Biomedical subjects

A Z Jamurtas

Publications and source records attributed to A Z Jamurtas.

13 recordsLinked to original sources

PubMed2007

The effect of eccentric exercise on position sense and joint reaction angle of the lower limbs.

Impaired position sense and impaired joint reaction angle of the lower limbs after muscle-damaging activities is a serious functional limitation that may lead to an increased risk of injury, particularly in older populations. The purpose of the present study was to examine whether position sense and joint reaction angle to release can be affected by eccentric exercise-induced muscle damage. Twelve women underwent an isokinetic exercise session of the lower limb. Isometric peak torque, delayed-onset muscle soreness, serum creatine kinase, position sense, and knee joint reaction angle to release were examined before, immediately after, and 24, 48, and 72 h post-exercise. Due to the effect of eccentric exercise, subjects persistently placed their lower limb at a more extended position, representing a shorter knee extensor muscle. Eccentric exercise increased the knee reaction angle of the lower limb after release from 0 degrees and 15 degrees but not from 30 degrees and 45 degrees . Position sense and joint reaction to release were similarly affected by eccentric exercise and independently of visual feedback. Position sense was impaired only immediately post-exercise (probably due to muscle fatigue), whereas impairment of the reaction angle to release persisted up to 3 days post-exercise (probably due to muscle damage). Attenuation of position sense and joint reaction angle of the lower limbs after damaging activities is a serious functional limitation that may lead to an increase risk of injury, particularly in older populations.

Adult↗

PubMed2006

The effects of acute exercise on serum adiponectin and resistin levels and their relation to insulin sensitivity in overweight males.

The purpose of this study was to investigate the effects of a submaximal aerobic exercise bout on adiponectin and resistin levels as well as insulin sensitivity, until 48 h post-exercise in healthy overweight males. Nine subjects performed an exercise bout at an intensity corresponding to approximately 65% of their maximal oxygen consumption for 45 min. Adiponectin, resistin, cortisol, insulin, glucose and insulin sensitivity were measured prior to exercise, immediately after exercise as well as 24 and 48 h after exercise. Data were analyzed using repeated measures ANOVA while Pearson's correlations were performed to identify possible relationship among the assessed variables. There were no significant differences for adiponectin (microg ml(-1)) [pre, 3.61(0.73); post, 3.15(0.43); 24 h, 3.15(0.81); 48 h, 3.37(0.76)] or resistin (ng ml(-1)) [pre, 0.19(0.03); post, 0.13(0.03); 24 h, 0.23(0.04); 48 h, 0.23(0.03)] across time. Insulin sensitivity increased and insulin concentration decreased significantly only immediately after exercise. Furthermore, no significant correlations were observed among the variables assessed except for the expected between insulin level and insulin sensitivity. These results indicate that a submaximal aerobic workout does not result in significant changes in adiponectin and resistin up to 48 h post-exercise. Furthermore, it appears that adiponectin or resistin is not associated with insulin sensitivity.

Adiponectin↗

PubMed2006

Comparison of the blood redox status between long-distance and short-distance runners.

Exercise increases the production of reactive oxygen species, which may damage a number of cell constituents. Organisms have developed a sophisticated antioxidant system for protection against reactive oxygen species. Our aim was to compare the adaptive responses of antioxidant mechanisms and the blood redox status of two groups of athletes, long-distance and short-distance runners. Thiobarbituric acid reactive substances, catalase activity and total antioxidant capacity was measured in the serum, while reduced and oxidized glutathione as well as their ratio were determined in blood hemolysates. Serum catalase activity (P<0.001) was found to be three times higher in long-distance compared to short-distance runners (25.4 vs. 8.9 micromol x min(-3) x ml(-1)), whereas the two groups did not differ in the other markers. Catalase activity also correlated significantly with maximal oxygen consumption in long-distance runners. In conclusion, we report here that long-distance and short-distance runners exhibit similar blood redox status judged by several oxidative stress indices, except for the much higher activity of catalase in long-distance runners. This different effect of the two training modules on catalase activity of long-distance runners might be partly due to the high oxygen load imposed during their repeated prolonged exercise bouts.

