Similar improvements in 5-km performance and maximal oxygen uptake with submaximal and maximal 10-20-30 training in runners, but increase in muscle oxidative phosphorylation occur only with maximal effort training.

OBJECTIVE: The aim of the present study was to examine whether 10-20-30 training (consecutive 1-min intervals consisting of 30 s at low-speed, 20 s at moderate-speed, and 10 s at high-speed), performed with submaximal effort during the 10-s high-speed runs, would lead to improved performance as well as increased maximum oxygen uptake (VO2 -max) and muscle oxidative phosphorylation (OXPHOS). In addition, to examine to what extent the effects would compare to 10-20-30 running conducted with maximal effort. DESIGN: Nineteen males were randomly assigned to 10-20-30 running performed with either submaximal (SUBMAX; n = 11) or maximal (MAX; n = 8) effort, which was conducted three times/week for 6 weeks (intervention; INT). Before and after INT, subjects completed a 5-km running test and a VO2 -max test, and a biopsy was obtained from m. vastus lateralis. RESULTS: After compared to before INT, SUBMAX and MAX improved (p < 0.05) 5-km performance by 3.0% (20.8 ± 0.4 (means±SE) vs. 21.5 ± 0.4 min) and 2.3% (21.2 ± 0.4 vs. 21.6 ± 0.4 min), respectively, and VO2 -max was ~7% higher (p < 0.01) in both SUBMAX (57.0 ± 1.3 vs. 53.5 ± 1.1 mL/min/kg) and MAX (57.8 ± 1.2 vs. 53.7 ± 0.9 mL/min/kg), with no difference in the changes between groups. In SUBMAX, muscle OXPHOS was unchanged, whereas in MAX, muscle OXPHOS subunits (I-IV) and total OXPHOS (5.5 ± 0.3 vs 4.7 ± 0.3 A.U.) were 9%-29% higher (p < 0.05) after compared to before INT. CONCLUSION: Conducting 10-20-30 training with a non-maximal effort during the 10-s high-speed runs is as efficient in improving 5-km performance and VO2 -max as maximal effort exercise, whereas increase in muscle OXPHOS occur only when the 10-s high-speed runs are performed with maximal effort.

Active Relative to Passive Ischemic Preconditioning Enhances Intense Endurance Performance in Well-Trained Men.

PURPOSE: This study tested the hypothesis of whether ischemic exercise preconditioning (IPC-Ex) elicits a better intense endurance exercise performance than traditional ischemic preconditioning at rest (IPC-rest) and a SHAM procedure. METHODS: Twelve men (average V˙O2max ∼61 mL·kg-1·min-1) performed 3 trials on separate days, each consisting of either IPC-Ex (3 × 2-min cycling at ∼40 W with a bilateral-leg cuff pressure of ∼180 mm Hg), IPC-rest (4 × 5-min supine rest at 220 mm Hg), or SHAM (4 × 5-min supine rest at <10 mm Hg) followed by a standardized warm-up and a 4-minute maximal cycling performance test. Power output, blood lactate, potassium, pH, rating of perceived exertion, oxygen uptake, and gross efficiency were assessed. RESULTS: Mean power during the performance test was higher in IPC-Ex versus IPC-rest (+4%; P = .002; 95% CI, +5 to 18 W). No difference was found between IPC-rest and SHAM (-2%; P = .10; 95% CI, -12 to 1 W) or between IPC-Ex and SHAM (+2%; P = .09; 95% CI, -1 to 13 W). The rating of perceived exertion increased following the IPC-procedure in IPC-Ex versus IPC-rest and SHAM (P < .001). During warm-up, IPC-Ex elevated blood pH versus IPC-rest and SHAM (P ≤ .027), with no trial differences for blood potassium (P > .09) or cycling efficiency (P ≥ .24). Eight subjects anticipated IPC-Ex to be best for their performance. Four subjects favored SHAM. CONCLUSIONS: Performance in a 4-minute maximal test was better following IPC-Ex than IPC-rest and tended to be better than SHAM. The IPC procedures did not affect blood potassium, while pH was transiently elevated only by IPC-Ex. The performance-enhancing effect of IPC-Ex versus IPC-rest may be attributed to a placebo effect, improved pH regulation, and/or a change in the perception of effort.

