The effect of guar gum addition to a semisolid meal on appetite related to blood glucose, in dieting men.

OBJECTIVE: To investigate whether addition of modified guar gum (GG) to a low-energy semisolid meal might be effective on appetite by modifying the response of blood glucose and other blood parameters. DESIGN: Three intervention periods of 2 weeks each, separated by washout periods of 4 weeks. Randomized and cross-over design. SUBJECTS: Fifteen overweight male subjects (mean+/-s.d.; age, 44+/-9 y; body mass index, 28.6+/-1.8 kg/m(2)). INTERVENTION: Subjects consumed a low-energy diet divided over three times a day, consisting of a semisolid meal with (SSM+) or without (SSM) addition of 2.5 g GG, or a solid meal (SM) with the same energy content (947 kJ) and macronutrient composition, plus a dinner of the subject's own choice. At the end of each intervention, time and number of meal initiations, dynamics of blood glucose and other blood parameters, and appetite ratings such as hunger and satiety were determined in a time-blinded situation. RESULTS: The changes in blood glucose from meal initiation to blood glucose peak and from peak to nadir were smaller with SSM+ and SM compared to SSM. Satiety before the third meal was higher with SSM+ and SM compared to SSM (P<0.01). Meal pattern, general appetite and total energy intake were similar for all treatments. CONCLUSIONS: We conclude that, similar to SM, SSM+ resulted in a more moderate change in blood glucose compared to SSM and positively affected satiety before the third meal, while general appetite, total energy intake and meal pattern did not differ.

The effect of addition of modified guar gum to a low-energy semisolid meal on appetite and body weight loss.

OBJECTIVE: To investigate the effect of addition of modified guar gum (GG) to a low-energy semisolid meal on appetite and body weight (BW) loss. SUBJECTS: Twenty eight mainly overweight male volunteers (age, 19-56 y; body mass index, 29+/-2 kg x m(-2); BW, 89.4+/-9.2 kg). DESIGN: Baseline of one week with self-selected diet. Three treatments of 2 weeks with a low-energy diet divided over three times a day, consisting of a semisolid meal with (SSM+) or without GG (SSM) or a solid meal (SM) with the same energy content (947 kJ) and macronutrient composition, and a dinner of the subject's own choice. Washout periods lasted 4 weeks. RESULTS: Compared to baseline values, reduction in energy intake and BW loss were similar for SSM+, SSM and SM. Appetite (hunger, desire to eat or estimation of how much one could eat) was increased in SSM and in SM compared to baseline, but not in SSM+. Satiety and fullness in SSM+, SSM and SM were similar to baseline. Any intervention was more effective on BW loss when it took place the first time compared to the second and third times (2.6+/-0.2 kg, 1.7+/-0.2 kg and 1.1+/-0.2 kg, respectively; P<0.001). The SM-SSM+-SSM sequence was more effective on BW loss compared to the SSM+-SSM-SM sequence (5.6+/-1.0 and 2.5+/-0.6 kg, respectively; P<0.05). CONCLUSION: All the three treatments were equally effective with respect to BW loss. GG addition to a semisolid meal prevented an increase in appetite, hunger and desire to eat, which increase was present in the other treatments. However, differences between treatments were not statistically significant. The order effect shows that repeated 2-week bouts of dieting become increasingly ineffective. The sequence SM-SSM+-SSM was more effective than the sequence SSM+-SSM-SM, probably because compliance was relatively higher with the SSM+ or SSM diet, and compliance decreased towards the end of the complete experiment.

Influence of exercise and menstrual cycle phase on plasma homocyst(e)ine levels in young women--a prospective study.

