Vitamin D supplementation affects the IGF system in men after acute exercise.

OBJECTIVE: Contradictory data between the Insulin-Like Growth Factor System (IGF) system and exercise may be due to alteration in IGF binding proteins. Vitamin D (D) deficiency has been related to muscle weakness and Insulin Like Growth Factor Binding Protein 3 (IGFBP3). A Vit. D and acute exercise merge is proposed to modify the IGF system. DESIGN: D insufficient and deficient men (39.0±8.6yo with serum D (25OH D) 20.0±7.7ng/mL) did 1h of stretching (ST), aerobic (AB), and resistance (RT) exercises, before and after 28d of 4000IU/d Vit. D3 (D, n=6) or Placebo (P, n=7). ST, a time/attention control visit, interchanged unreceptive movements. AB was moderate intensity treadmill walking. RT rotated moderate strength 50% 1-RM repetitions (15, 10) of squat, bench press, leg press, and lat pull down. Serum Total IGF1 (TIGF1), Insulin Like Growth Factor Binding Protein 1 (IGFBP1), and IGFBP3 were measured before (T1, fasting), immediately after (T2), and 2h post (T3) exercise. RESULTS: After ST, IGFBP3 was greater in the D group at T2 (2948, 2130ng/mL; p<0.03) and T3 (3087, 2212; p<0.02). During RT, TIGF1 decreased in the Placebo (P) group from T1 to T3 (151.4, 107.3ng/mL; p<0.05), while IGFBP1 increased in the D group from T1 to T3 (26.5, 96.2ng/mL; p<0.05). RT IGFBP3 was greater at T1, T2, and T3 in the D group (2932.5, 2110.7; p<0.03), (3163.9, 2392.5; p<0.04), and (3355.3, 2353.1; p<0.01). In AB, IGFBP3 was greater in the D group at T2 (3128.6, 2226.3.0; p<0.04) and T3 (2949.7, 2135.1; p<0.05). CONCLUSION: D supplementation amplified IGFBP3 after low or moderate activity which may increase the delivery of IGF1 to tissues. Resistance exercise with D not only increased IGFBP3 and IGFBP1 levels but also conserved TIGF1 levels, possibly shifting the IGF system for enriched muscle well-being.

Endurance exercise training in myostatin null mice.

The growth factor myostatin (Mstn) is a negative regulator of skeletal muscle mass. Mstn(-/-) muscles are hypertrophied, stronger, and more glycolytic than Mstn(+/+) muscles, suggesting that they might not perform endurance exercise as well as Mstn(+/+) mice. Indeed, it has previously been shown that treadmill exercise training reduces triceps weight in Mstn(-/-) mice. To analyze the response of Mstn(-/-) muscle to endurance exercise in detail, we carried out endurance training over 4 weeks to examine muscle mass, histology, and oxidative enzyme activity. We found that muscle mass was reduced with training in several muscles from both genotypes, with no evidence of muscle damage. Citrate synthase activity was increased with training in control and mutant mice. Non-trained Mstn(-/-) mice did, however, have lower maximal exercise capacity compared with Mstn(+/+) mice. These results show that Mstn(-/-) muscle retains the metabolic plasticity necessary to adapt normally to endurance training.

Basal, but not overload-induced, myonuclear addition is attenuated by NG-nitro-L-arginine methyl ester (L-NAME) administration.

The purpose of this study was to examine the effect of blocking nitric oxide synthase (NOS) activity via NG-nitro-L-arginine methyl ester (L-NAME) on myonuclear addition in skeletal muscle under basal and overloaded conditions. Female Sprague-Dawley rats (approx. 220 g) were placed into 1 of the following 4 groups (n = 7-9/group): 7-day skeletal muscle overload (O), sham operation (S), skeletal muscle overload with L-NAME treatment (OLN), and sham operation with L-NAME treatment (SLN). Plantaris muscles were overloaded via bilateral surgical ablation of the gastrocnemius muscles and L-NAME (0.75 mg/mL) was administered in the animals' daily drinking water starting 2 days prior to surgery and continued until sacrifice. Myonuclear addition was assessed as subsarcolemmal incorporation of nuclei labeled with 5-bromo-2'-deoxyuridine (approx. 25 mg.(kg body mass)-1.day-1) delivered via osmotic pump during the overload period. As expected, muscle wet mass, total protein content, fiber cross-sectional area, and myonuclear addition were significantly higher (p

Oral contraceptive use and exercise-induced muscle damage and recovery.

Endogenous estrogen appears to attenuate muscle damage in animals; however, similar evidence in humans is not as strong. This investigation tested the hypothesis that women taking oral contraceptives, thereby having higher exogenous estrogen levels, would be more susceptible to damage or have an attenuated recovery from exercise-induced muscle damage. Muscle damage in women taking combined estrogen and progesterone oral contraceptives (OC) were compared to noncontraceptive users (NOC) after 50 eccentric muscle contractions of the elbow flexors. Measures of maximal isometric strength (MIS), range of motion (ROM), arm circumference (CIR), soreness (SOR), and serum creatine kinase (CK) activity were taken pre- and for 5 days post-exercise. All measures following exercises were similar between groups with the exception of MIS. Force recovery began 2 days post-exercise in the NOC group, while in the OC group strength did not start to return to normal until 4 days post-exercise (p < 0.05). Women taking oral contraceptives had a delayed strength recovery after eccentric exercise.