Aerobic-interval exercise with blood flow restriction potentiates early markers of metabolic health in man.

AIM: This study examined whether aerobic-interval exercise with blood flow restriction (BFR) potentiates early markers of metabolic health compared to exercise with systemic hypoxia or normoxia in man. METHODS: In a randomized-crossover fashion, eight healthy men completed nine 2-minute running bouts at 105% of their lactate threshold on three occasions separated by one week, either with BFR (BFR-trial), systemic hypoxia (HYP-trial) or normoxia (control; CON-trial). Near-infrared spectroscopy was used to assess the muscle level of hypoxia. A muscle biopsy was collected at rest and 3 hours after exercise to quantify genes involved in cholesterol synthesis (PGC-1α2), glucose disposal (GLUT4) and capillary growth (HIF-1α; VEGFA), as well as mitochondrial respiration (PGC-1α2/3), uncoupling (UCP3) and expansion (p53; COXIV-1/2; CS; AMPKα1/2). RESULTS: The muscle level of hypoxia was matched between the BFR-trial and HYP-trial (~90%; P > .05), which was greater than the CON-trial (~70%; P < .05). PGC-1α2 increased most in the BFR-trial (16-fold vs CON-trial; 11-fold vs HYP-trial; P < .05). GLUT4 and VEGFA selectively increased by 2.0 and 3.4-fold, respectively in BFR-trial (P < .05), which was greater than CON-trial (1.2 and 1.3 fold) and HYP-trial (1.2 and 1.8 fold; P < .05). UCP3 increased more in BFR-trial than the HYP-trial (4.3 vs 1.6 fold), but was not different between BFR-trial and CON-trial (2.1 fold) or between CON-trial and HYP-trial (P > .05). No trial differences were evident for other genes (P > .05). CONCLUSION: Independent of the muscle level of hypoxia, BFR-exercise potentiates early markers of metabolic health associated with the regulation of cholesterol production and glucose homeostasis in man.

Blood flow restriction training and the high-performance athlete: science to application.

The manipulation of blood flow in conjunction with skeletal muscle contraction has greatly informed the physiological understanding of muscle fatigue, blood pressure reflexes, and metabolism in humans. Recent interest in using intentional blood flow restriction (BFR) has focused on elucidating how exercise during periods of reduced blood flow affects typical training adaptations. A large initial appeal for BFR training was driven by studies demonstrating rapid increases in muscle size, strength, and endurance capacity, even when notably low intensities and resistances, which would typically be incapable of stimulating change in healthy populations, were used. The incorporation of BFR exercise into the training of strength- and endurance-trained athletes has recently been shown to provide additive training effects that augment skeletal muscle and cardiovascular adaptations. Recent observations suggest BFR exercise alters acute physiological stressors such as local muscle oxygen availability and vascular shear stress, which may lead to adaptations that are not easily attained with conventional training. This review explores these concepts and summarizes both the evidence base and knowledge gaps regarding the application of BFR training for athletes.

Blood-flow-restricted exercise: Strategies for enhancing muscle adaptation and performance in the endurance-trained athlete.

