The 'repeated bout effect'(RBE) is an adaptation whereby a single eccentric (ECC) exercise session protects against muscle damage during subsequent ECC exercise bouts and is characterized by faster strength recovery and a reduction in soreness and inflammation. The purpose was to determine if the protective capacity of the RBE is greater when both bouts of ECC exercise are performed at the same compared to a different velocity of contraction as well as at a fast or slow velocity. Thirty-one right handed participants were randomly assigned to perform an initial unilateral bout of either fast (180°/s) or slow (30°/s) maximal isokinetic ECC elbow flexion. Three weeks later 16 participants completed a repeated bout of ECC exercise at the same velocity as the initial bout (SAME)(FAST-FAST[n=8] and SLOW-SLOW[n=8]), while 15 participants completed a bout at the corresponding different velocity (DIFF) (FAST-SLOW[n=8] and SLOW-FAST[n=7]). Elbow flexor function and damage was measured prior to, immediately after, and at 24, 48, and 72 hours post exercise. Dependant variables included maximal voluntary contraction (MVC) isometric strength (Dynamometer), muscle thickness (MT; Ultrasound), delayed onset muscle soreness (DOMS; Visual Analog Scale), biceps and triceps electromyography (EMG), percent activation (Interpolated twitch), and twitch torque. There were no group differences for height, weight, training experience, or total work performed during the ECC bouts (p>0.05). After the repeated bout, there was a significant reduction in MVC strength, MT, and DOMS at 24, 48, and 72 hours, pooled across participants (p<0.05). After the repeated bout, MVC strength recovered faster only for the SAME group. There were no differences between groups for MT, DOMS, EMG, ITT, and TT. The analysis revealed neither fast nor slow contractions offered greater protection against muscle damage when the repeated bout was not completed at the same velocity. Since a faster recovery of strength is velocity specific this suggests there may be a neural contribution to the repeated bout effect.

The 'repeated bout effect'(RBE) is an adaptation whereby a single eccentric (ECC) exercise session protects against muscle damage during subsequent ECC exercise bouts and is characterized by faster strength recovery and a reduction in soreness and inflammation. The purpose was to determine if the protective capacity of the RBE is greater when both bouts of ECC exercise are performed at the same compared to a different velocity of contraction as well as at a fast or slow velocity. Thirty-one right handed participants were randomly assigned to perform an initial unilateral bout of either fast (180°/s) or slow (30°/s) maximal isokinetic ECC elbow flexion. Three weeks later 16 participants completed a repeated bout of ECC exercise at the same velocity as the initial bout (SAME)(FAST-FAST[n=8] and SLOW-SLOW[n=8]), while 15 participants completed a bout at the corresponding different velocity (DIFF) (FAST-SLOW[n=8] and SLOW-FAST[n=7]). Elbow flexor function and damage was measured prior to, immediately after, and at 24, 48, and 72 hours post exercise. Dependant variables included maximal voluntary contraction (MVC) isometric strength (Dynamometer), muscle thickness (MT; Ultrasound), delayed onset muscle soreness (DOMS; Visual Analog Scale), biceps and triceps electromyography (EMG), percent activation (Interpolated twitch), and twitch torque. There were no group differences for height, weight, training experience, or total work performed during the ECC bouts (p>0.05). After the repeated bout, there was a significant reduction in MVC strength, MT, and DOMS at 24, 48, and 72 hours, pooled across participants (p<0.05). After the repeated bout, MVC strength recovered faster only for the SAME group. There were no differences between groups for MT, DOMS, EMG, ITT, and TT. The analysis revealed neither fast nor slow contractions offered greater protection against muscle damage when the repeated bout was not completed at the same velocity. Since a faster recovery of strength is velocity specific this suggests there may be a neural contribution to the repeated bout effect.

Delayed Onset Muscle Soreness (DOMS) is a common response to activities involving lengthening contractions. Muscle inflammation is associated with DOMS and may play an integral role in protecting a muscle from damage and soreness in response to subsequent bouts of lengthening contractions. Research in animals has shown that prior exposure to passive stretching and isometric contractions of a muscle resulting in muscle inflammation attenuates the muscle inflammatory response following subsequent bouts of lengthening contractions. The purpose of this study was to determine whether passive stretching and isometric contractions in humans would reduce DOMS following a typical bout of resistance exercise. METHODS: Thirty untrained male subjects were assigned to a control (C), stretching (S) or isometric (I) contraction group (n=10/group). In the week prior to the typical resistance training bout subjects in S and I were exposed to 3 separate sessions involving 5 minutes of passive stretching or maximal isometric contractions, respectively. Passive and active soreness, thigh girth, and relaxed knee angle were assessed prior to intervention and on days 1, 2, 4, and 8 following the bout of resistance exercise. RESULTS: Passive and active muscle soreness increased similarly in all groups. However, active soreness returned higher values than passive soreness at several time points following resistance exercise. Peak soreness occurred at 48h post exercise. Thigh girth and relaxed knee angle reached their highest values at 5 minutes following resistance exercise however there were no differences between the groups. CONCLUSIONS: The present study demonstrates that a typical bout of resistance exercise is sufficient to cause measurable levels of DOMS in untrained subjects and that subjects are more sensitive to active measures of DOMS compared to a passive assessment. Nevertheless the passive stretching and isometric contraction interventions did nothing to reduce DOMS in the current subjects.