Plasma total homocysteine (tHcy) has been identified as an independent risk factor for cardiovascular diseases (CVD). The difference in tHcy between the sexes has most often been related to the sex hormones, but also to a higher muscle mass in men. The purpose of this study was to assess the effects of acute exercise, brief exhaustive training, and menstrual cycle phase on circulating plasma tHcy concentrations. Fifteen untrained eumenorrheic women (mean age [+/-SD]: 18.7+/-0.4 yr, body fat: 25.8+/-3.4%, VO2max: 43.8+/-2.3 ml x kg(-1) x min(-1)) volunteered for the present study, which covered two menstrual cycles. During the second cycle the subjects participated in two exhaustive 5-day training programs on a cycle ergometer: one in the follicular (FPh) and one in the luteal phase (LPh). Pre- and posttraining plasma tHcy and total estrogen (E) responses were determined in blood samples obtained immediately before, during and immediately after incremental exercise to exhaustion. tHcy levels showed a large between-subject variation, but differences between FPh and LPh levels were consistent (P=0.063). Mean tHcy levels at rest were 9.44+/-1.65 micromol/L and 8.93+/-1.71 micromol/L during the FPh and LPh, respectively. Brief exhaustive training did not elicit any changes in plasma tHcy concentrations, although posttraining LPh E levels were lower (P<0.01). Overall, the differences between FPh and LPh values for tHcy and E were attenuated by training. Acute exercise increased plasma tHcy concentrations (P<0.001). At exhaustion, tHcy levels increased by 17% and 16% during the FPh and LPh, respectively. This was also significantly above tHcy levels at submaximal exercise (P=0.044). After a short period of training tHcy levels did not increase as much during acute exercise as they did before training; however, the increments were still significant (P=0.048). In conclusion, acute exercise in women produces significant increases in plasma tHcy concentrations, whereas brief exhaustive training does not significantly alter plasma tHcy levels. Our findings also suggest that plasma tHcy concentrations are menstrual cycle phase-dependent and that there is a close association between estrogen status and tHcy levels.

Responsiveness of plasma 2- and 4-hydroxycatecholestrogens to training and to graduate submaximal and maximal exercise in an untrained woman. Interuniversity Project on Reproductive Endocrinology in Women and Exercise.

A single-subject experimental design was used to obtain some preliminary findings on the plasma responses of catecholestrogens (CE) to acute exercise and brief, but exhaustive training on a cycle ergometer. One previously untrained eumenorrheic female (body fat: 26% VO2max: 43.3 ml x kg(-1) x min[-1]) participated in this study. Resting CE levels were for "total" (unconjugated + conjugated) 2-hydroxyestrogens (2-OHE) 162pg/ ml and 350 pg/ml in the follicular (FPh) and luteal phase (LPh), respectively. Plasma total 4-hydroxyestrogen (4-OHE) levels were 41 pg/ml in the FPh and 66 pg/ml in the LPh. For "total" 2-methoxyestrogens (2-MeOE), we found 257 pgl/ml in the FPh and 374 pg/ml in the LPh. Resting levels of 2-hydroxy CE following a period of brief, intensive training were decreased during the LPh (2-OHE: -38%; 2-MeOE: -19%), whereas 4-hydroxy CE were unaffected. After training, the formation of CE as expressed by the 2-OHE:E and 4-OHE:E ratios, was increased by 75% and 200% at rest, respectively. CE activity or O-methylation, as estimated from the 2-MeOE:2-OHE ratio, was higher following training (FPh: +22%; LPh: +30%). During acute exercise before training, we observed a small rise proportional to the exercise intensity in the plasma "total" primary estrogen concentrations (FPh: +28%; LPh: +16%), and no changes in either 2-OHE or 2 MeOE levels. Plasma concentrations of 4-OHE, however, doubled during maximal exercise intensity. The 2-OHE:E and 2-MeOE:2-OHE ratios did not alter during incremental exercise. Training effects on acute exercise responses were only noticed for 4-OHE, which contrary to pre-training conditions, now progressively decreased. The major findings of this study are that in response to training: a) during rest, a greater proportion of CE are formed from a lower amount of precursor hormone, b) the rate of O-methylation of CE increases.

Responses of catecholestrogen metabolism to acute graded exercise in normal menstruating women before and after training.