NEW FINDINGS: What is the topic of this review? Blood-flow-restricted (BFR) exercise represents a potential approach to augment the adaptive response to training and improve performance in endurance-trained individuals. What advances does it highlight? When combined with low-load resistance exercise, low- and moderate-intensity endurance exercise and sprint interval exercise, BFR can provide an augmented acute stimulus for angiogenesis and mitochondrial biogenesis. These augmented acute responses can translate into enhanced capillary supply and mitochondrial function, and subsequent endurance-type performance, although this might depend on the nature of the exercise stimulus. There is a requirement to clarify whether BFR training interventions can be used by high-performance endurance athletes within their structured training programme. ABSTRACT: A key objective of the training programme for an endurance athlete is to optimize the underlying physiological determinants of performance. Training-induced adaptations are governed by physiological and metabolic stressors, which initiate transcriptional and translational signalling cascades to increase the abundance and/or function of proteins to improve physiological function. One important consideration is that training adaptations are reduced as training status increases, which is reflected at the molecular level as a blunting of the acute signalling response to exercise. This review examines blood-flow-restricted (BFR) exercise as a strategy for augmenting exercise-induced stressors and subsequent molecular signalling responses to enhance the physiological characteristics of the endurance athlete. Focus is placed on the processes of capillary growth and mitochondrial biogenesis. Recent evidence supports that BFR exercise presents an intensified training stimulus beyond that of performing the same exercise alone. We suggest that this has the potential to induce enhanced physiological adaptations, including increases in capillary supply and mitochondrial function, which can contribute to an improvement in performance of endurance exercise. There is, however, a lack of consensus regarding the potency of BFR training, which is invariably attributable to the different modes, intensities and durations of exercise and BFR methods. Further studies are needed to confirm its potential in the endurance-trained athlete.

The effect of blood-flow-restricted interval training on lactate and H+ dynamics during dynamic exercise in man.

AIM: To assess how blood-flow-restricted (BFR) interval-training affects the capacity of the leg muscles for pH regulation during dynamic exercise in physically trained men. METHODS: Ten men (age: 25 ± 4y; V˙O2max : 50 ± 5 mL∙kg-1 ∙min-1 ) completed a 6-wk interval-cycling intervention (INT) with one leg under BFR (BFR-leg; ~180 mmHg) and the other without BFR (CON-leg). Before and after INT, thigh net H+ -release (lactate-dependent, lactate-independent and sum) and blood acid/base variables were measured during knee-extensor exercise at 25% (Ex25) and 90% (Ex90) of incremental peak power output. A muscle biopsy was collected before and after Ex90 to determine pH, lactate and density of H+ -transport/buffering systems. RESULTS: After INT, net H+ release (BFR-leg: 15 ± 2; CON-leg: 13 ± 3; mmol·min-1 ; Mean ± 95% CI), net lactate-independent H+ release (BFR-leg: 8 ± 1; CON-leg: 4 ± 1; mmol·min-1 ) and net lactate-dependent H+ release (BFR-leg: 9 ± 3; CON-leg: 10 ± 3; mmol·min-1 ) were similar between legs during Ex90 (P > .05), despite a ~142% lower muscle intracellular-to-interstitial lactate gradient in BFR-leg (-3 ± 4 vs 6 ± 6 mmol·L-1 ; P < .05). In recovery from Ex90, net lactate-dependent H+ efflux decreased in BFR-leg with INT (P < .05 vs CON-leg) owing to lowered muscle lactate production (~58% vs CON-leg, P < .05). Net H+ gradient was not different between legs (~19%, P > .05; BFR-leg: 48 ± 30; CON-leg: 44 ± 23; mmol·L-1 ). In BFR-leg, NHE1 density was higher than in CON-leg (~45%; P < .05) and correlated with total-net H+ -release (r = 0.71; P = .031) and lactate-independent H+ release (r = 0.74; P = .023) after INT, where arterial [ HCO3- ] and standard base excess in Ex25 were higher in BFR-leg than CON-leg. CONCLUSION: Compared to a training control, BFR-interval training increases the capacity for pH regulation during dynamic exercise mainly via enhancement of muscle lactate-dependent H+ -transport function and blood H+ -buffering capacity.

Training with blood flow restriction increases femoral artery diameter and thigh oxygen delivery during knee-extensor exercise in recreationally trained men.

