JNK regulates muscle remodeling via myostatin/SMAD inhibition.

Skeletal muscle has a remarkable plasticity to adapt and remodel in response to environmental cues, such as physical exercise. Endurance exercise stimulates improvements in muscle oxidative capacity, while resistance exercise induces muscle growth. Here we show that the c-Jun N-terminal kinase (JNK) is a molecular switch that when active, stimulates muscle fibers to grow, resulting in increased muscle mass. Conversely, when muscle JNK activation is suppressed, an alternative remodeling program is initiated, resulting in smaller, more oxidative muscle fibers, and enhanced aerobic fitness. When muscle is exposed to mechanical stress, JNK initiates muscle growth via phosphorylation of the transcription factor, SMAD2, at specific linker region residues leading to inhibition of the growth suppressor, myostatin. In human skeletal muscle, this JNK/SMAD signaling axis is activated by resistance exercise, but not endurance exercise. We conclude that JNK acts as a key mediator of muscle remodeling during exercise via regulation of myostatin/SMAD signaling.

Ammonium Chloride Ingestion Attenuates Exercise-Induced mRNA Levels in Human Muscle.

Minimizing the decrease in intracellular pH during high-intensity exercise training promotes greater improvements in mitochondrial respiration. This raises the intriguing hypothesis that pH may affect the exercise-induced transcription of genes that regulate mitochondrial biogenesis. Eight males performed 10x2-min cycle intervals at 80% VO2speak intensity on two occasions separated by ~2 weeks. Participants ingested either ammonium chloride (ACID) or calcium carbonate (PLA) the day before and on the day of the exercise trial in a randomized, counterbalanced order, using a crossover design. Biopsies were taken from the vastus lateralis muscle before and after exercise. The mRNA level of peroxisome proliferator-activated receptor co-activator 1α (PGC-1α), citrate synthase, cytochome c and FOXO1 was elevated at rest following ACID (P<0.05). During the PLA condition, the mRNA content of mitochondrial- and glucose-regulating proteins was elevated immediately following exercise (P<0.05). In the early phase (0-2 h) of post-exercise recovery during ACID, PGC-1α, citrate synthase, cytochome C, FOXO1, GLUT4, and HKII mRNA levels were not different from resting levels (P>0.05); the difference in PGC-1α mRNA content 2 h post-exercise between ACID and PLA was not significant (P = 0.08). Thus, metabolic acidosis abolished the early post-exercise increase of PGC-1α mRNA and the mRNA of downstream mitochondrial and glucose-regulating proteins. These findings indicate that metabolic acidosis may affect mitochondrial biogenesis, with divergent responses in resting and post-exercise skeletal muscle.

Changes in mitochondrial function and mitochondria associated protein expression in response to 2-weeks of high intensity interval training.

PURPOSE: High-intensity short-duration interval training (HIT) stimulates functional and metabolic adaptation in skeletal muscle, but the influence of HIT on mitochondrial function remains poorly studied in humans. Mitochondrial metabolism as well as mitochondrial-associated protein expression were tested in untrained participants performing HIT over a 2-week period. METHODS: Eight males performed a single-leg cycling protocol (12 × 1 min intervals at 120% peak power output, 90 s recovery, 4 days/week). Muscle biopsies (vastus lateralis) were taken pre- and post-HIT. Mitochondrial respiration in permeabilized fibers, citrate synthase (CS) activity and protein expression of peroxisome proliferator-activated receptor gamma coactivator (PGC-1α) and respiratory complex components were measured. RESULTS: HIT training improved peak power and time to fatigue. Increases in absolute oxidative phosphorylation (OXPHOS) capacities and CS activity were observed, but not in the ratio of CCO to the electron transport system (CCO/ETS), the respiratory control ratios (RCR-1 and RCR-2) or mitochondrial-associated protein expression. Specific increases in OXPHOS flux were not apparent after normalization to CS, indicating that gross changes mainly resulted from increased mitochondrial mass. CONCLUSION: Over only 2 weeks HIT significantly increased mitochondrial function in skeletal muscle independently of detectable changes in mitochondrial-associated and mitogenic protein expression.

Sex differences in acute translational repressor 4E-BP1 activity and sprint performance in response to repeated-sprint exercise in team sport athletes.

