Estratti Termogenici

[Anabolic]

Salve ragazzi volevo capire bene il miglio modo di farsi un prodotto termogenico in casa.
Allora per l' ossidazione dei grassi:
ALC
se si vuole perdere il grasso viscerale [beta 3]:
octopamina hcl, se conoscete prodotti validi li aspetto

per le catecolamine:
caffeina o the verde

per la lipolisi:
forskolina,

per i beta 2
yohimbe,


Ho pensato di fare due termogenici:
1 al inizio per il viscerale
octopamina hcl, alc,forskolina,

2 dopo un pò di tempo per perdere anche il grasso sotocutaneo
alc, octopamina hcl, alc, forskolina, caffeina, the verde, yohimbe


P.S.
i blocattori dei recettori degli estrogeni possono essere utili per il grasso ginodeo
tipo indole 3 carbinoli?

[homer]

a ke livello di grasso sei?

[Guru]

L'octopamina è un bluff, risparmia soldi.

La yohimbina e lo yohimbè non sono utilizzabili.

L'indolo-3-carbinolo, ed il sulforafano, sono composti interessanti che potrebbero funzionare.
In particolare il sulforafano ha talmente tanti effetti, anche antiossidanti e protettivi, che si potrebbe usare anche solo per quello.

Un buon mix lipolitico potrebbe essere costituito da:

• estratto di the verde ad alta titolazione di egcg
• acetilcarnitina
• forscolina(da coleus)
• capsaicina(da pepe di caienna)
• bioperina(da pepe nero)
• calcio
• complesso di antiossidanti

[BLACKEAGLE]

Originariamente inviato da Guru

L'octopamina è un bluff, risparmia soldi.

La yohimbina e lo yohimbè non sono utilizzabili.

L'indolo-3-carbinolo, ed il sulforafano, sono composti interessanti che potrebbero funzionare.
In particolare il sulforafano ha talmente tanti effetti, anche antiossidanti e protettivi, che si potrebbe usare anche solo per quello.

Un buon mix lipolitico potrebbe essere costituito da:

• estratto di the verde ad alta titolazione di egcg
• acetilcarnitina
• forscolina(da coleus)
• capsaicina(da pepe di caienna)
• bioperina(da pepe nero)
• calcio
• complesso di antiossidanti

Fidatevi delle ditte serie come la san e la muscletech.

[NoMoreTrouble]

ma non sarebbe pericoloso andare ad intaccare il grasso viscerale?
non è quel grasso che per esempio serve al sostegno di organo come i reni?
in quest' ottica non è piu produttivo cercare di diminuire il grasso sottocutaneo?

[Antò]

Bene..cercate di capire che quando si parla di sostanze illegali in italia siete pregati di postare su "ergogenic drugs". Sposto il 3ad

[Antò]

Forskolina-> inibisce l'adenyl cyclase mantenendo elevato il livello di Camp e quindi la risposta cellulare all'azione degli ormoni. Aumenta la produzione di testo nelle gonadi rendendo + sensibili i recettori alle gonodotropine

Tyrosina/l-dopa/geramine/nicotine->aumentano il livello di dopamina

adrenosterone (11OXO)->a basso dosaggio (150mg/die) blocca la conversione di cortisono in cortisolo. Ottimo per la lipolisi a livello del grasso viscerale. Ad alti dosaggi è un proormone dell'11-keto-testosterone

Acido arachidonico->inibisce la produzione di testo a livello gonadico inibendo il Camp, ma aumenta la conversione di testo in DHT mantenendo elevata l'attività della 5-reductase. Ottimo questo per incrementi di forza e densità muscolare. Inoltre migliora la velocità di riparazione tissutale e dovrebbe essere un forte attivatore dei ppar-alfa migliorando la lipolisi ed inibendo la lipogenesi

Questo, per adesso, sarebbe la mia idea di Bodyrecomp stack..