It has been hypothesized that exercise-related hypo-estrogenemia occurs as a consequence of increased competition of catecholestrogens (CE) for catechol-O-methyltransferase (COMT). This may result in higher norepinephrine (NE) concentrations, which could interfere with normal gonadotropin pulsatility. The present study investigates the effects of training on CE responses to acute exercise stress. Nine untrained eumenorrheic women (mean percentage of body fat +/-SD: 24.8 +/- 3.1%) volunteered for an intensive 5-day training program. Resting, submaximal, and maximal (tmax) exercise plasma CE, estrogen, and catecholamine responses were determined pre- and post training in both the follicular (FPh) and luteal phase (LPh). Acute exercise stress increased total primary estrogens (E) but had little effect on total 2-hydroxyestrogens (2-OHE) and 2-hydroxyestrogen-monomethylethers (2-MeOE) (= O-methylated CE after competition for catechol-O-methyltransferase). This pattern was not significantly changed by training. However, posttraining LPh mean (+/-SE) plasma E, 2-OHE, and 2-MeOE concentrations were significantly lower (P < 0.05) at each exercise intensity (for 2-OHE: 332 +/- 47 vs. 422 +/- 57 pg/mL at tmax; for 2-MeOE: 317 +/- 26 vs. 354 +/- 34 pg/mL at tmax). Training produced opposite effects on 2-OHE:E ratios (an estimation of CE formation) during acute exercise in the FPh (reduction) and LPh (increase). The 2-MeOE:2-OHE ratio (an estimation of CE activity) showed significantly higher values at tmax in both menstrual phases after training (FPh: +11%; LPh: +23%; P < 0.05). After training, NE values were significantly higher (P < 0.05). The major findings of this study were that: training lowers absolute concentrations of plasma estrogens and CE; the acute exercise challenge altered plasma estrogens but had little effect on CE; estimation of the formation and activity of CE suggests that formation and O-methylation of CE proportionately increases. These findings may be of importance for NE-mediated effects on gonadotropin release.

Heat stress protects aged hypertrophied and nonhypertrophied rat hearts against ischemic damage.

To explore the effects of heat stress (HS) in aged hypertrophied and nonhypertrophied rat hearts, postischemic recovery was investigated 15 mo after aortic constriction (AoB) or sham operation (Sham). Twenty-four hours after HS (42 degrees C; 15 min) or control treatment (normothermia), global ischemia was induced for 20 min in isolated AoB hearts and for 20 or 30 min in Sham hearts. After HS, postischemic recovery after 20-min ischemia in AoB hearts and 30-min ischemia in Sham hearts, respectively, was significantly better than in corresponding controls. In AoB hearts, cardiac output (CO), left ventricular developed pressure (LVDP), and the positive maximal first derivative of left ventricular pressure (+dP/dtmax) recovered to 33 +/- 26 (means +/- SD), 87 +/- 5, and 72 +/- 12%, respectively, after HS and to 5 +/- 8, 22 +/- 39, and 17 +/- 29% of preischemic values, respectively, in controls. Postischemic arrhythmias were significantly reduced in HS hypertrophied hearts, but creatine kinase (CK) loss was not reduced. In Sham hearts subjected to 30 min ischemia, CO, LVDP, and +dP/dtmax recovered to 20 +/- 20, 75 +/- 8, and 59 +/- 15%, respectively, after HS and to 3 +/- 8, 21 +/- 32, and 16 +/- 32% of preischemic values, respectively, in controls. Duration of arrhythmias and CK loss were not reduced in the heated hearts. When Sham hearts were subjected to only 20-min ischemia, functional recovery was not different in HS and control hearts, indicating that HS pretreatment extends the ischemic interval before irreversible injury occurs in the heart. In all HS Sham hearts, the myocardial 72-kDa HS protein (HSP 70) content was significantly increased. However, in HS AoB hearts, HSP 70 levels were not significantly different from the values in the control hearts. These results indicate that HS pretreatment induces cardioprotection in aged hypertrophied and nonhypertrophied rat hearts, which, however, cannot be unequivocally related to increased HSP 70 tissue contents.

4-Hydroxycatecholestrogen metabolism responses to exercise and training: possible implications for menstrual cycle irregularities and breast cancer.