OBJECTIVES: The physiological requirements underlying soccer-specific exercise are incomplete and sex-based comparisons are sparse. The aim of this study was to determine the effects of a repeated-sprint protocol on the translational repressor 4E-BP1 and sprint performance in male and female soccer players. DESIGN: Cross-over design involving eight female and seven male university soccer players. METHODS: Participants performed four bouts of 6 × 30-m maximal sprints spread equally over 40 min. Heart rate, sprint time and sprint decrement were measured for each sprint and during the course of each bout. Venous blood samples and muscle biopsies from the vastus lateralis were taken at rest, at 15 min and 2h post-exercise. RESULTS: While males maintained a faster mean sprint time for each bout (P < 0.05) females exhibited a greater decrement in sprint performance for each bout (P < 0.05), indicating a superior maintenance of sprint performance in males, with no sex differences for heart rate or lactate. Muscle analyses revealed sex differences in resting total (P < 0.05) and phosphorylated (P < 0.05) 4E-BP1 Thr37/46, and 15 min post-exercise the 4E-BP1 Thr37/46 ratio decreased below resting levels in males only (P < 0.05), indicative of a decreased translation initiation following repeated sprints. CONCLUSIONS: We show that females have a larger sprint decrement indicating that males have a superior ability to recover sprint performance. Sex differences in resting 4E-BP1 Thr37/46 suggest diversity in the training-induced phenotype of the muscle of males and females competing in equivalent levels of team-sport competition.

Cytokine mRNA expression responses to resistance, aerobic, and concurrent exercise in sedentary middle-aged men.

Concurrent resistance and aerobic exercise (CE) is recommended to ageing populations, though is postulated to induce diminished acute molecular responses. Given that contraction-induced cytokine mRNA expression reportedly mediates remunerative postexercise molecular responses, it is necessary to determine whether cytokine mRNA expression may be diminished after CE. Eight middle-aged men (age, 53.3 ±1.8 years; body mass index, 29.4 ± 1.4 kg·m(-2)) randomly completed (balanced for completion order) 8 × 8 leg extensions at 70% maximal strength (RE), 40 min of cycling at 55% of peak aerobic workload (AE), or (workload-matched) 50% RE and 50% AE (CE). Muscle (vastus lateralis) was obtained pre-exercise, and at 1 h and 4 h postexercise, and analyzed for changes of glycogen concentration, tumor necrosis factor (TNF)α, TNF receptor-1 and -2 (TNF-R1 and TNF-R2, respectively), interleukin (IL)-6, IL-6R, IL-1ß, and IL-1 receptor-antagonist (IL-1ra). All exercise modes upregulated cytokine mRNA expression at 1 h postexercise comparably (TNFα, TNF-R1, TNF-R2, IL-1ß, IL-6) (p < 0.05). Expression remained elevated at 4 h after RE and AE (p < 0.05), though returned to pre-exercise levels after CE (p > 0.05). Moreover, AE and RE upregulated IL-1ß and IL-1ra expression, whereas CE upregulated IL-1ß expression only (p < 0.05). Only AE reduced muscle glycogen concentration (p < 0.05), whilst upregulating receptor expression the greatest; though, IL-6R expression remained unchanged after all modes (p > 0.05). In conclusion, in middle-aged men, all modes induced commensurate cytokine mRNA expression at 1 h postexercise; however, only CE resulted in ameliorated expression at 4 h postexercise. Whether the RE or AE components of CE are independently or cumulatively sufficient to upregulate cytokine responses, or whether they collectively inhibit cytokine mRNA expression, remains to be determined.

Comparative effects of single-mode vs. duration-matched concurrent exercise training on body composition, low-grade inflammation, and glucose regulation in sedentary, overweight, middle-aged men.