[Anabolic]

scusa ma usando forskolina e l' acido arachidonico aumenta o diminuisce il camp, non ho capito bene come agiscono il bioperine e la capsaicina.
Per i recettori beta 3 non esiste niente? preferisco prima bruciare grasso viscerale sull adome e poi quello sottocutaneo.
Il sulforano e l' indole 3 carbinoli cosa fanno quando si legano ai recettori degli estrogeni? gli estrogeni ci sono ma non si deposita il grasso a livello ginodeo

[Antò]

Originariamente inviato da Anabolic

scusa ma usando forskolina e l' acido arachidonico aumenta o diminuisce il camp, non ho capito bene come agiscono il bioperine e la capsaicina.
Per i recettori beta 3 non esiste niente? preferisco prima bruciare grasso viscerale sull adome e poi quello sottocutaneo.
Il sulforano e l' indole 3 carbinoli cosa fanno quando si legano ai recettori degli estrogeni? gli estrogeni ci sono ma non si deposita il grasso a livello ginodeo

Specific effect of arachidonic acid on 17beta-hydroxysteroid dehydrogenase in rat Leydig cells.

Marinero MJ, Penalva V, Oliva JL, Colás B, Prieto JC, López-Ruiz MP.
Unidad de Neuroendocrinologia Molecular, Departamento de Bioquímica y Biología Molecular, Universidad de Alcalá, Alcalá de Henares-Madrid, Spain.
It is well known that arachidonic acid (AA) acts as an intratesticular factor regulating luteinizing hormone-mediated testicular steroidogenesis. The present studies were conducted to determine the effect of AA on steroidogenic enzymes in rat Leydig cells. Exogenously added AA significantly inhibited 22(R)-hydroxy-cholesterol-stimulated testosterone production, which is a clear indication that AA is acting at some point after cholesterol transport to the inner mitochondrial membrane. AA failed to block the conversion of 22(R)-hydroxycholesterol to pregnenolone, indicating that the cytochrome P-450 side-chain cleavage enzyme complex is not the site of inhibition. The present results demonstrate that only 17beta-hydroxysteroid dehydrogenase seems to be involved in the AA action, since nearly 60% inhibition of testosterone production was found when the cells were incubated with androstenedione. Furthermore, no effect of AA was found when androstenediol was used as substrate in the testosterone synthesis, which indicates that 3beta-hydroxysteroid dehydrogenase is not affected by AA. The conversion of AA to its metabolites is not required for its action on 17beta-hydroxysteroid dehydrogenase and the activation of protein kinase C is not involved in the inhibitory effect.
PMID: 9475159 [PubMed - indexed for MEDLINE]




Involvement of arachidonic acid and the lipoxygenase pathway in mediating luteinizing hormone-induced testosterone synthesis in rat Leydig cells.

Mele PG, Dada LA, Paz C, Neuman I, Cymeryng CB, Mendez CF, Finkielstein CV, Cornejo Maciel F, Podestá EJ.
Department of Biochemistry, School of Medicine, University of Buenos Aires, Argentina.
Evidence has been introduced linking the lipoxygenase products and steroidogenesis in Leydig cells, thereby supporting that this pathway may be a common event in the hormonal control of steroid synthesis. On the other hand, it has also been reported that lipoxygenase products of arachidonic acid (AA) may not be involved in Leydig cells steroidogenesis. In this paper, we investigated the effects of PLA2 and lipoxygenase pathway inhibitors on steroidogenesis in rat testis Leydig cells. The effects of two structurally unrelated PLA2 inhibitors (4-bromophenacyl bromide (BPB) and quinacrine) were determined. BPB blocked the LH- and Bt2cAMP-stimulated testosterone production but had no effect on 22(4)-OH-cholesterol conversion to testosterone. Quinacrine caused a dose-dependent inhibition of LH- and Bt2cAMP-induced steroidogenesis. The effects of different lipoxygenase pathway inhibitors (nordihydroguaiaretic acid (NDGA), 5,8,11,14-eicosatetraynoic acid (ETYA), caffeic acid and esculetin) have also been determined. Both NDGA and ETYA inhibited LH- and Bt2cAMP-stimulated steroid synthesis in a dose-related manner. Furthermore caffeic acid and esculetin also blocked the LH-stimulated testosterone production. Moreover, exogenous AA induced a dose-dependent increase of testosterone secretion which was inhibited by NDGA. Our results strongly support the previous concept that the lipoxygenase pathway is involved in the mechanism of action of LH on testis Leydig cells.
PMID: 9187535 [PubMed - indexed for MEDLINE]




Different sites of action of arachidonic acid on steroidogenesis in rat Leydig cells.

