Consumption of a Western diet rich in saturated fats is associated with obesity and insulin resistance. In some insulin-resistant phenotypes this is associated with accumulation of skeletal muscle fatty acids. We examined the effects of diets high in saturated fatty acids (Sat) or n-6 polyunsaturated fatty acids (PUFA) on skeletal muscle fatty acid metabolite accumulation and whole-body insulin sensitivity. Male Sprague-Dawley rats were fed a chow diet (16% calories from fat, Con) or a diet high (53%) in Sat or PUFA for 8 wk. Insulin sensitivity was assessed by fasting plasma glucose and insulin and glucose tolerance via an oral glucose tolerance test. Muscle ceramide and diacylglycerol (DAG) levels and triacylglycerol (TAG) fatty acids were also measured. Both high-fat diets increased plasma free fatty acid levels by 30%. Compared with Con, Sat-fed rats were insulin resistant, whereas PUFA-treated rats showed improved insulin sensitivity. Sat caused a 125% increase in muscle DAG and a small increase in TAG. Although PUFA also resulted in a small increase in DAG, the excess fatty acids were primarily directed toward TAG storage (105% above Con). Ceramide content was unaffected by either high-fat diet. To examine the effects of fatty acids on cellular lipid storage and glucose uptake in vitro, rat L6 myotubes were incubated for 5 h with saturated and polyunsaturated fatty acids. After treatment of L6 myotubes with palmitate (C16:0), the ceramide and DAG content were increased by two- and fivefold, respectively, concomitant with reduced insulin-stimulated glucose uptake. In contrast, treatment of these cells with linoleate (C18:2) did not alter DAG, ceramide levels, and glucose uptake compared with controls (no added fatty acids). Both 16:0 and 18:2 treatments increased myotube TAG levels (C18:2 vs. C16:0, P < 0.05). These results indicate that increasing dietary Sat induces insulin resistance with concomitant increases in muscle DAG. Diets rich in n-6 PUFA appear to prevent insulin resistance by directing fat into TAG, rather than other lipid metabolites.

Ultra-marathon running is frequently associated with muscle fibre damage. However, ultra-marathon related information is scarce. The present study evaluated muscle and cartilage biomarkers, and cytokine secretion during a 200 km running event. Venous blood samples from 54 trained male ultra-marathon runners (mean +/- SD, 45.7 +/- 5.1 years). Plasma creatine phosphokinase (CPK), lactate dehydrogenase (LDH), aspartate aminotransferase (AST), alanine aminotransferase (ALT), lactate, glucose, high-sensitivity C-reactive protein (Hs-CRP), interleukin-6 (IL-6), TNF- proportional, variant and serum cartilage oligomeric matrix protein (COMP) content were determined before, midway and immediately after the race. CPK increased 90-fold (19-fold at 100 km) from pre-race value and LDH increased 3.7-fold (2.2-fold at 100 km). AST increased 15-fold (5-fold at 100 km) and ALT increased 3.9-fold (2-fold at 100 km). Blood lactate and glucose levels did not change significantly. Hs-CRP increased 23-fold (3-fold at 100 km) and IL-6 increased 121-fold at 100 km, and then remained stable up to 200 km, whereas TNF- proportional, variant did not change significantly. Serum COMP increased 3-fold (1.3-fold at 100 km). Post-run CPK was correlated with LDH (r = 0.62, P < 0.001), Hs-CRP (r = 0.45, P < 0.001), ALT (r = 0.89, P < 0.001), AST (r = 0.97, P < 0.001), and IL-6 (r = 0.61, P < 0.001). The present study demonstrated that blood biomarkers related to muscle and cartilage damage and inflammation were increased during a 200 km run and that this was particularly marked during the second half of the event. Ultra-marathon running clearly has a major impact on muscle and cartilage structures.

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Carnosine (Carn) occurs in high concentrations in skeletal muscle is a potent physico-chemical buffer of H+ over the physiological range. Recent research has demonstrated that 6.4 g x day(-1) of beta-alanine (beta-ala) can significantly increase skeletal muscle Carn concentrations (M-[Carn]) whilst the resultant change in buffering capacity has been shown to be paralleled by significant improvements in anaerobic and aerobic measures of exercise performance. Muscle carnosine increase has also been linked to increased work done during resistance training. Prior research has suggested that strength training may also increase M-[Carn] although this is disputed by other studies. The aim of this investigation is to assess the effect of 10 weeks resistance training on M-[Carn], and, secondly, to investigate if increased M-[Carn] brought about through beta-ala supplementation had a positive effect on training responses. Twenty-six Vietnamese sports science students completed the study. The subjects completed a 10-week resistance-training program whilst consuming 6.4 g x day(-1) of beta-ala (beta-ALG) or a matched dose of a placebo (PLG). Subjects were assessed prior to and after training for whole body strength, isokinetic force production, muscular endurance, body composition. beta-Alanine supplemented subjects increased M-[Carn] by 12.81 +/- 7.97 mmol x kg(-1) dry muscle whilst there was no change in PLG subjects. There was no significant effect of beta-ala supplementation on any of the exercise parameters measured, mass or % body fat. In conclusion, 10 weeks of resistance training alone did not change M-[Carn].

Marathon running is frequently associated with numerous cellular changes, but little information is available on the effects of exercise-mediated prolonged impact-stress on cartilage integrity. This study was undertaken to evaluate muscle and cartilage damage with different running distances. Twenty male marathoners and ultra-marathoners participated in the study. Serum COMP and plasma CPK and hs-CRP were measured as markers of cartilage and muscle damage and inflammation. Serum COMP was increased 1.6-fold at 10 km during a marathon race and declined to the pre-race level after 2 days recovery. In contrast, serum COMP was increased 1.9-fold after a 200-km race and maintained until day 3 of recovery, only returning to the pre-race level on day 6. Plasma CPK was increased at 10 km of the marathon race and up to threefold at the end of the race. This was further increased on day 1, only returning to pre-race level on day 6. Plasma CPK was increased 35-fold at the end of the 200-km race and remained increased until day 5. There was no change in plasma hs-CRP during the marathon race, but this was increased 3.4-fold by day 1, returning to the pre-race level on day 4. Plasma hs-CRP increased 40-fold by the end of the 200-km race and was still increased on day 6 of recovery. Therefore, longer distance running may induce more impact-stress both on muscle and cartilage. Further, the required time for recovery may vary with running distance and the tissue type, e.g. cartilage or skeletal muscle as in this case.