The effect of duration-matched concurrent exercise training (CET) (50% resistance (RET) and 50% endurance (EET) training) on physiological training outcomes in untrained middle-aged men remains to be elucidated. Forty-seven men (age, 48.1 ± 6.8 years; body mass index, 30.4 ± 4.1 kg·m(-2)) were randomized into 12-weeks of EET (40-60 min of cycling), RET (10 exercises; 3-4 sets × 8-10 repetitions), CET (50% serial completion of RET and EET), or control condition. The following were determined: intervention-based changes in fitness and strength; abdominal visceral adipose tissue (VAT), total body fat (TB-FM) and fat-free (TB-FFM) mass; plasma cytokines (C-reactive protein (CRP), tumor necrosis factor-α (TNFα) interleukin-6 (IL-6)); muscle protein content of p110α and glucose transporter 4 (GLUT4); mRNA expression of GLUT4, peroxisome proliferator-activated receptor-γ coactivator-1α-ß, cytochrome c oxidase, hexokinase II, citrate synthase; oral glucose tolerance; and estimated insulin sensitivity. CET promoted commensurate improvements of aerobic capacity and muscular strength and reduced VAT and TB-FM equivalently to EET and RET (p < 0.05), yet only RET increased TB-FFM (p < 0.05). Although TNFα and IL-6 were reduced after all training interventions (p < 0.05), CRP remained unchanged (p > 0.05). EET reduced area under the curve for glucose, insulin, and C-peptide, whilst CET and RET respectively reduced insulin and C-peptide, and C-peptide only (p < 0.05). Notwithstanding increased insulin sensitivity index after all training interventions (p < 0.05), no change presented for GLUT4 or p110α total protein, or chronic mRNA expression of the studied mitochondrial genes (p > 0.05). In middle-aged men, 12 weeks of duration-matched CET promoted commensurate changes in fitness and strength, abdominal VAT, plasma cytokines and insulin sensitivity, and an equidistant glucose tolerance response to EET and RET; despite no change of measured muscle mechanisms associative to insulin action, glucose transport, and mitochondrial function.

Altering the rest interval during high-intensity interval training does not affect muscle or performance adaptations.

It has been hypothesized that exercise-induced changes in metabolites and ions are crucial in the adaptation of contracting muscle. We tested this hypothesis by comparing adaptations to two different interval-training protocols (differing only in the rest duration between intervals), which provoked different perturbations in muscle metabolites and acid-base status. Prior to and immediately after training, 12 women performed the following tests: (1) a graded exercise test to determine peak oxygen uptake (V(O2)); (2) a high-intensity exercise bout (followed 60 s later by a repeated-sprint-ability test; and (3) a repeat of the high-intensity exercise bout alone with muscle biopsies pre-exercise, immediately postexercise and after 60 s of recovery. Subjects performed 5 weeks (3 days per week) of training, with either a short (1 min; HIT-1) or a long rest period (3 min; HIT-3) between intervals; training intensity and volume were matched. Muscle [H(+)] (155 ± 15 versus 125 ± 8 nmol l(-1); P < 0.05) and muscle lactate content (84.2 ± 7.9 versus 46.9 ± 3.1 mmol (g wet weight)(-1)) were both higher after HIT-1, while muscle phosphocreatine (PCr) content (52.8 ± 8.3 versus 63.4 ± 9.8 mmol (g wet weight)(-1)) was lower. There were no significant differences between the two groups regarding the increases in , repeated-sprint performance or muscle Na(+),K(+)-ATPase content. Following training, both groups had a significant decrease in postexercise muscle [H(+)] and lactate content, but not postexercise ATP or PCr. Postexercise PCr resynthesis increased following both training methods. In conclusion, intense interval training results in marked improvements in muscle Na(+),K(+)-ATPase content, PCr resynthesis and . However, manipulation of the rest period during intense interval training did not affect these changes.

Concurrent resistance and aerobic exercise stimulates both myofibrillar and mitochondrial protein synthesis in sedentary middle-aged men.

