Post-eccentric exercise blunted hGH response.

The purpose of the present study was to test if a previous acute concentric exercise bout blunts hGH response after an eccentric exercise bout. Nine healthy untrained male university students (25.4+/-0.5 yr, 176.5+/-1.2 cm, and 79.4+/-2.0 kg) performed a concentric exercise bout followed by an eccentric exercise bout one week later. Serum human growth hormone (hGH), creatine kinase (CK), and lactate were measured before, immediately and up to 32 h after both exercise bouts. Higher lactate values were observed immediately, 5 and 10 min after the concentric bout (70%, 119%, and 142%, respectively, p<0.05) than the eccentric bout. There was a CK main time effect at 8 and 32 h after the exercise bouts compared to baseline values (p<0.002). However, peak serum CK effect size was higher after the concentric than the eccentric exercise bout, 1.3 and 0.9, respectively. hGH increased after both exercise bouts, however it reached significance only at immediately (207%), 5 min (256%), 10 min (276%), 20 min (300%), and 40 min (168%) after the concentric exercise bout (p<0.05). Our findings suggest that a previous concentric exercise bout may blunt the anabolic response expected after an eccentric exercise bout.

Hyperglycemia activates glucose transport in rat skeletal muscle via a Ca(2+)-dependent mechanism.

We investigated the acute effect of hyperglycemia on 3-O-methylglucose transport in isolated rat epitrochlearis muscles. High levels of glucose (20 mmol/l) induced an approximately twofold increase in the rate of glucose transport when compared with muscles exposed to a low level of glucose (8 mmol/l) (P < 0.001). The hyperglycemic effect was additive to the effects of both insulin and exercise on the glucose transport rates. Dantrolene (25 mumol/l), a potent inhibitor of Ca2+ release from the sarcoplasmic reticulum, blocked the ability of hyperglycemia to increase glucose transport by 73% (P < 0.01). Although dantrolene had no effect on the non-insulin-stimulated or the insulin-stimulated glucose transport rates during normoglycemic conditions, the effect of exercise was completely blocked in the presence of dantrolene (P < 0.01). Inhibition of phosphatidylinositol (PI) 3-kinase by wortmannin (500 nmol/l) had no effect on the activation of glucose transport by hyperglycemia, whereas the insulin-stimulated glucose transport was completely abolished (P < 0.001). These findings suggest that hyperglycemia activates glucose transport by a Ca(2+)-dependent activation of glucose transport does not involve the activation of PI 3-kinase and is separate from the mass-action effect of glucose on glucose transport.

The influence of fructose feeding on physical performance.

Athletic competition requires great energy expenditure and the ability to maintain performance depends on an adequate supply of metabolic fuels, which has led to the use of dietary supplements. Much of the data concerning fructose supplementation is contradictory in nature, but it shows that fructose feeding before or during exercise can enhance performance under certain conditions. Preexercise nutrition seems to be the most important condition to be met. It has been theorized that prefeeding elevates liver glycogen and spares muscle glycogen, which prolongs activity. There is also good evidence to indicate that the addition of fructose to the diet during ultraendurance events can improve performance by 126%. The gastrointestinal discomfort created by large amounts of fructose can hinder performance and has limited research with this supplement. Therefore, even though positive effects have been demonstrated, more research is needed to determine the role that fructose can play in enhancing athletic performance.

The influence of high-resistance training on glucose tolerance in young and elderly subjects.