Marinero MJ, Colas B, Prieto JC, López-Ruiz MP.
Departmento de Bioquímica y Biologia Molecular, Universidad de Alcalá, Alcalá de Henares, Madrid, Spain.
The present study in purified rat Leydig cells shows that arachidonic acid may act as an intratesticular factor regulating LH-mediated testicular steroidogenesis. Arachidonic acid decreased, in a dose-dependent manner, the LH-stimulated cAMP and testosterone levels, over 2 h incubation. Incubation of Leydig cells with arachidonic acid did not modify 125I-hCG binding to the cells as compared to control, showing that the action of arachidonic acid is not related to a decrease of hCG binding to the cells. Forskolin-stimulated cAMP and testosterone production were inhibited by 51.65 and 70.9%, respectively, in the presence of arachidonic acid (100 microM), although the ED50 for the diterpene was not changed. When isobutyl-methyl-xanthine was added to the incubation medium, the same percentage of inhibition was found indicating that arachidonic acid inhibition of cAMP production is not due to stimulation of Leydig cell phosphodiesterase activity. Pretreatment of the cells with pertussis toxin, to inactivate Gi, was also without effect on arachidonic acid inhibition of LH-stimulated cAMP production, but pertussis toxin abolished the inhibitory effects of arachidonic acid when adenylate cyclase was stimulated with forskolin. However, arachidonic acid addition resulted in inhibition of LH- and forskolin-stimulated testosterone production, even if the cells were pretreated with pertussis toxin. It can be concluded that: (1) The inhibitory effect of arachidonic acid is neither due to a decrease of hCG binding to Leydig cells nor to a stimulation of cell phosphodiesterase activity; (2) arachidonic acid modulates cAMP production at two different levels, either by activation of Gi protein and by inhibition of Gs protein or adenylate cyclase; (3) the effect of arachidonic acid on steroidogenesis is also beyond cAMP formation.
PMID: 8735605 [PubMed - indexed for MEDLINE]



Come vedi ciò che ho affermato è da prendere con le pinze. L'AA potrebe inibire la steroidogenesi secondo varie vie metaboliche, ma potrebbe stimolarla via le ciclossigenasi. L'ultimo studio nn lo porenderei molto in considerazione visto che è stato eseguito in vitro e l'AA è stato "sparato" direto nelle gonadi, se vedi i primi 2 studi l'AA seggue varie vie metaboliche rpima di stimolare/inibire le varie vie metaboliche.
Bisognerà fare altre ricerche, ma nn credo che l'inibizione del Camp sia così profonda con uno stack foscolina/AA



Dei beta 3 nn te ne deve fregar de meno. Il cortisolo e gli androgeni aumentano il grasso viscerale.
Meglio il DIM rispetto all'I3C. Il DIM è il metabolita dell' I3C ed ha maggiore biodisponibilità visto che nn deve subire alcuna conversione. Il DIM ha solo la capacità di evitare la conversione degli estrogeni nella loro forma 17beta la quale ha maggiore "attività recettoriale".

Il dosaggio è circa 1gr al giorno per avere i maggiori benefici..

[ikuape86]

anto' la yohimbina è una anfetamina o no? credo di non ma non ne sono sicuro

[Anabolic]

we antò allora l' AA dovrebbe diminuire il camp e la forskolina aumentarlo se si prendono tutte e due assieme forse lo si mantiene.
Per il dim si torva in integratori e quale il nome completo??
scusa ma il 2° studio dice che aumenta il TT o sbaglio?

antò ma hai provato l' AA ha avuto effetti su di te?

Saluti Alberto

[Anabolic]

anzi diminuisce il TT

[Anabolic]

antò mi spieghi i vari studi

[Antò]

Originariamente inviato da Antò

Specific effect of arachidonic acid on 17beta-hydroxysteroid dehydrogenase in rat Leydig cells.