OBJECTIVE: To investigate the behavior of C4-substituted estrogens, the so-called catecholestrogens, in response to acute exercise and training. The 4-hydroxyestrogens are known to have both a strong estrogenic potency and affinity for catechol-O-methyltransferase (COMT), the enzyme that deactivates catecholamines. DESIGN: A prospective trial covering three menstrual cycles: a control cycle, a moderate training cycle, and a heavy training cycle. PARTICIPANT(S): Six untrained, healthy, eumenorrheic women (mean pretraining maximum oxygen uptake: 40.9 +/- 4.9 mL/kg per minute, body fat: 27.9% +/- 3.6%) volunteered for this study. INTERVENTION(S): An incremental exercise test to exhaustion on a cycle ergometer, in the follicular and luteal phases, before and after a brief but exhaustive training program. MAIN OUTCOME MEASURE(S): Hormone measurements included follicular and luteal phase plasma E2, LH, catecholamines, PRL, total unconjugated and conjugated estrogens, total 4-hydroxyestrogens (4-OHE), and 4-hydroxyestrogen-monomethylethers (4-MeOE). RESULT(S): Pretraining baseline 4-OHE levels were significantly higher in the luteal phase (66 +/- 9 pg/mL; mean +/- SEM) than in the follicular phase (51 +/- 7 pg/mL). Pretraining and post-training baseline 4-MeOE values were below minimal detection limits (< 35 pg/mL). During incremental exercise, catecholamines, PRL, E2, unconjugated and conjugated estrogens, 4-OHE, and 4-MeOE always increased (the increases in 4-OHE during exercise were more pronounced before training, contrary to the 4-MeOE being most increased after training). The baseline 4-MeOE:4-OHE ratio (a measure of catecholestrogen activity) significantly increased with progressive training. CONCLUSION(S): Because 4-OHE have been shown to be able to control the hypothalamic gonadotropin oscillator and to stimulate the luteolytic prostaglandin PGF2 alpha, the acute exercise-induced increases of 4-OHE and their positive correlation with lactate levels may indicate a key process in the pathogenesis of exercise-associated menstrual irregularities. In addition, 4-OHE, when insufficiently O-methylated, are known to be capable of raising mutagenic superoxide free radicals and causing DNA damage that may lead to breast cancer. The results of the present study also may be of significance for the apparent protective effects of sports participation against cancer of the breast.

Plasma 2-hydroxycatecholestrogen responses to acute submaximal and maximal exercise in untrained women.

Exercise-induced menstrual problems are accompanied by an increase in catecholestrogen (CE) formation. It has been hypothesized that hypoestrogenemia may be secondary to an increased turnover from estrogens to CE, which then may disrupt luteinizing hormone release. In addition, the strong affinity of CE for the catecholamine-deactivating enzyme catechol-O-methyltransferase (COMT) has led to speculations about their possible role in safeguarding norepinephrine from premature decomposition during exercise. We investigated whether acute exercise on a cycle ergometer produces any changes in CE homeostasis. Nine untrained eumenorrheic women (body fat, 24.8 +/- 3.1%) volunteered for this study. Baseline plasma CE averages for total 2-hydroxyestrogens (2-OHE) were 218 +/- 29 (SE) pg/ml during the follicular phase (FPh) and 420 +/- 58 pg/ml during the luteal phase (LPh). 2-Methoxyestrogens (2-MeOE) measured 257 +/- 17 pg/ml in the FPh and 339 +/- 39 pg/ml in the LPh. During incremental exercise, total estrogens (E) increased, but 2-OHE and 2-MeOE levels did not significantly change in either phase. The 2-OHE/E ratio (measure of CE turnover) decreased during exercise in both menstrual phases, whereas the 2-MeOE/2-OHE ratio (correlates with COMT activity) did not significantly change. These findings suggest that there is insufficient evidence to conclude that brief incremental exercise in untrained eumenorrheic females acutely produces increased CE formation.

Effects of a training program on resting plasma 2-hydroxycatecholestrogen levels in eumenorrheic women.

Catecholestrogens (CE) represent a major metabolic pathway in estrogen metabolism. Previous information on CE and training is limited to two cross-sectional studies that did not involve standardized training. Our purpose, by means of a prospective design, was to evaluate the effects of a brief, exhaustive training program on resting plasma concentrations of 2-hydroxy CE. The experimental design spanned two menstrual cycles; a control cycle and a training cycle. The subjects were nine previously untrained, eumenorrheic women [body fat: 24.8 +/- 1.0 (SE) %]. Data were collected during the follicular (FPh) and the luteal phases (LPh). Posttraining FPh and LPh tests were held the day after the last day of a 5-day period of training on a cycle ergometer. Total 2-hydroxyestrogens (2-OHE) averaged 200 +/- 29 pg/ml during the FPh and 420 +/- 54 pg/ml during the LPh (P < 0.05). Levels of total 2-methoxyestrogens (2-MeOE) were 237 +/- 32 pg/ml during the FPh and 339 +/- 26 pg/ml during the LPh (P < 0.05). After training, although the plasma levels of 2-OHE significantly decreased (21%; P < 0.05) during the LPh, the actual CE formation (as estimated from the 2-OHE-to-total estrogens ratio) increased (+ 29%; P < 0.05). CE activity, as expressed by the 2-MeOE-to-2-OHE ratio, showed significantly higher values in both phases (FPh, + 14%; LPh, + 13%; P < 0.05). At the same time, resting levels of norepinephrine (NE) were increased by 42% (P < 0.05). CE strongly inhibit biological decomposition of NE by catechol-O-methyltransferase (COMT). Results of the present study suggest that, in response to training, CE are increasingly competing with the enzyme COMT, thus preventing premature NE deactivation.

