Bone loss over 1 year of training and competition in female cyclists.

OBJECTIVE: To observe changes in hip, spine, and tibia bone characteristics in female cyclists over the course of 1 year of training. DESIGN: Prospective observational study. SETTING: Laboratory. PARTICIPANTS: Female cyclists (n = 14) aged 26-41 years with at least 1 year of competition history and intent to compete in 10 or more races in the coming year. ASSESSMENT OF RISK FACTORS: Women who train and compete in road cycling as their primary sport. MAIN OUTCOME MEASURES: Total body fat-free and fat mass and lumbar spine and proximal femur areal bone mineral density (aBMD) and bone mineral content (BMC) assessments by dual-energy x-ray absorptiometry. Volumetric BMD and BMC of the tibia were measured by peripheral quantitative computed tomography at sites corresponding to 4%, 38%, 66%, and 96% of tibia length. Time points were baseline and after 12 months of training and competition. RESULTS: Weight and body composition did not change significantly over 12 months. Total hip aBMD and BMC decreased by -1.4% ± 1.9% and -2.1% ± 2.3% (P < 0.02) and subtrochanter aBMD and BMC decreased by -2.1% ± 2.0% and -3.3% ± 3.7% (P < 0.01). There was a significant decrease in lumbar spine BMC (-1.1% ± 1.9%; P = 0.03). There were no significant bone changes in the tibia (P > 0.11). CONCLUSIONS: Bone loss in female cyclists was site specific and similar in magnitude to losses previously reported in male cyclists. Research is needed to understand the mechanisms for bone loss in cyclists.

Prolonged maternal amino acid infusion in late-gestation pregnant sheep increases fetal amino acid oxidation.

Protein supplementation during human pregnancy does not improve fetal growth and may increase small-for-gestational-age birth rates and mortality. To define possible mechanisms, sheep with twin pregnancies were infused with amino acids (AA group, n = 7) or saline (C group, n = 4) for 4 days during late gestation. In the AA group, fetal plasma leucine, isoleucine, valine, and lysine concentrations were increased (P < 0.05), and threonine was decreased (P < 0.05). In the AA group, fetal arterial pH (7.365 +/- 0.007 day 0 vs. 7.336 +/- 0.012 day 4, P < 0.005), hemoglobin-oxygen saturation (46.2 +/- 2.6 vs. 37.8 +/- 3.6%, P < 0.005), and total oxygen content (3.17 +/- 0.17 vs. 2.49 +/- 0.20 mmol/l, P < 0.0001) were decreased on day 4 compared with day 0. Fetal leucine disposal did not change (9.22 +/- 0.73 vs. 8.09 +/- 0.63 micromol x min(-1) x kg(-1), AA vs. C), but the rate of leucine oxidation increased 43% in the AA group (2.63 +/- 0.16 vs. 1.84 +/- 0.24 micromol x min(-1) x kg(-1), P < 0.05). Fetal oxygen utilization tended to be increased in the AA group (327 +/- 23 vs. 250 +/- 29 micromol x min(-1) x kg(-1), P = 0.06). Rates of leucine incorporation into fetal protein (5.19 +/- 0.97 vs. 5.47 +/- 0.89 micromol x min(-1) x kg(-1), AA vs. C), release from protein breakdown (4.20 +/- 0.95 vs. 4.62 +/- 0.74 micromol x min(-1) x kg(-1)), and protein accretion (1.00 +/- 0.30 vs. 0.85 +/- 0.25 micromol x min(-1) x kg(-1)) did not change. Consistent with these data, there was no change in the fetal skeletal muscle ubiquitin ligases MaFBx1 or MuRF1 or in the protein synthesis regulators 4E-BP1, eEF2, eIF2alpha, and p70(S6K). Decreased concentrations of certain essential amino acids, increased amino acid oxidation, fetal acidosis, and fetal hypoxia are possible mechanisms to explain fetal toxicity during maternal amino acid supplementation.

Effects of modafinil and sleep loss on physiological parameters.

