Concurrent training is defined as simultaneously incorporating both resistance and endurance exercise within a periodized training regime. Despite the potential additive benefits of combining these divergent exercise modes with regards to disease prevention and athletic performance, current evidence suggests that this approach may attenuate gains in muscle mass, strength, and power compared with undertaking resistance training alone. This has been variously described as the interference effect or concurrent training effect. In recent years, understanding of the molecular mechanisms mediating training adaptation in skeletal muscle has emerged and provided potential mechanistic insight into the concurrent training effect. Although it appears that various molecular signaling responses induced in skeletal muscle by endurance exercise can inhibit pathways regulating protein synthesis and stimulate protein breakdown, human studies to date have not observed such molecular 'interference' following acute concurrent exercise that might explain compromised muscle hypertrophy following concurrent training. However, given the multitude of potential concurrent training variables and the limitations of existing evidence, the potential roles of individual training variables in acute and chronic interference are not fully elucidated. The present review explores current evidence for the molecular basis of the specificity of training adaptation and the concurrent interference phenomenon. Additionally, insights provided by molecular and performance-based concurrent training studies regarding the role of individual training variables (i.e., within-session exercise order, between-mode recovery, endurance training volume, intensity, and modality) in the concurrent interference effect are discussed, along with the limitations of our current understanding of this complex paradigm.

Hamstring strain injuries are amongst the most common and problematic injuries in a wide range of sports that involve high speed running. The comparatively high rate of hamstring injury recurrence is arguably the most concerning aspect of these injuries. A number of modifiable and nonmodifiable risk factors are proposed to predispose athletes to hamstring strains. Potentially, the persistence of risk factors and the development of maladaptations following injury may explain injury recurrence. Here, the role of neuromuscular inhibition following injury is discussed as a potential mechanism for several maladaptations associated with hamstring re-injury. These maladaptations include eccentric hamstring weakness, selective hamstring atrophy and shifts in the knee flexor torque-joint angle relationship. Current evidence indicates that athletes return to competition after hamstring injury having developed maladaptations that predispose them to further injury. When rehabilitating athletes to return to competition following hamstring strain injury, the role of neuromuscular inhibition in re-injury should be considered.

We determined the effects of cold water immersion (CWI) on long-term adaptations and post-exercise molecular responses in skeletal muscle before and after resistance training. Sixteen men (22.9 ± 4.6 y; 85.1 ± 17.9 kg; mean ± SD) performed resistance training (3 day/wk) for 7 wk, with each session followed by either CWI [15 min at 10°C, CWI (COLD) group, n = 8] or passive recovery (15 min at 23°C, control group, n = 8). Exercise performance [one-repetition maximum (1-RM) leg press and bench press, countermovement jump, squat jump, and ballistic push-up], body composition (dual X-ray absorptiometry), and post-exercise (i.e., +1 and +48 h) molecular responses were assessed before and after training. Improvements in 1-RM leg press were similar between groups [130 ± 69 kg, pooled effect size (ES): 1.53 ± 90% confidence interval (CI) 0.49], whereas increases in type II muscle fiber cross-sectional area were attenuated with CWI (−1,959 ± 1,675 µM2 ; ES: −1.37 ± 0.99). Post-exercise mechanistic target of rapamycin complex 1 signaling (rps6 phosphorylation) was blunted for COLD at post-training (POST) +1 h (−0.4-fold, ES: −0.69 ± 0.86) and POST +48 h (−0.2-fold, ES: −1.33 ± 0.82), whereas basal protein degradation markers (FOX-O1 protein content) were increased (1.3-fold, ES: 2.17 ± 2.22). Training-induced increases in heat shock protein (HSP) 27 protein content were attenuated for COLD (−0.8-fold, ES: −0.94 ± 0.82), which also reduced total HSP72 protein content (−0.7-fold, ES: −0.79 ± 0.57). CWI blunted resistance training-induced muscle fiber hypertrophy, but not maximal strength, potentially via reduced skeletal muscle protein anabolism and increased catabolism. Post-exercise CWI should therefore be avoided if muscle hypertrophy is desired. NEW & NOTEWORTHY This study adds to existing evidence that post-exercise cold water immersion attenuates muscle fiber growth with resistance training, which is potentially mediated by attenuated post-exercise increases in markers of skeletal muscle anabolism coupled with increased catabolism and suggests that blunted muscle fiber growth with cold water immersion does not necessarily translate to impaired strength development.