Aging is associated with a decrease in glucose tolerance. In younger subjects both high and low intensity forms of exercise have been shown to improve glucose tolerance. The purpose of this investigation was to determine whether or not strength training in elderly subjects would have a positive effect upon glucose and insulin responsiveness following a glucose feeding. The medical history of each subject and an exercise stress test were given prior to the establishment of the two age groups: those individuals with contra-indications for exercise were not tested further. An oral glucose tolerance test, 100 g, was administered to six young (23 +/- 1 year) and 9 elderly (63 +/- 1 year) male subjects before and after 12 weeks of a supervised progressive resistance weight lifting program, which employed Nautilus equipment. All the major muscle groups of the body were exercised and a three set, six-eight repetition, training protocol was followed. Blood samples were taken at 0, 30, 60, 120 and 180 min; after centrifugation (1169 g for 15 min) the serum was frozen for analysis of glucose and insulin. Percent body fat was determined by skin calipers and the Lean Body Mass estimated. The 6 Rep max for the leg press, leg extension and bench press machines were used to determine the strength gains made for the 12 weeks of training. The results show that both the young and elderly subjects had a significant increase (P less than 0.05) in LBM and a significant decrease (P less than 0.05) in percent body fat with training. In the young these changes occurred without a significant change in body weight, whereas the elderly had a significant increase (P less than 0.05) in body weight. In terms of strength, both the young and elderly showed significant gains (P less than 0.05) following training. The training protocol had little effect on the glucose response, but did significantly lower (P less than 0.05) the plasma insulin response to a glucose load. In response to a 100 g oral glucose load insulin declined regardless of age, with the insulin sum of the young and elderly being, 31.8% and 32.6% lower, respectively, after training. Although strength training improved glucose tolerance in both age groups, the response of the elderly subjects was well below that of the young. In conclusion, the data present here demonstrate that 12 weeks of high resistance strength training improved the overall physical fitness level of both the young and elderly participants of this study, but did not affect age related differences.

Effects of progressive resistance training on growth hormone and testosterone levels in young and elderly subjects.

We observed the response of serum growth hormone (GH) and testosterone (T) to a progressive resistance strength training program. Basal levels (after a 12-h fast) of GH and T were measured in young (23 years) and elderly (63 years) subjects before and after a 12-week training program. The response of GH and T to an acute bout of exercise was also measured. The exercise training, which involved all the major muscle groups, was conducted on Nautilus equipment and required 45-60 min for completion. The subjects completed three sets of lifts with 8-10 Reps/set. Blood was drawn from an anticubital vein, centrifuged (1169 g) for 15 min and the serum frozen for later analysis. The acute exercise blood samples were taken immediately before and after the exercise and at 15 min post-exercise during week 1 and 12. The hormone assay was carried out with radioimmunoassay kits for GH and T. The basal level of GH increased by 44.9% in the young and by only 3% in the elderly but neither change was significant. In response to a single exercise session GH levels in the young went from 0.85 +/- 0.13 to 4.19 +/- 1.45 ng/ml before training and from 1.45 +/- 0.11 to 8.61 +/- 2.55 after training. Each response was significant (P less than 0.05) as were the pre-post differences (P less than 0.001). In the elderly the response was not as great, values increasing from 1.00 +/- 0.09 to 2.92 +/- 0.65 ng/ml before training and from 1.50 +/- 0.06 to 3.43 +/- 0.64 ng/ml after training were recorded. These differences represented significant increases (P less than 0.05) but did not demonstrate pre- to post-changes. Basal levels of T decreased in both groups, but were not significant. The T response to an acute bout of exercise was not significant but did increase in both age groups. In conclusion, the data presented here indicate that strength training can induce growth hormone and testosterone release, regardless of age, but that the elderly response does not equal that of the young.

Ageing, exercise and food restriction: effects on skeletal muscle glucose uptake.

We investigated the effects of ageing, exercise and food restriction on glucose uptake by muscles perfused with physiological concentrations of insulin and glucose in male Long-Evans rats. The rate of glucose uptake by hindlimb muscles perfused with medium containing 50 microU@ml insulin and 8 mM glucose was the same in 9-10 month-, 18 month-, and 24-month-old rats. Rats exercised by means of swimming 3 h/day, 5 days/week, had significantly higher rates of muscle glucose uptake than did the sedentary freely eating rats. Paired-weight sedentary rats, that were food restricted so as to keep their weights in the same range as those of the swimmers, had a hindlimb glucose uptake rate similar to that of the swimmers, and greater than that of the sedentary freely eating rats. The 24-month-old sedentary freely eating rats showed a trend toward a higher plasma glucose response and a lower plasma insulin response to a glucose tolerance test. The 24-month-old swimmers showed no deterioration in glucose tolerance compared to the 9-10 month-old rats. Our findings argue against the concept that ageing results in skeletal muscle insulin resistance in rats.

