Although Asian women have lower bone mineral mass than white women, when weight, height, and other factors are controlled, bone mineral density and mass do not differ between Asian and white women.

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