We determined myofibrillar and mitochondrial protein fractional synthesis rates (FSR), intramuscular signaling protein phosphorylation, and mRNA expression responses after isolated bouts of resistance exercise (RE), aerobic exercise (AE), or in combination [termed concurrent exercise (CE)] in sedentary middle-aged men. Eight subjects (age = 53.3 ± 1.8 yr; body mass index = 29.4 ± 1.4 kg·m(2)) randomly completed 8 × 8 leg extension repetitions at 70% of one repetition-maximum, 40 min of cycling at 55% peak aerobic power output (AE), or (consecutively) 50% of the RE and AE trials (CE). Biopsies were obtained (during a primed, constant infusion of l-[ring-(13)C(6)]phenylalanine) while fasted, and at 1 and 4 h following postexercise ingestion of 20 g of protein. All trials increased mitochondrial FSR above fasted rates (RE = 1.3-fold; AE = 1.5; CE = 1.4; P < 0.05), although only CE (2.2) and RE (1.8) increased myofibrillar FSR (P < 0.05). At 1 h postexercise, phosphorylation of Akt on Ser(473) (CE = 7.7; RE = 4.6) and Thr(308) (CE = 4.4; RE = 2.9), and PRAS40 on Thr(246) (CE = 3.8; AE = 2.5) increased (P < 0.05), with CE greater than AE for Akt Ser(473)-Thr(308) and greater than RE for PRAS40 (P < 0.05). Despite increased phosphorylation of Akt-PRAS40, phosphorylation of mammalian target of rapamycin (Ser(2448)) remained unchanged (P > 0.05), while rpS6 (Ser(235/236)) increased only in RE (10.4) (P < 0.05). CE and AE both resulted in increased peroxisome proliferator receptor-γ coactivator 1-α (PGC1α) expression at 1 h (CE = 2.9; AE = 2.8; P < 0.05) and 4 h (CE = 2.6; AE = 2.4) and PGC1ß expression at 4 h (CE = 2.1; AE = 2.6; P < 0.05). These data suggest that CE-induced acute stimulation of myofibrillar and mitochondrial FSR, protein signaling, and mRNA expression are equivalent to either isolate mode (RE or AE). These results occurred without an interference effect on muscle protein subfractional synthesis rates, protein signaling, or mRNA expression.

The recovery of repeated-sprint exercise is associated with PCr resynthesis, while muscle pH and EMG amplitude remain depressed.

The physiological equivalents of power output maintenance and recovery during repeated-sprint exercise (RSE) remain to be fully elucidated. In an attempt to improve our understanding of the determinants of RSE performance we therefore aimed to determine its recovery following exhaustive exercise (which affected intramuscular and neural factors) concomitantly with those of intramuscular concentrations of adenosine triphosphate [ATP], phosphocreatine [PCr] and pH values and electromyography (EMG) activity (a proxy for net motor unit activity) changes. Eight young men performed 10, 6-s all-out sprints on a cycle ergometer, interspersed with 30 s of recovery, followed, after 6 min of passive recovery, by five 6-s sprints, again interspersed by 30 s of passive recovery. Biopsies of the vastus lateralis were obtained at rest, immediately after the first 10 sprints and after 6 min of recovery. EMG activity of the vastus lateralis was obtained from surface electrodes throughout exercise. Total work (TW), [ATP], [PCr], pH and EMG amplitude decreased significantly throughout the first ten sprints (P<0.05). After 6 min of recovery, TW during sprint 11 recovered to 86.3±7.7% of sprint 1. ATP and PCr were resynthesized to 92.6±6.0% and 85.3±10.3% of the resting value, respectively, but muscle pH and EMG amplitude remained depressed. PCr resynthesis was correlated with TW done in sprint 11 (r = 0.79, P<0.05) and TW done during sprints 11 to 15 (r = 0.67, P<0.05). There was a ∼2-fold greater decrease in the TW/EMG ratio in the last five sprints (sprint 11 to 15) than in the first five sprints (sprint 1 to 5) resulting in a disproportionate decrease in mechanical power (i.e., TW) in relation to EMG. Thus, we conclude that the inability to produce power output during repeated sprints is mostly mediated by intramuscular fatigue signals probably related with the control of PCr metabolism.

Randomised controlled trial of informal team sports for cardiorespiratory fitness and health benefit in Pacific adults.

INTRODUCTION: Rates of obesity, Type 2 diabetes and cardiovascular disease are high among Pacific people in New Zealand. Physical activity is recommended in the prevention and management of these conditions. Community-based, 'small-sided game' group activities may be an effective and culturally appropriate way to promote physical activity within Pacific communities. AIM: To assess the effectiveness of small-sided games-based exercise on fitness and health parameters among Pacific adults over four weeks. METHODS: Twenty untrained (13 female) Pacific adults were randomised to intervention or control. Intervention participants were offered 45 minutes of small-sided games three times per week for four weeks. Control participants were offered one-month gym membership after the trial. Primary outcomes included cardiorespiratory fitness (VO2peak) and leg strength (maximal concentric force of quadriceps at 60°/second) measured at baseline and four weeks. Secondary outcomes included glycaemia, lipid profile, blood pressure (BP), and inflammatory markers. Multivariable regression models were used to assess differences between groups, adjusting for baseline values, age and gender. RESULTS: At baseline, mean age was 34.8 years (SD 12.6), BMI 36.3 (6.7), systolic BP 127.7 mmHg (12.1), HbA1c 6.1% (1.9), VO2peak 2.5 L/min (0.6) and leg strength 170.0 N.m (57.4). Sixteen participants completed the trial. Change in outcomes were greater in intervention than control participants in absolute VO2peak (0.9 L/min (p=0.003)), leg strength (17.8 N.m (p=0.04)) and HDL (0.12 mmol/L (p=0.02)). There were no other significant differences. DISCUSSION: Small-sided games appear to be a promising means for improving the health and cardiorespiratory fitness and reducing the risk of diabetes and cardiovascular disease in Pacific adults.