Yes / The ability of skeletal muscle to adapt to eccentric contractions has been suggested to be blunted in older muscle. If eccentric exercise is to be a safe and efficient training mode for older adults, preclinical studies need to establish if older muscle can effectively adapt and if not, determine the molecular signatures that are causing this impairment. The purpose of this study was to quantify the extent age impacts functional adaptations of muscle and identify genetic signatures associated with adaptation (or lack thereof). The anterior crural muscles of young (4 mo) and older (28 mo) female mice performed repeated bouts of eccentric contractions in vivo (50 contractions/wk for 5 wk) and isometric torque was measured across the initial and final bouts. Transcriptomics was completed by RNA-sequencing 1 wk following the fifth bout to identify common and differentially regulated genes. When torques post eccentric contractions were compared after the first and fifth bouts, young muscle exhibited a robust ability to adapt, increasing isometric torque 20%-36%, whereas isometric torque of older muscle decreased up to 18% (P ≤ 0.047). Using differential gene expression, young and older muscles shared some common transcriptional changes in response to eccentric exercise training, whereas other transcripts appeared to be age dependent. That is, the ability to express particular genes after repeated bouts of eccentric contractions was not the same between ages. These molecular signatures may reveal, in part, why older muscles do not appear to be as adaptive to exercise training as young muscles.NEW & NOTEWORTHY The ability to adapt to exercise training may help prevent and combat sarcopenia. Here, we demonstrate young mouse muscles get stronger whereas older mouse muscles become weaker after repeated bouts of eccentric contractions, and that numerous genes were differentially expressed between age groups following training. These results highlight that molecular and functional plasticity is not fixed in skeletal muscle with advancing age, and the ability to handle or cope with physical stress may be impaired. / The full-text of this article will be released for public view at the end of the publisher embargo on 1 Nov 2024.

This study determined if insulin resistance (IR), induced by an acute bout of eccentrically-biased contractions that resulted in muscle injury, was attenuated following a repeated bout of contractions. Female subjects (n = 10, age 24.7 ± 3.0 yr, weight 64.9 ± 7.4 kg, height 1.67 ± 0.02 m, body fat 29.1 ± 1.9 %) performed two 30 minute bouts of downhill treadmill running (DTR 1 and DTR 2, -12 % grade, 8.0 mph) separated by 14 days. Oral glucose tolerance tests (OGTT) were administered at baseline and 48 hours following DTR 1 and DTR 2, with IR assessed by calculation of insulin and glucose areas under the curve (AUC). Maximum isometric quadriceps strength (MVC), muscle soreness (SOR), and serum creatine kinase (CK) were assessed pre-, immediately post-, and 48 hours post-DTR 1 and DTR 2 to determine the presence of muscle injury. Compared to baseline OGTT, insulin and glucose AUC (37.6 ± 8.4 and 21.4 ± 4.7 % increase, respectively), and peak insulin (44.1 ± 5.1 vs. 31.6 ± 4.0 uU·mL-1) and glucose (6.5 ± 0.4 vs. 5.5 ± 0.4 mmol·L-1) were elevated following DTR 1. These same insulin and glucose measures showed no increase above baseline 48 hours following DTR 2 (p > 0.05). MVC was reduced to a greater degree immediately following DTR 1 (16.7 ± 2.6 vs. 8.6 ± 1.2 % decline) and, although demonstrating a significant degree of recovery, remained reduced by 9.4 ± 2.7 % 48 hours following exercise. In contrast, MVC made a full recovery back to baseline values 48 hours after DTR 2. SOR was elevated to a greater degree 48 hours following DTR 1 than after DTR 2 (48.08 ± 6.16 vs. 12.70 ± 3.24 mm). There was a tendency for an attenuated serum CK response 48 hours following DTR 2 (812.8 ± 365.1 vs. 162.5 ± 42.5 U·L-1, p = 0.08). In conclusion, a novel bout of eccentrically-biased contractions resulting in a moderate degree of muscle injury confers a protective effect, whereby a subsequent bout of contractions 14 days later results in complete elimination of the IR observed following the initial bout.

Skeletal muscle is prone to damage from a range of stimuli. The muscle repair process that ensues is complex, involving several phases and requiring the participation of many different cell types. Among the cells involved are various immune cells including neutrophils, macrophages, monocytes, and eosinophils. More recently, T cells were added to this list of immune cells known to participate in effective muscle repair from traumatic injuries in mice. We recently published data showing that T cells also accumulate in human muscle following contraction-induced damage. These data suggested that T cells might be involved an adaptation known as the repeated bout effect that renders muscle protected from future damage after an initial exposure. This document contains research on the role of the immune system, particularly T cells, in the "repeated bout effect."

