Mid Sweden University

As aerobic exercise (AE) may interfere with adaptations to resistance exercise (RE), this study explored acute and chronic responses to consecutive AE (similar to 45 min cycling) and RE (4 X 7 maximal knee extensions) vs. RE only. Ten men performed acute unilateral AE + RE interspersed by 15 min recovery. The contralateral leg was subjected to RE. This exercise paradigm was then implemented in a 5-wk training program. Protein phosphorylation, gene expression, and glycogen content were assessed in biopsies obtained from the vastus lateralis muscle of both legs immediately before and 3 h after acute RE. Quadriceps muscle size and in vivo torque were measured, and muscle samples were analyzed for citrate synthase activity and glycogen concentration, before and after training. Acute AE reduced glycogen content (32%; P < 0.05) and increased (P < 0.05) phosphorylation of AMPK (1.5-fold) and rpS6 (1.3-fold). Phosphorylation of p70S6K and 4E-BP1 remained unchanged. Myostatin gene expression was downregulated after acute AE + RE but not RE. Muscle size showed greater (P < 0.05) increase after AE + RE (6%) than RE (3%) training. Citrate synthase activity (18%) and endurance performance (22%) increased (P < 0.05) after AE + RE but not RE. While training increased (P < 0.05) in vivo muscle strength in both legs, normalized and concentric torque increased after RE only. Thus AE activates AMPK, reduces glycogen stores, and impairs the progression of concentric force, yet muscle hypertrophic responses to chronic RE training appear not to be compromised.

Purpose: This study assessed markers of muscle damage and training adaptations to eccentric-overload flywheel resistance exercise (RE) in men and women. Methods: Dynamic strength (1 RM), jump performance, maximal power at different percentages of 1 RM, and muscle mass in three different portions of the thigh were assessed in 16 men and 16 women before and after 6 weeks (15 sessions) of flywheel supine squat RE training. Plasma creatine kinase (CK) and lactate dehydrogenase (LDH) concentrations were measured before, 24, 48 and 72 h after the first and the last training session. Results: After training, increases in 1 RM were somewhat greater (interaction P < 0.001) in men (25 %) than in women (20 %). Squat and drop jump height and power performance at 50, 60, 70 and 80 % of 1 RM increased after training in both sexes (P < 0.05). Power improvement at 80 % of 1 RM was greater (interaction P < 0.02) in men than women. Muscle mass increased ~5 % in both groups (P < 0.05). CK increased in men after the first training session (P < 0.001), whereas the response in women was unaltered. In both sexes, LDH concentration was greater after the first training session compared with basal values (P < 0.05). After the last session, CK and LDH remained at baseline in both groups. Conclusions: These results suggest that although improvements in maximal strength and power at high loads may be slightly greater for men, eccentric-overload RE training induces comparable and favorable gains in strength, power, and muscle mass in both men and women. Equally important, it appears muscle damage does not interfere with the adaptations triggered by this training paradigm. © 2014 Springer-Verlag Berlin Heidelberg.