Marinero MJ, Penalva V, Oliva JL, Colás B, Prieto JC, López-Ruiz MP.
Unidad de Neuroendocrinologia Molecular, Departamento de Bioquímica y Biología Molecular, Universidad de Alcalá, Alcalá de Henares-Madrid, Spain.
It is well known that arachidonic acid (AA) acts as an intratesticular factor regulating luteinizing hormone-mediated testicular steroidogenesis. The present studies were conducted to determine the effect of AA on steroidogenic enzymes in rat Leydig cells. Exogenously added AA significantly inhibited 22(R)-hydroxy-cholesterol-stimulated testosterone production, which is a clear indication that AA is acting at some point after cholesterol transport to the inner mitochondrial membrane. AA failed to block the conversion of 22(R)-hydroxycholesterol to pregnenolone, indicating that the cytochrome P-450 side-chain cleavage enzyme complex is not the site of inhibition. The present results demonstrate that only 17beta-hydroxysteroid dehydrogenase seems to be involved in the AA action, since nearly 60% inhibition of testosterone production was found when the cells were incubated with androstenedione. Furthermore, no effect of AA was found when androstenediol was used as substrate in the testosterone synthesis, which indicates that 3beta-hydroxysteroid dehydrogenase is not affected by AA. The conversion of AA to its metabolites is not required for its action on 17beta-hydroxysteroid dehydrogenase and the activation of protein kinase C is not involved in the inhibitory effect.
PMID: 9475159 [PubMed - indexed for MEDLINE]

L'AA sembra inibire l'enzima 17beta-idrossisteroidi deidrogenasi, quello che converte l'androstenendione in testo, ma nn l'enzima 3beta che converte l'androstediol in testo. Stusio in vitro, nn gli darei molto peso

Originariamente inviato da Antò

Involvement of arachidonic acid and the lipoxygenase pathway in mediating luteinizing hormone-induced testosterone synthesis in rat Leydig cells.

Mele PG, Dada LA, Paz C, Neuman I, Cymeryng CB, Mendez CF, Finkielstein CV, Cornejo Maciel F, Podestá EJ.
Department of Biochemistry, School of Medicine, University of Buenos Aires, Argentina.
Evidence has been introduced linking the lipoxygenase products and steroidogenesis in Leydig cells, thereby supporting that this pathway may be a common event in the hormonal control of steroid synthesis. On the other hand, it has also been reported that lipoxygenase products of arachidonic acid (AA) may not be involved in Leydig cells steroidogenesis. In this paper, we investigated the effects of PLA2 and lipoxygenase pathway inhibitors on steroidogenesis in rat testis Leydig cells. The effects of two structurally unrelated PLA2 inhibitors (4-bromophenacyl bromide (BPB) and quinacrine) were determined. BPB blocked the LH- and Bt2cAMP-stimulated testosterone production but had no effect on 22(4)-OH-cholesterol conversion to testosterone. Quinacrine caused a dose-dependent inhibition of LH- and Bt2cAMP-induced steroidogenesis. The effects of different lipoxygenase pathway inhibitors (nordihydroguaiaretic acid (NDGA), 5,8,11,14-eicosatetraynoic acid (ETYA), caffeic acid and esculetin) have also been determined. Both NDGA and ETYA inhibited LH- and Bt2cAMP-stimulated steroid synthesis in a dose-related manner. Furthermore caffeic acid and esculetin also blocked the LH-stimulated testosterone production. Moreover, exogenous AA induced a dose-dependent increase of testosterone secretion which was inhibited by NDGA. Our results strongly support the previous concept that the lipoxygenase pathway is involved in the mechanism of action of LH on testis Leydig cells.
PMID: 9187535 [PubMed - indexed for MEDLINE]

L'AA sembra aumentare la steroidogenesi indicando un chiaro legame tra le lipossigenasi è l'azione dell'LH nelle gonadi.
Questo studio contraddice i precedenti o meglio fa un pò di luce sul fato che l'AA nn antagonizza l'azione dell'LH sui recettori gonadici, ma alzi lo supporta. Un blocco delle lipossigenasi inibisce la steroidogenesi.

Originariamente inviato da Antò

Different sites of action of arachidonic acid on steroidogenesis in rat Leydig cells.