The effect of graduated compression stockings on running performance.

The aim of this study was to examine the effects of wearing different grades of graduated compression stockings (GCS) on 10-km running performance. After an initial familiarization run, 9 male and 3 female competitive runners (VO2max 68.7 ± 5.8 ml·kg⁻¹·min⁻¹) completed 4 10-km time trials on an outdoor 400-m track wearing either control (0 mm Hg; Con), low (12-15 mm Hg; Low), medium (18-21 mm Hg; Med), or high (23-32 mm Hg; Hi) GCS in a randomized counterbalanced order. Leg power was assessed pre and postrun via countermovement jump using a jump mat. Blood-lactate concentration was assessed pre and postrun, whereas heart rate was monitored continuously during exercise. Perceptual scales were used to assess the comfort, tightness, and any pain associated with wearing GCS. There were no significant differences in performance time between trials (p = 0.99). The change in pre to postexercise jump performance was lower in Low and Med than in Con (p < 0.05). Mean heart rate (p = 0.99) and blood lactate (p = 1.00) were not different between trials. Participants rated Con and Low as more comfortable than Med and Hi (p < 0.01), Med and Hi were rated as tighter than Low (p < 0.01), all GCS were rated as tighter than Con (p < 0.01), and Hi was associated with the most pain (p < 0.01). In conclusion, GCS worn by competitive runners during 10-km time trials did not affect performance time; however Low and Med GCS resulted in greater maintenance of leg power after endurance exercise. Athletes rated low-grade GCS as most comfortable garments to wear during exercise.

Intermittent-sprint performance and muscle glycogen after 30 h of sleep deprivation.

PURPOSE: The aim of this study was to determine the effects of 30 h of sleep deprivation on consecutive-day intermittent-sprint performance and muscle glycogen content. METHODS: Ten male, team-sport athletes performed a single-day "baseline" session and two consecutive-day experimental trials separated either by a normal night's sleep (CONT1 and CONT2) or no sleep (SDEP1 and SDEP2). Each session included a 30-min graded exercise run and 50-min intermittent-sprint exercise protocol, including a 15-m maximal sprint every minute and self-paced exercise bouts of varying intensities. Muscle biopsies were extracted before and after exercise during the baseline session and before exercise on day 2 during experimental trials. Voluntary force and activation of the right quadriceps, nude mass, HR, core temperature, capillary blood lactate and glucose, RPE, and a modified POMS were recorded before, after, and during the exercise protocols. RESULTS: Mean sprint times were slower on SDEP2 (2.78±0.17 s) compared with SDEP1 (2.70±0.16 s) and CONT2 (2.74±0.15 s, P<0.05). Distance covered during self-paced exercise was reduced during SDEP2 during the initial 10 min compared with SDEP1 and during the final 10 min compared with CONT2 (P<0.05). Muscle glycogen concentration was lower before exercise on SDEP2 (209±60 mmol·kg dry weight) compared with CONT2 (274±54 mmol·kg dry weight, P=0.05). Voluntary force and activation were reduced on day 2 of both conditions; however, both were lower in SDEP2 compared with CONT2 (P<0.05). Sleep loss did not affect RPE but negatively affected POMS ratings (P<0.05). CONCLUSIONS: Sleep loss and associated reductions in muscle glycogen and perceptual stress reduced sprint performance and slowed pacing strategies during intermittent-sprint exercise for male team-sport athletes.

Adaptations to skeletal muscle with endurance exercise training in the acutely fed versus overnight-fasted state.

