1. Time course of phosphatidylcholine release following eccentric exercise
Jake Bernards, Nick Carney, Lauren K. Kirlin, Alison Nguyen, Simon G. Madsen, Denise Gallagher, Martin S. Pedersen, Michael J. Buono, Fred W. Kolkhorst
School of Exercise and Nutritional Sciences, San Diego State University
Abstract
Methods
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Creatine kinase (CK) is the most widely used biomarker of muscle damage. However, after exercise-induced muscle damage, CK does not peak in the bloodstream until hr. Phosphatidylcholine (PC) is a type of phospholipid found principally in the outer layer of the plasma membrane. The purpose of this pilot study was to observe whether PC is also released into the blood in response to exercise-induced muscle damage and whether it follows a time course similar to that of CK release. Five subjects participated in 30 min of downhill treadmill running at 7 mph at a 10% decline. Venous blood was drawn prior to exercise and again at 6, 12, 24, and 48-hr post-exercise. Subjects rated their perceived muscle soreness at the same times. Although subjects’ reported muscle soreness after exercise (p < 0.10), there were no significant change for the plasma CK or PC responses (p > 0.10) This suggests that the exercise protocol was inadequate to cause significant muscle damage.
5 subjects (4 males and 1 female), 25.6 ± 1.8 yr
Exercise protocol: 30 min of downhill treadmill running (10%) at 7 mph
Venous blood sampled at pre-exercise and 6, 12, 24 and 48 hr post- exercise
Perceived muscle soreness evaluated at same time periods using a Likert 0 to 6 scale (0 = absence of soreness, 6 = inability to move)
CK and PC assessed using a colorimetric spectrophotometric assay kit
Data analyzed using a repeated measures ANOVA
Figure 2. Mean PC and CK response to downhill running; pre-exercise and 6, 12, 24, and 48 hours post-exercise.
Introduction
Results
Discussion
Creatine kinase (CK) is an enzyme normally found in the cytosol and mitochondria of tissues where energy demand is high. CK catalyzes phosphocreatine in our tissues producing ATP for activity. In muscle, this reaction is reversible thus allowing ATP to be quickly and readily available for physical activity from PCr and ADP.1 Following eccentric exercise that damages muscle sarcomeres, CK is released into the blood; thus it is often used as a biomarker of muscular damage, particularly after damage to the heart muscle. Furthermore, after muscle damage, the appearance of CK is delayed and does not peak until hours post-exercise in humans. However, actual damage to the muscle from physical exercise does not correlate well to CK or perceived muscular soreness (DOMS) in individuals.
Phosphatidylcholine (PC) is a type of phospholipid containing choline which constitutes up to 50% of the phospholipid bilayer membrane found in humans and plants. Particularly found in the outer portions of the plasma membrane.2 – need a transition to next paragraph
Purpose: Therefore, the aim of this study was to examine a different biomarker, Phosphatidylcholine (PC), over the course of 48 hours following DOMS inducing exercise.
DOMS increased significantly over the 48-hr (p < 0.1; Figure 1)
Creatine kinase was unaffected by the exercise (p > 0.1; Figure 2)
Phosphatidylcholine was unaffected by the exercise (p < 0.18; Figure 2).
Results from the study indicated there was a significant response in DOMS 6 hr following the exercise protocol. However, there were no significant differences in CK or PC concentrations through 48-hr post-exercise, although PC was trending towards significance at the 12-hr reading. One possible explanation as to why there was not a significant increase in PC and CK concentrations following exercise is that the exercise intensity was insufficient. All subjects involved in the study exercise regularly that included eccentric exercise. Muscles adapt to eccentric exercise whereas even a single bout of eccentric exercise minimizes damage from future bouts of eccentric exercise for up to 10 weeks.4
With there being no response of CK or PC, a new question arises, why did subjects still become sore following exercise? Creatine kinase is known to have a high variability from person to person in response to exercise.5 Some individuals are responders while others are non-responders of CK release to eccentric exercise. If the exercise protocol was difficult enough to elicit small amounts of muscle damage (suggested by the significant difference in DOMS) then PC is not a good biomarker for low levels of muscle damage.
Limitations of this study include a small sample size along with different people running the various assays.
Figure 1. Average perceived muscle soreness rating at pre-exercise and at 6, 12, 24 and 48 hr post-exercise. Scale ranges from 0 (complete absence of soreness) to 6 (soreness causing inability to move).
References
1 Bittl JA, Ingwall JS. Reaction rates of creatine kinase and ATP synthesis in the isolated rat heart. A 31P NMR
magnetization transfer study. J Biol Chem. 1985;260(6):3512–3517.
2 Lucy, J. A. (1980). IS THERE A MEMBRANE DEFECT IN MUSCLE AND OTHER CELLS ? British Medical Bulletin,
36(2), 187–192.
3 English KL, Loehr JA, Lee SMC, Smith SM. Early-phase musculoskeletal adaptations to different levels of eccentric resistance after 8 weeks of lower body training. European Journal of Applied Physiology Nosaka K, Clarkson PM, McGuiggin ME, Byrne JM. Time course of muscle adaptation after high force eccentric exercise. Eur J Appl Physiol Occup Physiol. 1991;63(1):70– Totsuka, M., Nakaji, S., Suzuki, K., Sugawara, K., & Sato, K. (2002). Break point of serum creatine kinase release after endurance exercise. Journal of Applied Physiology : 1985), 93(4), 1280–1286