Marinero MJ, Colas B, Prieto JC, López-Ruiz MP.
Departmento de Bioquímica y Biologia Molecular, Universidad de Alcalá, Alcalá de Henares, Madrid, Spain.
The present study in purified rat Leydig cells shows that arachidonic acid may act as an intratesticular factor regulating LH-mediated testicular steroidogenesis. Arachidonic acid decreased, in a dose-dependent manner, the LH-stimulated cAMP and testosterone levels, over 2 h incubation. Incubation of Leydig cells with arachidonic acid did not modify 125I-hCG binding to the cells as compared to control, showing that the action of arachidonic acid is not related to a decrease of hCG binding to the cells. Forskolin-stimulated cAMP and testosterone production were inhibited by 51.65 and 70.9%, respectively, in the presence of arachidonic acid (100 microM), although the ED50 for the diterpene was not changed. When isobutyl-methyl-xanthine was added to the incubation medium, the same percentage of inhibition was found indicating that arachidonic acid inhibition of cAMP production is not due to stimulation of Leydig cell phosphodiesterase activity. Pretreatment of the cells with pertussis toxin, to inactivate Gi, was also without effect on arachidonic acid inhibition of LH-stimulated cAMP production, but pertussis toxin abolished the inhibitory effects of arachidonic acid when adenylate cyclase was stimulated with forskolin. However, arachidonic acid addition resulted in inhibition of LH- and forskolin-stimulated testosterone production, even if the cells were pretreated with pertussis toxin. It can be concluded that: (1) The inhibitory effect of arachidonic acid is neither due to a decrease of hCG binding to Leydig cells nor to a stimulation of cell phosphodiesterase activity; (2) arachidonic acid modulates cAMP production at two different levels, either by activation of Gi protein and by inhibition of Gs protein or adenylate cyclase; (3) the effect of arachidonic acid on steroidogenesis is also beyond cAMP formation.
PMID: 8735605 [PubMed - indexed for MEDLINE]

Questo è meno chiaro. La foscolina aumenta il Camp aumentando l'adenylatecyclase, l'AA contrasta tale attivazione della foscolina, ma, guardando gli studi precedenti sembra che l'inibizione della steroidogenesi da parte dell'AA dipenda solo dalla sua capacità di modulare il Camp. Per essere + chiaro: se usiamo solo AA avremo un aumento della steroidogenesi, penso, a livelli fisiologici, se utilizziamo solo foscolina avremo una sovraregolazione del Camp e quindi un aumento oltre i parametri fisiologici della steroidogensi. Utilizzando AA e foscolina blocchiamo la capacità di quest'ultima di sovraregolare la produzione di testo da parte delle gonadi. La foscolina è una sostanza molto potente, aumenta l'adenylatecyclase in tutti i tessuti aumentando di molto, si parla di circa il 50%, la risposta cellulare agli ormoni. Questi è ciò che penso



[/quote]

[Anabolic]

cosa ne pensi di questi studi li ho trovati sul sito del x-factor ma sono reali se vedi i risultati non sono particolari

Performance and body composition changes after 50 days of concomitant arachidonic acid supplementation and resistance training.

M Iosia, M Roberts, C Kerksick, B Campbell, T Harvey, C Wilborn, R Wilson, M. Greenwood, D Willoughby and R Kreider. Exercise & Sport Nutrition Laboratory, Center for Exercise, Nutrition & Preventive Health Research, Baylor University, Waco, TX 76798-7313. Mike_Iosia@baylor.edu.

