Post by John A. Casler on Jul 9, 2009 10:21:09 GMT -8
This is from Jamie Carruthers as posted to SuperTraining
To visit SUPERTRAINING FORUM
health.groups.yahoo.com/group/Supertraining/?yguid=44276758
DO ANTIOXIDANTS ENHANCE OR SUPPRESS TRAINING INDUCED ADAPTATIONS?
PHILP, A.
UNIVERSITY OF DUNDEE
14th annual Congress of the
EUROPEAN COLLEGE OF SPORT SCIENCE
Oslo/Norway, June 24-27, 2009
BOOK OF ABSTRACTS
Exercise involves a complex series of cellular events, which combine to mediate skeletal muscle adaptation. Muscle contraction evokes
signal transduction pathways regulated by calcium and ATP fluctuations as well as a stress response leading to systemic release of
hormones, and the muscle specific generation of reactive oxygen species and cytokines. As a general process, this response can be
termed exercise specific inflammation and recent research suggests that this transient inflammatory response is a key factor in exercise
adaptation (Petersen and Pedersen, 2005). If inflammation is prolonged however, such as during repetitive periods of intense training, or
sustained exhaustive exercise, deleterious effects develop within the working muscle suggesting that the range over which inflammation
is beneficial is small. Radicals and reactive oxygen species (ROS) are molecules that initiate damaging oxidation reactions within the cell
(Powers et al., 2004). ROS generation has been linked with exercise induced oxidative injury and muscle fatigue due to an imbalance
between oxidant production and the antioxidant capacity of the cell (Powers and Jackson, 2008). There are a number of enzymatic and
non-enzymatic defence systems, or antioxidants, in mammalian skeletal muscle which reduce free radicals and reactive oxygen species
production. Importantly, dietary antioxidants work in synergy with these endogenous antioxidants to offset ROS induced oxidative stress.
With this in mind, recreational and elite athletes supplement with antioxidant agents, in the belief that they will protect the athlete against
exercise-induced damage, local inflammation and enhance post exercise recovery.
However, recent research suggests that dietary
antioxidants may in fact suppress ROS mediated signalling essential for exercise-induced adaptation (Powers and Jackson, 2008). Specifically
it appears that ROS generation is important for kinase activity of the AMP-dependent kinase (AMPK), the mitogen activated protein
kinases (p38 and p42/44) and their downstream targets NF-κB and the transcriptional co-activator PGC-1รก (Gomez-Cabrera et al.,
2005; Irrcher et al., 2009). Therefore, whether antioxidants enhance or interfere with training adaptation and whether training regimes
and nutritional interventions should be adjusted to account for ROS action in response to exercise remains a controversial issue.
References
Petersen, AM and Pedersen, BK (2005) J. Appl. Physiol. 98(4): 1154-62.
Powers, SK et al., (2004) J. Sports Sciences. 22: 81-94.
Powers, SK and Jackson, MJ (2008) Physiol. Rev. 88: 1243-76
Gomez-Cabrera, M-C et al., (2005) J. Physiol. 567.1: 113-20
Irrcher, I et al., (2009) Am. J. Physiol. Cell Physiol. 296: C116-23
=======================
Jamie Carruthers
Wakefield, UK
To visit SUPERTRAINING FORUM
health.groups.yahoo.com/group/Supertraining/?yguid=44276758
DO ANTIOXIDANTS ENHANCE OR SUPPRESS TRAINING INDUCED ADAPTATIONS?
PHILP, A.
UNIVERSITY OF DUNDEE
14th annual Congress of the
EUROPEAN COLLEGE OF SPORT SCIENCE
Oslo/Norway, June 24-27, 2009
BOOK OF ABSTRACTS
Exercise involves a complex series of cellular events, which combine to mediate skeletal muscle adaptation. Muscle contraction evokes
signal transduction pathways regulated by calcium and ATP fluctuations as well as a stress response leading to systemic release of
hormones, and the muscle specific generation of reactive oxygen species and cytokines. As a general process, this response can be
termed exercise specific inflammation and recent research suggests that this transient inflammatory response is a key factor in exercise
adaptation (Petersen and Pedersen, 2005). If inflammation is prolonged however, such as during repetitive periods of intense training, or
sustained exhaustive exercise, deleterious effects develop within the working muscle suggesting that the range over which inflammation
is beneficial is small. Radicals and reactive oxygen species (ROS) are molecules that initiate damaging oxidation reactions within the cell
(Powers et al., 2004). ROS generation has been linked with exercise induced oxidative injury and muscle fatigue due to an imbalance
between oxidant production and the antioxidant capacity of the cell (Powers and Jackson, 2008). There are a number of enzymatic and
non-enzymatic defence systems, or antioxidants, in mammalian skeletal muscle which reduce free radicals and reactive oxygen species
production. Importantly, dietary antioxidants work in synergy with these endogenous antioxidants to offset ROS induced oxidative stress.
With this in mind, recreational and elite athletes supplement with antioxidant agents, in the belief that they will protect the athlete against
exercise-induced damage, local inflammation and enhance post exercise recovery.
However, recent research suggests that dietary
antioxidants may in fact suppress ROS mediated signalling essential for exercise-induced adaptation (Powers and Jackson, 2008). Specifically
it appears that ROS generation is important for kinase activity of the AMP-dependent kinase (AMPK), the mitogen activated protein
kinases (p38 and p42/44) and their downstream targets NF-κB and the transcriptional co-activator PGC-1รก (Gomez-Cabrera et al.,
2005; Irrcher et al., 2009). Therefore, whether antioxidants enhance or interfere with training adaptation and whether training regimes
and nutritional interventions should be adjusted to account for ROS action in response to exercise remains a controversial issue.
References
Petersen, AM and Pedersen, BK (2005) J. Appl. Physiol. 98(4): 1154-62.
Powers, SK et al., (2004) J. Sports Sciences. 22: 81-94.
Powers, SK and Jackson, MJ (2008) Physiol. Rev. 88: 1243-76
Gomez-Cabrera, M-C et al., (2005) J. Physiol. 567.1: 113-20
Irrcher, I et al., (2009) Am. J. Physiol. Cell Physiol. 296: C116-23
=======================
Jamie Carruthers
Wakefield, UK