No description available.

This study examined effects of carbohydrate (C), carbohydrate-protein (CP), or placebo (P) beverages following eccentric resistance exercise on muscle damage by serum creatine kinase (CK), muscle protein breakdown by urinary 3-methylhistidine (3MH), muscle soreness, isokinetic muscle strength, muscle glycogen resynthesis, and serum hormones. Untrained males (N=26) underwent a 9-day controlled meat-free diet and 24 hr urine collections. To reduce glycogen, subjects cycled for 40 min at 70% of VO_2peakfollowed by 5 cycling sprints on day 4 evening. On day 5, fasted subjects performed 100 eccentric leg flexions at 120% of 1-RM and drank C (n=8, 1.25 g C/kg), CP (n=9, 0.875 g C/kg, 0.375 g protein/kg), or P (n=9) beverages immediate post-exercise (IPE) and 2 hr later. Muscle biopsies were taken IPE on day 5, and days 6 and 8 mornings. Blood was obtained days 4-10 fasted plus IPE, 3 hr, and 6 hr post-exercise on day 5. At 3 hr on day 5, insulin was higher for CP (24.6 ( 15.5 &amp;#181;IU/ml) and C (17.2 +/- 10.9 &amp;#181;IU/ml) than P (5.3 +/- 0.4 &amp;#181;IU/ml, p<.05). Glycogen was low on day 5, partially recovered on day 6, and normal by day 8 (p<.01) with no difference among groups. Isokinetic quadriceps peak torque at 60^o/s decreased 24% on day 6 and remained depressed by 21% on d 8 (p<.01) for all groups. Soreness peaked on day 7 and CK on day 8 (p<.01) with no differences by group. CK increased (p<.01) over day 5 (delta CP 24.6 +/- 19.1, delta P 39.2 +/- 71.6, delta C 70.8 +/- 60.4 U/L) and was highest for C (p<.05). On day 5, CP had lowest 3MH (193.0 +/- 13.8 &amp;#181;mol/d) versus C (251.1 +/- 22.5 &amp;#181;mol/d, p<.05). Testosterone at 3 hr on day 5 was lower for C (4.2 +/- 0.3 ng/ml) and CP (4.3 +/- 0.3 ng/ml) versus P (5.1 +/- 0.2 ng/ml, p<.05). In summary, glycogen, muscle strength and soreness were unaffected by beverage. However, a CP beverage may be beneficial for reducing muscle damage and protein breakdown on the day of eccentric resistance exercise. / Ph. D.

Aim: The purpose of this study was to investigate the influence of docosahexaenoic acid (DHA) on muscle damage and inflammation following an acute eccentric exercise bout. Methods: A double-blind placebo-controlled, study was performed using 41 healthy, untrained males aged 18-28 y who consumed either 2 g/d DHA or placebo (PL, corn oil) for 32 days. Supplements were consumed for 28 days prior to exercise. Participants completed an eccentric exercise procedure of the elbow flexors at 140% of 1-RM (6 sets x 10 repetitions). The time under tension (TUT) for each set of eccentric contractions was recorded manually from the investigators voice commands. Fasted blood samples for prostaglandin E2 (PGE2), interleukin-6 (IL-6), interleukin-1 receptor antagonist (IL1-ra), C-reactive protein and creatine kinase (CK) were assessed on days 1, 2 and 4. Fasted serum DHA was measured at baseline (day -28) and on day 1. Peak isometric strength of the elbow flexors, delayed-onset muscle soreness, and range of motion were measured on day 1 prior to exercise and days 2, 3, and 4 following exercise. Results: DHA significantly reduced natural log of CK (p<0.05) response over 4 d. Additionally, IL-6 area under the curve (AUC) was reduced for DHA compared to PL (3.6 ± 2.5 pg/mL vs. 5.3 ± 2.7 pg/mL) (p<0.05). TUT/set was higher in the DHA group compared to placebo (p<0.05). There were no other significant differences between treatments. Conclusion: DHA supplementation produced lower indicators of muscle damage (CK) and inflammation (IL-6 AUC). DHA supplementation resulted in greater TUT/set. / Master of Science

No description available.

Thesis (Ph. D.)--University of Washington, 1998. / Vita. Includes bibliographical references (leaves [137]-139).

