Sunlight exposure increases vitamin D sufficiency in growing pigs fed a diet formulated to exceed requirements.

Traditional confinement practices limit exposure to sunlight and vitamin D synthesis, and vitamin insufficiency occurs even with dietary supplementation. The aim of this study was to determine the effect of limited sun exposure on serum concentration of vitamin D and the expression of vitamin D synthesizing enzymes in the liver and kidney of pigs on a vitamin D sufficient diet. White-pigmented grower pigs (29.7 ± 2.3 kg) fed 15% CP diet ad libitum providing >1,200 IU vitamin D3/kg of feed were exposed to sunlight for 1 h each day at solar noon for 14 d at the spring equinox (March pigs, n = 10) or summer solstice (June pigs, n = 5) and again before slaughter in June (March pigs) and September (June pigs). Blood for the analysis of 25(OH)D was collected before and after sunlight exposure. Traditionally housed pigs served as controls. After initial sun exposure, blood samples were collected from June pigs daily for 5 d and weekly for 8 wk to determine vitamin D3 and 25(OH)D decay, respectively. Kidney and liver samples were collected from the June pigs at slaughter after sun exposure for analysis of messenger RNA expression of vitamin D binding protein and synthesizing/degrading enzymes. Average daily gain (ADG) was not influenced (P > 0.5) by sunlight exposure. June pigs had fewer days on feed, lower (P = 0.003) ADG and were slaughtered at a lighter (P < 0.001) weight. Exposure to sunlight increased (P < 0.001) 25(OH) vitamin D for all pigs. March pigs, obtained from a Midwest producer, had lower (P < 0.001) concentration of 25(OH)D than June pigs born on-farm. Initial sunlight exposure increased serum concentration of 25(OH)D in March pigs by 200% and June pigs by 67%. Serum concentration of vitamin D3 was decreased (P < 0.05) by 72 h with 25(OH)D decreased (P < 0.05) by wk 4 after exposure. Expression of vitamin D binding protein, vitamin D synthesizing CYP2R1, CYP27A1, CYP2D25, or degrading enzyme CYP24A1 were not influenced (P ≥ 0.19) by sunlight exposure. Expression of CYP27B1 was decreased (P = 0.04) in the kidney but tended to be increased (P = 0.06) in the liver after sun exposure. These results suggest limited sun exposure can efficiently increase serum concentration of vitamin D in growing pigs with varying levels of vitamin sufficiency. The lack of major changes in vitamin synthesizing enzymes suggests the 14-d exposure period did not saturate the capacity of slaughter-weight pigs to synthesize vitamin D.

Intrahepatic and intramyocellular lipids are determinants of insulin resistance in prepubertal children.

AIMS/HYPOTHESIS: We hypothesised that ectopic fat deposition is present in liver and skeletal muscle before puberty and that both are potentially important factors in the early pathogenesis of insulin resistance. METHODS: Proton magnetic resonance spectroscopy was used to evaluate intramyocellular and intrahepatic lipids in 50 male and 42 female multi-ethnic, prepubertal (Tanner < 2) children (8.1 ± 0.8 years; 35.4 ± 10.7 kg; 27.9 ± 8.3% body fat; means ± SD). Intramyocellular lipid was measured in soleus muscle and intrahepatic lipid in the middle right lobe. Abdominal fat was measured by magnetic resonance imaging, body fat by dual energy X-ray absorptiometry, and insulin resistance using homeostatic model assessment. RESULTS: Intrahepatic lipid ranged from 0.11% to 4.6% relative to the liver water signal (mean 0.79 ± 0.79%) whereas intramyocellular lipid ranged from 0.13% to 1.86% relative to the muscle water signal (mean 0.51 ± 0.28%). Intramyocellular and intrahepatic lipids were significantly correlated with total adiposity (r = 0.49 and 0.59), abdominal adiposity (r = 0.44 and 0.54), and each other (r = 0.39, p < 0.05, Spearman). Both intramyocellular and intrahepatic lipid were positively correlated with fasting insulin (r = 0.37 and 0.38 respectively) and insulin resistance (r = 0.37 and 0.37; p < 0.01). After adjustment for race and sex, the relations between ectopic fat and insulin resistance remained, whereas both disappeared when further adjusted for body fat or BMI z scores. CONCLUSIONS/INTERPRETATIONS: These results suggest that typical relations between body composition, ectopic fat and insulin resistance are present in children before puberty. Thus, interventions aimed at reducing adiposity have the potential to decrease ectopic fat accumulation, delay the onset of insulin resistance and decrease the risk for development of type 2 diabetes in children.

Relation between in vivo and in vitro measurements of skeletal muscle oxidative metabolism.