Exercise-induced changes in enzymatic O-methylation of catecholestrogens by erythrocytes of eumenorrheic women.

The present study was designed to assess the effects of acute exercise and short-term intensive training on catechol-O-methyltransferase (COMT) activity. COMT inactivates catecholamines and converts primary catecholestrogens (CE) into their O-methylated form yielding the 2- (2-MeOE) and 4-methoxyestrogens (4-MeOE). Blood samples were obtained from 15 previously untrained eumenorrheic women (mean +/- SE, VO2max: 43.8 mL x kg-1 x min-1 +/- 0.6) before and after a 5-d intensive training period, at rest and during incremental exercise. COMT activity was determined in the erythrocytes (RBC-COMT) after incubation of blood lysate with primary CE. The formation of both 2- and 4-MeOE was significantly higher (P < 0.05) during the luteal (LPh) than during the follicular phase (FPh). The amount of 2-MeOE formed (FPh: 4.2 +/- 0.2%; LPh: 4.9 +/- 0.2%) was significantly greater than the produced amount of 4-MeOE (FPh: 1.4 +/- 0.1%; LPh: 1.5 +/- 0.1%) (P < 0.05). Both before and after training, incremental exercise did not significantly alter RBC-COMT activity although we observed a trend for RBC-COMT activity increasing proportionally with the exercise intensity. After a brief period of exhaustive training, during rest the formation of 2-MeOE (FPh: +16.7%, LPh: +15.7%) and 4-MeOE (FPh: +28.6%; LPh: +40%) was significantly (P < 0.05) increased. The results of the present study are consistent with earlier findings reporting increased plasma concentrations of O-methylated CE following training. It is concluded that RBC-COMT activity is increased by brief intensive training, but not by acute exercise. We speculate that an increase in COMT-catalyzed O-methylation of CE may indicate that less COMT is available to deactivate norepinephrine.

Structural muscle damage and muscle strength after incremental number of isometric and forced lengthening contractions.

Exercise-induced muscle damage is characterized by histological changes, like Z-line streaming, inflammatory response and decreased muscle function reflected in a prolonged decline in maximal isometric muscle strength after eccentric work. It is assumed that force decrement is mainly related to the amount of structural damage. However, the relationship between number of eccentric contractions, magnitude of structural damage and force decrement is not very well documented. Therefore we studied the effect of an increasing number of both isometric and eccentric (forced lengthening) contractions on histological parameters of muscle damage and maximal isometric force in an experimental in situ rat model. Tibialis anterior muscles of male Wistar rats were subjected to an increasing number of either isometric or eccentric contractions and were examined for histological markers of muscle damage. The present study shows that muscle damage increases progressively with the number of forced lengthening contractions. Maximal isometric torque was found to decline after both types of exercise. However, the decline after forced lengthening exercise was more pronounced. Only a weak relationship between percentage of histological muscle damage and isometric torque after forced lengthening contractions was found. The findings of the present study suggest that the decline in muscle force after eccentric exercise may partly be attributed to other factors than structural damage.

Modulation of glycogen metabolism of rat skeletal muscles by endurance training and testosterone treatment.

The effects of training and/or testosterone treatment on glycogen content and the activities of glycogen synthase, glycogen phosphorylase, and fructose-6-phosphate kinase were studied in extensor digitorum longus (EDL) and soleus muscles of intact adult female rats. One group of rats remained sedentary, whereas another group was trained for 7 weeks. Thereafter, both the sedentary and trained rats were subdivided into two control and four testosterone-treated subgroups. Testosterone was administered by a silastic implant. Training was continued for 2 weeks. On the final day of the experiment rats from one trained control and one trained testosterone-treated subgroup ran for 60 min submaximally. Upon testosterone treatment of sedentary rats the glycogen concentration was not changed. However, in the soleus, but not in the EDL, the glycogen content was increased by training (P < 0.05) which could, at least partly, be explained by a decrease in activity of active glycogen phosphorylase (P < 0.05). In the EDL of trained rats testosterone treatment increased glycogen content significantly by both an increase in activity of active glycogen synthase and a decrease in activity of active glycogen phosphorylase (P < 0.05). In the EDL and soleus of testosterone-treated animals from the exercised subgroup a significant sparing of glycogen was observed, which could be explained by an increase in activity of active glycogen synthase and, in the soleus, could also be explained by a concerted decrease in active glycogen phosphorylase (P < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Use of the intact mouse skeletal-muscle preparation for metabolic studies. Evaluation of the model.