We determined the effect of concurrent training incorporating either high-intensity interval training (HIT) or moderate-intensity continuous training (MICT) on maximal strength, counter-movement jump (CMJ) performance, and body composition adaptations, compared with single-mode resistance training (RT). Twenty-three recreationally-active males (mean ± SD: age, 29.6 ± 5.5 y; trueV˙O2peak, 44 ± 11 mL kg−1·min−1) underwent 8 weeks (3 sessions·wk−1) of either: (1) HIT combined with RT (HIT+RT group, n = 8), (2) work-matched MICT combined with RT (MICT+RT group, n = 7), or (3) RT performed alone (RT group, n = 8). Measures of aerobic capacity, maximal (1-RM) strength, CMJ performance and body composition (DXA) were obtained before (PRE), mid-way (MID), and after (POST) training. Maximal (one-repetition maximum [1-RM]) leg press strength was improved from PRE to POST for RT (mean change ± 90% confidence interval; 38.5 ± 8.5%; effect size [ES] ± 90% confidence interval; 1.26 ± 0.24; P < 0.001), HIT+RT (28.7 ± 5.3%; ES, 1.17 ± 0.19; P < 0.001), and MICT+RT (27.5 ± 4.6%, ES, 0.81 ± 0.12; P < 0.001); however, the magnitude of this change was greater for RT vs. both HIT+RT (7.4 ± 8.7%; ES, 0.40 ± 0.40) and MICT+RT (8.2 ± 9.9%; ES, 0.60 ± 0.45). There were no substantial between-group differences in 1-RM bench press strength gain. RT induced greater changes in peak CMJ force vs. HIT+RT (6.8 ± 4.5%; ES, 0.41 ± 0.28) and MICT+RT (9.9 ± 11.2%; ES, 0.54 ± 0.65), and greater improvements in maximal CMJ rate of force development (RFD) vs. HIT+RT (24.1 ± 26.1%; ES, 0.72 ± 0.88). Lower-body lean mass was similarly increased for RT (4.1 ± 2.0%; ES; 0.33 ± 0.16; P = 0.023) and MICT+RT (3.6 ± 2.4%; ES; 0.45 ± 0.30; P = 0.052); however, this change was attenuated for HIT+RT (1.8 ± 1.6%; ES; 0.13 ± 0.12; P = 0.069). We conclude that concurrent training incorporating either HIT or work-matched MICT similarly attenuates improvements in maximal lower-body strength and indices of CMJ performance compared with RT performed alone. This suggests endurance training intensity is not a critical mediator of interference to maximal strength gain during short-term concurrent training.

Fyfe JJ, Bishop DJ, Zacharewicz E, Russell AP, Stepto NK. Concurrent exercise incorporating high-intensity interval or continuous training modulates mTORC1 signaling and microRNA expression in human skeletal muscle. Am J Physiol Regul Integr Comp Physiol 310: R1297-R1311, 2016. First published April 13, 2016 doi:10.1152/ajpregu.00479.2015.-We compared the effects of concurrent exercise, incorporating either high-intensity interval training (HIT) or moderate-intensity continuous training (MICT), on mechanistic target of rapamycin complex 1 (mTORC1) signaling and microRNA expression in skeletal muscle, relative to resistance exercise (RE) alone. Eight males (mean Ϯ SD: age, 27 Ϯ 4 yr; V O2 peak, 45.7 Ϯ 9 ml·kg Ϫ1 ·min Ϫ1 ) performed three experimental trials in a randomized order: 1) RE (8 ϫ 5 leg press repetitions at 80% 1-repetition maximum) performed alone and RE preceded by either 2) HIT cycling [10 ϫ 2 min at 120% lactate threshold (LT); HIT ϩ RE] or 3) work-matched MICT cycling (30 min at 80% LT; MICT ϩ RE). Vastus lateralis muscle biopsies were obtained immediately before RE, either without (REST) or with (POST) preceding endurance exercise and ϩ1 h (RE ϩ 1 h) and ϩ3 h (RE ϩ 3 h) after RE. Prior HIT and MICT similarly reduced muscle glycogen content and increased ACC Ser79 and p70S6K Thr389 phosphorylation before subsequent RE (i.e., at POST). Compared with MICT, HIT induced greater mTOR Ser2448 and rps6 Ser235/236 phosphorylation at POST. REinduced increases in p70S6K and rps6 phosphorylation were not influenced by prior HIT or MICT; however, mTOR phosphorylation was reduced at RE ϩ 1 h for MICT ϩ RE vs. both HIT ϩ RE and RE. Expression of miR-133a, miR-378, and miR-486 was reduced at RE ϩ 1 h for HIT ϩ RE vs. both MICT ϩ RE and RE. Postexercise mTORC1 signaling following RE is therefore not compromised by prior HIT or MICT, and concurrent exercise incorporating HIT, but not MICT, reduces postexercise expression of miRNAs implicated in skeletal muscle adaptation to RE. concurrent training; interference; exercise intensity; high-intensity interval training; continuous training INCORPORATING BOTH RESISTANCE (RE) and endurance exercise into a periodized training program is termed concurrent training (56). Compared with undertaking RE alone, concurrent training attenuates skeletal muscle hypertrophy and maximal strength development in some (10,19,33,48,53), but not all (5,58,63,75,76), studies. Given that skeletal muscle mass plays an important role in overall metabolic health (87), and many athletes require elements of strength and muscle hypertrophy, concomitantly with a high aerobic capacity (47), minimizing interference during concurrent training has implications for optimizing both health and performance outcomes.