Hey guys, we have known for awhile that you can lift more weight on your eccentric movements, and the eccentric phase is largely responsible for our DOMS. This has great implications for the rationale behind doing slow negatives and doubles.
There are several reasons for increased muscle damage during the eccentric phase which have nothing to do with lactic acid build up. Blood and muscle lactate should return to normal within 30-60min. after exercise and the concentric phase produces about 2/3 more lactic acid then the eccentric so if lactic acid was a cause of DOMS we would see this much more with the concentric movement which we dont.
The research and reasons for this are very interesting and may have something to do with the increased force production per fiber. The research shows the eccentric phase increases muscle soreness because of built up damage to the muscle membrane, streaming of the Z-lines, Excitation-Contraction coupling failure - http://www.blackwell-synergy.com/doi...3.2001.0571a.x
Also, the hypothesis that the type II-Z fibers having zero to a low oxidative capacity predisposes them to damage which is explained in the following study:
NUMEROUS INVESTIGATIONS DEMONSTRATE that skeletal muscle injury and soreness result from the forced lengthening of activated muscle [i.e., eccentric contraction (EC)]. Experimental models involving both humans (6, 9) and animals (1, 21) have identified a number of factors that affect the initial injury itself as well as subsequent tissue deterioration. For example, mechanical stress (38) and strain (14) have both been shown to be strong predictors of the magnitude of force loss after EC. After the initial injury, inflammation causes further tissue deterioration (4, 5, 22).
EC-induced injury is also fiber type specific. For example, using the rat downhill running model, preferential damage of the deep vastus intermedius muscle fibers was shown (35) and was interpreted as indicating preferential activation of these fibers. In eccentric exercise of human quadriceps muscles, Fridén and co-workers (10) demonstrated a greater incidence of myofibrillar disruption to the ultrastructurally identified type 2B fibers compared with either type 2A or type 1 fibers. They also interpreted the decreased isokinetic torque observed at high angular velocities as indicating selective type 2B fiber damage. Lieber and Fridén (13) demonstrated selective damage of histochemically identified type fast glycolytic (FG) fibers in the rabbit tibialis anterior (TA) muscle after 30 min of cyclic EC. On the basis of this observation, they hypothesized that the low oxidative capacity of FG fibers predisposed them to injury either due to rigor cross-bridge formation or to initiation of degradative cellular events associated with loss of cellular adenylate charge (cytosolic [ATP]/[ADP] and [Pi]) that may serve as a stimulus for lactate production or may activate cellular degradative processes during and after cyclic EC. The appeal of this hypothesis was that it provided a metabolic basis for the observed protective effect of eccentric training before eccentric exercise (9). However, this hypothesis has not been tested. It is possible that the eccentric action itself causes cellular changes independent of cellular metabolism, such as increased sarcomere number (23) or increased cytoskeletal strength (2), that may be protective against EC-induced muscle injury. Thus the purpose of this study was to increase muscle oxidative capacity to test the hypothesis that muscle damage resulting from EC is a function of oxidative capacity. Brief versions of this work have been presented (25, 26).
The question is whywhywhy??
Why does the lengthening of a muscle fiber produce more tension and more force then the shortening (concentric) phase?