Female cadets maintained a significantly more fat-predominant fuel metabolism than did male cadets in response to sustained exercise and semistarvation.

Moderate exercise appears to stimulate the immune system, but there is good evidence that intense exercise can cause immune deficiency. In the present study the authors examined the effect of continuous physical exercise (35% of VO2 max), calorie deficiency and sleep deprivation on the immune system of young men participating in a 5–7 days military training course. There was a two–three fold increase of neutrophils from day 1, the values remained high and decreased slightly at the end of the course. Monocyte counts also increased with a pattern similar to that of neutrophils. Eosinophils decreased to 30% of control and lymphocyte numbers decreased by 30–40%. All the major subgroups (CD4 T cells , CD8 T cells, B cells, NK cells) were reduced. Neutrophil function, as tested by measuring chemotaxis, was significantly stimulated during the first days of the course, in particular in the group with the lowest calorie intake. The mitogenic response of lymphocytes to PHA and Con A was variable, ranging from stimulation during one course to no effect in another course. Serum levels of immunoglobulins decreased significantly during the course. IgG was reduced by 6–7%, IgA by 10–20% and IgM by 20–35%. The authors found no changes of interleukin 1, 2 and 4 during the course, but a (12–20%) reduction (P<0.01) of interleukin 6 , and an increase (P<0.01) of granulocyte–macrophage colony stimulating factor. Altogether the results from the ranger course present a mixed‐up picture. The non‐specific phagocyte‐related immunity was enhanced. On the other hand, the data indicate that even a moderate physical activity, around the clock, caused significant suppression of a number of parameters reflecting the status of the specific, lymphocyte‐related immunity. It is noteworthy, however, that there was no significantly increased infection rate during the course or in the first 4–5 weeks thereafter.

The intention of the study was to investigate a possible correlation between increase in circulating blood level of beta‐endorphin and decrease in pain perception after short‐term intensive physical exercise. In addition, we wanted to see if plasma beta‐endorphin level and pain perception were influenced by regular physical or mental training and if there was any difference in response between trained and untrained subjects. Twenty physically trained males were studied before and after a 6‐month intervention period while practising regular physical endurance training. Eleven of them were randomized to perform daily additional mental training (ACEM meditation). Nine untrained males served as control subjects and were investigated only at baseline. All participants were tested for maximum oxygen uptake (VO2max) during treadmill exercise, and pain perception measured by an ischaemic pain test was performed just before and after VO2max. Blood samples analysed for beta‐endorphin were drawn before and after the tests. There was a substantial decrease of 47 per cent (p < 0.005) in basal plasma beta‐endorphin level after the intervention. The plasma beta‐endorphin level increased two‐fold (p < 0.01) in response to the VO2max test. The subjects experienced post‐exercise hypoalgesia (p < 0.001), but there was no correlation between the exercise‐associated opioid hyperendemia and the hypoalgesia. No difference was found between trained and untrained subjects regarding the circulating blood level of beta‐endorphin or the exercise‐induced hypoalgesia. Practising regular meditation had no influence on beta‐endorphin level or pain tolerance level. Peripheral beta‐endorphin level and pain perception are modulated by intensive physical exercise and by regular physical, but not by mental training. It could be speculated that the observed initial high basal level of beta‐endorphin is due to pre‐experimental stress and tension. Copyright © 2001 John Wiley & Sons, Ltd.