The influence of training-detraining upon the heart, muscle and adipose tissue of female rats.

The purpose of this study was to measure the effects of a 10 week training, 3 week detraining cycle upon heart, muscle and adipose tissue of the rat. Specific pathogen-free female Wistar rats, 175 g at the onset of the experiments, were separated into three treatment groups; Sedentary Control (SC), Trained (T) and Detrained (DT). Animals from the T group were killed at 2, 4, 6, 8 and 10 weeks and animals from the DT group were killed at 7, 14 and 21 days after the last day of training. Unweighted swimming--6 h/day, 5 day/week, was the form of training employed. The animals, after being sacrificed, were anesthetized with nembutal (45 mg/kg body wt.) and muscle samples and heart removed. These tissues were frozen and analyzed at a later date for succinate dehydrogenase (SDH) activity (muscles), total protein (TP), total hydroxylprotein (TH) and wet and dry weight (heart). Adipose tissue was removed last, digested in collagenase (5 mg/ml) and the isolated cells used to measured 2-[3H]deoxyglucose uptake (DOG) and the conversion of D-[1-14C]glucose (C-1) and D-[6-14C]glucose (C-6) to CO2. The results of this study show that 10 weeks of endurance training induced myocardial hypertrophy (P less than 0.05) which involved increases in both TP and TH, the heart of the trained animals having 20.8% more protein and a 28.5% more hydroxlprotein than the sedentary controls. With detraining hypertrophy was lost within 21 days. Training maintained fat cell size at its pre-trained diameter, while inactivity allowed growth in the adipocytes of the control animals. The uptake of DOG and the conversion of glucose C-1 and glucose C-6 to CO2, were significantly (P less than 0.05) higher in the adipocytes of trained animals indicating that they were more responsive to insulin than the sedentary controls, which corresponded to increases in the respiratory enzyme levels of the muscles. During the first 7 days of detraining DOG uptake and both C-1 and C-6 glucose oxidation remained elevated. In conclusion the results of this study clearly demonstrate that there is a direct relationship between adiposity and training that can be related to the insulin responsiveness of the adipose tissue.

Ageing, exercise and food restriction: effects on body composition.

This study was undertaken to reevaluate the effect of ageing on body composition and to compare the effects of exercise and food restriction on body fat content in rats. Body fat content increased progressively between ages 12 and 28 months in sedentary freely eating male Long-Evans rats. A program of 3 h of swimming/day caused body weight to plateau at a level approximately 20% below that of the freely eating sedentary rats, primarily due to a more than 100 g lower body fat content in the swimmers. Lean body mass and protein content decreased progressively with ageing; in the sedentary animals, this decrease was significant by 18 months. The swimming protected against the decline in lean body mass and protein content up to age 18 months, but did not prevent a large decrease in lean body mass between ages 18 and 24 months. Food restriction that kept the sedentary rats at the same weight as the swimmers had its major effect on body fat content, which was approximately 40% lower than in the sedentary freely eating rats at all ages. The differences in body composition between the swimmers and food restricted sedentary animals were relatively small and consisted primarily of a lower body fat content in the swimmers. In conclusion, our results show that lean body mass declines with ageing in rats and that this loss of lean tissue is counterbalanced by an increase in fat. Exercise is highly effective in minimizing the increase in body fat, and may delay the decline in lean body mass, with ageing.

The effects of exercise mode, swimming vs. running, upon bone growth in the rapidly growing female rat.

