This study compared muscle-tendon behavior, muscle oxygenation, and muscle activity between eccentric and concentric cycling exercise at the same work output to investigate why metabolic demand is lower during eccentric cycling than with concentric cycling. Eleven untrained men (27.1 ± 7.0 y) performed concentric cycling (CONC) and eccentric cycling (ECC) for 10 min (60 rpm) at 65% of the maximal concentric cycling power output (191 ± 45 W) 4 wk apart. During cycling, oxygen consumption (V̇o₂), heart rate (HR), vastus lateralis (VL) tissue total hemoglobin (tHb), and oxygenation index (TOI) were recorded, and muscle-tendon behavior was assessed using ultrasonography. The surface electromyogram (EMG) was recorded from VL, vastus medialis (VM), rectus femoris (RF), and biceps femoris (BF) muscles, and cycling torque and knee joint angle during each revolution were also recorded. Average V̇o₂ (−65 ± 7%) and HR (−35 ± 9%) were lower and average TOI was greater (16 ± 1%) during ECC than CONC, but tHb was similar between bouts. Positive and negative cycling peak crank torques were greater (32 ± 21 and 48 ± 24%, respectively) during ECC than CONC, but muscle-tendon unit and fascicle and tendinous tissue length changes during pedal revolutions were similar between CONC and ECC. VL, VM, RF, and BF peak EMG amplitudes were smaller (24 ± 15, 22 ± 18, 16 ± 17, and 18 ± 9%, respectively) during ECC than CONC. These results suggest that the lower metabolic cost of eccentric compared with concentric cycling was due mainly to a lower level of muscle activation per torque output. NEW & NOTEWORTHY This study shows that lower oxygen consumption of eccentric compared with concentric cycling at the same workload is explained by lower muscle activity of agonist and antagonist muscles during eccentric compared with during concentric cycling.

Ycling bouts to test the hypothesis that muscle–tendon behavior would be different between bouts and would be associated with the protective effect. Methods Eleven untrained men (27.1 ± 7.0 yr) performed two bouts of eccentric cycling (ECC1 and ECC2) separated by 2 wk for 10 min at 65% of maximal concentric workload (191.9 ± 44.2 W) each. Muscle soreness (by visual analog scale) and maximal voluntary isometric contraction (MVC) torque of the knee extensors were assessed before and 1–2 d after exercise. Using ultrasonography, VL fascicle length and angle changes during cycling were assessed, and tendinous tissue (TT) length changes were estimated. VL EMG amplitude, crank torque, and knee joint angles were measured during cycling. Results Soreness was greater (P < 0.0001) after ECC1 than ECC2, although MVC changes were not different between bouts (P = 0.47). No significant differences in peak EMG amplitude (normalized to EMG during MVC), crank peak torque, or knee angles were evident between bouts. However, fascicle elongation was 16% less during ECC2 than ECC1 (P < 0.01), indicating less fascicle strain in ECC2. Maximum TT length occurred at a smaller knee joint angle during ECC2 than ECC1 (P = 0.055). Conclusion These results suggest that a lesser fascicle elongation and earlier TT elongation were associated with reduced muscle soreness after ECC2 than ECC1; thus, changes in muscle–tendon behavior may be an important mechanism underpinning the protective effect....

Skeletal muscle is the largest tissue in the human body, comprising approximately 40% of body mass. After damage or injury, a healthy skeletal muscle is often fully regenerated; however, with aging and chronic diseases, the regeneration process is usually incomplete, resulting in the formation of fibrotic tissue, infiltration of intermuscular adipose tissue, and loss of muscle mass and strength, leading to a reduction in functional performance and quality of life. Accumulating evidence has shown that omega-3 (n-3) polyunsaturated fatty acids (PUFAs) and their lipid mediators (i.e., oxylipins and endocannabinoids) have the potential to enhance muscle regeneration by positively modulating the local and systemic inflammatory response to muscle injury. This review explores the process of muscle regeneration and how it is affected by acute and chronic inflammatory conditions, focusing on the potential role of n-3 PUFAs and their derivatives as positive modulators of skeletal muscle healing and regeneration.

Purpose: The aim of this review was to (1) characterize the time-course of markers of exercise-induced muscle damage (EIMD) based on the level of maximal voluntary contraction torque loss at 24-48h post-exercise (MVC_loss24-48h), (2) identify factors (e.g., exercise and population characteristics) affecting the level of MVC_loss24-48h, and (3) evaluate the appropriateness of EIMD markers as indicators of MVC_loss24-48h. Methods: Magnitude of change of each EIMD markers was normalized using the standardized mean differences method to compare the results from different studies. Time-course of EIMD markers were characterized according to three levels of MVC_loss24-48h based on a clustering analysis of the 141 studies included. Association between MVC_loss24-48h levels and participant´s characteristics or exercise type/modalities were assessed. Meta-regressions were performed to investigate the associations between MVC_loss24-48h and EIMD markers changes at 96h after exercise. Results: Time-course of EIMD markers recovery differs between levels of MVC_loss24-48h. Training status and exercise type/modality were associated with MVC_loss24-48h level (p<0.05). MVC_loss24-48h was correlated to changes in myoglobin concentration (<6h), jump height (24h) and range of motion (48h) (p<0.001). Conclusion: As the exercise could differently affect markers as function of the EIMD severity (i.e., MVC_loss24-48h levels), different markers should be used as function of the timing of measurement. Mb concentration should be used during the first hours after the exercise (<6h), whereas jump height (24h) and range of motion (48h) could be used as surrogate for maximal voluntary contraction later. Moreover, training status and exercise type/modality could influence the magnitude of MVC_loss24-48h.