Minimising carbohydrate (CHO) status in the peri-training period may accelerate the training adaptations normally observed. The aim of this study was to compare adaptations to endurance training undertaken in the acutely CHO fed and overnight-fasted states. Eight female and six male untrained, healthy participants: aged 26.6+/-5.8 years (mean+/-SD); height 174.7+/-7.6 cm; weight 75.3+/-11.4 kg; VO(2max) 3.48+/-0.67 l/min; were randomly divided into two training groups and undertook four weeks of five days per week endurance cycle ergometer training in either the overnight-fasted (FAST) or acutely fed (FED) state. FAST training had no effect on RER or plasma glucose, lactate and FFA concentrations during subsequent submaximal exercise. Training-induced changes in Vastus lateralis citrate synthase (CS) and 3-hydroxy-CoA dehydrogenase (HAD) activities were not different between training groups (P=0.655 and 0.549, respectively), but when the effect of gender was considered, men responded better to FAST and women responded better to FED. The FAST group showed a significantly greater training-induced increase in VO(2max) and resting muscle glycogen concentration than FED (P=0.014 and P=0.047 respectively), but there was no gender interaction. In conclusion, these results suggest that (a) meal ingestion prior to daily exercise can modify some of the exercise training-induced adaptations normally seen with endurance training compared to when daily exercise is undertaken in the overnight-fasted state; and (b) the extent of these adaptations in skeletal muscle differ slightly between men and women.

Physiological effects of wearing graduated compression stockings during running.

This study examined the effect of wearing different grades of graduated compression stockings (GCS) on physiological and perceptual measures during and following treadmill running in competitive runners. Nine males and one female performed three 40-min treadmill runs (80 +/- 5% maximal oxygen uptake) wearing either control (0 mmHg; CON), low (12-15 mmHg; LO-GCS), or high (23-32 mmHg; HI-GCS) grade GCS in a double-blind counterbalanced order. Oxygen uptake, heart rate and blood lactate were measured. Perceptual scales were used pre- and post-run to assess comfort, tightness and any pain associated with wearing GCS. Changes in muscle function, soreness and damage were determined pre-run, immediately after running and 24 and 48 h post-run by measuring creatine kinase and myoglobin, counter-movement jump height, perceived soreness diagrams, and pressure sensitivity. There were no significant differences between trials for oxygen uptake, heart rate or blood lactate during exercise. HI-GCS was perceived as tighter (P < 0.05) and more pain-inducing (P < 0.05) than the other interventions; CON and LO-GCS were rated more comfortable than HI-GCS (P < 0.05). Creatine kinase (P < 0.05), myoglobin (P < 0.05) and jump height (P < 0.05) were higher and pressure sensitivity was more pronounced (P < 0.05) immediately after running but not after 24 and 48 h. Only four participants reported muscle soreness during recovery from running and there were no differences in muscle function between trials. In conclusion, healthy runners wearing GCS did not experience any physiological benefits during or following treadmill running. However, athletes felt more comfortable wearing low-grade GCS whilst running.

Early time course of Akt phosphorylation after endurance and resistance exercise.

PURPOSE: The aim of this study was to determine the early time course of exercise-induced signaling after divergent contractile activity associated with resistance and endurance exercise. METHODS: Sixteen male subjects were randomly assigned to either a cycling (CYC; n = 8, 60 min, 70% V˙O2peak) or resistance (REX; n = 8, 8 x 5 leg extension, 80% one-repetition maximum, 3-min recovery) exercise group. Serial muscle biopsies were obtained from vastus lateralis at rest before, immediately after, and after 15, 30, and 60 min of passive recovery to determine early signaling responses after exercise. RESULTS: There were comparable increases from rest in Akt(Thr308/Ser473) and mTOR(Ser2448) phosphorylation during the postexercise time course that peaked 30-60 min after both CYC and REX (P < 0.05). There were also similar patterns in p70S6K(Thr389) and 4E-BP1(Thr37/46) phosphorylation, but a greater magnitude of effect was observed for REX and CYC, respectively (P < 0.05). However, AMPK(Thr172) phosphorylation was only significantly elevated after CYC (P < 0.05), and we observed divergent responses for glycogen synthase(Ser641) and AS160 phosphorylation that were enhanced after CYC but not REX (P < 0.05). CONCLUSIONS: We show a similar time course for Akt-mTOR-S6K phosphorylation during the initial 60-min recovery period after divergent contractile stimuli. Conversely, enhanced phosphorylation status of proteins that promote glucose transport and glycogen synthesis only occurred after endurance exercise. Our results indicate that endurance and resistance exercise initiate translational signaling, but high-load, low-repetition contractile activity failed to promote phosphorylation of pathways regulating glucose metabolism.