OBJECTIVE: The purpose of this study was to determine the effects of modafinil administration on physical performance, thermoregulation, and total energy expenditure (TEE) during continued wakefulness in Air Force operators. METHODS: Participants (N = 12) were randomly assigned to the modafinil or placebo group. Participants performed physical performance and testing during 72 hours of wakefulness. RESULTS: There were no differences between groups for physical performance. Oral temperature was higher for modafinil compared to placebo (36.5 +/- 0.2 degrees C versus 36.3 +/- 0.2 degrees C for modafinil and placebo, respectively, p < 0.05). Daily water turnover (8.8 +/- 1.0 L x day(-1) and 9.0 +/- 1.5 L x day(-1)) and total energy expenditure (19.4 +/- 3.7 and 19.9 +/- 2.1 MJ) were similar between the modafinil and placebo groups, respectively. CONCLUSION: modafinil did not improve physical performance. Despite elevating oral temperature, water turnover and TEE were similar between treatments. These findings suggest it is unnecessary for operators taking modafinil to carry additional fluids and/or food.

Exercise increases the proportion of fat utilization during short-term consumption of a high-fat diet.

BACKGROUND: Increases in energy substrate oxidation occur at different rates after an increase in either fat or carbohydrate intake. Adaptations to increased fat intake are relatively slow and are influenced by activity level. OBJECTIVE: We tested the hypothesis that increased levels of daily activity, as influenced by added exercise, would have a graded effect on the rate of compensatory adjustment to a short-term high-fat diet. DESIGN: Daily total energy expenditure and macronutrient oxidation were measured at 3 physical activity levels (PALs) by using a whole-room indirect calorimeter in 10 adult women as they transitioned from a 1-d low-fat (30% of energy) control diet to a 4-d high-fat (50% of energy) diet. The 3 PALs (1.4, 1.6, and 1.8) were provided daily by increases in bicycle ergometer exercise time. RESULTS: An increase in physical activity led to a greater increase in the nonprotein respiratory exchange ratio (-0.047 +/- 0.02, -0.064 +/- 0.02, and -0.071 +/- 0.02; P < 0.0001) and 24-h fat oxidation (113 +/- 24, 125 +/- 19, and 147 +/- 20 g/d; P < 0.0001) for PALs of 1.4, 1.6, and 1.8, respectively, after the transition from the low-fat control diet to the high-fat diet. Random-effects analysis found a significant (P = 0.003) relation between PAL and the compensatory fat oxidation response to a high-fat diet. CONCLUSIONS: Amounts of exercise consistent with the Institute of Medicine's recommendations reduce the time required to match fat oxidation to a change in the percentage of fat in the diet. Because short-term consumption of high-fat diets is thought to contribute to excess fat accumulation, regular exercise should be protective and should help maintain a healthy body composition.

Calcium supplementation and parathyroid hormone response to vigorous walking in postmenopausal women.

INTRODUCTION: Disruptions in calcium (Ca) homeostasis during exercise may influence skeletal adaptations to exercise training. In young men, vigorous cycling causes increases in parathyroid hormone (PTH) and bone resorption (C-terminal telopeptides of type I collagen [CTX]); responses are attenuated by Ca supplementation. The study aimed to determine whether vigorous walking causes similar increases in PTH and CTX in older women and how the timing of Ca supplementation before and during exercise influences these responses. METHODS: In experiment 1, 10 women (61 ± 4 yr) consumed 125 mL of either a Ca-fortified (1 g·L) or control beverage every 15 min during exercise starting 60 min before and continuing during 60 min of exercise. In experiment 2, 23 women (61 ± 4 yr) consumed 200 mL of a Ca-fortified (1 g·L) or control beverage every 15 min starting 15 min before and continuing during 60 min of exercise. The exercise was treadmill walking at 75%-80% V˙O2peak. RESULTS: In experiment 1, serum ionized Ca decreased in the control condition (P < 0.001), but not with Ca supplementation. PTH increased after exercise on both days (Ca, P = 0.05; control, P = 0.009) but was attenuated by Ca supplementation (8.3 vs 26.1 pg·mL; P = 0.03). CTX increased only on the control day (P = 0.02). In experiment 2, serum ionized Ca decreased on Ca and control days (Ca and control, P < 0.001), but less so on the Ca day (P = 0.04). PTH (Ca and control, P < 0.001) and CTX (Ca, P = 0.02; control P = 0.007) increased on the Ca and control day, and there were no differences in the changes. CONCLUSION: The timing of Ca supplementation may be a key mediator of Ca homeostasis during acute exercise. Further research is necessary to determine how this influences skeletal adaptations to training.

