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.

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.

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.

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.

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.

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.

High-intensity exercise acutely decreases the membrane content of MCT1 and MCT4 and buffer capacity in human skeletal muscle.

The regulation of intracellular pH during intense muscle contractions occurs via a number of different transport systems [e.g., monocarboxylate transporters (MCTs)] and via intracellular buffering (beta m(in vitro)). The aim of this study was to investigate the effects of an acute bout of high-intensity exercise on both MCT relative abundance and beta m(in vitro) in humans. Six active women volunteered for this study. Biopsies of the vastus lateralis were obtained at rest and immediately after 45 s of exercise at 200% of maximum O2 uptake. Beta m(in vitro) was determined by titration, and MCT relative abundance was determined in membrane preparations by Western blots. High-intensity exercise was associated with a significant decrease in both MCT1 (-24%) and MCT4 (-26%) and a decrease in beta m(in vitro) (-11%; 135 +/- 3 to 120 +/- 2 micromol H+ x g dry muscle(-1) x pH(-1); P < 0.05). These changes were consistently observed in all subjects, and there was a significant correlation between changes in MCT1 and MCT4 relative abundance (R2 = 0.92; P < 0.05). In conclusion, a single bout of high-intensity exercise decreased both MCT relative abundance in membrane preparations and beta m(in vitro). Until the time course of these changes has been established, researchers should consider the possibility that observed training-induced changes in MCT and beta m(in vitro) may be influenced by the acute effects of the last exercise bout, if the biopsy is taken soon after the completion of the training program. The implications that these findings have for lactate (and H+) transport following acute, exhaustive exercise warrant further investigation.

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).

Effects of chronic NaHCO3 ingestion during interval training on changes to muscle buffer capacity, metabolism, and short-term endurance performance.

This study determined the effects of altering the H(+) concentration during interval training, by ingesting NaHCO(3) (Alk-T) or a placebo (Pla-T), on changes in muscle buffer capacity (beta m), endurance performance, and muscle metabolites. Pre- and posttraining peak O(2) uptake (V(O2 peak)), lactate threshold (LT), and time to fatigue at 100% pretraining V(O2 peak) intensity were assessed in 16 recreationally active women. Subjects were matched on the LT, were randomly placed into the Alk-T (n = 8) or Pla-T (n = 8) groups, and performed 8 wk (3 days/wk) of six to twelve 2-min cycle intervals at 140-170% of their LT, ingesting NaHCO(3) or a placebo before each training session (work matched between groups). Both groups had improvements in beta m (19 vs. 9%; P < 0.05) and V(O2 peak) (22 vs. 17%; P < 0.05) after the training period, with no differences between groups. There was a significant correlation between pretraining beta m and percent change in beta m (r = -0.70, P < 0.05). There were greater improvements in both the LT (26 vs. 15%; P = 0.05) and time to fatigue (164 vs. 123%; P = 0.05) after Alk-T, compared with Pla-T. There were no changes to pre- or postexercise ATP, phosphocreatine, creatine, and intracellular lactate concentrations, or pH(i) after training. Our findings suggest that training intensity, rather than the accumulation of H(+) during training, may be more important to improvements in beta m. The group ingesting NaHCO(3) before each training session had larger improvements in the LT and endurance performance, possibly because of a reduced metabolic acidosis during training and a greater improvement in muscle oxidative capacity.

Effects of resistance training on H+ regulation, buffer capacity, and repeated sprints.

PURPOSE: We investigated the effects of resistance training on muscle buffer capacity, H regulation, and repeated-sprint ability (RSA). METHODS: Sixteen recreationally active females performed a graded exercise test to determine VO2peak and the lactate threshold (LT), a repeated-sprint test (5 x 6 s, every 30 s) to determine RSA, and a 60-s high-intensity exercise test based on their pretraining RSA score (CIT60; continuous cycling at approximately 160% VO2peak). Muscle biopsies (vastus lateralis) were sampled before and immediately after CIT60. Subjects were then randomly assigned to either a high-repetition (three to five sets of 15-20 reps) short-rest (20 s) resistance-training group or to a control group. RESULTS: Training did not result in significant improvements in VO2peak (P > 0.05) but did improve the LT, leg strength, and RSA (P < 0.05). There were no significant improvements in muscle buffer capacity after training (P > 0.05); however, there was a significant reduction in H in the muscle and blood after high-intensity exercise (CIT60) (P < 0.05), CONCLUSIONS: High-repetition, short-rest, resistance training does not improve muscle buffer capacity in active females, but it does reduce H accumulation during high-intensity exercise (approximately 160% VO2peak). It is likely that increases in strength, LT, and ion regulation contributed to the improved RSA.

Effects of high-intensity interval training on the VO2 response during severe exercise.

