In 2014, 6 collegiate swimmers were hospitalized for symptomatic exertional rhabdomyolysis.
To serially monitor and assess relationships between skeletal muscle membrane disruption, upper body soreness (UBS) and lower body soreness (LBS), and stress during the first 6 weeks (timepoints) of preseason training in collegiate male and female swimmers.
Prospective observational study.
Upper and lower body soreness rating (0-10); testosterone (T), cortisol (C), and T/C ratio.
Main Outcome Measures:
Creatine kinase (CK) and myoglobin (over time) versus independent variables.
Weekly training load consisted of ∼87% swimming, ∼5% running, and ∼8% weight training, which increased from 15.8 hours to 20.5 total training hours per week over the first 6 weeks of training. Muscle damage in collegiate swimmers was modest and peaked after the first week of training (week 2) for men (CK = 438 ± 259 U/L; P < 0.0001; r2 = 0.28; myoglobin = 47 ± 18 ng/mL; P = 0.001; r2 = 0.22) and women (CK = 446 ± 723 U/L; P < 0.01; r2 = 0.13; myoglobin = 63 ± 140 ng/mL, not significant) with high variability. Data were presented as peak mean ± SD, significant P value, and r2 from repeated-measures analysis of variance. A temporal disconnect was noted between muscle damage and UBS, which peaked at week 5 in both men (5 ± 2; P < 0.0001; r2 = 0.44) and women (6 ± 2; P < 0.0001; r2 = 0.57). The serum cortisol level decreased over time, which peaked at week 1 (baseline) in men (15 ± 6 μg/dL; P = 0.0004; r2 = 0.38) and women (19 ± 10 μg/dL; P < 0.0001; r2 = 0.49). The testosterone level remained unchanged, which promoted an anabolic hormonal environment that peaked at week 6 (increasing T/C ratio) in men (58 ± 32; P = 0.0003; r2 = 0.31) and women (4 ± 3; P = 0.04; r2 = 0.18) despite gradual increases in training and soreness.
Muscle soreness does not parallel muscle membrane disruption. A 1-week “transition” period is required for muscles to adapt to intense/novel training.