With energy intake restriction and exercise remaining the key diet and lifestyle approaches to weight loss, this is not without potential negative implications for body composition, metabolic health, and quality and quantity of life. Ideally, weight loss should be derived almost exclusively from the fat mass compartment as this is the main driver of metabolic disease, however, several studies have shown that there is an accompanying loss of tissue from the fat-free compartment, especially skeletal muscle. Population groups including post-menopausal women, the elderly, those with metabolic disease and athletes may be particularly at risk of skeletal muscle loss when following a weight management programme. Research studies that have addressed this issue across a range of population groups are reviewed with a focus upon the contribution of resistance and endurance forms of exercise and a higher intake dietary protein above the current guideline of 0.8 g/kg body weight/day. While findings can be contradictory, overall, the consensus appears that fat-free and skeletal muscle masses can be preserved, albeit to varying degrees by including both forms of exercise (but especially resistance forms) in the weight management intervention. Equally, higher intakes of protein can protect loss of these body compartments, acting either separately or synergistically with exercise. Elderly individuals in particular may benefit most from this approach. Thus, the evidence supports the recommendations for intakes of protein above the current guidelines of 0.8 g/kg body weight/d for the healthy elderly population to also be incorporated into the dietary prescription for weight management in this age group.

Both the unspecific and the specific branch of the immune system are triggered and governed by contact and by a set of cytokines, including interleukin-1 (IL-1), interleukin-6 (IL-6), and tumor necrosis factor (TNF). These mediators, which are produced by activated macrophages and other cells, have also multiple (pleiotropic) effects on different cells and organs. While TNF and IL-1 have strongly proinflammatory effects and seem to play a critical role in clinical situations such as septic shock, IL-6 has more restorative effects by being the main inducer of the acute phase response of the liver. The monokines also induce fever and release of ACTH in the brain. Strenuous exercise leads to a significant elevation of cytokines in the serum thereby eliciting an acute phase response. Analysis of systemic cytokines in the serum of marathon runners by the 7TD1 cell line assay revealed that the observed activity is very likely IL-6.

Although regular physical activity is recommended for prevention of cardiovascular diseases, no data are available on its antiatherosclerotic effects in the general population. To determine whether progressive aerobic exercise compared with usual activity slows progression of atherosclerosis in men. A 6-year randomized, controlled trial. Eastern Finland. 140 middle-aged men randomly selected from the population registry. Low- to moderate-intensity aerobic exercise. Atherosclerosis was quantitated ultrasonographically as the mean intima-media thickness in the carotid artery at baseline and at years 2 through 6. On the basis of intention-to-treat analyses, a 19.5% net increase (P < 0.001) in ventilatory aerobic threshold was evident in the exercise group after 6 years. High-sensitivity C-reactive protein levels were statistically nonsignificantly lower in the exercise group than in the control group (P > 0.2). The progression of intima-media thickness in the carotid artery did not differ between the study groups (P > 0.2). A subgroup analysis that excluded men taking statins showed that the 6-year progression of intima-media thickness, adjusted for smoking and annual measures of low-density lipoprotein cholesterol level, systolic blood pressure, and waist circumference, was 40% less in the exercise group (0.12 mm [95% CI, -0.010 to 0.26 mm]) than in the control group (0.20 mm [CI, 0.05 to 0.35 mm]). Only middle-aged white men were included. The intervention included mainly aerobic exercises. Aerobic physical exercise did not attenuate progression of atherosclerosis, except in a subgroup of men not taking statins.

Fifteen athletes were investigated 24 h before, 1 h after, and 20 h after an exhaustive exercise stress test (mean duration 68 min). Testing for cytokines was done in serum, urine, and the supernatants of whole blood cell cultures, which were stimulated with lipopolysaccharide (LPS), concanavalin A(Con A), or phythaemagglutinin (PHA). Elevated levels of interleukin 6 (IL-6) and soluble IL-2 receptor (sIL-2R) were found 1 h after the run in both serum and urine samples. TNF-α in serum was also increased, whereas IL-2 in urine was decreased after the exercise. All other testings in serum and urine(including IFN-γ) gave borderline or negative results. In cell cultures, the LPS-induced release of the inflammatory cytokines TNF-α, IL-1, and IL-6 was suppressed 1 h after exercise. Also, the Con-A-induced and LPS-induced release of IFN-γ, and the PHA-induced release of IL-2 were suppressed 1 h after exercise. In contrast, Con-A-induced release of IL-2 was mildly increased after the run. We conclude that exercise of the intensity and duration described here causes an activation of the immune system, which is immediately counter-regulated. Twenty hours after the exercise, most of the observed changes were back to pre-exercise levels, indicating only a short duration for this suppressive counter-regulation.