ABSTRACT 1

Arachidonic acid (AA) is a polyunsaturated omega-6 (0-6) fatty acid that is stored within skeletal muscle phospholipids and has been purported to stimulate changes in strength and body composition while resistance training. The purpose of this study was to determine if 50 days of concomitant resistance training and AA supplementation affects performance and/or body composition adaptations in previously resistance-trained males. Thirty-one subjects (22.1 ± 5.0 yrs, 178.9 ± 3.4 cm, 86.1 ± 13.0 kg, 18.1 ± 6.4 % body fat) were randomly assigned to ingest either a corn oil placebo (P: n=16) or AA (n=15). All subjects ingested a total of four capsules each day by ingesting one 0.25 gram capsule every four hours for a total daily dose of 1 gram•d-1 and were given a supplemental protein powder in order attain a protein intake of 2 g•kg-1•d-1. Each subject completed two upper-body and two lower-body workouts each week in a split-body fashion. Total training volumes were calculated from training logs. Body mass, body composition using DEXA, bench press one-repetition maximum (1RM), leg press 1RM and Wingate anaerobic capacity tests were completed at 0, 25 and 50 days. Data were analyzed using repeated measures ANOVA and are presented as mean ± SD changes from baseline after 50-days. No significant differences (p>0.05) between groups were noted for training volume. Training significantly increased body mass (p<0.01), DEXA lean mass (p<0.001), bench press 1RM (p<0.001), leg press 1RM (p<0.001), Wingate average power (p<0.001) and Wingate total work (p<0.001) indicating that the subjects experienced positive training adaptations. No significant group x time interaction effects were observed among groups in changes in body mass (AA: 1.6 ± 2.3; P: 1.0 ± 2.1 kg, p=0.45), DEXA lean mass (AA: 1.2 ± 1.6; P: 1.0 ± 1.9 kg, p=0.71), or leg press 1RM (AA: 25.0 ± 24.7; P: 22.7 ± 34.0 kg, p=0.83). Statistical trends were seen in bench press 1RM (AA: 11.0 ± 6.2; P: 8.0 ± 8.0 kg, p=0.20), Wingate average power (AA: 37.9 ± 10.0; P: 17.0 ± 24.0 W, p=0.16), and Wingate total work (AA: 1292 ± 1206; P: 510 ± 1249 J, p=0.087). A significant group x time interaction effect was observed in Wingate relative peak power (AA: 1.2 ± 0.5; P: -0.2 ± 0.2 W•kg-1, p=0.015). In conclusion, AA supplementation during resistance-training promoted significant increases in relative peak power with other performance related variables approaching significance. These findings provide some preliminary evidence to support the use of AA as an ergogenic aid. More research is needed to explore the effects of AA supplementation on training adaptations.

Proceedings of the International Society of Sports Nutrition (ISSN) Conference June 15-17, 2006.





Hormonal and intramuscular adaptations over 50 days of concomitant arachidonic acid supplementation and resistance training.

Roberts, M, C Kerksick, L Taylor, M Iosia, B Campbell, C Wilborn, T Harvey, R Wilson, M. Greenwood, D Willoughby and R Kreider. Exercise & Sport Nutrition Laboratory, Center for Exercise, Nutrition & Preventive Health Research, Baylor University, Waco, TX 76798-7313. Mike_Roberts@baylor.edu.

ABSTRACT 2

Prostaglandins are derived from dietary arachidonic acid (AA) and up-regulate recovery mechanisms including inflammation and protein synthesis within skeletal muscle in response to resistance training. The purpose of this study was to determine if 50 days of concomitant resistance training and AA supplementation elicited changes in hormonal and/or intramuscular markers in resistance-trained males. Thirty-one subjects (22.1 ± 5.0 yrs, 86.1 ±1 3.0 kg, 178.9 ± 3.4 cm, 18.1 ± 6.4 % body fat) were randomly assigned to a placebo (P: n = 16; 1 g capsulated corn oil/day) or AA group (AA: n = 15; 1 g capsulated AA/day) and were given supplemental protein powder to ingest in order attain an adequate protein intake of 2 g/kg/day while participating in a 4 day/wk resistance training regimen (2 upper/ 2 lower). Fasting blood was taken on days 0, 25 and 50 and muscle biopsies were taken from the vastus lateralis on days 0 and 50. Prostaglandin E2 (PGE2), prostaglandin F2a (PGF2a), interleukin-6 (IL-6), free testosterone (fTEST), total testosterone (tTEST) and cortisol (CORT) were assessed with EIA while myosin heavy chain isoform (MHC I, -IIa, -IIx) and mRNA levels were detected using SDS-PAGE and real-time RT-PCR, respectively. Hormonal and MHC data were analyzed by ANOVA with repeated measures while independent t-tests were used to assess changes in MHC mRNA expression. Data are expressed as means ± SD changes from baseline after 50-days of supplementation for the AA and P groups, respectively. Statistical trends were found for PGE2 increases (98.5 ± 217; P -73.8 ± 273 pg/ml, p=0.063) and IL-6 decrements (-28.8 ± 47; 52.5 ± 45 pg/ml, p=0.067) in the AA group. A non-significant increase in PGF2a was also found in the AA group (AA: 45.2 ± 153; P: -33.6 ± 139 pg/ml, p=0.143). fTEST significantly decreased (p=0.03) in both groups over time with no differences among groups (AA: -2.99 ± 6; P -2.60 ± 8 pg/ml, p=0.88). There was no significant group or main effects for tTEST or CORT. MHC IIa levels significantly increased in both groups over time (p=0.009) with no differences among groups (AA: 120 ± 229; P 139 ± 262 ng/ml, p=0.84). There were no significant time or group x time effects for MHC I or MHC IIx levels. A significant decrement was observed in MHC IIx basal mRNA expression in the AA group (AA: -6.96 ± 24.28; P: -4.97 ± 10.88 %, p=0.02), while there was no significant time or interaction effects for MHC I or IIa expression. Results suggest that AA supplementation during resistance training may exert some potentially favorable alterations in an inflammatory marker, fasting hormonal, and gene expression patterns and that additional research is necessary to further examine this hypothesis.