Effect of consecutive repeated sprint and resistance exercise bouts on acute adaptive responses in human skeletal muscle.

We examined acute molecular responses in skeletal muscle to repeated sprint and resistance exercise bouts. Six men [age, 24.7 +/- 6.3 yr; body mass, 81.6 +/- 7.3 kg; peak oxygen uptake, 47 +/- 9.9 mlxkg(-1)xmin(-1); one repetition maximum (1-RM) leg extension 92.2 +/- 12.5 kg; means +/- SD] were randomly assigned to trials consisting of either resistance exercise (8 x 5 leg extension, 80% 1-RM) followed by repeated sprints (10 x 6 s, 0.75 Nxm torquexkg(-1)) or vice-versa. Muscle biopsies from vastus lateralis were obtained at rest, 15 min after each exercise bout, and following 3-h recovery to determine early signaling and mRNA responses. There was divergent exercise order-dependent phosphorylation of p70 S6K (S6K). Specifically, initial resistance exercise increased S6K phosphorylation ( approximately 75% P < 0.05), but there was no effect when resistance exercise was undertaken after sprints. Exercise decreased IGF-I mRNA following 3-h recovery ( approximately 50%, P = 0.06) independent of order, while muscle RING finger mRNA was elevated with a moderate exercise order effect (P < 0.01). When resistance exercise was followed by repeated sprints PGC-1alpha mRNA was increased (REX1-SPR2; P = 0.02) with a modest distinction between exercise orders. Repeated sprints may promote acute interference on resistance exercise responses by attenuating translation initiation signaling and exacerbating ubiquitin ligase expression. Indeed, repeated sprints appear to generate the overriding acute exercise-induced response when undertaking concurrent repeated sprint and resistance exercise. Accordingly, we suggest that sprint-activities are isolated from resistance training and that adequate recovery time is considered within periodized training plans that incorporate these divergent exercise modes.

High-intensity exercise decreases muscle buffer capacity via a decrease in protein buffering in human skeletal muscle.

We have previously reported an acute decrease in muscle buffer capacity (betam(in vitro)) following high-intensity exercise. The aim of this study was to identify which muscle buffers are affected by acute exercise and the effects of exercise type and a training intervention on these changes. Whole muscle and non-protein betam(in vitro) were measured in male endurance athletes (VO(2max) = 59.8 +/- 5.8 mL kg(-1) min(-1)), and before and after training in male, team-sport athletes (VO(2max) = 55.6 +/- 5.5 mL kg(-1) min(-1)). Biopsies were obtained at rest and immediately after either time-to-fatigue at 120% VO(2max) (endurance athletes) or repeated sprints (team-sport athletes). High-intensity exercise was associated with a significant decrease in betam(in vitro) in endurance-trained males (146 +/- 9 to 138 +/- 7 mmol H(+) x kg d.w.(-1) x pH(-1)), and in male team-sport athletes both before (139 +/- 9 to 131 +/- 7 mmol H(+) x kg d.w.(-1) x pH(-1)) and after training (152 +/- 11 to 142 +/- 9 mmol H(+) x kg d.w.(-1) x pH(-1)). There were no acute changes in non-protein buffering capacity. There was a significant increase in betam(in vitro) following training, but this did not alter the post-exercise decrease in betam(in vitro). In conclusion, high-intensity exercise decreased betam(in vitro) independent of exercise type or an interval-training intervention; this was largely explained by a decrease in protein buffering. These findings have important implications when examining training-induced changes in betam(in vitro). Resting and post-exercise muscle samples cannot be used interchangeably to determine betam(in vitro), and researchers must ensure that post-training measurements of betam(in vitro) are not influenced by an acute decrease caused by the final training bout.

Effects of high-intensity training on muscle lactate transporters and postexercise recovery of muscle lactate and hydrogen ions in women.

