No abstract

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.

This randomized controlled trial examined body mass, body composition, energy balance and performance responses of previously sedentary overweight/obese women to a circuit-type integrated neuromuscular training program with alternative modalities. Forty-nine healthy overweight or class I obese females (36.4±4.4 yrs) were randomly assigned to either a control (N = 21), training (N = 14) or training-detraining (N = 14) group. In weeks 1–20, the training groups trained three times/week using 10–12 whole-body exercises of progressively increased intensity/volume, organized in timed interval circuit form. In weeks 21–40, the training group continued training whereas the training-detraining group not. Heart rate, perceived exertion, blood lactate, exertion, oxygen consumption and excess post-exercise oxygen consumption were measured for one session/phase/person and exercise energy expenditure was calculated. Energy intake, habitual physical activity, resting metabolic rate, body composition, body mass, strength and maximal oxygen consumption were measured at baseline, mid-intervention and post-intervention. A two-way repeated measures ANOVA was used to determine differences between three time points and three groups. In C, VO2max declined (p<0.013) and body fat (p<0.008), waist (p<0.059) and hip (p<0.012) circumferences increased after 40 weeks compared to baseline. Training reduced body mass (6%, p<0.001), body fat (~5.5%, p<0.001) and increased fat-free mass (1.2–3.4%, p<0.05), strength (27.2%, p<0.001) and endurance (26.8%, p<0.001) after a 10-month implementation period using a metabolic overload of only 5–12 metabolic equivalents of task-hours per week. Training induced a long-term negative energy balance during an exercise and a non-exercise day due to an elevation of resting metabolic rate (6%-10%, p<0.05) and exercise-related energy expenditure. Training had an 8% and 94% attrition and attendance rates, respectively. Training-induced gains were attenuated but not lost following a 5-month detraining. A 10-month implementation of a high-intensity interval type training program elicited both endurance and musculoskeletal gains and resulted in a long-term negative energy balance that induced a progressive and sustained reduction of body and fat mass.Trial Registration: ClinicalTrials.gov NCT03134781

The study of exercise-induced muscle damage (EIMD) is of paramount importance not only because it affects athletic performance but also because it is an excellent model to study the mechanisms governing muscle cachexia under various clinical conditions. Although, a large number of studies have investigated EIMD and its associated inflammatory response, several aspects of skeletal muscles responses remain unclear. In the first section of this article, the mechanisms of EIMD are reviewed in an attempt to follow the events that result in functional and structural alterations of skeletal muscle. In the second section, the inflammatory response associated with EIMD is presented with emphasis in leukocyte accumulation through mechanisms that are largely coordinated by pro- and anti-inflammatory cytokines released either by injured muscle itself or other cells. The practical applications of EIMD and the subsequent inflammatory response are discussed with respect to athletic performance. Specifically, the mechanisms leading to performance deterioration and development of muscle soreness are discussed. Emphasis is given to the factors affecting individual responses to EIMD and the resulting interindividual variability to this phenomenon.

beta-Endorphin, a 31-amino-acid peptide, is primarily synthesised in the anterior pituitary gland and cleaved from pro-opiomelanocortin, its larger precursor molecule. beta-Endorphin can be released into the circulation from the pituitary gland or can project into areas of the brain through nerve fibres. Exercise of sufficient intensity and duration has been demonstrated to increase circulating beta-endorphin levels. Previous reviews have presented the background of opioids and exercise and discussed the changes in beta-endorphin levels in response to aerobic and anaerobic exercise. The present review is to update the response of beta-endorphin to exercise. This review suggests that exercise-induced beta-endorphin alterations are related to type of exercise and special populations tested, and may differ in individuals with health problems. Additionally, some of the possible mechanisms which may induce beta-endorphin changes in the circulation include analgesia, lactate or base excess, and metabolic factors. Based on the type of exercise, different mechanisms may be involved in the regulation of beta-endorphin release during exercise.