The relationships between in vivo (31)P magnetic resonance spectroscopy (MRS) and in vitro markers of oxidative capacity (mitochondrial function) were determined in 27 women with varying levels of physical fitness. Following 90-s isometric plantar flexion exercises, calf muscle mitochondrial function was determined from the phosphocreatine (PCr) recovery time constant, the adenosine diphosphate (ADP) recovery time constant, the rate of change of PCr during the initial 14 s of recovery, and the apparent maximum rate of oxidative adenosine triphosphate (ATP) synthesis (Q(max)). Muscle fiber type distribution (I, IIa, IIx), citrate synthase (CS) activity, and cytochrome c oxidase (COX) activity were determined from a biopsy sample of lateral gastrocnemius. MRS markers of mitochondrial function correlated moderately (P < 0.05) with the percentage of type IIa oxidative fibers (r = 0.41 to 0.66) and CS activity (r = 0.48 to 0.64), but only weakly with COX activity (r = 0.03 to 0.26, P > 0.05). These results support the use of MRS to determine mitochondrial function in vivo.

Skeletal muscle metabolism in overweight and post-overweight women: an isometric exercise study using (31)P magnetic resonance spectroscopy.

OBJECTIVE: To investigate whether skeletal muscle anaerobic metabolism, oxidative metabolism or metabolic economy during controlled sub-maximal and near-maximal exercises is altered in overweight women after diet-induced weight reduction, and whether these parameters are different between normal-weight, obesity-prone and normal-weight obesity-resistant women with similar physical fitness levels. DESIGN: A prospective weight loss study of overweight women and their comparison with never overweight controls. SUBJECTS: Thirty overweight, nondiabetic, premenopausal women and 28 never overweight controls were included in this analysis. All were participating in a longitudinal investigation of the role of energy metabolism in the etiology of obesity. The overweight women were recruited specifically to have a positive family history of obesity and have a body mass index (BMI) between 27 and 30 kg/m(2) and were studied in the overweight state and after reduction to a normal weight. The never-overweight controls were recruited specifically to have no personal and family history of obesity and were group matched with the weight-reduced post-overweight subjects in terms of premenopausal status, age, BMI, race and sedentary lifestyle. MEASUREMENTS: All testing was performed following one month of weight maintenance and during the follicular phase of the menstrual cycle. Hydrostatic weighing was performed to measure body composition and a whole-body maximal oxygen uptake (VO(2max)) test was done to measure aerobic fitness. (31)P MRS was used to determine ATP production from oxidative phosphorylation (OxPhos), 'anaerobic' glycolysis (AnGly), and creatine kinase (CK), as well as muscle metabolic economy. The time constant of ADP (TC(ADP)), V(PCr) (ie the initial rate of PCr resynthesis following exercise), and Q(max) (ie the apparent maximal oxidative ATP production rate) were also calculated as additional markers of mitochondrial function. RESULTS: Diet-induced weight loss did not have any effects on the anaerobic metabolism markers (AnGly and CK). The aerobic metabolism markers calculated from the initial recovery data (OxPhos and V(PCr)) were unaffected by diet-induced weight loss. However, diet-induced weight loss resulted in improvements in the TC(ADP) and Q(max) in the post-overweight state as compared to their overweight state. There were no differences in any of the anaerobic (AnGly and CK) or oxidative metabolism markers (OxPhos, V(PCr), Q(max) and TC(ADP)) between the post-overweight and control groups. CONCLUSIONS: Once the overweight women were reduced to a normal-weight state, their skeletal muscle energy metabolism and economy was similar to the never overweight control women. In overweight women, oxidative metabolism or mitochondrial function may be limited by blood flow to the muscle following the cessation of exercise.

Muscle metabolic economy is inversely related to exercise intensity and type II myofiber distribution.

It is not known what causes the well-established inverse relationship between whole-body exercise economy and exercise intensity. The purpose of this study was to: (1) evaluate muscle exercise economy at 45%, 70%, and maximum isometric strength using 31P magnetic resonance spectroscopy (31P-MRS); and (2) determine the relationship between percent type II muscle fiber cross-section, whole-body exercise economy, and muscle exercise economy. Subjects included 32 premenopausal women. Muscle exercise economy was significantly different across the three exercise intensities (28.1 +/- 10.4, 24.8 +/- 8.2, and 20.2 +/- 7.5 N/cm2. mmol/L adenosine triphosphate [ATP] for the 45%, 70%, and maximum intensities, respectively). Percent type II muscle area was significantly related to whole-body metabolic economy during activities of daily living (r = -0.68) and 31P-MRS muscle metabolic economy during isometric plantar flexion (r = -0.53). These data suggest that skeletal muscle becomes less economical as force production increases, and that these decreases in metabolic economy may be related to increased dependence on inefficient type II muscle.

Evaluation of the strength-size relationship in vivo using various muscle size indices.

