In conclusion, the SQUASH is a fairly reliable and reasonably valid questionnaire and may be used to order subjects according to their level of physical activity in an adult population. Because the SQUASH is a short and simple questionnaire, it may proof to be a very useful tool for the evaluation of health enhancing physical activity in large populations.

OBJECTIVE: To investigate the long-term effects of changes in dietary carbohydrateafat ratio and simple vs complex carbohydrates. DESIGN: Randomized controlled multicentre trial (CARMEN), in which subjects were allocated for 6 months either to a seasonal control group (no intervention) or to one of three experimental groups: a control diet group (dietary intervention typical of the average national intake); a low-fat high simple carbohydrate group; or a low-fat high complex carbohydrate group. SUBJECTS: Three hundred and ninety eight moderately obese adults. MEASUREMENTS: The change in body weight was the primary outcome; changes in body composition and blood lipids were secondary outcomes. RESULTS: Body weight loss in the low-fat high simple carbohydrate and low-fat high complex carbohydrate groups was 0.9 kg (P`0.05) and 1.8 kg (P`0.001), while the control diet and seasonal control groups gained weight (0.8 and 0.1 kg, NS). Fat mass changed by 7 1.3 kg (P`0.01), 7 1.8 kg (P`0.001) and 0.6 kg (NS) in the low-fat high simple carbohydrate, low-fat high complex carbohydrate and control diet groups, respectively. Changes in blood lipids did not differ signi®cantly between the dietary treatment groups. CONCLUSION: Our ®ndings suggest that reduction of fat intake results in a modest but signi®cant reduction in body weight and body fatness. The concomitant increase in either simple or complex carbohydrates did not indicate signi®cant differences in weight change. No adverse effects on blood lipids were observed. These ®ndings underline the importance of this dietary change and its potential impact on the public health implications of obesity.

Lipotoxicity in skeletal muscle plays a critical role in the aetiology of insulin resistance and type 2 diabetes mellitus by interference of lipid metabolites with insulin signalling and action. The dynamics of lipid oxidation and fine tuning with fatty acid uptake and intramyocellular triacylglycerol turnover may be very important to limit the accumulation of lipid intermediates. The use of metabolic inflexibility, defined as the impaired capacity to increase fat oxidation upon increased fatty acid availability and to switch between fat and glucose as the primary fuel source after a meal, does more justice to the complexity of changes in fuel oxidation during the day. Fatty acid availability, uptake and oxidation all play a role in metabolic flexibility and insulin resistance. During high fatty acid availability, fatty acid transporters may limit cellular and mitochondrial fatty acid uptake and thus limit fat oxidation. After a meal, when the demand for fatty acids as fuel is low, an increased fractional extraction of lipids from plasma may promote intramyocellular lipid accumulation and insulin resistance. Furthermore, defects in fuel switching cluster together with impaired mitochondrial content and/or function. Lifestyle changes in dietary fat intake, physical activity and weight loss may improve metabolic flexibility in skeletal muscle, and thereby contribute to the prevention of type 2 diabetes.

This is the first part in a series of three articles about fat metabolism during exercise. In this part the mobilization of fatty acids and their metabolism will be discussed as well as the possible limiting steps of fat oxidation. It is known for a long time that fatty acids are an important fuel for contracting muscle. After lipolysis, fatty acids from adipose tissue have to be transported through the blood to the muscle. Fatty acids derived from circulating TG may also be used as a fuel but are believed to be less important during exercise. In the muscle the IMTG stores may also provide fatty acids for oxidation after stimulation of hormone sensitive lipase. In the muscle cell, fatty acids will be transported by carrier proteins (FABP), and after activation, fatty acyl CoA have to cross the mitochondrial membrane through the carnitine palmytoyl transferase system, after which the acyl CoA will be degraded to acetyl CoA for oxidation. The two steps that are most likely to limit fat oxidation are fatty acid mobilization from adipose tissue and transport of fatty acids into the mitochondria along with mitochondrial density and the muscles capacity to oxidize fatty acids.

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