KEY POINTS: Endurance-type training with blood flow restriction (BFR) increases maximum oxygen uptake ( V̇O2max ) and exercise endurance of humans. However, the physiological mechanisms behind this phenomenon remain uncertain. In the present study, we show that BFR-interval training reduces the peripheral resistance to oxygen transport during dynamic, submaximal exercise in recreationally-trained men, mainly by increasing convective oxygen delivery to contracting muscles. Accordingly, BFR-training increased oxygen uptake by, and concomitantly reduced net lactate release from, the contracting muscles during relative-intensity-matched exercise, at the same time as invoking a similar increase in diffusional oxygen conductance compared to the training control. Only BFR-training increased resting femoral artery diameter, whereas increases in oxygen transport and uptake were dissociated from changes in the skeletal muscle content of mitochondrial electron-transport proteins. Thus, physically trained men benefit from BFR-interval training by increasing leg convective oxygen transport and reducing lactate release, thereby improving the potential for increasing the percentage of V̇O2max that can be sustained throughout exercise. ABSTRACT: In the present study, we investigated the effect of training with blood flow restriction (BFR) on thigh oxygen transport and uptake, and lactate release, during exercise. Ten recreationally-trained men (50 ± 5 mL kg-1  min-1 ) completed 6 weeks of interval cycling with one leg under BFR (BFR-leg; pressure: ∼180 mmHg) and the other leg without BFR (CON-leg). Before and after the training intervention (INT), thigh oxygen delivery, extraction, uptake, diffusion capacity and lactate release were determined during knee-extensor exercise at 25% incremental peak power output (iPPO) (Ex1), followed by exercise to exhaustion at 90% pre-training iPPO (Ex2), by measurement of femoral-artery blood flow and femoral-arterial and -venous blood sampling. A muscle biopsy was obtained from legs before and after INT to determine mitochondrial electron-transport protein content. Femoral-artery diameter was also measured. In the BFR-leg, after INT, oxygen delivery and uptake were higher, and net lactate release was lower, during Ex1 (vs. CON-leg; P < 0.05), with an 11% larger increase in workload (vs. CON-leg; P < 0.05). During Ex2, after INT, oxygen delivery was higher, and oxygen extraction was lower, in the BFR-leg compared to the CON-leg (P < 0.05), resulting in an unaltered oxygen uptake (vs. CON-leg; P > 0.05). In the CON-leg, at both intensities, oxygen delivery, extraction, uptake and lactate release remained unchanged (P > 0.05). Resting femoral artery diameter increased with INT only in the BFR-leg (∼4%; P < 0.05). Oxygen diffusion capacity was similarly raised in legs (P < 0.05). Mitochondrial protein content remained unchanged in legs (P > 0.05). Thus, BFR-interval training enhances oxygen utilization by, and lowers lactate release from, submaximally-exercising muscles of recreationally-trained men mainly by increasing leg convective oxygen transport.

Blood flow-restricted training enhances thigh glucose uptake during exercise and muscle antioxidant function in humans.

This study examined the effects of blood-flow-restricted (BFR)-training on thigh glucose uptake at rest and during exercise in humans and the muscular mechanisms involved. Ten active men (~25 y; VO2max ~50 mL/kg/min) completed six weeks of training, where one leg trained with BFR (cuff pressure: ~180 mmHg) and the other leg without BFR. Before and after training, thigh glucose uptake was determined at rest and during exercise at 25% and 90% of leg incremental peak power output by sampling of femoral arterial and venous blood and measurement of femoral arterial blood flow. Furthermore, resting muscle samples were collected. After training, thigh glucose uptake during exercise was higher than before training only in the BFR-trained leg (p < 0.05) due to increased glucose extraction (p < 0.05). Further, BFR-training substantially improved time to exhaustion during exhaustive exercise (11 ±â€¯5% vs. CON-leg; p = 0.001). After but not before training, NAC infusion attenuated (~50-100%) leg net glucose uptake and extraction during exercise only in the BFR-trained leg, which coincided with an increased muscle abundance of Cu/Zn-SOD (39%), GPX-1 (29%), GLUT4 (28%), and nNOS (18%) (p < 0.05). Training did not affect Mn-SOD, catalase, and VEGF abundance in either leg (p > 0.05), although Mn-SOD was higher in BFR-leg vs. CON-leg after training (p < 0.05). The ratios of p-AMPK-Thr172/AMPK and p-ACC-Ser79/ACC, and p-ACC-Ser79, remained unchanged in both legs (p > 0.05), despite a higher p-AMPK-Thr172 in BFR-leg after training (38%; p < 0.05). In conclusion, BFR-training enhances glucose uptake by exercising muscles in humans probably due to an increase in antioxidant function, GLUT4 abundance, and/or NO availability.