PURPOSE: It is well accepted that maximum strength is related to muscle size. The primary purpose of this study was to determine whether anthropometric or dual-energy x-ray absorptiometry (DEXA) estimates of muscle size were valid predictors of plantar flexor maximum voluntary contraction (MVC) strength and could be used in lieu of more sophisticated techniques (e.g., magnetic resonance imaging (MRI)). Additionally, we compared the relationship among MVC and three MRI-determined muscle size measures; anatomical (ACSA) and physiological (PCSA) cross-sectional areas; and muscle volume (VOLm). METHODS: We measured plantar flexor MVC at 1.83 rad and various indices of muscle size: 1) body weight, 2) total body lean mass (LM) (DEXA), 3) lower leg LM (DEXA), 4) lower leg circumference, 5) estimated muscle+bone cross-sectional area (CSA) from circumference and calf skin-fold, 6) triceps surae ACSA, 7) triceps surae PCSA, and (8) triceps surae volume (VOLm), in 39 premenopausal women (mean +/- SD: 36 +/- 8 yr, 165 +/- 6 cm, and 65 +/- 9 kg). RESULTS: Zero-order correlations showed significant (P < 0.05) associations between MVC and total body LM (r = 0.365), lower leg LM (r = 0.381), circumference (r = 0.584), estimated muscle+bone CSA (r = 0.447), ACSA (r = 0.733), PCSA (r = 0.715), and VOLm (r = 0.649). By using the Fisher Z-transformation, ACSA and PCSA correlated significantly higher with MVC (P < 0.05) than anthropometric and DEXA indices. Further, only ACSA and PCSA regressed to the origin, indicating the ability to predict MVC was greatest with these two measures. CONCLUSIONS: The MRI-determined muscle size indices, which were specific to the triceps surae, correlated with strength better than whole limb anthropometric and DEXA indices. In this group of women, both ACSA and PCSA appeared superior to VOLm for predicting strength. PCSA was not found to be more precise than ACSA. ACSA appears to provide adequate precision for estimating plantar flexor specific tension in vivo.

31P MRS measurement of mitochondrial function in skeletal muscle: reliability, force-level sensitivity and relation to whole body maximal oxygen uptake.

The reliability, relation to whole-body maximal oxygen uptake (VO(2max)), and force-level sensitivity of (31)P MRS markers of mitochondrial function were studied in 39 normal-weight women. Following 90 s isometric plantar-flexion exercises at 45, 70 and 100% of maximum voluntary contraction, skeletal muscle mitochondrial function was determined from the phosphocreatine recovery time constant (TC(PCr)), the ADP recovery time constant (TC(ADP)), and the rate of change in PCr during the first 14 s of recovery (OxPhos). VO(2max) was measured on a treadmill. Test-retest measurements were obtained in a subset of seven women. Overall, TC(PCr), TC(ADP) and OxPhos were reproducible for all exercises (coefficients of variation = 2.3-19.3%). With increasing force-level, TC(PCr) was prolonged (29.0 +/- 8.2, 31.9 +/- 9.0 and 35.4 +/- 9.5 s), OxPhos was increased (0.159 +/- 0.081, 0.247 +/- 0.090 and 0.310 +/- 0.114), and TC(ADP) was shortened (22.4 +/- 7.9, 21.3 +/- 6.2, and 19.5 +/- 6.7; p < 0.01). All MRS markers of mitochondrial function were correlated with VO(2max) (r = 0.41-0.72; p < 0.05). These results suggest that measurements of TC(PCr), TC(ADP) and OxPhos yield reproducible results that correlate with whole-body VO(2max) and that vary in force-level sensitivity.

Effect of weight reduction, obesity predisposition, and aerobic fitness on skeletal muscle mitochondrial function.

We used (31)P magnetic resonance spectroscopy to measure maximal mitochondrial function in 12 obesity-prone women before and after diet-induced weight reduction and in 12 matched, never-obese, and 7 endurance-trained controls. Mitochondrial function was modeled after maximum-effort plantar flexion from the phosphocreatine recovery time constant (TC(PCr)), the ADP recovery time constant (TC(ADP)), and the rate of change in PCr during the first 14 s of recovery (OxPhos). Weight reduction was not associated with a significant change in mitochondrial function by TC(PCr), TC(ADP), or OxPhos. Mitochondrial function was not different between postobese and never-obese controls by TC(PCr) [35.1 +/- 2.5 (SE) vs. 34.6 +/- 2.5 s], TC(ADP) (22.9 +/- 1.8 vs. 21.2 +/- 1.8 s), or OxPhos (0.26 +/- 0. 03 vs. 0.25 +/- 0.03 mM ATP/s), postobese vs. never-obese, respectively. However, TC(ADP) was significantly faster (14.5 +/- 2. 3 s), and OxPhos was significantly higher (0.38 +/- 0.04 mM ATP/s) in the endurance-trained group. These results suggest that maximal mitochondrial function is not impaired in normal-weight obesity-prone women relative to their never-obese counterparts but is increased in endurance-trained women.