Thesis (Ph. D.)--University of Missouri--Columbia, 1996. / Typescript. Vita. Includes bibliographical references (leaves: 138-156). Also available on the Internet.

No description available.

Thesis (PhD (Biomedical Sciences. Medical Physiology))--University of Stellenbosch, 2010. / ENGLISH ABSTRACT: Background: There has been a dramatic increase in the use of dietary creatine supplementation among sports men and women, and by clinicians as a therapeutic agent in muscular and neurological diseases. The effects of creatine have been studied extensively in skeletal muscle, but knowledge of its myocardial effects is limited. Objectives: To investigate the effects of dietary creatine supplementation with and without exercise on 1) basal cardiac function, 2) susceptibility to ischaemia/reperfusion injury and 3) myocardial protein expression and phosphorylation and 4) mitochondrial oxidative function. Methods: Male Wistar rats were randomly divided into control or creatine supplemented groups. Half of each group was exercise trained by swimming for a period of 8 weeks, 5 days per week. At the end of the 8 weeks the open field test was performed and blood corticosterone levels were measured by RIA to determine whether the swim training protocol had any effects on stress levels of the rats. Afterwards hearts were excised and either freeze-clamped for biochemical and molecular analysis or perfused on the isolated heart perfusion system to assess function and tolerance to ischaemia and reperfusion. Five series of experiments were performed: (i) Mechanical function was documented before and after 20 minutes global ischaemia using the work heart model, (ii) A H2O filled balloon connected to a pressure transducer was inserted into the left ventricle to measure LVDP and ischaemic contracture in the Langendorff model, (iii) The left coronary artery was ligated for 35 minutes and infarct size determined after 30 minutes of reperfusion by conventional TTC staining methods. (iv) Mitochondrial oxidative capacity was quantified. (v) High pressure liquid chromatography (HPLC) and Western Blot analysis were performed on blood and heart tissue for determination of high energy phosphates and protein expression and phosphorylation. Results: Neither the behavioural studies nor the corticosterone levels showed any evidence of stress in the groups investigated. Hearts from creatine supplemented sedentary (33.5 ± 4.5%), creatine supplemented exercised rats (18.22 ± 6.2%) as well as control exercised rats (26.1 ± 5.9%) had poorer aortic output recoveries than the sedentary control group (55.9 ± 4.35% p < 0.01) and there was also greater ischaemic contracture in the creatine supplemented exercised group compared to the sedentary control group (10.4 ± 4.23 mmHg vs 31.63 ± 4.74 mmHg). There were no differences in either infarct size or in mitochondrial oxygen consumption between the groups. HPLC analysis revealed elevated phosphocreatine content (44.51 ±14.65 vs 8.19 ±4.93 nmol/gram wet weight, p < 0.05) as well as elevated ATP levels (781.1 ±58.82 vs 482.1 ±75.86 nmol/gram wet weight, p<0.05) in blood from creatine supplemented vs control sedentary rats. These high energy phosphate elevations were not evident in heart tissue and creatine tranporter expression was not altered by creatine supplementation. GLUT4 and phosphorylated AMPK and PKB/Akt were all significantly higher in the creatine supplemented exercised hearts compared to the control sedentary hearts. Conclusion: This study suggests that creatine supplementation has no effects on basal cardiac function but reduces myocardial tolerance to ischaemia in hearts from exercise trained animals by increasing the ischaemic contracture and decreasing reperfusion aortic output. Exercise training alone also significantly decreased aortic output recovery. However, the exact mechanisms for these adverse myocardial effects are unknown and need further investigation. / AFRIKAANSE OPSOMMING: Agtergrond: Die gebruik van kreatien as dieetaanvulling het in die afgelope aantal jaar dramaties toegeneem onder sportlui, sowel as mediese