A fast, reliable and sample-sparing method to identify fibre types of single muscle fibres.

Many skeletal muscle proteins are present in a cell-specific or fibre-type dependent manner. Stimuli such as exercise, aging, and disease have been reported to result in fibre-specific responses in protein abundances. Thus, fibre-type-specific determination of the content of specific proteins provides enhanced mechanistic understanding of muscle physiology and biochemistry compared with typically performed whole-muscle homogenate analyses. This analysis, however, is laborious and typically not performed. We present a novel dot blotting method for easy and rapid determination of skeletal muscle fibre type based on myosin heavy chain (MHC) isoform presence. Requiring only small amounts of starting muscle tissue (i.e., 2-10 mg wet weight), muscle fibre type is determined in one-tenth of a 1-3-mm fibre segment, with the remainder of each segment pooled with fibre segments of the same type (I or II) for subsequent protein quantification by western blotting. This method, which we validated using standard western blotting, is much simpler and cheaper than previous methods and is adaptable for laboratories routinely performing biochemical analyses. Use of dot blotting for fibre typing will facilitate investigations of fibre-specific responses to diverse stimuli, which will advance our understanding of skeletal muscle physiology and biochemistry.

Cycling with blood flow restriction improves performance and muscle K+ regulation and alters the effect of anti-oxidant infusion in humans.

KEY POINTS: Training with blood flow restriction (BFR) is a well-recognized strategy for promoting muscle hypertrophy and strength. However, its potential to enhance muscle function during sustained, intense exercise remains largely unexplored. In the present study, we report that interval training with BFR augments improvements in performance and reduces net K+ release from contracting muscles during high-intensity exercise in active men. A better K+ regulation after BFR-training is associated with an elevated blood flow to exercising muscles and altered muscle anti-oxidant function, as indicated by a higher reduced to oxidized glutathione (GSH:GSSG) ratio, compared to control, as well as an increased thigh net K+ release during intense exercise with concomitant anti-oxidant infusion. Training with BFR also invoked fibre type-specific adaptations in the abundance of Na+ ,K+ -ATPase isoforms (α1 , ß1 , phospholemman/FXYD1). Thus, BFR-training enhances performance and K+ regulation during intense exercise, which may be a result of adaptations in anti-oxidant function, blood flow and Na+ ,K+ -ATPase-isoform abundance at the fibre-type level. ABSTRACT: We examined whether blood flow restriction (BFR) augments training-induced improvements in K+ regulation and performance during intense exercise in men, and also whether these adaptations are associated with an altered muscle anti-oxidant function, blood flow and/or with fibre type-dependent changes in Na+ ,K+ -ATPase-isoform abundance. Ten recreationally-active men (25 ± 4 years, 49.7 ± 5.3 mL kg-1  min-1 ) performed 6 weeks of interval cycling, where one leg trained without BFR (control; CON-leg) and the other trained with BFR (BFR-leg, pressure: ∼180 mmHg). Before and after training, femoral arterial and venous K+ concentrations and artery blood flow were measured during single-leg knee-extensor exercise at 25% (Ex1) and 90% of thigh incremental peak power (Ex2) with i.v. infusion of N-acetylcysteine (NAC) or placebo (saline) and a resting muscle biopsy was collected. After training, performance increased more in BFR-leg (23%) than in CON-leg (12%, P < 0.05), whereas K+ release during Ex2 was attenuated only from BFR-leg (P < 0.05). The muscle GSH:GSSG ratio at rest and blood flow during exercise was higher in BFR-leg than in CON-leg after training (P < 0.05). After training, NAC increased resting muscle GSH concentration and thigh net K+ release during Ex2 only in BFR-leg (P < 0.05), whereas the abundance of Na+ ,K+ -ATPase-isoform α1 in type II (51%), ß1 in type I (33%), and FXYD1 in type I (108%) and type II (60%) fibres was higher in BFR-leg than in CON-leg (P < 0.05). Thus, training with BFR elicited greater improvements in performance and reduced thigh K+ release during intense exercise, which were associated with adaptations in muscle anti-oxidant function, blood flow and Na+ ,K+ -ATPase-isoform abundance at the fibre-type level.