This study examined the effect of high-intensity interval training on the VO2 response during severe, constant-load exercise. Prior to, and following training, 10 females (V O2 peak 37.4+/-6.0 mL kg-1 min-1) performed a graded exercise test to determine VO2 peak and lactate threshold (LT) and a 6 min cycle test (CT) at the pre-training VO2 peak intensity. Training involved high-intensity intervals (2 min work, 1 min rest) performed 3x week for 8 weeks. Breath-by-breath data from 0 to 6 min during the CT were smoothed using 5s averages and fit to a bi-exponential model starting from 20s. Training resulted in significant improvements in VO2 max (2.34+/-0.37-2.78+/-0.30 L min-1), power at VO2 max (170+/-26-204+/-25 W) and power at LT (113+/-17-136+/-20 W) (p<0.05). Following training, the VO2 response showed a significant increase in the amplitude of the primary phase (A1) (1396+/-103-1695+/-100 mL min-1; p<0.05) and end-exercise VO2 (VO2 EE), with no difference (p>0.05) in the time constants of either phase or the amplitude of the slow component (318+/-67-380+/-48 mL; p=0.15). In conjunction, accumulated oxygen deficit (AOD) (43.7+/-9.8-17.2+/-2.8 mL O2 eq kg-1) and anaerobic contribution to the CT (19.4+/-4.4-7.2+/-1.2%) were significantly reduced. In contrast to previous moderate-intensity research, a high-intensity interval training program increased A1 and VO2 EE for the same absolute exercise intensity, decreasing the AOD during a severe-intensity CT.

Effects of high- and moderate-intensity training on metabolism and repeated sprints.

PURPOSE: We compared the effects of high-intensity interval (HIT) and moderate-intensity continuous (MIT) training (matched for total work) on changes in repeated-sprint ability (RSA) and muscle metabolism. METHODS: Pre- and posttraining, VO(2peak), lactate threshold (LT), and RSA (5 x 6-s sprints, every 30 s) were assessed in 20 females. Before and immediately after the RSA test, muscle biopsies were taken from the vastus lateralis. Subjects were matched on RSA, randomly placed into the HIT (N = 10) or MIT (N = 10) group and performed 5 wk (3 d.wk(-1)) of cycle training; performing either HIT (6-10, 2-min intervals at 120-140% LT) or MIT (continuous, 20-30 min at 80-95% LT). RESULTS: Both groups had significant improvements in VO(2peak) (10-12%; P < 0.05) and LT (8-10%; P < 0.05), with no significant differences between them. Both groups also had significant increases in RSA total work (kJ) (P < 0.05), with a significantly greater increase following HIT than MIT (13 vs 8.5%, respectively; P < 0.05). There was a significant decrease in resting [ATP] and an increase in postexercise [La(-)](b) for both groups, but no significant differences between them. There were no significant changes in resting or postexercise [PCr], [Cr], muscle [La(-)], or [H(+)] after the training period. CONCLUSIONS: When total work is matched, HIT results in greater improvements in RSA than MIT. This results from an improved ability to maintain performance during consecutive sprints, which is not explained by differences in work done during the first sprint, aerobic fitness or metabolite accumulation at the end of the sprints.

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.

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.

Induced metabolic alkalosis affects muscle metabolism and repeated-sprint ability.

PURPOSE: The purpose of this study was to assess the effects of induced metabolic alkalosis, via sodium bicarbonate (NaHCO3) ingestion, on muscle metabolism and power output during repeated short-duration cycle sprints. METHODS: : Ten active females (mean +/- SD: age = 19 +/- 2 yr, VO2max = 41.0 +/- 8.8 mL x kg x min ) ingested either 0.3 g x kg NaHCO3 or 0.207 g x kg of NaCl (CON), in a double-blind, random, counterbalanced order, 90 min before performing a repeated-sprint ability (RSA) test (5 x 6-s all-out cycle sprints every 30 s). RESULTS: Compared with CON, there was a significant increase in resting blood bicarbonate concentration [HCO3] (23.6 +/- 1.1 vs 30.0 +/- 3.0 mmol x L ) and pH (7.42 +/- 0.02 vs 7.50 +/- 0.04), but no significant difference in resting lactate concentration [La] (0.8 +/- 0.2 vs 0.8 +/- 0.3 mmol x L ) during the NaHCO3 trial. Muscle biopsies revealed no significant difference in resting muscle [La], pH, or buffer capacity (beta(in vitro)) between trials (P > 0.05). Compared with CON, the NaHCO3 trial resulted in a significant increase in total work (15.7 +/- 3.0 vs 16.5 +/- 3.1 kJ) and a significant improvement in work and power output in sprints 3, 4, and 5. Despite no significant difference in posttest muscle pH between conditions, the NaHCO3 trial resulted in significantly greater posttest muscle [La]. CONCLUSIONS: As NaHCO3 ingestion does not increase resting muscle pH or beta(in vitro), it is likely that the improved performance is a result of the greater extracellular buffer concentration increasing H efflux from the muscles into the blood. The significant increase in posttest muscle [La] in NaHCO3 suggests that an increased anaerobic energy contribution is one mechanism by which NaHCO3 ingestion improved RSA.

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.

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.

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.