Abstract:BackgroundPhosphatidic acid (PA) has been reported to activate the mammalian target of rapamycin (mTOR) signaling pathway and is thought to enhance the anabolic effects of resistance training. The purpose of this pilot study was to examine if oral phosphatidic acid administration can enhance strength, muscle thickness and lean tissue accruement during an 8-week resistance training program.MethodsSixteen resistance-trained men were randomly assigned to a group that either consumed 750 mg of PA (n = 7, 23.1 ± 4.… Show more
“…Previous studies have used narrow field‐of‐view imaging snapshots at both the VL0 and VL5 locations to quantify MT, PA, and FL in the VL. However, little consensus exists regarding the rationale for anatomical landmark selection during ultrasound assessment of the VL.…”
“…Previous studies have used narrow field‐of‐view imaging snapshots at both the VL0 and VL5 locations to quantify MT, PA, and FL in the VL. However, little consensus exists regarding the rationale for anatomical landmark selection during ultrasound assessment of the VL.…”
“…However, since the repeatability of measurement was not so good (the CV of repeated measurements was 13.5%), it may be the reason for the lack of changes in pennation angle. Hoffman et al 92) found an increase in VL thickness after resistance training for 8 weeks, but did not find such an increase in its pennation angle. Because the subjects in Hoffman et al 92) were resistance-trained men, and because adaptation of the pennation angle of VL was large within several weeks from the beginning of the training program 46) , the lack of change in the pennation angle of VL may have been due to its low responsiveness.…”
Section: Evidence Against Pennation Angle Changementioning
confidence: 92%
“…Hoffman et al 92) found an increase in VL thickness after resistance training for 8 weeks, but did not find such an increase in its pennation angle. Because the subjects in Hoffman et al 92) were resistance-trained men, and because adaptation of the pennation angle of VL was large within several weeks from the beginning of the training program 46) , the lack of change in the pennation angle of VL may have been due to its low responsiveness. Lack of pennation angle adaptation was also demonstrated in MG 93,94) and BF 56) , but these studies did not provide data on changes in muscle size.…”
Section: Evidence Against Pennation Angle Changementioning
confidence: 92%
“…Some studies failed to find a change in pennation angle despite significant muscle hypertrophy 9,43,91,92) . Rutherford and Jones 9) measured the pennation angle of VL and VI before and after knee extension training for 12 weeks, and failed to find significant changes in either of the two muscles.…”
Section: Evidence Against Pennation Angle Changementioning
The present review summarizes current evidence and unresolved issues regarding training-induced changes in the architecture of human skeletal muscles. As architectural parameters, we focused on the fascicle length and pennation angle, which are related to force-generating capability of pennate muscles. Cross-sectional studies in sport athletes suggested changes in both the parameters following chronic sport-specific activities. Longitudinal training intervention experiments indicated direct evidence of the plasticity of the two parameters induced by resistance training, but no consensus has been reached regarding the factors influencing those changes. Considering the importance of fascicle arrangement on muscle function, future studies are required to explain the underpinning mechanisms of the adaptation.
“…With regards to human studies, one resistance exercise training study has employed oral supplementation of PA, producing an increase in lean body mass compared to placebo (Hoffman et al, 2012). …”
Section: How Can a Mechanical Signal Elicited By Resistance Exercise mentioning
Loss of skeletal muscle myofibrillar protein with disease and/or inactivity can severely deteriorate muscle strength and function. Strategies to counteract wasting of muscle myofibrillar protein are therefore desirable and invite for considerations on the potential superiority of specific modes of resistance exercise and/or the adequacy of low load resistance exercise regimens as well as underlying mechanisms. In this regard, delineation of the potentially mechanosensitive molecular mechanisms underlying muscle protein synthesis (MPS), may contribute to an understanding on how differentiated resistance exercise can transduce a mechanical signal into stimulation of muscle accretion. Recent findings suggest specific upstream exercise-induced mechano-sensitive myocellular signaling pathways to converge on mammalian target of rapamycin complex 1 (mTORC1), to influence MPS. This may e.g. implicate mechanical activation of signaling through a diacylglycerol kinase (DGKζ)-phosphatidic acid (PA) axis or implicate integrin deformation to signal through a Focal adhesion kinase (FAK)-Tuberous Sclerosis Complex 2 (TSC2)-Ras homolog enriched in brain (Rheb) axis. Moreover, since initiation of translation is reliant on mRNA, it is also relevant to consider potentially mechanosensitive signaling pathways involved in muscle myofibrillar gene transcription and whether some of these pathways converge with those affecting mTORC1 activation for MPS. In this regard, recent findings suggest how mechanical stress may implicate integrin deformation and/or actin dynamics to signal through a Ras homolog gene family member A protein (RhoA)-striated muscle activator of Rho signaling (STARS) axis or implicate deformation of Notch to affect Bone Morphogenetic Protein (BMP) signaling through a small mother of decapentaplegic (Smad) axis.
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