As contrações excêntricas causam lesão muscular envolvendo a ruptura dos sarcômeros. Todavia, uma sessão repetida de exercício excêntrico acarreta na redução dessa lesão. Esse mecanismo protetor é conhecido como efeito da carga repetida (ECR). Visando contribuir para o melhor entendimento do ECR, em especial, a expressão de genes pró e anti-inflamatórios após o dano promovido pelo exercício excêntrico, camundongos foram submetidos a uma ou duas sessões de exercício. Os músculos sóleos foram avaliados após 24 horas e 3 dias. A análise histológica mostra que houve lesão de fibras dos animais submetidos à 1ª sessão, com atenuação do dano após a 2ª sessão. A expressão gênica das citocinas pró-inflamatórias (TNF-&alpha;, iNOS e IL-1&beta;) e anti-inflamatórias (IL-10, YM1, Fizz-1 e Arginase-1) foi alta em 24 h após a 1ª sessão, e reduziu aos níveis basais em 24 h após a 2ª sessão. Nossos resultados sugerem que a elevação da expressão gênica dessas citocinas no músculo antes da 2ª sessão pode ter contribuído para o ECR. / The eccentric contractions cause muscle injury involving rupture of the sarcomeres, with subsequent activation of proteolysis. However, repeated session of eccentric exercise cause attenuation of this damage. This protective mechanism is known as \"repeated bout effect\" (RBE). In order to contribute to a better understanding of the RBE, in particular, the gene expression of pro and anti-inflammatory after injury induced by eccentric exercise, mice were subjected to one or two sessions of exercise and soleus muscles were evaluated after 24 h or 3 days. Histological analysis shows that there was injury of myofiber from animals subjected to the 1st session, with attenuation of damage after 2nd session. The gene expression of pro-inflammatory (TNF-&alpha;, iNOS and IL-1&beta;) and anti-inflammatory (IL-10, YM1, Fizz-1 and Arginase-1) cytokines was high at 24h after the 1st session, and reduced to baseline levels at 24 h after 2nd session. Our results suggest that the elevated gene expression of these cytokines in muscle before the 2nd session may have contributed to the RBE.

Performance of a series of eccentric contractions produces adverse effects including muscle weakness, delayed onset muscle soreness (DOMS), fluid accumulation and decreased muscle function. The repeated bout effect is a physiological adaptation observed when a single-bout of eccentric exercise protects against muscle damage from subsequent eccentric bouts. Similar to the repeated bout effect, increases in flexibility have been linked to attenuations in acute muscle damage, muscle fatigue and strength loss after eccentric exercise. Purpose: The purpose of this study was to examine the muscle physiological responses to eccentric strength training after first priming the muscles with either a period of static flexibility training or a single intense bout of eccentric exercise performed weeks earlier; and compare these to the responses from eccentric strength training when no prior intervention is administered. Methods: Twenty-five participants were randomly assigned to a flexibility (F) (n=8), a single-bout (SB) (n=9), or a control (C) (n=8) group. The design consisted of two 4-week phases; 1) priming intervention, 2) eccentric training. The priming intervention included static stretching (3x/week; 30mins/day) (F), a single-bout of eccentric exercise (SB) or no priming intervention (C). All groups proceeded to complete eccentric training of the knee flexors using isotonic contractions (%load progressively increased over training period) on a dynamometer following the priming intervention phase. Testing was completed at baseline, post-priming intervention and post-eccentric training, in conjunction with data being collected during the acute eccentric training phase (0hr, 24hr, 48hr; post-bout 1 and 4). Dependent measures included muscle thickness, isometric maximal voluntary contraction (MVC), eccentric and concentric MVC, optimal angle, active range of motion (ROM), passive ROM, maximal power, electromyography (EMG) and delayed onset muscle soreness (DOMS). Results: Acute data during the eccentric training phase revealed a significant reduction in DOMS for both the F and SB groups compared to the C following the first bout of eccentric exercise (p<0.05). The F also had reduced soreness in comparison to both the SB and C post fourth bout of eccentric exercise (p<0.05). The F group demonstrated attenuated loss in isometric strength (post fourth bout) and maximal power (post first bout) during eccentric training compared to the C group (p<0.05). However, there was no significant difference between groups across all dependent variables following the eccentric training phase. Conclusion: This is the first study to directly compare the protective effects observed with static flexibility training to that of a single-bout of eccentric exercise throughout a subsequent eccentric training regime. Although differences in muscle soreness, strength and maximal power occurred during the acute stages of eccentric training, there appeared to be no significant advantage of either protective priming method at the end of eccentric training.