Exercise-Induced Muscle Injury Results in Elevations in Aerobic and Anaerobic Metabolism during Submaximal Treadmill Running

Abstract

Exercise-induced muscle injury results in strength reductions, which may require individuals to work at a higher relative intensity to perform a given submaximal exercise. Manifestations of such increased work intensity could include increased VO2, blood lactate concentrations, VE, and VCO2. PURPOSE: To test the hypothesis that exercise-induced muscle injury will result in elevations in both aerobic and anaerobic metabolism during submaximal level treadmill running and to correlate the magnitude of functional reductions with any observed metabolic alterations. METHODS: Male recreational athletes (n = 12) aged 28 ± 6 yrs participated in this study. Subjects performed identical submaximal treadmill protocols 1 d before (STR1) and 2 d after (STR2) a 30-min downhill run. The submaximal running protocol consisted of two 15-min runs (at velocities corresponding to 60% or 75% VO2peak) separated by 10 min rest. Changes in metabolism and injury markers were determined by repeated measures ANOVA and Bonferroni post hoc mean comparisons tests. The alpha level was set at 0.05. RESULTS: The downhill run reduced the quadriceps muscles strength immediately (21 ± 2%) and at 2 d (12 ± 2%). Muscle soreness was increased from pre-injury values of 3 ± 2 mm to 2 d post-injury values of 56 ± 5 mm on a 100 mm scale. CK activity was increased by 55 ± 16% 2 d post-injury. At the 60% VO2peak intensity, VO2, VE, and VCO2 were elevated by 4 ± 1, 12 ± 3, and 5 ± 2% respectively through the first 3 min during STR2 compared to STR1. Mean VE and VCO2 were 9+3 and 3 ± 1 % greater during STR2 at the 60% VO2peak intensity compared to STR1 values. The percent change in blood lactate concentration (pre to post 15 min run) increased by 61 ± 16% during the post-injury 60% run compared to STR1. The magnitude of strength deficit was negatively correlated with the magnitude of change in lactate accumulation at the 60% VO2peak intensity (r = −0.65, p = .03). No significant metabolic alterations occurred from pre- to post-injury at the 75% VO2peak intensity. Although, during the first 3 min of exercise at this intensity VO2 (p = .08) and VE (p = .07) tended to be increased. Mean VE (p = 0.06) was 9 ± 3% greater during STR2 at the 75% VO2peak intensity compared to STR1 values. The percent change in blood lactate accumulation (p = .09) increased by 77 ± 39% during the post-injury run compared to STR1. CONCLUSION: Exercise-induced muscle injury results in a transitory increase in aerobic metabolism and a greater reliance on anaerobic metabolism during submaximal running at 60% VO2peak intensity. The magnitude of strength deficits may be indicative of the degree of elevation of anaerobic metabolism.