The purpose of this study was to compare the effects of two programs of endurance training, of equal duration and intensity, on bone development in female rats. Thirty-eight female Wistar rats were randomly assigned to one of three groups: run-trained (RUN), swim-trained (SWIM) or control (CON). The RUN group ran at a speed of 27 m/min up an 8 degrees incline. Swim trained animals swam with 2% of body weight attached to their tails. Training sessions were 2 h/day, 5 days/week and were conducted over a 10-week period. Hindlimb and forelimb muscles were removed upon sacrifice and analyzed for citrate synthase (CS) activity, liver (LG) and muscle (MG) glycogen. The parametrial fat pads were removed, digested with collagenase, and 2-deoxy-D-[3H]glucose uptake measured in isolated cells. Bone weight, length, diameter, ponderal index and bone mineral content (BMC) were measured in the femur and humerus of each animal. The LG, MG, fat cell volume, glucose uptake of the adipocyte and adrenal weight data indicate that the training response was identical. The CS activity of the muscles indicated that mechanical and recruitment patterns of the upper and lower body differ and could be responsible for bone development patterns found in this study. Exercise had a minimal effect on bone growth in the run-trained animals but did stimulate development in the swim-trained animals. The humerus of the SWIM was significantly (P < 0.05) heavier, wider and had a greater BMC when compared with those of the RUN and CON rats. The results of this study indicate that the muscular forces applied by the swim training protocol produced greater bone adaptations than the forces applied by a running protocol of equal duration and intensity.

The effects of phospholipase C inhibition on insulin-stimulated glucose transport in skeletal muscle.

Previous research has demonstrated that phospholipase C (PLC) is involved in insulin-stimulated glucose transport in 3T3-L1 adipocytes. The purpose of the current investigation was to determine if PLC is also involved in insulin-stimulated glucose uptake in rat skeletal muscle. To that end, we used an in vitro muscle preparation of the rat soleus muscle to test the effects of the PLC inhibitor, U73122, on glucose transport. The PLC inhibitor, U73122, led to a concentration-dependent inhibition of insulin (0.6 nmol/L)-stimulated glucose transport, whereas it had no effect on basal glucose transport. Specifically 10, 20, 50, and 150 micromol/L U73122 inhibited insulin (0.6 nmol/L)-stimulated glucose transport approximately 17%, 20%, 26%, and 38%, respectively, while an equal molar concentration of U73343 (inactive form of U73122) and/or carrier media (dimethyl sulfoxide [DMSO]) did not influence glucose uptake. A secondary aim of this investigation was to determine if increasing the concentration of insulin from a physiologic concentration (0.6 nmol/L) to a supraphysiologic concentration (6.0 nmol/L) could ameliorate the inhibitory effects of U73122. A 10-fold increase in insulin eliminated the inhibitory effects of U73122 on insulin-stimulated glucose uptake in soleus muscle. In summary, this preliminary report provides evidence to suggest that a PLC signaling mechanism modifies insulin-stimulated glucose uptake in skeletal muscle via its influence on insulin sensitivity.

Glucose uptake and oxidation in fat cells of trained and sedentary pregnant rats.

The purpose of this investigation was to examine the relationship between an exercise program and fetal development to determine whether training could influence insulin sensitivity in the pregnant rat. Prior to impregnation one group of animals was exercise trained on a Quinton shock-stimulus rodent treadmill. The exercised group was trained to run 5 days/wk, for 2.0 h/day at 31 m/min up an 8 degree incline for 8 wk before mating. Following mating the training intensity was reduced to 27 m/min up a 5 degree incline, and the exercise period decreased to 1 h/day. On day 19 of gestation, 24 h postexercise for the trained mothers, the animals were killed in the fed state and the parametrial fat pads were removed. The parametrial depot of the trained mother was smaller than the sedentary control dam. This was due to a change in cell size and did not involve alterations in cell number. Isolated adipocytes of the parametrial fat pads were used to measure the rates of 2-deoxy-D-[3H]glucose uptake and D-[1-14C]glucose oxidation to 14CO2. The results indicated that the adipocytes from the dam trained prior to and during pregnancy were significantly (P less than 0.05) more responsive to insulin than those of animals remaining sedentary during the same period. At the maximal insulin concentration tested, the fat cells from trained mothers were able to take up and metabolize approximately twice as much glucose as the sedentary control dams. However, the increase in insulin responsiveness induced by the training program did not match the changes observed in trained nonpregnant rats of prior investigations.

Influence of early nutrition on growth and adipose tissue characteristics in male and female rats.