Aerobic exercise (AE) may interfere with muscle adaptations induced by resistance exercise (RE). Three experimental campaigns were conducted to explore the influence of AE on molecular, functional and muscular adaptations to acute and chronic RE. Twenty-nine men performed unilateral knee extensor RE preceded by AE (AE+RE). The contralateral leg did RE only. First, the influence of acute AE on muscle molecular responses to RE performed 6 h later was studied. Subsequently, this exercise regimen was implemented over 5 weeks training. The relationships between acute and chronic outcomes were examined and molecular responses to acute exercise were assessed in untrained and trained muscle. Finally, acute and chronic responses to AE+RE, interspersed by only 15 min recovery, were investigated.Phosphorylation of mTOR and p70S6K was greater after AE+RE than after RE. In parallel, myostatin was suppressed for a longer time after AE+RE. These results suggest that AE+RE enhance skeletal muscle anabolic environment more than RE alone (Paper I). After 5 weeks training, improvements in muscle strength and power were similar across legs. However, AE+RE prompted a greater increase in muscle size than RE, suggesting that AE potentiates the hypertrophic stimulus to RE training without altering muscle function progress (Paper II). Consistent with changes in whole-muscle size, AE+RE showed greater anabolic molecular responses than RE. As chronic training blunted this effect, it appears that AE offers a synergistic hypertrophic stimulus to RE only during short-term training (Paper III). Although putative regulators of hypertrophy such as p70S6K, myostatin and PGC-1a4 were examined, no molecular marker correlated with changes in muscle size, strength or power induced by training. Hence, this study challenges the concept that single molecular markers are viable predictors of training-induced muscle adaptations (Paper III–IV). When recovery time between exercise bouts was reduced to 15 min, AE+RE still produced a more substantial increase in muscle size than RE. However, progression of concentric strength was blunted. Thus, while restored muscle function between exercise bouts is a prerequisite for achieving maximal gains in strength and power, incomplete recovery appears not to compromise muscle hypertrophy (Paper V).Collectively, the results suggest that outcomes of AE+RE are impacted by chronic training and time allowed for recovery between exercise modes. Yet, the current study offers no support to the view that AE interferes with muscle hypertrophy induced by RE.

Introduction: A truncated PGC-1 alpha splice variant (PGC-1 alpha 4) has been implicated in the regulation of resistance exercise (RE)-induced muscle hypertrophy, and basal expression levels said to be augmented in response to concurrent aerobic (AE) and RE training.Aim: The current study investigated human muscle truncated and non-truncated PGC-1a transcripts in response to both acute and chronic RE, and with or without preceding AE (AE+RE).Methods: Ten men performed 5 weeks of unilateral AE+RE and RE training.Before (untrained) and after (trained) this intervention, PGC-1a transcripts were assessed in vastus lateralis muscle biopsies obtained before and 3 h after acute RE, with or without preceding AE.Additionally, samples were collected 72 h after the last exercise bout of the training programme.Results: The truncated splice variant increased (P < 0.05) its expression after acute exercise regardless of mode. However, the expression was greater (P < 0.05) after AE+RE than RE. Other PGC-1a transcripts showed similar response. Truncated transcripts originated from both the alternative and proximal promoter, and AE+RE increasedPGC-1 alpha expression from both promoter sites. RE induced transcripts from the alternative promoter only. PGC-1 alpha expressions after acute exercise were comparable across isoforms in both untrained and trained muscle. Steady-state levels of isoforms were unchanged after 5-week training (P > 0.05). Exercise-induced expression of PGC-1a variants did not correlate with changes in muscle size or strength (P > 0.05).Conclusion: Our results do not support the view that truncated PGC-1a coordinates exercise-induced hypertrophy in human skeletal muscle.Rather, all PGC-1 alpha isoforms appear to be regulated transiently in response to acute exercise and regardless of mode.

AimThis study assessed and compared acute muscle molecular responses before and after 5-week training, employing either aerobic (AE) and resistance exercise (RE) or RE only. MethodsTen men performed one-legged RE, while the contralateral limb performed AE followed by RE 6h later (AE+RE). Before (untrained) and after (trained) the intervention, acute bouts of RE were performed with or without preceding AE. Biopsies were obtained from m. vastus lateralis of each leg pre- and 3h post-RE to determine mRNA levels of VEGF, PGC-1, MuRF-1, atrogin-1, myostatin and phosphorylation of mTOR, p70S6K, rpS6 and eEF2. ResultsPGC-1 and VEGF expression increased (P<0.05) after acute RE in the untrained, but not the trained state. These markers showed greater response after AE+RE than RE in either condition. Myostatin was lower after AE+RE than RE, both before and after training. AE+RE showed higher MuRF-1 and atrogin-1 expression than RE in the untrained, not the trained state. Exercise increased (P<0.05) p70S6K phosphorylation both before and after training, yet this increase tended to be more prominent for AE+RE than RE before training. Phosphorylation of p70S6K was greater in trained muscle. Changes in these markers did not correlate with exercise-induced alterations in strength or muscle size. ConclusionConcurrent exercise in untrained skeletal muscle prompts global molecular responses consistent with resulting whole muscle adaptations. Yet, training blunts the more robust anabolic response shown after AE+RE compared with RE. This study challenges the concept that single molecular markers could predict training-induced changes in muscle size or strength.

