Unaccustomed eccentric exercise has a profound impact on muscle structure and function. However, it is not known whether associated microvascular dysfunction disrupts the matching of O2 delivery (Qo2) to O2 utilization (Vo2). Near-infrared spectroscopy (NIRS) was used to test the hypothesis that eccentric exercise-induced muscle damage would elevate the muscle Qo2:Vo2 ratio during severe-intensity exercise while preserving the speed of the Vo2 kinetics at exercise onset. Nine physically active men completed "step" tests to severe-intensity exercise from an unloaded baseline on a cycle ergometer before (Pre) and 48 h after (Post) eccentric exercise (100 squats with a load corresponding to 70% of body mass). NIRS and breath-by-breath pulmonary Vo2 were measured continuously during the exercise tests and subsequently modeled using standard nonlinear regression techniques. There were no changes in phase II pulmonary Vo2 kinetics following the onset of exercise (time constant: Pre, 25 +/- 4 s; Post, 24 +/- 2 s; amplitude: Pre, 2.36 +/- 0.23 l/min; Post, 2.37 +/- 0.23 l/min; all P > 0.05). However, the primary (Pre, 14 +/- 3 s; Post, 19 +/- 3 s) and overall (Pre, 16 +/- 4 s; Post, 21 +/- 4 s) mean response time of the [HHb] response was significantly slower following eccentric exercise (P < 0.05). The slower [HHb] kinetics observed following eccentric exercise is consistent with an increased Qo2:Vo2 ratio during transitions to severe-intensity exercise. We propose that unchanged primary phase Vo2 kinetics are associated with an elevated Qo2:Vo2 ratio that preserves blood-myocyte O2 flux.

This study examined the effect of exercise-induced muscle damage (EIMD) on ventilatory and perceived exertion responses to cycle exercise. Ten healthy, physically active men cycled for 6 min at moderate intensity and to exhaustion at severe intensity before and 48 h after eccentric exercise (100 squats with a load corresponding to 70% of body mass). Changes in ventilation and ratings of perceived exertion (RPE) were calculated for each individual and expressed against time (moderate and severe exercise) and as a percentage of time to exhaustion (severe exercise). Ventilation increased during moderate exercise at 48 h V(E); 34.5 +/- 5.0 to 36.3 +/- 3.8 l min(-1), P < 0.05) but increases in RPE were not significant. During severe exercise at 48 h, time to exhaustion (TTE) was reduced and V(E) (87.1 +/- 14.1 to 93.8 +/- 11.7 l min(-1)) and RPE (15.5 +/- 1.3 to 16.1 +/- 1.4) were elevated (P < 0.05). When expressed as a percentage of TTE, the differences in ventilation and RPE values disappeared. Findings indicate that the augmented ventilatory response to cycle exercise following EIMD may be an important cue in informing effort perception during high-intensity exercise but not during moderate-intensity exercise.

The study examined which of a number of different magnetic resonance (MR) methods were sensitive to detecting muscle damage induced by eccentric exercise. Seventeen healthy, physically active participants, with muscle damage confirmed by non-MR methods were tested 24 h after performing eccentric exercise. Techniques investigated whether damage could be detected within the quadriceps muscle as a whole, and individually within the rectus femoris, vastus lateralis (VL), vastus medialis (VM), and vastus intermedius (VI). Relative to baseline values, significant changes were seen in leg and muscle cross-sectional areas and volumes and the resting inorganic phosphate concentration. Significant time effects over all muscles were also seen in the transverse relaxation time (T2) and apparent diffusion coefficient (ADC) values, with individually significant changes seen in the VL, VM, and VI for T2 and in the VI for ADC. A significant correlation was found between muscle volume and the average T2 change (r = 0.59) but not between T2 and ADC or Pi alterations. There were no significant time effects over all muscles for magnetization transfer contrast images, for baseline pH, phosphocreatine (PCr), phosphodiester, or ATP metabolite concentrations or the time constant describing the rate of PCr recovery following exercise.

We used ³¹P-magnetic resonance spectroscopy to test the hypothesis that exercise-induced muscle damage (EIMD) alters the muscle metabolic response to dynamic exercise, and that this contributes to the observed reduction in exercise tolerance following EIMD in humans. Ten healthy, physically active men performed incremental knee extensor exercise inside the bore of a whole body 1.5-T superconducting magnet before (pre) and 48 h after (post) performing 100 squats with a load corresponding to 70% of body mass. There were significant changes in all markers of muscle damage [perceived muscle soreness, creatine kinase activity (434% increase at 24 h), and isokinetic peak torque (16% decrease at 24 h)] following eccentric exercise. Muscle phosphocreatine concentration ([PCr]) and pH values during incremental exercise were not different pre- and post-EIMD (P > 0.05). However, resting inorganic phosphate concentration ([P(i)]; pre: 4.7 ± 0.8; post: 6.7 ± 1.7 mM; P < 0.01) and, consequently, [P(i)]/[PCr] values (pre: 0.12 ± 0.02; post: 0.18 ± 0.05; P < 0.01) were significantly elevated following EIMD. These mean differences were maintained during incremental exercise (P < 0.05). Time to exhaustion was significantly reduced following EIMD (519 ± 56 and 459 ± 63 s, pre- and post-EIMD, respectively, P < 0.001). End-exercise pH (pre: 6.75 ± 0.04; post: 6.83 ± 0.04; P < 0.05) and [PCr] (pre: 7.2 ± 1.7; post: 14.5 ± 2.1 mM; P < 0.01) were higher, but end-exercise [P(i)] was not significantly different (pre: 19.7 ± 1.9; post: 21.1 ± 2.6 mM, P > 0.05) following EIMD. The results indicate that alterations in phosphate metabolism, specifically the elevated [P(i)] at rest and throughout exercise, may contribute to the reduced exercise tolerance observed following EIMD.

We tested the hypothesis that exercise-induced muscle damage would increase the ventilatory (V(E)) response to incremental/ramp cycle exercise (lower the gas exchange threshold) without altering the blood lactate profile, thereby dissociating the gas exchange and lactate thresholds. Ten physically active men completed maximal incremental cycle tests before (pre) and 48 h after (post) performing eccentric exercise comprising 100 squats. Pulmonary gas exchange was measured breath-by-breath and fingertip blood sampled at 1-min intervals for determination of blood lactate concentration. The gas exchange threshold occurred at a lower work rate (pre: 136 ± 27 W; post: 105 ± 19 W; P < 0.05) and oxygen uptake (VO(2)) (pre: 1.58 ± 0.26 litres · min(-1); post: 1.41 ± 0.14 litres · min(-1); P < 0.05) after eccentric exercise. However, the lactate threshold occurred at a similar work rate (pre: 161 ± 19 W; post: 158 ± 22 W; P > 0.05) and VO(2) (pre: 1.90 ± 0.20 litres · min(-1); post: 1.88 ± 0.15 litres · min(-1); P > 0.05) after eccentric exercise. These findings demonstrate that exercise-induced muscle damage dissociates the V(E) response to incremental/ramp exercise from the blood lactate response, indicating that V(E) may be controlled by additional or altered neurogenic stimuli following eccentric exercise. Thus, due consideration of prior eccentric exercise should be made when using the gas exchange threshold to provide a non-invasive estimation of the lactate threshold.