Adaptation, Physiological↗

PubMed2005

Leptin and adiponectin responses in overweight inactive elderly following resistance training and detraining are intensity related.

CONTEXT: Adiponectin and leptin are closely related to weight control and energy balance, whereas exercise affects elderly metabolic regulation and functional capacity. OBJECTIVE: The objective of this study was to investigate leptin and adiponectin responses in elderly males after exercise training and detraining. DESIGN: The study design was a 1-yr randomized controlled trial. SETTING: The study was performed at the Laboratory of Physical Education and Sport Science Department. PARTICIPANTS: Fifty inactive men [age, 65-78 yr; body mass index (BMI), 28.7-30.2 kg/m2] were recruited from a volunteer database by word of mouth and fliers sent to medical practitioners, physiotherapists, and nursing homes in the local community. INTERVENTION(S): Participants were randomly assigned to a control (n = 10), low-intensity (n = 14), moderate-intensity (n = 12), or high-intensity training (HI; n = 14) group. Resistance training (6 months, 3 d/wk, 10 exercises/three sets) was followed by 6 months of detraining. MAIN OUTCOME MEASURE(S): Strength, exercise energy cost, skinfold sum, body weight, maximal oxygen consumption, resting metabolic rate (RMR), and plasma leptin and adiponectin were determined at baseline and after training and detraining. RESULTS: Strength, maximal oxygen consumption, RMR, and exercise energy cost increased (P < 0.05) after training in an intensity-dependent manner. Skinfold sum and BMI were reduced by resistance training (P < 0.05), with HI being more effective (P < 0.05) than moderate-intensity/low-intensity training. Leptin was diminished (P < 0.05) by all treatments, whereas adiponectin increased (P < 0.05) only in HI. Detraining maintained training-induced changes only in HI. The percent leptin decrease was associated (P < 0.05) with the percent BMI decrease and the percent RMR increase, whereas the percent adiponectin increase was associated (P < 0.05) with the percent BMI decrease. CONCLUSIONS: Resistance training and detraining may alter leptin and adiponectin responses in an intensity-dependent manner. Leptin and adiponectin changes were strongly associated with RMR and anthropometric changes.

Adiponectin↗

PubMed2005

The effects of muscle damage on running economy in healthy males.

Published information on aspects related to muscle damage and running economy is both limited and contradictory. To contribute to the current debate, we investigated the effects of an eccentric exercise session on selected muscle damage indices in relation to running economy using 10 (mean age 23 +/- 1 years) healthy male volunteers. The eccentric exercise session consisted of 120 (12 x 10) maximal voluntary repetitions by each randomly selected leg at the angular velocity of 1.05 rad . s (-1). Muscle damage (creatine kinase, delayed onset muscle soreness, range of movement, and eccentric, concentric and isometric [at 60 degrees and 110 degrees knee flexion] peak torque) and running economy (oxygen consumption, pulmonary ventilation, respiratory exchange ratio and breaths per minute during treadmill running at 133 and 200 m . min (-1)) indicators, were assessed pre-, 24-, 48-, 72- as well as 96-h after exercise. All muscle damage indicators revealed significant changes at almost all time-points of assessment compared to pre-exercise data (p < 0.05). However, none of the running economy parameters disclosed any significant change throughout the study (p > 0.05). It was concluded that changes in muscle damage and muscle performance as measured in this study are not reflected by concomitant alterations in running economy at submaximal intensities.

Adult↗

PubMed2004

The effects of a single bout of exercise on resting energy expenditure and respiratory exchange ratio.