The purpose of this investigation was to assess the effects of early nutrition on adipose tissue characteristics and growth by altering litter size. After birth, rats were redistributed into large (15-18 pups), control (10 pups), or small (4 pups) litters. During the postweaning phase of growth half of the small-litter animals were pair-fed to animals raised in large litters for 5 wk and then allowed to feed ad libitum until they were 80 days of age. The small-litter males gained weight at a more rapid rate than the other litter types, both before and after weaning, and attained a final body weight twofold greater than the other groups. The small-litter males had significantly higher (P less than 0.05) numbers of adipocytes per epididymal fat pad than the other litter groups with 60.4, 51.4, and 79.0% greater cell number per pad than control, large, and pair-fed animals, respectively. Limiting food intake to small-litter animals after weaning (pair-fed) inhibited this growth and prevented fat cell proliferation. Litter manipulation had significant effects on male rats, but the same treatment did not influence female rats. Litter size influenced fat cell characteristics but had little effect on the adipocytes' ability to take up or metabolize glucose. The major finding, in terms of insulin responsiveness, was the difference between the sexes. The uptake of tritiated 2-deoxyglucose by the fat cells of female litter groups was significantly higher than that of the males whether insulin was present or not, whereas the conversion of [1-14C]glucose to CO2 by the adipocytes of females was lower than that of the males.(ABSTRACT TRUNCATED AT 250 WORDS)

Adipocyte insulin resistance: effects of aging, obesity, exercise, and food restriction.

This study examined the effects of aging, exercise training, and food restriction on epididymal fat cell size and resistance to insulin in rats. The exercise group was given access to voluntary running wheels at age 6 mo. The rats were studied at ages 12 and 28 mo. Sedentary free-eating (SFE) rats were obese and their fat cells were extremely insulin resistant, showing minimal increases in glucose oxidation and 2-deoxy-D-glucose (2-DOG) uptake in response to high insulin concentrations. The runners' adipocytes were smaller and had a greater responsiveness to insulin (approximately 9-fold for 2-DOG uptake and approximately 30-fold for glucose oxidation) than those of the SFE rats. Sedentary rats that were food restricted to keep their body weights the same as those of the runners had fat cells that were intermediate both in size and insulin responsiveness relative to those of the SFE rats and runners. There was a close correlation between fat cell size and responsiveness to insulin of 2-DOG uptake and glucose oxidation independent of age. There were no significant differences in fat cell size, insulin sensitivity, or insulin responsiveness between the adult (12 mo) and old (28 mo) rats in the same treatment groups. We conclude that aging alone has little or no effect on the responsiveness to insulin of glucose metabolism in fat cells and that the insulin resistance of adipocytes from obese older rats is due to fat cell hypertrophy, not aging. Exercise is effective in protecting against development of fat cell hypertrophy and insulin resistance.

Influence of exercise training on maternal and fetal morphological characteristics in the rat.

Evidence in both humans and animals has shown that exercise before or during pregnancy may effect fetal outcome. The purpose of this investigation was to examine the effects of an exercise program on fetal development in the rat. Prior to impregnation one group of animals was exercise-trained on a Quinton shock-stimulus rodent treadmill. The exercised group was trained to run 5 days/wk, for 2.0 h/day at 31 m/min up an 8 degree incline for 8 wk before mating. Following mating the training intensity was reduced to 27 m/min up a 5 degree incline, and the exercise period decreased to 1 h/day. On day 19 of gestation, 24 h postexercise for the trained mothers, the animals were killed in the fed state and the maternal and fetal characteristics were measured. The sedentary controls gained significantly (P less than 0.05) more body weight during pregnancy. This can be attributed to three factors: higher number of fetuses, 14.83 +/- 0.04 vs. 12.2 +/- 0.85 for the trained; larger litter weights, 44.25 +/- 4.97 vs. 26.17 +/- 1.82 g/dam for the trained; and slightly larger lipid stores. In addition to having fewer pups the trained mothers had a greater number of fetal resorptions; 0.9/dam as opposed to 0.17/dam for the sedentary control. Analysis of fetal body composition showed no difference in total body water, protein, or fat between the pups of sedentary and trained dams. The results of this study indicate that exercise training prior to and during pregnancy influences fetal development in the rat.

Effects of resistance exercise on glucose tolerance in normal and glucose-intolerant subjects.

