Are the hamstrings from the drive leg or landing leg more active in baseball pitchers? An electromyographic study.

BACKGROUND: Ulnar collateral ligament reconstruction (UCLR) has become a common procedure among baseball players of all levels. There are several graft choices in performing UCLR, one of which is a hamstring (gracilis or semitendinosus) autograft. It is unclear whether the hamstring muscle from a pitcher's drive leg (ipsilateral side of the UCLR) or landing leg (contralateral side of the UCLR) is more active during the pitching motion. We hypothesized that the landing leg semitendinosus will be more electromyographically active than the drive leg. METHODS: Healthy, elite male pitchers aged 16-21 years were recruited. Sixteen pitchers (average age, 17.6 ± 1.6 years; 67% threw right handed) underwent electromyographic analysis. Pitchers threw 5 fastballs at 100% effort from the wind-up with electromyographic analysis of every pitch. Activation of the semitendinosus and biceps femoris in both legs was compared within pitchers and between pitchers. RESULTS: Hamstring activity was higher in the drive leg than in the landing leg during each phase and in sum, although the difference was significant only during the double support phase (P = .021). On within-pitcher analysis, 10 of 16 pitchers had significantly more sum hamstring activity in the drive leg than in the landing leg, while only 4 of 16 had more activity in the landing leg (P = .043). CONCLUSION: During the baseball pitch, muscle activity of the semitendinosus was higher in the drive leg than in the landing leg in most pitchers. Surgeons performing UCLR using hamstring autograft should consider harvesting the graft from the pitcher's landing leg to minimize disruption to the athlete's pitching motion.

Muscle soreness and delayed-onset muscle soreness.

Immediate and delayed-onset muscle soreness differ mainly in chronology of presentation. Both conditions share the same quality of pain, eliciting and relieving activities and a varying degree of functional deficits. There is no single mechanism for muscle soreness; instead, it is a culmination of 6 different mechanisms. The developing pathway of DOMS begins with microtrauma to muscles and then surrounding connective tissues. Microtrauma is then followed by an inflammatory process and subsequent shifts of fluid and electrolytes. Throughout the progression of these events, muscle spasms may be present, exacerbating the overall condition. There are a multitude of modalities to manage the associated symptoms of immediate soreness and DOMS. Outcomes of each modality seem to be as diverse as the modalities themselves. The judicious use of NSAIDs and continued exercise are suggested to be the most reliable methods and recommended. This review article and each study cited, however, represent just one part of the clinician's decisionmaking process. Careful affirmation of temporary deficits from muscle soreness is not to be taken lightly, nor is the advisement and medical management of muscle soreness prescribed by the clinician.