We investigated the effects of a single bout of aerobic and resistance exercise of similar relative intensity and duration on resting energy expenditure (REE) and substrate utilisation. Ten young healthy males volunteered [age 22 (1.8) years, weight 76 (7.9) kg, height 176 (4.1) cm, percentage body fat 10.5 (4.0)%; mean (SEM)]. They randomly underwent three conditions in which they either lifted weights for 60 min at 70-75% of 1-RM (WL), ran for 60 min at 70-75% of maximal oxygen intake (R) or did not exercise (C). REE and substrate utilisation, determined via respiratory exchange ratio ( R), were measured prior to exercise, and 10, 24, 48 and 72 h post-exercise. It was revealed that REE was significantly elevated ( P<0.05) 10 and 24 h after the end of WL [2,124 (78) and 2,081 (76) kcal, respectively] compared to pre-exercise [1,972 (82) kcal]. REE was also significantly increased ( P<0.05) 10 and 48 h after the completion of R [2,150 (73) and 1,995 (74) kcal, respectively] compared to pre-exercise data [1,862 (70) kcal]. R was lower 10 and 24 h following either WL or R [0.813 (0.043); 0.843 (0.040) and 0.818 (0.021); 0.832 (0.021), respectively] compared to baseline measurements [0.870 (0.025) and 0.876 (0.04), respectively]. Creatine kinase was significantly elevated ( P<0.05) 24 h after both WL and R, whereas delayed onset muscle soreness became significantly elevated ( P<0.05) 24 h after only WL. There were no significant changes for any treatment in thyroid hormones (T(3) and T(4)). These results suggest that a single bout of either WL or R exercise, characterised by the same relative intensity and duration, increase REE and fat oxidation for at least 24 h post-exercise.

Adult↗

PubMed2001

Beta-endorphin infusion during exercise in rats does not alter hepatic or muscle glycogen.

The aim of this study was to determine whether beta-endorphin infusion influences liver or muscle glycogen concentration during exercise. Thirty-two rats (Harlan Co., IN, USA) with a body mass of 265-290 g were assigned at random to four groups, each of eight rats: (1) beta-endorphin infusion for 90 min at rest; (2) beta-endorphin infusion for 90 min while running on a rodent treadmill at 22 m x min(-1) and 0% grade; (3) saline infusion (0.9% NaCl) for 90 min at rest; and (4) saline infusion for 90 min while running on a rodent treadmill at 22 m x min(-1) and 0% grade. Beta-endorphin infusion elevated plasma beta-endorphin concentration by 2.5-fold at rest compared with saline infusion at rest, and by two-fold after exercise compared with saline infusion after exercise. Beta-endorphin infusion attenuated exercise-induced glucose concentration but did not alter the fasting hepatic glycogen concentration at rest or after exercise compared with saline infusion. Fasting hepatic glycogen decreased significantly as a result of 90 min of exercise independent of treatment. Deep intermedius muscle glycogen concentration at rest was similar after 90 min of both beta-endorphin and saline infusion and decreased significantly as a result of 90 min of exercise independent of treatment. Our results suggest that liver and muscle glycogenolysis is not responsible for the differences in plasma glucose with beta-endorphin infusion during exercise.

Animals↗

PubMed2000

Perceived stress and blood pressure in early adolescent children.

The objective of this investigation was to determine the individual contributions of perceived daily, major, and total stressors to blood pressure in early adolescent children. Toward this goal, cardiovascular risk factors were assessed in 74 6th-grade students. Height and body weight, measured in standard fashion, were used to calculate body mass index (BMI). Waist and hip circumferences and triceps and calf skinfolds were taken to determine the distribution and percentage of body fat, respectively. Seated resting blood pressure was obtained using a mercury sphygmomanometer. The dietary sodium-to-potassium ratio was calculated from a food intake questionnaire. Family history of hypertension was self-reported by participant's parents, and physical activity and perceived stress levels were determined by questionnaire. When added to the hierarchical regression models, the perceived stress variables did not significantly predict any additional variance in systolic or diastolic blood pressure in this early adolescent sample. Additionally, bivariate correlations between the stress variables and blood pressure were nonsignificant. The nonpsychological hypertension risk factors accounted for 25%-35% of the total variance in systolic and diastolic blood pressure. Further, regression analyses revealed that with the exception of BMI and the sodium-to-potassium ratio, no other risk factors were independent predictors of systolic or diastolic blood pressure. Further identification and understanding of environmental precursors of childhood hypertension is recommended.

Adolescent↗

PubMed2000

Beta-endorphin infusion during exercise in rats: blood metabolic effects.