Proceedings of the International Society of Sports Nutrition (ISSN) Conference June 15-17, 2006.





Changes in whole blood and clinical safety markers over 50 days of concomitant arachidonic acid supplementation and resistance training.

Wilborn, C, M Roberts, C Kerksick, M Iosia, L Taylor, B Campbell, T Harvey, R Wilson, M. Greenwood, D Willoughby and R Kreider. Exercise & Sport Nutrition Laboratory, Center for Exercise, Nutrition & Preventive Health Research, Baylor University, Waco, TX 76798-7313. Colin_Wilborn@baylor.edu.

ABSTRACT 3

Prostaglandins are derived from dietary arachidonic acid (AA) and up-regulate recovery mechanisms including inflammation and protein synthesis within skeletal muscle in response to resistance training. The purpose of this study was to determine if 50 days of concomitant resistance training and AA supplementation elicited changes in immune and serum clinical safety markers in resistance-trained males. Thirty-one subjects (22.1 ± 5.0 yrs, 86.1 ±1 3.0 kg, 178.9 ± 3.4 cm, 18.1 ± 6.4 % body fat) were randomly assigned to a placebo (P: n = 16; 1 g capsulated corn oil/day) or AA group (AA: n = 15; 1 g capsulated AA/day) and were given supplemental protein powder to ingest in order attain an adequate protein intake of 2 g/kg/day while participating in a 4 day/wk resistance training regimen (2 upper/ 2 lower). Fasting blood was taken on days 0, 25 and 50. Immune markers were measured from whole blood using flow cytometric analysis (Abbott Cell Dyne 3500) while serum markers were measured from separated serum using nephelometric analysis (Dade Dimension XRL). Data was analyzed by ANOVA with repeated measures and significant changes (p=0.05) are expressed as means ± SD changes from baseline after 50-days of supplementation for the AA and P groups, respectively. There were no significant group x time interactions in immune markers including white blood cell count (p=0.12), neutrophil count (p=0.17), lymphocyte count (p=0.20) or neutrophil: lymphocyte ratio (p=0.49). There were also no significant group x time interactions with red blood cell count (p=0.49), hemoglobin concentration (p=0.65) or hematocrit % (p=0.79). No significant group x time interactions were evident for liver enzyme levels including alanine aminotransferase (p=0.53) or gamma-glutamyl transferase (p=0.40) nor was there significant a group x time interaction for serum albumin (p=0.43). There was a statistical trend for the decrement in the liver enzyme aspartate aminotransferase in the P group (AA: 4.0 ± 11.2 U/L; P: -10.5 ± 27.7 U/L, p=0.07) but values remained well-within normal limits. No significant group x time interactions were evident for kidney function and/or catabolic indicators including blood urea nitrogen (BUN; p=0.21), creatinine (p=0.41) or BUN:creatinine ratio (p=0.41). None of the thirty-one subjects reported any adverse side effects over the 50-day trial. These results suggest that AA supplementation during an extended period of resistance training is physiologically well-tolerated and does not alter whole blood, liver or kidney clinical safety markers.

Proceedings of the International Society of Sports Nutrition (ISSN) Conference June 15-17, 2006.