נק' מוניטין:
131
חופרים עליו יותר מדי, גוגל עמוס וגועש במחקרים יותר מדי רעש וצלצולים הבאתי לכאן את הדברים המענינים תאכלס דעות? מישהו ניסה?
THE EFFECTS OF ARACHIDONIC ACID SUPPLEMENTATION ON MYOTUBE DEVELOPMENT
David Bisterfeldt, Howard Hughes Medical Institute Student Researcher Allison Wilson , Ph.D. Department Chair Biological Sciences Craig Broeder, Ph.D. FACSM, FNAASO
Director Activities of Daily Living Performance Enhancement Research Center Director of the Masters of Clinical Exercise Physiology Program
BENEDICTINE UNIVERSITY. DEPARTMENT OF BIOLOGICAL SCIENCES. LISLE, IL
The current cell-culture studies we are conducting are designed to determine what effects arachidonic acid (AA) may have on the development and molecular constitutions involved in the differentiated myoblast to skeletal muscle myotube cells in vitro. We are targeting three specific areas of muscle growth including actin-myosin cell development-cell fusion, androgen receptor expression, and how protein cell-signaling activities are affected by various AA concentrations. To date, we have focused on the myotube hypertrophy and cell fusion effects of AA using immunohistochemical staining of myosin and actin.
We are also in the final stages of setting up the optimum in-vitro model for identifying androgen receptor expression with and without AA added to our cell-culture medium.
Cell di erentiation, myosin hypertrophy and fusion studies using C C myoblasts Precursor muscle cells cells were conducted initially. These C C cells were replenished with either fresh 10% fetal bovine serum (FBS) or the appropriate 2% horse serum (HS) media (containing no AA or 12.5 μM, 25 μM, or 50 μM AA) and then incubated for 96, 120, or 144 hours. These results indicated that the best differentiation was noted for at 144 hour incubation time in 2% HS and when comparing 25 μM or 50 μM AA to control cultures. Thus, a 144 hour incubation times were used as the experimental condition for all measurements.
For the myosin hypertrophy and fusion studies, the same experimental conditions described above were used. Thus far, we have observed clear phenotypic changes in C2C12 cells to myotubes whose medium contains arachidonic acid. These changes occurred most notable in 25 μM and 50 μM concentrations. The myotubes have an increased lateral diameter, enhanced levels of myosin deposition, and a greater concentration of nuclei than controls
(Figures 1 and 2). These results suggest that arachidonic acid may play a role in enhancing protein synthesis and myotube development at the cellular level. Moreover, we observed increased levels of nuclear fusion suggesting arachidonic acid may augment a muscle’s hypertrophic response through enhanced cellular myotube growth in our mouse myoblast cell-culture model.
Proceedings of the International Society of Sports Nutrition (ISSN) Conference June 15-17, 2006.
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.
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.
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.
New Paper on Arachidonic Acid Supplementation
A paper on the supplementation of arachidonic acid (AA) was recently published in the British Journal of Nutrition (British Journal of Nutrition (2007), 98, 451–453). This article is of interest to the athletic community supplementing arachidonic acid for a number of reasons, most notably its focus on safety, its close examination of the buildup and depletion of arachidonic acid in the body, and its use of AA combined with a high intake of Omega-3 fatty acids. Key to this review was a study published in the same journal in April of 2007 by Kusumoto et al. (Br J Nutr. 2007 Sep;98(3):626-35. Epub 2007 Apr 20), which involved the supplementation of arachidonic acid (840mg/d) in a group of 24 healthy Japanese men that consumed high amounts of fish in their diet. This is the first paper of its kind, as most previous investigations of arachidonic acid supplementation safety involved Westerners with low daily intakes of Omega-3 fatty acids. Habitual daily intakes of DHA and EPA in this study ranged from 42 to 691mg and 98 to 991mg, respectively. The average intakes were about 310mg and 550 mg per day. Among the findings were the following.
2-Week Buildup Window:
It took 2 weeks for maximum arachidonic acid levels to be achieved in serum phospholipids. This was the first study to closely examine the time it took to reach peak levels with AA supplementations, and reinforces anecdotal observations of a 2-3 week “loading” window before significant results are noted with supplementation in bodybuilders/athletes.
4-Week Washout:
Arachidonic acid levels remained elevated for a few weeks after supplementation was discontinued. They reached their pretreated levels after 4 weeks. This may also explain why some continue to notice progress in the immediate weeks following AA discontinuation.
Omega-3’s Had No Effect:
Peak arachidonic acid levels were similar in this study to other studies where AA was given to subjects with low dietary levels of Omega-3 fatty acids. At these levels there did not appear to be any significant Omega-3 antagonism of arachidonic acid. This study reinforces the anecdotal observations that low doses of fish oil or regular fish consumption do not appear to appreciably diminish the results of arachidonic acid supplementation.
Arachidonic Acid Supplementation is Safe:
This paper one again takes a review of the safety of arachidonic acid supplementation, with interest in its effects on many areas of health including inflammation, immune functioning, lipids, blood pressure, platelet aggregation, glucose concentrations, liver function, and bleeding time, and notes that arachidonic acid supplementation appears to be perfectly safe in healthy subjects. When noting the inclusion of the most recent AA study (Kusumoto), the British Journal of Nutrition review states:
“Taken together with earlier studies, this study suggests that, rather than being harmful, moderately increased arachidonic acid intake is probably harmless in healthy adults, although the effect of intakes above 1.5g/d are not known and the effect of increased intake in diseased individuals is not known.”