This study tested the hypothesis that chronic aerobic and resistance exercise (AE+RE) would elicit greater muscle hypertrophy than resistance exercise only (RE). Ten men (25±4 yrs) performed 5 wks unilateral knee extensor AE+RE. The opposing limb was subjected to RE. AE completed 6 hrs prior to RE, consisted of ~45 min one-legged cycle ergometry. RE comprised 4 x 7 maximal concentric-eccentric knee extensions. Various indices of in vivo knee extensor function were measured before and after training. Magnetic resonance imaging (MRI) assessed m. quadricep femoris (QF) cross-sectional area (CSA), volume, and signal intensity (SI). Biopsies obtained from m. vastus lateralis determined fiber CSA, enzyme levels and gene expression of myostatin, atrogin-1, MuRF-1, PGC-1α and VEGF. Increases (P < 0.05) in isometric strength and peak power, respectively were comparable in AE+RE (9 and 29%) and RE (11 and 24%). AE+RE showed greater increase (14%; P < 0.05) in QF volume than RE (8%). Muscle fiber CSA increased 17% after AE+RE (P < 0.05) and 9% after RE (P > 0.05). QF SI increased (12%; P < 0.05) after AE+RE, but not RE. Neither AE+RE nor RE showed altered mRNA-levels. Citrate Synthase activity increased (P < 0.05) after AE+RE. The results suggest that the increased aerobic capacity shown with AE+RE, was accompanied by a more robust increase in muscle size compared with RE. While this response was not carried over to greater improvement in muscle function, it remains that intense AE can be executed prior to RE without compromising performance outcome.

LUNDBERG, T. R., R. FERNANDEZ-GONZALO, T. GUSTAFSSON, and P. A. TESCH. Aerobic Exercise Alters Skeletal Muscle Molecular Responses to Resistance Exercise. Med. Sci. Sports Exerc., Vol. 44, No. 9, pp. 1680-1688, 2012. Purpose: This study assessed the influence of an acute aerobic exercise bout on molecular responses to subsequent resistance exercise (RE). Methods: Nine physically active men performed a 45-min one-legged cycle ergometry exercise and 4 x 7 maximal concentric eccentric knee extensions for each leg 6 h later. Thus, one limb was subjected to aerobic and resistance exercise (AE+RE), and the contralateral limb to resistance exercise (RE) only. Knee extensor peak power was determined. Biopsies were obtained from the m vastus lateralis before (PRE) and 15 mm (POST1) and 3 h after RE. Analysis determined glycogen content, mRNA levels (vascular endothelial growth factor, peroxisome proliferator activated receptor-gamma coactivator-1, muscle RING-finger protein-1, atrogin-1, myostatin), and phosphorylated proteins (mammalian target of rapamycin, p70S6 kinase, ribosomal protein S6, eukaryotic elongation factor 2). Results: Peak power was similar in AE + RE and RE. After RE, the time course of glycogen utilization and protein signaling was similar across legs. However, phosphorylation of mammalian target of rapamycin and p70S6 kinase was elevated in AE + RE versus RE (main effect, P < 0.05). Vascular endothelial growth factor and peroxisome proliferator activated receptor-gamma coactivator-1 were higher in AE + RE than in RE at PRE and POST1 (P < 0.05). Myostatin was lower in AE + RE versus RE at PRE and POST1 (P < 0.05) and downregulated after resistance exercise only. Atrogin-1 was higher in AE + RE than in RE at PRE and POST1 (P < 0.05) and decreased after RE in AE + RE. Muscle RING-finger protein-1 was similar across legs. No difference for any marker was evident 3 h after RE. Conclusions: These results suggest that acute aerobic exercise alters molecular events regulating muscle protein turnover during the early recovery period from subsequent RE.