UNLABELLED: Beta-endorphin (betaE) bolus (0.05 mg x kg(-1)) infusion (0.05 mg x kg(-1) x h(-1)) was previously shown in rats to attenuate the decline in plasma glucose during exercise. PURPOSE: The present investigation compared betaE and saline infusion in rats without a bolus of betaE to determine whether 1) the attenuation in the glucose decline was attributable to the type of administration (bolus betaE + continuous betaE infusion vs continuous betaE infusion), and 2) whether circulating catecholamines or FFAs were in part involved in the glucose decline. METHODS: Forty untrained Sprague-Dawley rats were randomly assigned to one of four treatments: 1) betaE infusion at rest (betaR), 2) betaE infusion during exercise (betaX), 3) saline infusion at rest (SR), and 4) saline infusion during exercise (SX). Infusions (betaE or saline) with running (22 m x min(-1), 0% grade) lasted 90 min. RESULTS: A 2 x 2 ANOVA indicated betaE infusion significantly attenuated the decline in plasma glucose due to exercise at 90 min (SX = 4.16 +/- 0.1 vs betaX = 4.61 +/- 0.1 mM). BetaE infusion elevated plasma betaE about 2.5-fold at rest compared with SR and two-fold after exercise (betaX) compared with SX. BetaE infusion had no effect at rest on any of the other variables measured. Exercise significantly increased catecholamines, FFAs and glucagon compared with resting levels. BetaE infusion enhanced the glucagon response to exercise (SX = 577 +/- 67.5 vs betaX = 913 +/- 153 ng x L(-1), P < 0.02). Epinephrine and norepinephrine and FFAs were similar with betaE infusion either at rest or during exercise compared with saline infusion. CONCLUSION: These results suggest that betaE infusion independent of the betaE bolus can attenuate the decline in glucose during exercise by enhancing glucagon levels and the betaE infusion did not influence circulating catecholamines or FFA's response to exercise.

Animals↗

PubMed1999

Effect of exercise during the follicular and luteal phases on indices of oxidative stress in healthy women.

PURPOSE: Eleven healthy nonsmoking women (24+/-1.1 yr) exercised for 30 min at 75-80% VO2max during the follicular (F) and luteal (L) phases of their menstrual cycle to determine whether menstrual phase influenced indices of oxidative stress. METHODS: Subjects completed the exercise in a randomized order. Subjects reported between 0800 and 0900 in a postabsorptive state, rested for 15-30 min, and had a venous blood sample obtained by Vacutainer before and after exercise. RESULTS: Resting estradiol was 54.4+/-12.0 pg.mL(-1) for F phase and was significantly higher in L phase (147.2+/-25.5 pg.mL(-1)). Plasma malondialdehyde and thiobarbituric acid substances were no different before and after exercise independent of menstrual cycle phase. No differences in resting blood total glutathione (TGSH), oxidized glutathione (GSSG), and reduced glutathione (GSH) were evident comparing the F and L phases. After exercise, TGSH decreased (P = 0.03) but reached significance only in the F phase = 8.1 %(P = 0.04), L phase = 2.5% (P = 0. 15). Exercise increased GSSG 10.5% in F (P = 0.15) and 27.8% in L phases(P = 0.01). GSH decreased after exercise independent of menstrual phase (F = 17%, L = 16%, P = 0.01). CONCLUSION: These data suggest that 30 min of moderate-intensity exercise in female subjects can result in mild oxidative stress as indicated by blood glutathione status and that menstrual cycle phase has minimal influences on these exercise responses.

Adult↗

PubMed1998

Gender effect on beta-endorphin response to exercise.