1. We examined the isolated mouse skeletal-muscle model in vitro, commonly used by many investigators, for its suitability for metabolic studies. 2. Despite the fact that pH, O2 saturation, osmolality and the release of the enzyme creatine kinase remained stable, histochemical studies showed large cores devoid of glycogen, suggesting that the incubated muscle had lost its viability. 3. This study indicates that caution should be exercised when interpreting the results of studies with intact isolated mouse muscles.

Plasma urea, creatinine, uric acid, albumin, and total protein concentrations before and after 15-, 25-, and 42-km contests.

One hundred fourteen volunteers (34 +/- 8 years) took part in an endurance training study to be completed after 18-20 months with a marathon. Ultimately, 60 males and 18 females achieved that goal. The training program, carefully supervised, was divided into three periods with a maximum of 45, 70, and 110 km/week training volume and concluded with contests of 15, 25, and 42.2 km, respectively. The competitive distance always exceeded the maximal distance covered in any previous training session. Three days before and 3 and 5 days after each race 35 subjects were selected to perform a progressive treadmill test and the remaining subjects participated in field tests of 400 and 1000 m. Before and after three contests of 15, 25, and 42.195 km the plasma concentration of urea, creatinine, uric acid, albumin, and total protein were determined. Both sexes demonstrated an increase of the plasma concentrations of urea, creatinine, and uric acid after the contests. Plasma albumin concentration decreased 2 days after the contests and total protein did not change. In females the decrease of the elevated plasma urea concentration after the marathon from the 1st day to the 3rd day post-exercise was faster than in males. The increase of plasma creatinine and uric acid concentrations were hardly dependent on the contest's distance.

Structural and ultrastructural changes in skeletal muscle associated with long-distance training and running.

The histological and ultrastructural features of 21 males and 8 females were monitored during an 18- to 20-month training period, during which the training distance was gradually increased. The training period was divided into three periods of 6, 5, and 7 months, respectively. The first, second, and third periods were concluded with a 15-, 25-, 42-km road race, respectively. The competitive distance always exceeded the maximal distance covered in any previous training session. Percutaneous biopsies were taken from the vastus lateralis muscle 5 days before each contest as well as 0.5-6 h post-contest and 8-9 days post-contest. No shift in fiber type was observed during the training period from the 15-km contest until the 42-km contest nor were any changes in fiber diameter observed. Histological examination demonstrated a gradual increase in degenerative changes during the training period, which occurred in type I as well as in type II fibers. Ultrastructural examination revealed irregular Z-lines and hypercontraction immediately after exercise. No damage to the sarcolemma was detected. The number of degenerative changes after each contest was not higher than before each race. It is concluded that long-distance running is associated with transient minor pathological changes in skeletal muscle, which are related to the total distance covered per week rather than the intensity of the exercise.

Plasma activity of muscle enzymes: quantification of skeletal muscle damage and relationship with metabolic variables.

One hundred fourteen sedentary volunteers (34 +/- 8 years) took part in an endurance training study to be completed after 18-20 months with a marathon. Ultimately, 60 males and 18 females achieved that goal. The training program, carefully supervised, was divided into three periods with a maximum of 45-, 70-, and 110-km week training volume and concluded with a performance race of 15, 25, and 42.2 km, respectively. Three days before and 3 and 5 days after each race, 35 subjects were selected to perform a progressive treadmill test and the remaining subjects participated in field tests of 400 and 1000 m. A significant decrease in half-life time of CK enzyme plasma activity after running long distances in the course of the study from 20 h to 13 h was observed. Based on plasma enzyme activity and supposing that the total enzyme content left the muscle fiber, the estimated amount of muscle damage was found to be small. A gender difference in plasma enzyme activity increase (females demonstrated a lower increase) occurred only after the marathon.

Exercise-induced changes in the percentage of free testosterone and estradiol in trained and untrained women.

