Supplementation with a whey protein hydrolysate enhances recovery of muscle force-generating capacity following eccentric exercise.

There is evidence that protein hydrolysates can speed tissue repair following damage and may therefore be useful for accelerating recovery from exercise induced muscle damage. The potential for a hydrolysate (WPI(HD)) of whey protein isolate (WPI) to speed recovery following eccentric exercise was evaluated by assessing effects on recovery of peak isometric torque (PIT). In a double-blind randomised parallel trial, 28 sedentary males had muscle soreness (MS), serum creatine kinase (CK) activity, plasma TNFalpha, and PIT assessed at baseline and after 100 maximal eccentric contractions (ECC) of their knee extensors. Participants then consumed 250 ml of flavoured water (FW; n=11), or FW containing 25 g WPI (n=11) or 25 g WPI(HD) (n=6) and the assessments were repeated 1, 2, 6 and 24h later. PIT decreased approximately 23% following ECC, remained suppressed in FW and WPI, but recovered fully in WPI(HD) by 6h (P=0.006, treatment x time interaction). MS increased following ECC (P<0.001 for time), and remained elevated with no difference between groups (P=0.61). TNFalpha and CK did not change (P>0.45). WPI(HD) may be a useful supplement for assisting athletes to recover from fatiguing eccentric exercise.

Dietary phospholipid-rich dairy milk extract reduces hepatomegaly, hepatic steatosis and hyperlipidemia in mice fed a high-fat diet.

Recent studies have suggested that milk and certain dairy food components have the potential to protect against cardiovascular disease. In order to determine whether the addition of milk-derived phospholipids to the diet results in an improvement in metabolic and cardiovascular risk factors, we studied four groups (n=10) of C57BL/6 mice that were fed: (1) a normal non-purified diet (N); (2) the normal non-purified diet supplemented with phospholipid-rich dairy milk extract (PLRDME, 2.5% by wt) (NPL); (3) a high-fat semi-purified diet (HF) containing 21% butterfat+0.15% cholesterol by wt; or (4) HF supplemented with 2.5% by wt PLRDME (HFPL). Dietary PLRDME supplementation did not have a significant effect on metabolic parameters in mice fed the N diet. In contrast, in high-fat fed mice, PLRDME caused a significant decrease in: (a) liver wt (1.57+/-0.06 g vs. 1.20+/-0.04 g, P<0.001), (b) total liver lipid (255+/-22 mg vs. 127+/-13 mg, P<0.001, (c) liver triglyceride (TG) and total cholesterol (TC) 236+/-25 micromol/g vs. 130+/-8 micromol/g (P<0.01), 40+/-7 micromol/g vs. 21+/-2 micromol/g (P<0.05), respectively); and serum lipids (TG: 1.4+/-0.1 mmol/L vs. 1.1+/-0.1 mmol/L, P=0.01; TC: 4.6+/-0.2 mmol/L vs. 3.6+/-0.2 mmol/L, P<0.001; and PL: 3.3+/-0.1 mmol/L vs. 2.6+/-0.1 mmol/L, P<0.01). These data indicate that dietary PLRDME has a beneficial effect on hepatomegaly, hepatic steatosis and elevated serum lipid levels in mice fed a high-fat diet, providing evidence that PLRDME might be of therapeutic value in human subjects as a hepatoprotective or cardioprotective nutraceutical.