Mackey AL
The influence of anti-inflammatory medication on exercise-induced myogenic precursor cell responses in humans.
J Appl Physiol. 2007 Apr 26;
The consumption of nonsteroidal anti-inflammatory drugs (NSAIDs) is widespread among athletes when faced with muscle soreness or injury, but the effects of NSAIDs on satellite cell activity in humans are unknown. In order to investigate this, 14 healthy male endurance athletes (mean VO2peak: 62 ml.kg(-1).min(-1)) volunteered for the study which involved running 36 km. They were divided into two groups, and received either 100 mg indomethacin per day or placebo. Muscle biopsies collected before the run and on days 1, 3, and 8 afterwards were analysed for satellite cells by immunohistochemistry with the aid of neural cell adhesion molecule (NCAM) and fetal antigen-1 (FA1) antibodies. Muscle biopsies were also collected from untrained individuals for comparison. Compared to pre-exercise levels, a 27% increase in the number of NCAM+ cells was observed on day 8 post exercise in the placebo group (P < 0.05), while levels remained similar at all time points in the NSAID group. No change was seen in the proportion of FA1+ cells, although lower levels were found in the muscle of endurance trained athletes when compared to untrained individuals (P < 0.05). These results suggest that ingestion of anti-inflammatory drugs attenuates the exercise-induced increase in satellite cell number, supporting the role of the cyclooxygenase pathway in satellite cell activity. Key words: skeletal muscle, NSAID, Running, Fetal Antigen-1, NCAM.
Although this was studied on ET subjects it still has some interesting impacts, which I'll point out.
1. This particular NSAID did indeed show an attenuation in Sat cell activity.
2. And more importantly where I am concerned, this study shows that the proportion of NCAM+ cells stained by FA1 in trained subjects were in a lower proportion than untrained. Obviously indicating a higher resistance to the training and again points to a reduced training effect.
3. There was a higher FA1 staining in precursor cells resident outside the basal lamina, something that may prove to be very interesting in future sat cell studies as it's yet to be known exactly where all sat cells reside and the impact or contribution from various populations. Why is this important? It has been suggested that there is a finite number of sat cells and that constant or rather repeated damage causing increased differeniation would reduce the available populations. This study now adds in the possiblity that the population used may be different and called upon via different effects and modes of proliferation.
4. So even though the results support the hyopthesis, NSAIDs = bad for sat cell proliferation (or at least this particluar NSAID), it shows us something else as well.
Now whether or not this will be repeated in weight trained subjects, we'll have to wait and see.
The influence of anti-inflammatory medication on exercise-induced myogenic precursor cell responses in humans.
J Appl Physiol. 2007 Apr 26;
The consumption of nonsteroidal anti-inflammatory drugs (NSAIDs) is widespread among athletes when faced with muscle soreness or injury, but the effects of NSAIDs on satellite cell activity in humans are unknown. In order to investigate this, 14 healthy male endurance athletes (mean VO2peak: 62 ml.kg(-1).min(-1)) volunteered for the study which involved running 36 km. They were divided into two groups, and received either 100 mg indomethacin per day or placebo. Muscle biopsies collected before the run and on days 1, 3, and 8 afterwards were analysed for satellite cells by immunohistochemistry with the aid of neural cell adhesion molecule (NCAM) and fetal antigen-1 (FA1) antibodies. Muscle biopsies were also collected from untrained individuals for comparison. Compared to pre-exercise levels, a 27% increase in the number of NCAM+ cells was observed on day 8 post exercise in the placebo group (P < 0.05), while levels remained similar at all time points in the NSAID group. No change was seen in the proportion of FA1+ cells, although lower levels were found in the muscle of endurance trained athletes when compared to untrained individuals (P < 0.05). These results suggest that ingestion of anti-inflammatory drugs attenuates the exercise-induced increase in satellite cell number, supporting the role of the cyclooxygenase pathway in satellite cell activity. Key words: skeletal muscle, NSAID, Running, Fetal Antigen-1, NCAM.
Although this was studied on ET subjects it still has some interesting impacts, which I'll point out.
1. This particular NSAID did indeed show an attenuation in Sat cell activity.
2. And more importantly where I am concerned, this study shows that the proportion of NCAM+ cells stained by FA1 in trained subjects were in a lower proportion than untrained. Obviously indicating a higher resistance to the training and again points to a reduced training effect.
3. There was a higher FA1 staining in precursor cells resident outside the basal lamina, something that may prove to be very interesting in future sat cell studies as it's yet to be known exactly where all sat cells reside and the impact or contribution from various populations. Why is this important? It has been suggested that there is a finite number of sat cells and that constant or rather repeated damage causing increased differeniation would reduce the available populations. This study now adds in the possiblity that the population used may be different and called upon via different effects and modes of proliferation.
4. So even though the results support the hyopthesis, NSAIDs = bad for sat cell proliferation (or at least this particluar NSAID), it shows us something else as well.
Now whether or not this will be repeated in weight trained subjects, we'll have to wait and see.