Acute calcium ingestion attenuates exercise-induced disruption of calcium homeostasis.

PURPOSE: Exercise is associated with a decrease in bone mineral density under certain conditions. One potential mechanism is increased bone resorption due to an exercise-induced increase in parathyroid hormone (PTH), possibly triggered by dermal calcium loss. The purpose of this investigation was to determine whether calcium supplementation either before or during exercise attenuates exercise-induced increases in PTH and C-terminal telopeptide of Type I collagen (CTX; a marker of bone resorption). METHODS: Male endurance athletes (n = 20) completed three 35-km cycling time trials under differing calcium supplementation conditions: 1) 1000 mg of calcium 20 min before exercise and placebo during, 2) placebo before and 250 mg of calcium every 15 min during exercise (1000 mg total), or 3) placebo before and during exercise. Calcium was delivered in a 1000-mg·L(-1) solution. Supplementation was double-blinded, and trials were performed in random order. PTH, CTX, bone-specific alkaline phosphatase (BAP; a marker of bone formation), and ionized calcium (iCa) were measured before and immediately after exercise. RESULTS: CTX increased and iCa decreased similarly in response to exercise under all test conditions. When compared with placebo, calcium supplementation before exercise attenuated the increase in PTH (mean ± SE: 55.8 ± 15.0 vs 74.0 ± 14.2 pg·mL(-1), P = 0.04); there was a similar trend (58.0 ± 17.4, P = 0.07) for calcium supplementation during exercise. There were no effects of calcium on changes in CTX, BAP, and iCa. CONCLUSIONS: Calcium supplementation before exercise attenuated the disruption of PTH. Further research is needed to determine the effects of repeated increases in PTH and CTX on bone (i.e., exercise training) and whether calcium supplementation can diminish any exercise-induced demineralization.

Effect of prior acute exercise on trafficking of dietary fat away from adipose tissue.

OBJECTIVE: Increasing fat content in an isocaloric diet is associated with positive fat imbalance. Exercise attenuates this process, and the authors hypothesized the attenuation was a result of altered postprandial lipid trafficking. DESIGN: To investigate the effects of prior exercise and nutritional state on the metabolic fate of dietary fat, a study was designed with 4 treatment arms. Energy-balance modifications (fed or fasted) ± exercise were followed by postexercise feeding of 1-14C oleic acid to Sprague-Dawley rats. Fed rats were fed 6 hr before treatment, whereas fasted rats were fasted for 15 hr before treatment with the primary variable being exercise. MEASUREMENTS: 14C content of gastrointestinal tract, plasma, breath, muscle (soleus, vastus lateralis [VL], and extensor digitorum longus), liver, and adipose tissue (retroperitoneal and epididymal) was measured at 5 time points postdose (1, 2, 4, 8, and 24 hr). RESULTS: Compared with matched unexercised controls, fed rats undergoing acute exercise significantly increased recovery of 14C in breath (p = .005) and plasma (p = .001), and trends of increasing 14C recovery occurred in VL (p = .07) and soleus (p = .06). Acute exercise significantly increased recovery of 14C in breath (p = .003), VL (p = .04), and soleus (p = .03) in the fasted study. Acute exercise significantly decreased the trafficking of dietary tracer into adipose tissue in only the fed study (p < .0001). CONCLUSION: Although the effect of acute exercise on trafficking dietary fat away from adipose tissue was greater in the fed group than in the fasted, acute exercise had beneficial effects on adipose tissue's collecting dietary fat when fed or fasted.