We have studied the effect of exercise on the percentage of free plasma estradiol 17-beta (E2) and testosterone (T) in 13 untrained (UT) and 8 trained (marathon runners, MR) eumenorrheic women. All women performed a standardized bicycle ergometer (UT) or treadmill (MR) test in the follicular and luteal phases of their menstrual cycles (15-min consecutive work loads of 60%, 70%, and 80% VO2 max to exhaustion). Blood was drawn through an indwelling venous catheter at 15 and 2 min before and immediately after exercise. Free E2 and T was assayed by centrifugal ultrafiltration using undiluted plasma at 37 degrees C (basal samples) and 39 degrees C (exercise samples). Statistical analysis was performed by a two-tailed paired t test. In the UT, the basal percentage of free E2 was measured to be 1.55% +/- 0.24% (mean +/- SD) in the follicular phase and 1.62% +/- 0.32% in the luteal phase (differences NS). In the MR, these values were 1.22% +/- 0.25% and 1.25% +/- 0.12% for the follicular and luteal phases, respectively. The differences between the groups were not significant. Exercise did not provoke significant changes in free E2 in either of the groups. Constrastingly, exercise induced a significant (P less than 0.02) increase in the percentage of free T from 1.56% +/- 0.27% to 2.1% +/- 0.36% and from 1.6% +/- 0.27% to 2.12% +/- 0.33% in the UT in the follicular and luteal phases, respectively. In the MR, the free percentage of T increased from 1.04% +/- 0.39% to 1.6% +/-0.16% (follicular phase) and from 1.24% +/- 0.22% to 1.67% +/- 0.18% (P less than 0.02).

Effect of a 3-month endurance training program on metabolic and multiple hormonal responses to exercise.

We have investigated the effect of a 3-month endurance training program (running and cycling) on plasma hormone responses during standardized bicycle ergometer work (15-min consecutive work loads of 60%, 70%, 80%, and eventually 90% VO2 max) in eight previously untrained eumenorrheic women. The subjects were investigated before and after training both in the follicular and luteal phases of the menstrual cycle (between the 7th-10th and 20th-25th days of their menstrual cycle, respectively). Blood was obtained 15 and 2 min before the onset of exercise and at the end of each work load from an indwelling catheter. In each sample, the plasma concentrations of estradiol 17 beta (E2), progesterone (P), testosterone (T), androstenedione (delta 4-A), dehydroepiandrosterone sulfate (DHEA-S), prolactin (PRL), and adrenocorticotropic hormone (ACTH) were assayed in duplicate by RIA; lactate was assayed as well. The hormone concentrations were expressed in absolute as well as in relative values. After training basal DHEA-S and ACTH levels were significantly (P less than 0.05) lower in both phases of the menstrual cycle, whereas basal luteal phase E2 and T levels were significantly (0.05 greater than P greater than 0.01) lower after training. Exercise induced significant increments in the relative values of all hormones in both phases (0.05 greater than P greater than 0.001). After training, T and DHEA-S increased relatively more pronounced (0.05 greater than P greater than 0.02) in the follicular and luteal phase, respectively.

Influence of liquid and solid meals on muscle glycogen resynthesis, plasma fuel hormone response, and maximal physical working capacity.

The effect of forced liquid (L) or solid (S) carbohydrate (CHO)-rich feedings on plasma glucose, insulin, and glycogenesis after glycogen depletion was investigated. The relationship between glycogen restoration and maximal physical working capacity (MPWC) was studied as well. Eight males performed two experiments, with 2 weeks interval, on a bicycle ergometer. In each experiment, MPWC was determined in a graded test, which was immediately followed by interval work until exhaustion. After exercise cessation (EC), the subjects started to consume a standardized amount of concentrated L or CHO-rich food. Insulin and glucose concentration in blood were determined. Muscle glycogen was determined before, immediately after, 5 h after, and 22 h after EC. MPWC was determined again 22 h after EC. Four subjects performed a third experiment, in which solid food consumption was left ad libitum (AL). A rapid glycogen repletion was found 5 h after EC, i.e., from 72 +/- 40 to 198 +/- 38 mmol/kg in the S, and from 69 +/- 39 to 192 +/- 40 mmol/kg in the L experiment. The higher plasma glucose and insulin levels (P less than 0.05) during the 5 h after EC in the S experiments did not elicit a difference in glycogen repletion. Glycogen synthesis rate in the AL experiment was lower (P less than 0.05) than in the L and S experiments. Glycogen restoration in the L and S experiments was complete 22 h after depletion. However, despite repletion of glycogen, MPWC was decreased (P less than 0.05) in both experiments.(ABSTRACT TRUNCATED AT 250 WORDS)