praktisyns wat dit as ‘n terapeutiese middel vir die behandeling van spier- en neurologiese siektes aanwend. Die effekte van kreatien op skeletspier is reeds deeglik ondersoek, maar inligting aangaande die miokardiale effekte van die preperaat is beperk. Doelwitte: Om die effekte van kreatien dieetaanvulling met of sonder oefening ten opsigte van die volgende aspekte te ondersoek: 1) basislyn miokardiale funksie, 2) vatbaarheid vir iskemie/herperfusie besering, 3) proteïenuitdrukking en -fosforilering in die miokardium en 4) mitochondriale oksidatiewe funksie. Metodes: Manlike Wistar rotte is ewekansig in kontrole of kreatien aanvullings groepe verdeel. Helfte van elke groep is aan oefening in die vorm van swemsessies, vir ‘n periode van 8 weke, 5 dae per week blootgestel. Gedrags- en biochemiese toetse is aangewend om die moontlike effek van die swemprotokol op die rotte se stres vlakke te bepaal. In hierdie verband is die oop area toets gebruik, asook bloed kortikosteroon vlakke gemeet deur radioaktiewe immuunessais. Harte is daarna uit die rotte gedissekteer en gevriesklamp vir biochemiese en molekulêre analise, of geperfuseer op die geïsoleerde werkhart perfusiesisteem om sodoende funksie en weerstand teen iskemie en herperfusie beskadeging te bepaal. Vyf eksperimentele reekse is uitgevoer: (i) Meganiese funksie is noteer voor en na 20 minute globale isgemie in die werkhart model; (ii) ‘n Water gevulde plastiek ballon, gekoppel aan ‘n druk omsetter, is in die linker ventrikel geplaas om sodoende linker ventrikulêre ontwikkelde druk (LVDP), asook iskemiese kontraktuur te meet; (iii) Linker koronêre arterie afbinding is vir ‘n periode van 35 minute toegepas en die infarktgrootte bepaal na 30 minute herperfusie deur gebruik te maak van standaard kleuringsmetodes; (iv) Mitochondriale oksidatiewe kapasiteit is gemeet; (v) Hoë druk vloeistof chromatografie (HPLC) en Western Blot analises is uitgevoer op bloed en hartweefsel vir die bepaling van hoë energie fosfate (HEFe), sowel as proteïenuitdrukking en -fosforilering. Resultate: Beide gedragsstudies en kortikosteroonvlakke het geen teken van stres in die betrokke groepe getoon nie. Die groep blootgestel aan kreatienaanvulling en oefening se harte het na iskemie funksioneel swakker herstel as harte van die onaktiewe kontrole groep (18.22±6.2% vs 55.9±4.35%; p<0.01), asook ‘n groter ikgemiese kontraktuur in vergelyking met die onaktiewe kontrole groep ontwikkel (31.63±4.74 mmHg vs 10.4±4.23 mmHg). Daar was geen verskille in infarktgrootte of mitochondriale suurstofverbruik tussen die verskillende groepe waargeneem nie. HPLC analise het verhoogde fosfokreatien (44.51±14.65 vs 8.19±4.93 nmol/gram nat gewig, p<0.05) en adenosientrifosfaat (ATP) bloedvlakke (781.1±58.82 vs 482.1±75.86 nmol/gram nat gewig, p<0.05) in kreatien aanvullings vergelyk met die kontrole groepe getoon. Daar was egter geen meetbare veranderings in HEF vlakke in hartweefsel nie. Gepaardgaande hiermee het kreatienaanvulling geen effek gehad op die uitdrukking va die kreatien transporter nie. In vergelyking met onaktiewe kontrole harte was GLUT4, en fosforileerde AMPK en PKB/ Akt beduidend hoër in harte van geoefende rotte met kreatienaangevulling. Gevolgtrekking: Hierdie data dui daarop dat kreatienaanvulling geen effek op basislyn miokardiale funksie het nie. Kreatienaanvulling het egter die miokardium se weerstand teen iskemiese skade verlaag in harte van rotte blootgestel aan oefening: iskemiese kontraktuur is verhoog en aorta-uitset tydens herperfusie is verlaag. Die presiese meganismes hierby betrokke is egter onbekend en vereis dus verdere studie. / Division of Medical Physiology (University of Stellenbosch), The National Research Foundation and the Harry Crossley Fund for financial support.

Thesis (doctoral)--University of Jyväskylä, 1994. / Thesis is based on six separately published papers which are reprinted at end. Includes bibliographical references.

Thesis (doctoral)--University of Jyväskylä, 1994. / Thesis is based on six separately published papers which are reprinted at end. Includes bibliographical references.