THE EFFECTS OF ARACHIDONIC ACID SUPPLEMENTATION ON MYOTUBE DEVELOPMENT
David Bisterfeldt, Howard Hughes Medical Institute Student Researcher Allison Wilson , Ph.D. Department Chair Biological Sciences Craig Broeder, Ph.D. FACSM, FNAASO
Director Activities of Daily Living Performance Enhancement Research Center Director of the Masters of Clinical Exercise Physiology Program
BENEDICTINE UNIVERSITY. DEPARTMENT OF BIOLOGICAL SCIENCES. LISLE, IL
The current cell-culture studies we are conducting are designed to determine what effects arachidonic acid (AA) may have on the development and molecular constitutions involved in the differentiated myoblast to skeletal muscle myotube cells in vitro. We are targeting three specific areas of muscle growth including actin-myosin cell development-cell fusion, androgen receptor expression, and how protein cell-signaling activities are affected by various AA concentrations. To date, we have focused on the myotube hypertrophy and cell fusion effects of AA using immunohistochemical staining of myosin and actin.
We are also in the final stages of setting up the optimum in-vitro model for identifying androgen receptor expression with and without AA added to our cell-culture medium.
Cell di erentiation, myosin hypertrophy and fusion studies using C C myoblasts Precursor muscle cells cells were conducted initially. These C C cells were replenished with either fresh 10% fetal bovine serum (FBS) or the appropriate 2% horse serum (HS) media (containing no AA or 12.5 μM, 25 μM, or 50 μM AA) and then incubated for 96, 120, or 144 hours. These results indicated that the best differentiation was noted for at 144 hour incubation time in 2% HS and when comparing 25 μM or 50 μM AA to control cultures. Thus, a 144 hour incubation times were used as the experimental condition for all measurements.
For the myosin hypertrophy and fusion studies, the same experimental conditions described above were used. Thus far, we have observed clear phenotypic changes in C2C12 cells to myotubes whose medium contains arachidonic acid. These changes occurred most notable in 25 μM and 50 μM concentrations. The myotubes have an increased lateral diameter, enhanced levels of myosin deposition, and a greater concentration of nuclei than controls
(Figures 1 and 2). These results suggest that arachidonic acid may play a role in enhancing protein synthesis and myotube development at the cellular level. Moreover, we observed increased levels of nuclear fusion suggesting arachidonic acid may augment a muscle’s hypertrophic response through enhanced cellular myotube growth in our mouse myoblast cell-culture model.
Proceedings of the International Society of Sports Nutrition (ISSN) Conference June 15-17, 2006.
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.
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.
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.
New Paper on Arachidonic Acid Supplementation
A paper on the supplementation of arachidonic acid (AA) was recently published in the British Journal of Nutrition (British Journal of Nutrition (2007), 98, 451–453). This article is of interest to the athletic community supplementing arachidonic acid for a number of reasons, most notably its focus on safety, its close examination of the buildup and depletion of arachidonic acid in the body, and its use of AA combined with a high intake of Omega-3 fatty acids. Key to this review was a study published in the same journal in April of 2007 by Kusumoto et al. (Br J Nutr. 2007 Sep;98(3):626-35. Epub 2007 Apr 20), which involved the supplementation of arachidonic acid (840mg/d) in a group of 24 healthy Japanese men that consumed high amounts of fish in their diet. This is the first paper of its kind, as most previous investigations of arachidonic acid supplementation safety involved Westerners with low daily intakes of Omega-3 fatty acids. Habitual daily intakes of DHA and EPA in this study ranged from 42 to 691mg and 98 to 991mg, respectively. The average intakes were about 310mg and 550 mg per day. Among the findings were the following.
2-Week Buildup Window:
It took 2 weeks for maximum arachidonic acid levels to be achieved in serum phospholipids. This was the first study to closely examine the time it took to reach peak levels with AA supplementations, and reinforces anecdotal observations of a 2-3 week “loading” window before significant results are noted with supplementation in bodybuilders/athletes.
4-Week Washout:
Arachidonic acid levels remained elevated for a few weeks after supplementation was discontinued. They reached their pretreated levels after 4 weeks. This may also explain why some continue to notice progress in the immediate weeks following AA discontinuation.
Omega-3’s Had No Effect:
Peak arachidonic acid levels were similar in this study to other studies where AA was given to subjects with low dietary levels of Omega-3 fatty acids. At these levels there did not appear to be any significant Omega-3 antagonism of arachidonic acid. This study reinforces the anecdotal observations that low doses of fish oil or regular fish consumption do not appear to appreciably diminish the results of arachidonic acid supplementation.
Arachidonic Acid Supplementation is Safe:
This paper one again takes a review of the safety of arachidonic acid supplementation, with interest in its effects on many areas of health including inflammation, immune functioning, lipids, blood pressure, platelet aggregation, glucose concentrations, liver function, and bleeding time, and notes that arachidonic acid supplementation appears to be perfectly safe in healthy subjects. When noting the inclusion of the most recent AA study (Kusumoto), the British Journal of Nutrition review states:
“Taken together with earlier studies, this study suggests that, rather than being harmful, moderately increased arachidonic acid intake is probably harmless in healthy adults, although the effect of intakes above 1.5g/d are not known and the effect of increased intake in diseased individuals is not known.”
