Many exercise models have demonstrated associations between eccentric muscle actions and muscle damage. However, the magnitude of muscle damage varies among the models. It appears that responses to eccentric exercise are different between leg and arm muscles but this has not been systematically clarified. This study compared leg and arm eccentric exercises of the same relative intensity for indices of muscle damage. Eleven healthy untrained males [Age: 21.2 (1.0) years, Height: 179.4 (3.0) cm, Weight: 78.4 (3.1) kg] performed a sub-maximal eccentric exercise of the knee extensors (LEGS) and the elbow flexors (ARMS), separately. Both LEGS and ARMS consisted of six sets of 12 repetitions with an intensity corresponding to 75% of the predetermined maximal eccentric peak torque (EPT) of each muscle. Range of motion (ROM), delayed onset muscle soreness (DOMS), serum creatine kinase (CK) and lactate dehydrogenase (LDH) activities, myoglobin (Mb) concentration, and muscle strength [EPT and isometric peak torque (IPT)] were assessed before and 24, 48, 72, and 96 h following exercise. Significant (P < 0.05) changes in DOMS and ROM were observed up to 96 h after both exercise bouts, and the magnitude of the change was similar between LEGS and ARMS. Increases in CK and Mb were significantly (P < 0.05) larger after ARMS than LEGS at 72 and 96 h post-exercise. EPT and IPT were significantly (P < 0.05) lower than the baseline up to 96 h post-exercise for ARMS but were fully recovered by 96 h post-exercise for LEGS. Decreases in muscle strength were significantly (p < 0.05) larger following ARMS than LEGS at 48, 72, and 96 h post-exercise for EPT, and from 24 h to 96 h post-exercise for IPT. These results suggest that the magnitude of muscle damage is greater and the recovery of muscle function was slower after eccentric exercise of arm elbow flexors than the knee extensors.

The objectives of the present investigation were to study the inflammatory and performance responses after an acute bout of intense plyometric exercise during a prolonged recovery period. Participants were randomly assigned to either an experimental group (P, n = 12) that performed intense plyometric exercises or a control group (C, n = 12) that rested. The delayed onset of muscle soreness (DOMS), knee range of motion (KROM), creatine kinase (CK) and lactate dehydrogenase (LDH) activities, white blood cell count, C reactive protein (CRP), uric acid (UA), cortisol, testosterone, IL-6, IL-1b strength (isometric and isokinetic), and countermovement (CMJ) and static (SJ) jumping performance were measured at rest, immediately postexercise and at 24, 48, 72, 96, and 120 hours of recovery. Lactate was measured at rest and postexercise. Strength remained unchanged throughout recovery, but CMJ and SJ declined (p < 0.05) by 8-20%. P induced a marked rise in DOMS, CK, and LDH (peaked 24-48 hours postexercise) and a KROM decline. An acute-phase inflammatory response consisting of leukocytosis (postexercise and at 24 hours), an IL-6, IL-1b, CRP, and cortisol elevation (during the first 24 hours of recovery) and a delayed increase of UA (peaked at 48 hours) and testosterone (peaked at 72 hours) was observed in P. The results of this investigation indicate that performing an acute bout of intense plyometric exercise may induce a short-term muscle damage and marked but transient inflammatory responses. Jumping performance seems to deteriorate for as long as 72 hours postexercise, whereas strength appears to remain unchanged. The acute-phase inflammatory response after a plyometric exercise protocol appears to follow the same pattern as in other exercise models. These results clearly indicate the need of sufficient recovery between successive plyometric exercise training sessions.

The aim of the present study was to examine the effect of acute plyometric exercise on indices of muscle damage and collagen breakdown. Nine untrained men performed an intense bout of plyometric jumping exercises (experimental group) and nine men remained at rest (control group). Seven days before and 24, 48, and 72 hours after plyometric exercise or rest, several physiological and biochemical indices of muscle damage and two biochemical indices of collagen damage were determined. No significant changes in concentric and eccentric peak torque of knee extensors and flexors or flexion and extension range of motion were found after the plyometric exercise. Delayed-onset muscle soreness increased 48 hours after exercise. Creatine kinase increased 48 and 72 hours post exercise, whereas lactate dehydrogenase increased 24, 48, and 72 hours post exercise. Serum hydroxyproline increased 24 hours post exercise, peaked at 48 hours, and remained elevated up to 72 hours post exercise. Hydroxylysine (which was measured only before exercise and at 48 hours) was found increased 48 hours post exercise. No differences were found in any physiological or biochemical index in the control group. Intense plyometric exercise increased muscle damage, delayed-onset muscle soreness, and serum indices of collagen breakdown without a concomitant decrease in the functional capacity of muscles. Hydroxyproline and hydroxylysine levels in serum seem promising measures for describing exercise-induced collagen degradation. Coaches need to keep in mind that by using plyometric activities, despite the increased muscle damage and collagen turnover that follow, it is not necessarily accompanied by decreases in skeletal muscle capacity.

Although low levels of reactive oxygen species (ROS) are beneficial for the organism ensuring normal cell and vascular function, the overproduction of ROS and increased oxidative stress levels play a significant role in the onset and progression of cardiovascular diseases (CVDs). This paper aims at providing a thorough review of the available literature investigating the effects of acute and chronic exercise training and detraining on redox regulation, in the context of CVDs. An acute bout of either cardiovascular or resistance exercise training induces a transient oxidative stress and inflammatory response accompanied by reduced antioxidant capacity and enhanced oxidative damage. There is evidence showing that these responses to exercise are proportional to exercise intensity and inversely related to an individual's physical conditioning status. However, when chronically performed, both types of exercise amplify the antioxidant defense mechanism, reduce oxidative stress and preserve redox status. On the other hand, detraining results in maladaptations within a time-frame that depends on the exercise training intensity and mode, as high-intensity training is superior to low-intensity and resistance training is superior to cardiovascular training in preserving exercise-induced adaptations during detraining periods. Collectively, these findings suggest that exercise training, either cardiovascular or resistance or even a combination of them, is a promising, safe and efficient tool in the prevention and treatment of CVDs.

We investigated the effects of a single bout of aerobic and resistance exercise of similar relative intensity and duration on resting energy expenditure (REE) and substrate utilisation. Ten young healthy males volunteered [age 22 (1.8) years, weight 76 (7.9) kg, height 176 (4.1) cm, percentage body fat 10.5 (4.0)%; mean (SEM)]. They randomly underwent three conditions in which they either lifted weights for 60 min at 70-75% of 1-RM (WL), ran for 60 min at 70-75% of maximal oxygen intake (R) or did not exercise (C). REE and substrate utilisation, determined via respiratory exchange ratio (R), were measured prior to exercise, and 10, 24, 48 and 72 h post-exercise. It was revealed that REE was significantly elevated (P<0.05) 10 and 24 h after the end of WL [2,124 (78) .04), respectively]. Creatine kinase was significantly elevated (P<0.05) 24 h after both WL and R, whereas delayed onset muscle soreness became significantly elevated (P<0.05) 24 h after only WL. There were no significant changes for any treatment in thyroid hormones (T 3 and T 4 ). These results suggest that a single bout of either WL or R exercise, characterised by the same relative intensity and duration, increase REE and fat oxidation for at least 24 h post-exercise.