This study was conducted to determine whether improvements in glucose tolerance could be observed after a single bout of resistance exercise in young (27.1 +/- 1.24 yr) control subjects, older (53.3 +/- 1.7 yr) patients with non-insulin-dependent diabetes mellitus (NIDDM), and older (50.7 +/- 1.9 yr) age-matched control subjects. Each subject was screened for fitness level and any contraindications to exercise before inclusion in the study. A 75-g oral glucose tolerance test was administered 2 wk after the subjects were screened, and the subjects were familiarized with the exercise equipment. The maximum weight that could be lifted with one repetition was determined on seven Nautilus machines that utilized the upper and lower body. After a 48-h rest period, a 3-set x 10-repetition protocol based on the subject's one repetition maximum was completed by each participant on each machine. Eighteen hours after the lifting protocol, a second oral glucose tolerance test was administered. There was no change in the pre- to post-exercise glucose levels in any of the treatment groups, but the total insulin responses (area under the curve) of the young control and NIDDM groups were significantly lower after exercise: from 6.93 +/- 0.8 x 10(3) to 5.38 +/- 0.65 x 10(3) pM in the young control group and from 9.83 +/- 1.95 x 10(3) to 7.77 +/- 1.50 x 10(3) pM in the NIDDM group. The postexercise C-peptide levels were unchanged in all groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Opioid antagonism alters blood glucose homeostasis during exercise in humans.

In an attempt to clarify the role of endogenous opioid peptides in substrate mobilization and hormonal responses to dynamic exercise, eight trained cyclists completed exercise trials at 90% of maximal O2 consumption (VO2max) until exhaustion and at 70% VO2max for 90 min. Trials were conducted after intravenous administration of the opiate antagonist naloxone (NAL, 0.1 mg/kg bolus + 0.1 mg.kg-1.h-1) or volume-matched saline (SAL) at each intensity. Serum glucose was maintained at significantly higher levels at 60 and 90 min of exercise in the 70%-NAL than in the 70%-SAL trial and at all points during exercise and at 30 and 60 min of recovery in the 90%-NAL than in the 90%-SAL trial. The serum insulin response to exercise was not altered by NAL administration at either intensity. Serum C-peptide was approximately 50% higher at 60 and 90 min of exercise in the 70%-NAL than in the 70%-SAL trial but was significantly lower during exercise in the 90%-NAL than in the 90%-SAL trial. The plasma glucagon response to exercise at 70% VO2max was not altered by NAL administration but was significantly elevated in the 90%-NAL vs. the 90%-SAL trial. Plasma epinephrine was 50-150% (approximately 2-3 nM) higher during exercise from 30 to 90 min of exercise in the 70%-NAL than in the 70%-SAL trial and was higher at termination (4.9 +/- 2.1 vs. 2.7 +/- 1.7 nM) in the 90%-NAL than in the 90%-SAL trial, although the difference in the 90% trial was not statistically significant.(ABSTRACT TRUNCATED AT 250 WORDS)

Evidence for the involvement of a phospholipase C--protein kinase C signaling pathway in insulin stimulated glucose transport in skeletal muscle.

The primary purpose of this investigation was to determine the relationship between phospholipase C (PLC) and diacylglycerol (DAG) sensitive protein kinase C isoforms in insulin signaling in skeletal muscle. Using an in vitro preparation of rat soleus muscle we found that insulin (0.6 nM) stimulated glucose transport was inhibited approximately 20 and 25% by the PKC inhibitor GF109203X and the phospholipase C inhibitor U73122 respectively (p<0.05). The combined effects of these inhibitors were no greater than the inhibitory effects of either compound alone. Western blot analysis revealed that insulin induced a redistribution of PKC beta II from the cytosol to the membrane that was reversed in the presence of GF109203X (1 microM) and U73122 (20 microM). Similarly, U73122 and GF109203X reversed the insulin induced increase in membrane associated phosphorylated (ser 660) PKC beta II. The novel finding of this investigation is that insulin induces an increase in PKC beta II translocation and phosphorylation through a U73122 sensitive pathway in quantatively the most important insulin responsive tissue, skeletal muscle. Furthermore, these results imply that PKC beta II may be one of the DAG sensitive isoforms involved in glucose transport.