PURPOSE: Twelve healthy men (26.4 yr) and women (26.8 yr) were compared at rest and after cycling for 25 min at 60 and 80% VO2max to determine whether gender and menstrual cycle influenced circulating beta-endorphin concentration (BE). METHODS: VO2max was determined on a cycle ergometer, and subjects completed the exercise in a randomized order. Women were tested in both the luteal (L) and follicular (F) phases of their menstrual cycle, which was confirmed by their blood estrogen levels. All tests were conducted in the morning after a 30-min rest (12-h postabsorptive). An indwelling venous catheter placed in a forearm vein enabled blood sampling at rest, 25 min of cycling, and 25 min of recovery. RESULTS: Resting BE was similar for men before both 60 and 80% intensities of exercise, 5.27 +/- 0.43 and 5.30 +/- 0.33 pmol.mL-1, respectively. BE was not significantly changed at 60% VO2max (6.54 +/- 0.33 pmol.mL-1) but significantly increased at 80% VO2max (11.90 +/- 1.98 pmol.mL-1). Women tended to have slightly lower BE during the L compared with F, but this did not reach significance (L = 4.40 +/- 0.22, F = 4.73 +/- 0.30 pmol.mL-1). Cycling at 60% VO2max did not significantly increase BE in the L (5.41 +/- 0.42 pmol.mL-1) nor the F (5.35 +/- 0.40 pmol.mL-1). Cycling at 80% VO2max increased BE to a similar extent in both the L and F phase, respectively (10.44 and 10.96). Although the BE concentrations tended to be slightly lower in women compared with men at 80% VO2max, this did not reach statistical significance. CONCLUSIONS: These data suggest that women cycling at 80% VO2max will have a similar BE response to men independent of their menstrual cycle. BE in women at rest and who exercise at lower exercise intensities may have slightly lower BE levels then men independent of the time of the women's menstrual cycle.

Adolescent↗

PubMed1997

Beta-endorphin infusion alters pancreatic hormone and glucose levels during exercise in rats.

beta-Endorphin (BE) infusion at rest can influence insulin and glucagon levels and thus may affect glucose availability during exercise. To clarify the effect of BE on levels of insulin, glucagon and glucose during exercise, 72 untrained male Sprague-Dawley rats were infused i.v. with either: (1) BE (bolus 0.05 mg.kg-1 + 0.05 mg.kg-1.h-1, n = 24); (2) naloxone (N, bolus 0.8 mg.kg-1 + 0.4 mg.kg-1, n = 24); or (3) volume-matched saline (S, n = 24). Six rats from each group were killed after 0, 60, 90 or 120 min of running at 22 m.min-1, at 0% gradient. BE infusion resulted in higher plasma glucose levels at 60 min [5.93 (0.32) mM] and 90 min [4,16 (0.29) mM] of exercise compared to S [4.62 (0.27) and 3.41 (0.26 mM] and N [4.97 (0.38) and 3.44 (0.25) mM]. Insulin levels decreased to a greater extent with BE [21.5 (0.9) and 18.3 (0.6) uIU.ml-1] at 60 and 90 min compared to S [24.5 (0.5) and 20.6 (0.6) uIU.ml-1] and N [24.5 (0.4) and 21.6 (0.7) uIU.ml-1] groups. Plasma C-peptide declined to a greater extent at 60 and 90 min of exercise with BE infusion compared to both S and N. BE infusion increased glucagon at all times during exercise compared to S and N. These data suggest that BE infusion during exercise influences plasma glucose by augmenting glucagon levels and attenuating insulin release.

Animals↗

PubMed1997

Beta-endorphin response to exercise. An update.

beta-Endorphin, a 31-amino-acid peptide, is primarily synthesised in the anterior pituitary gland and cleaved from pro-opiomelanocortin, its larger precursor molecule. beta-Endorphin can be released into the circulation from the pituitary gland or can project into areas of the brain through nerve fibres. Exercise of sufficient intensity and duration has been demonstrated to increase circulating beta-endorphin levels. Previous reviews have presented the background of opioids and exercise and discussed the changes in beta-endorphin levels in response to aerobic and anaerobic exercise. The present review is to update the response of beta-endorphin to exercise. This review suggests that exercise-induced beta-endorphin alterations are related to type of exercise and special populations tested, and may differ in individuals with health problems. Additionally, some of the possible mechanisms which may induce beta-endorphin changes in the circulation include analgesia, lactate or base excess, and metabolic factors. Based on the type of exercise, different mechanisms may be involved in the regulation of beta-endorphin release during exercise.

Animals↗