The purpose of this study was to investigate the effects of high-intensity interval training (3 days/wk for 5 wk), provoking large changes in muscle lactate and pH, on changes in intracellular buffer capacity (betam(in vitro)), monocarboxylate transporters (MCTs), and the decrease in muscle lactate and hydrogen ions (H+) after exercise in women. Before and after training, biopsies of the vastus lateralis were obtained at rest and immediately after and 60 s after 45 s of exercise at 190% of maximal O2 uptake. Muscle samples were analyzed for ATP, phosphocreatine (PCr), lactate, and H+; MCT1 and MCT4 relative abundance and betam(in vitro) were also determined in resting muscle only. Training provoked a large decrease in postexercise muscle pH (pH 6.81). After training, there was a significant decrease in betam(in vitro) (-11%) and no significant change in relative abundance of MCT1 (96 +/- 12%) or MCT4 (120 +/- 21%). During the 60-s recovery after exercise, training was associated with no change in the decrease in muscle lactate, a significantly smaller decrease in muscle H+, and increased PCr resynthesis. These results suggest that increases in betam(in vitro) and MCT relative abundance are not linked to the degree of muscle lactate and H+ accumulation during training. Furthermore, training that is very intense may actually lead to decreases in betam(in vitro). The smaller postexercise decrease in muscle H+ after training is a further novel finding and suggests that training that results in a decrease in H+ accumulation and an increase in PCr resynthesis can actually reduce the decrease in muscle H+ during the recovery from supramaximal exercise.

The effects of compression garments on intermittent exercise performance and recovery on consecutive days.

PURPOSE: The aim of this study was to determine whether compression garments improve intermittent-sprint performance and aid performance or self-reported recovery from high-intensity efforts on consecutive days. METHODS: Following familiarization, 14 male rugby players performed two randomized testing conditions (with or without garments) involving consecutive days of a simulated team sport exercise protocol, separated by 24 h of recovery within each condition and 2 weeks between conditions. Each day involved an 80-min high-intensity exercise circuit, with exercise performance determined by repeated 20-m sprints and peak power on a cart dynamometer (single-man scrum machine). Measures of nude mass, heart rate, skin and tympanic temperature, and blood lactate (La-) were recorded throughout each day; also, creatine kinase (CK) and muscle soreness were recorded each day and 48 h following exercise. RESULTS: No differences (P=.20 to 0.40) were present between conditions on either day of the exercise protocol for repeated 20-m sprint efforts or peak power on a cart dynamometer. Heart rate, tympanic temperature, and body mass did not significantly differ between conditions; however, skin temperature was higher under the compression garments. Although no differences (P=.50) in La- or CK were present, participants felt reduced levels of perceived muscle soreness in the ensuing 48 h postexercise when wearing the garments (2.5+/-1.7 vs 3.5+/-2.1 for garment and control; P=.01). CONCLUSIONS: The use of compression garments did not improve or hamper simulated team-sport activity on consecutive days. Despite benefits of reduced self-reported muscle soreness when wearing garments during and following exercise each day, no improvements in performance or recovery were apparent.

The relationship between the VO2 slow component, muscle metabolites and performance during very-heavy exhaustive exercise.

This study examined the relationship between the V O(2) response, particularly the slow component (SC), muscle metabolite changes and performance during very-heavy exhaustive exercise. Sixteen active females performed a graded exercise test to determine V O(2peak) and the lactate threshold followed 48h later by a constant-load cycle test to exhaustion (ET) at 85% V O(2peak) intensity. Muscle biopsies and capillary blood samples were obtained before and after the ET to determine changes in muscle ATP, pH, lactate and phosphocreatine and also plasma pH and lactate. Breath-by-breath data from the ET were smoothed using 5-s averages and fit to a three-component exponential model. The mean time to exhaustion (t(exh)) during the ET was 16.8 (+/-6.4) min. Results showed no correlation between the SC and t(exh) or any muscle metabolite changes (p>0.05). Significant correlations (p<0.05) were evident between t(exh) and tau; tau(0) (r=-0.54), tau(1) (r=-0.65), change in (Delta) pH(b) (r=-0.60), Delta[La(-)](b) (r=-0.58) and [La(-)](b post) (r=-0.64). Significant correlations (p<0.05) were also evident between tau(1) and [La(-)](b post) (r=0.54). Furthermore, a negative value resulted when the accumulated oxygen deficit was calculated for the entire duration of the ET. Results showed no association between the amplitude of the SC and t(ext) or to changes in muscle/blood metabolites, suggesting that the SC is not a determinant of high-intensity exercise tolerance. Furthermore, it is possible that a reduced perturbation of anaerobic energy sources, as a result of a faster tau(1), may have contributed to a longer t(exh).