Molecular stressors underlying exercise training-induced improvements in K+ regulation during exercise and Na+ ,K+ -ATPase adaptation in human skeletal muscle.

Despite substantial progress made towards a better understanding of the importance of skeletal muscle K+ regulation for human physical function and its association with several disease states (eg type-II diabetes and hypertension), the molecular basis underpinning adaptations in K+ regulation to various stimuli, including exercise training, remains inadequately explored in humans. In this review, the molecular mechanisms essential for enhancing skeletal muscle K+ regulation and its key determinants, including Na+ ,K+ -ATPase function and expression, by exercise training are examined. Special attention is paid to the following molecular stressors and signaling proteins: oxygenation, redox balance, hypoxia, reactive oxygen species, antioxidant function, Na+ ,K+ , and Ca2+ concentrations, anaerobic ATP turnover, AMPK, lactate, and mRNA expression. On this basis, an update on the effects of different types of exercise training on K+ regulation in humans is provided, focusing on recent discoveries about the muscle fibre-type-dependent regulation of Na+ ,K+ -ATPase-isoform expression. Furthermore, with special emphasis on blood-flow-restricted exercise as an exemplary model to modulate the key molecular mechanisms identified, it is discussed how training interventions may be designed to maximize improvements in K+ regulation in humans. The novel insights gained from this review may help us to better understand how exercise training and other strategies, such as pharmacological interventions, may be best designed to enhance K+ regulation and thus the physical function in humans.

Cold-water immersion after training sessions: effects on fiber type-specific adaptations in muscle K+ transport proteins to sprint-interval training in men.

Effects of regular use of cold-water immersion (CWI) on fiber type-specific adaptations in muscle K+ transport proteins to intense training, along with their relationship to changes in mRNA levels after the first training session, were investigated in humans. Nineteen recreationally active men (24 ± 6 yr, 79.5 ± 10.8 kg, 44.6 ± 5.8 ml·kg-1·min-1) completed six weeks of sprint-interval cycling, either without (passive rest; CON) or with training sessions followed by CWI (15 min at 10°C; COLD). Muscle biopsies were obtained before and after training to determine abundance of Na+, K+-ATPase isoforms (α1-3, ß1-3) and phospholemman (FXYD1) and after recovery treatments (+0 h and +3 h) on the first day of training to measure mRNA content. Training increased ( P < 0.05) the abundance of α1 and ß3 in both fiber types and ß1 in type-II fibers and decreased FXYD1 in type-I fibers, whereas α2 and α3 abundance was not altered by training ( P > 0.05). CWI after each session did not influence responses to training ( P > 0.05). However, α2 mRNA increased after the first session in COLD (+0 h, P < 0.05) but not in CON ( P > 0.05). In both conditions, α1 and ß3 mRNA increased (+3 h; P < 0.05) and ß2 mRNA decreased (+3 h; P < 0.05), whereas α3, ß1, and FXYD1 mRNA remained unchanged ( P > 0.05) after the first session. In summary, Na+,K+-ATPase isoforms are differently regulated in type I and II muscle fibers by sprint-interval training in humans, which, for most isoforms, do not associate with changes in mRNA levels after the first training session. CWI neither impairs nor improves protein adaptations to intense training of importance for muscle K+ regulation. NEW & NOTEWORTHY Although cold-water immersion (CWI) after training and competition has become a routine for many athletes, limited published evidence exists regarding its impact on training adaptation. Here, we show that CWI can be performed regularly without impairing training-induced adaptations at the fiber-type level important for muscle K+ handling. Furthermore, sprint-interval training invoked fiber type-specific adaptations in K+ transport proteins, which may explain the dissociated responses of whole-muscle protein levels and K+ transport function to training previously reported.

