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It is known that chronic endurance training leads to improvements in the lipoprotein profile, but less is known about changes that occur during postexercise recovery acutely. We analyzed triglyceride (TG), cholesterol classes and apolipoproteins in samples collected before, during and after individual moderate- and hard-intensity exercise sessions in men and women that were isoenergetic between intensities. Young healthy men (n = 9) and young healthy women (n = 9) were studied under three different conditions with diet unchanged between trials: (1) before, during and 3 h after 90 min of exercise at 45% VO2peak (E45); (2) before, during and 3 h after 60 min of exercise at 65% VO2peak (E65), and (3) in a time-matched sedentary control trial (C). At baseline, high-density lipoprotein cholesterol (HDL-C) was higher in women than men (P

Three weeks of caloric restriction alters protein metabolism in normal-weight young men. Am J Physiol Endocrinol Metab 289: E446-E455, 2005. First published May 3, 2005; doi:10.1152/ajpendo.00001.2005.--The effects of prolonged caloric restriction (CR) on protein kinetics in lean subjects has not been investigated previously. The purpose of this study was to test the hypotheses that 21 days of CR in lean subjects would 1) result in significant losses of lean mass despite a suppression in leucine turnover and oxidation and 2) negatively impact exercise performance. Nine young, normal-weight men [23 [+ or -] 5 y, 78.6 [+ or -] 5.7 kg, peak oxygen consumption (V[O.sub.2] peak) 45.2 [+ or -] 7.3 ml x [kg.sup.-1] x [min.sup.-1], mean [+ or -] SD] were underfed by 40% of the calories required to maintain body weight for 21 days and lost 3.8 [+ or -] 0.3 kg body wt and 2.0 [+ or -] 0.4 kg lean mass. Protein intake was kept at 1.2 g x [kg.sup.-1] x [day.sup.-1]. Leucine kinetics were measured using [alpha]-ketoisocaproic acid reciprocal pool model in the postabsorptive state during rest and 50 min of exercise (EX) at 50% of V[O.sub.2] peak. Body composition, basal metabolic rate (BMR), and exercise performance were measured throughout the intervention. At rest, leucine flux ([approximately equal to] 131 [micro]mol x [kg.sup.-1] x [h.sup.-1]) and oxidation ([R.sub.ox]; [approximately equal to] 19 [micro]mol x [kg.sup.-1] x [h.sup.-1]) did not differ pre- and post-CR. During EX, leucine flux (129 [+ or -] 6 vs. 121 [+ or -] 6) and [R.sub.ox] (54 [+ or -] 6 vs. 46 [+ or -] 8) were lower after CR than they were pre-CR. Nitrogen balance was negative throughout the intervention ([approximately equal to] 3.0g N/day), and BMR declined from 1,898 [+ or -] 262 to 1,670 [+ or -] 203 kcal/day. Aerobic performance (V[O.sub.2] peak, endurance cycling) was not impacted by CR, but arm flexion endurance decreased by 20%. In conclusion, 3 wk of caloric restriction reduced leucine flux and [R.sub.ox] during exercise in normal-weight young men. However, despite negative nitrogen balance and loss of lean mass, whole body exercise performance was well maintained in response to CR. energy intake; energy expenditure; leucine flux; exercise; nitrogen balance; lean mass

Diet-induced insulin resistance (IR) adversely affects human health and life span. We show that muscle-specific overexpression of human mitochondrial transcription factor A (TFAM) attenuates high-fat diet (HFD)-induced fat gain and IR in mice in conjunction with increased energy expenditure and reduced oxidative stress. These TFAM effects on muscle are shown to be exerted by molecular changes that are beyond its direct effect on mitochondrial DNA replication and transcription. TFAM augmented the muscle tricarboxylic acid cycle and citrate synthase facilitating energy expenditure. TFAM enhanced muscle glucose uptake despite increased fatty acid (FA) oxidation in concert with higher β-oxidation capacity to reduce the accumulation of IR-related carnitines and ceramides. TFAM also increased pAMPK expression, explaining enhanced PGC1α and PPARβ, and reversing HFD-induced GLUT4 and pAKT reductions. TFAM-induced mild uncoupling is shown to protect mitochondrial membrane potential against FA-induced uncontrolled depolarization. These coordinated changes conferred protection to TFAM mice against HFD-induced obesity and IR while reducing oxidative stress with potential translational opportunities. [ABSTRACT FROM AUTHOR]