A role for calcium/calmodulin kinase in insulin stimulated glucose transport.

Previous research has shown that the CAMK (calcium/calmodulin dependent protein kinase) inhibitor, KN62, can lead to reductions in insulin stimulated glucose transport. Although controversial, an L-type calcium channel mechanism has also been hypothesized to be involved in insulin stimulated glucose transport. The purpose of this report was to determine if 1) L-type calcium channels and CAMK are involved in a similar signaling pathway in the control of insulin stimulated glucose transport and 2) determine if insulin induces an increase in CAMKII phosphorylation through an L-type calcium channel dependent mechanism. Insulin stimulated glucose transport was significantly (p<0.05) inhibited to a similar extent ( approximately 30%) by both KN62 and nifedipine in rat soleus and epitrochelaris muscles. The new finding of these experiments was that the combined inhibitory effect of these two compounds was not greater than the effect of either inhibitor alone. To more accurately determine the interaction between CAMK and L-type calcium channels, we measured insulin induced changes in CAMKII phosphorylation using Western blot analysis. The novel finding of this set of experiments was that insulin induced an increase in phosphorylated CAMKII ( approximately 40%) in rat soleus muscle that was reversed in the presence of KN62 but not nifedipine. Taken together these results suggest that a CAMK signaling mechanism may be involved in insulin stimulated glucose transport in skeletal muscle through an L-type calcium channel independent mechanism.

The effect of exercise on serum and salivary cortisol in male children.

The purpose of this study was to examine serum and salivary cortisol responses to cycling exercise in male children, 10.6 +/- 0.2 yr (mean +/- SE). Each child performed a graded exercise test on a cycle ergometer to determine VO2max. On a separate day, a 30-min bout of exercise at 70% of VO2max was performed. Blood, obtained from a venous catheter, and saliva samples were collected at rest, at 15 and 30 min of exercise, and 15 min post-exercise. The mean serum cortisol level at 15 min (7.94 +/- 1.43 micrograms.dl-1) and 30 min (8.72 +/- 1.77 micrograms.dl-1) of exercise and at 15 min post-exercise (8.21 +/- 1.59 micrograms.dl-1) were significantly greater than rest (5.54 +/- 0.86 micrograms.dl-1). The increase in salivary cortisol levels over time approached (P = 0.08), but did not reach significance. However, effect size analyses indicated that the increase in salivary cortisol at 30 min of exercise (0.64) and 15 min post-exercise (0.62) was similar to the change in serum cortisol at these same two time points (0.72 and 0.66, respectively). Serum and salivary cortisol were correlated (P < 0.05) at 15 min of exercise (r = 0.77), 30 min of exercise (r = 0.90), and 15 min post-exercise (r = 0.84), but not at rest (r = 0.46). In conclusion, 30 min of submaximal exercise at 70% of VO2max significantly increased serum cortisol level; and salivary and serum cortisol are correlated during and after exercise.

Eating attitudes and energy intakes of female skaters.

PURPOSE: This study examined potential links between dietary intakes, body fatness, menstrual status, and hematological and serum iron status in 21 competitive female figure skaters aged 11-16 yr. METHODS: Attitudes toward dieting were assessed using the Eating Attitudes Test (EAT). Dietary intakes were based on 3-d food records. Percent body fat was calculated using measures of triceps, subscapular, suprailiac, pectoral, axillary, abdominal, and thigh skinfold measures. Blood iron status was measured using hematocrit (Hct), hemoglobin (Hgb), total iron binding capacity (TIBC), and serum iron. Menstrual status was based on a self-report questionnaire. RESULTS: Body weights and estimated energy intakes were all within normal range for this age group. Higher EAT scores were associated with lower micronutrient, but not lower energy intakes. Menstrual status and iron status were normal. No significant correlations between measures of body fatness, menstrual status, and hematological or serum iron status were observed. CONCLUSION: Although the measured indices of nutritional status were normal, adolescent athletes have higher energy needs than does the general population. Depending on energy expenditure levels, energy and nutrition intakes in the low normal range may put some athletes at risk for undernutrition.