Effect of speed endurance training and reduced training volume on running economy and single muscle fiber adaptations in trained runners.

The aim of the present study was to examine whether improved running economy with a period of speed endurance training and reduced training volume could be related to adaptations in specific muscle fibers. Twenty trained male (n = 14) and female (n = 6) runners (maximum oxygen consumption (VO2 -max): 56.4 ± 4.6 mL/min/kg) completed a 40-day intervention with 10 sessions of speed endurance training (5-10 × 30-sec maximal running) and a reduced (36%) volume of training. Before and after the intervention, a muscle biopsy was obtained at rest, and an incremental running test to exhaustion was performed. In addition, running at 60% vVO2 -max, and a 10-km run was performed in a normal and a muscle slow twitch (ST) glycogen-depleted condition. After compared to before the intervention, expression of mitochondrial uncoupling protein 3 (UCP3) was lower (P < 0.05) and dystrophin was higher (P < 0.05) in ST muscle fibers, and sarcoplasmic reticulum calcium ATPase 1 (SERCA1) was lower (P < 0.05) in fast twitch muscle fibers. Running economy at 60% vVO2 -max (11.6 ± 0.2 km/h) and at v10-km (13.7 ± 0.3 km/h) was ~2% better (P < 0.05) after the intervention in the normal condition, but unchanged in the ST glycogen-depleted condition. Ten kilometer performance was improved (P < 0.01) by 3.2% (43.7 ± 1.0 vs. 45.2 ± 1.2 min) and 3.9% (45.8 ± 1.2 vs. 47.7 ± 1.3 min) in the normal and the ST glycogen-depleted condition, respectively. VO2 -max was the same, but vVO2 -max was 2.0% higher (P < 0.05; 19.3 ± 0.3 vs. 18.9 ± 0.3 km/h) after than before the intervention. Thus, improved running economy with intense training may be related to changes in expression of proteins linked to energy consuming processes in primarily ST muscle fibers.

Effect of additional speed endurance training on performance and muscle adaptations.

PURPOSE: The present study examined the effect of additional speed endurance training (SET) during the season on muscle adaptations and performance of trained soccer players. METHODS: Eighteen subelite soccer players performed one session with six to nine 30-s intervals at an intensity of 90%-95% of maximal intensity (SET) a week for 5 wk (SET intervention). Before and after the SET intervention, the players carried out the Yo-Yo intermittent recovery level 2 (Yo-Yo IR2) test, a sprint test (10 and 30 m), and an agility test. In addition, seven of the players had a resting muscle biopsy specimen taken and they carried out a running protocol on a motorized treadmill before and after the SET intervention. RESULTS: After the SET intervention, the Yo-Yo IR2 test (n = 13) performance was 11% better (P < 0.05), whereas sprint (n = 15) and agility (n = 13) performances were unchanged. The expression of the monocarboxylate transporter 1 (n = 6) was 9% higher (P < 0.05). and the expression of the Na(+)/K(+) pump subunit ß(1) (n = 6) was 13% lower (P < 0.05) after the SET intervention. The Na(+)/K(+) pump subunits α(1), α(2), as well as the monocarboxylate transporter 4 and the Na(+)/H(+) exchanger 1 (n = 6) were unchanged. After the SET intervention, the relative number of Type IIx fibers and oxygen consumption at 10 km.h(-1) were lower (P < 0.05), whereas VO(2max) was unchanged. CONCLUSIONS: In conclusion, adding ∼30 min of SET once a week during the season for trained soccer players did lead to an improved ability to perform repeated high-intensity exercise, with a concomitant increase in the expression of monocarboxylate transporter 1 and an improved running economy.