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Purpose: To investigate metabolism and exercise economy during prolonged race simulation (>4 h) in a world-class, full-distance triathlete to help guide/adjust strategies for training, nutrition, hydration, and thermoregulation. Methods: Two experimental race-simulation days, designed to mimic the demands of a full-distance triathlon, were executed by a world-class male triathlete (MD; 25 y, body weight 82 kg, V ˙ O 2 max 6.2 L·min−1, blood lactate threshold ∼410 W, and 18 km · h−1 in cycling and running) who at the time ranked second in the world. Race simulation was performed 23 and 10 days prior to competing in Challenge Roth 2023, where MD won in a new world record/best time (7:24:40 h:min:s). Both test days lasted ∼4 to 5 hours with physiologic testing every ∼45 to 60 minutes in a "stationary" setting during cycling on a direct-mount trainer (∼320 W) and treadmill running (16 km · h−1), enabling gas exchange measurements ( V ˙ O 2 and respiratory exchange ratio) and other physiologic measurements of interest (ie, core temperature and heart rate). This was combined with "real activity" as repeated loops in an open-air field setting at expected race pace in swimming, biking, and running. Results: V ˙ O 2 was maintained at ∼4.2 L·min−1, with carbohydrates being the dominant fuel for oxidation as respiratory exchange ratio values dropped from ∼1 at the start of cycling to ∼0.85 during running. Cycling economy was stable, whereas a slight impairment in running economy occurred over time. Conclusion: High aerobic energy turnover and stable exercise economy can be maintained in a world-class record-breaking triathlete for prolonged period of time (+4 h), showcasing the importance of both for success in competition. [ABSTRACT FROM AUTHOR]

Fatigue resistance is vital for success in elite road cycling, as repeated, intense efforts challenge the athletes' ability to sustain peak performance throughout prolonged races. The present study combined recurrent performance testing and physiological measures during 6 h simulated racing with laboratory testing to investigate factors influencing fatigue resistance. Twelve male national elite cyclists (25 ± 3 years; 76 ± 6 kg and VO2max of 5.2 ± 0.5 L/min) completed incremental power and maximal fat oxidation tests. Subsequently, they underwent field testing with physiological measures and fatigue responses evaluated through peak sprint power and 5 km time trial (TT) testing after 0, 2, 4, and 6 h of exercise. Peak power declined from 1362 ± 176 W in first sprint to 1271 ± 152 W after 2 h (p < 0.01) and then stabilized. In contrast, TT mean power gradually declined from 412 ± 38 W in the first TT to 384 ± 41 W in the final trial, with individual losses ranging from 2% to 14% and moderately correlated (r2 = 0.45) to accumulated exercise time above lactate threshold. High carbohydrate intake (~90 g/h) maintained blood glucose levels, but post‐TT [lactate] decreased from 15.1 ± 2 mM to 7.1 ± 2.3 mM, while fat oxidation increased from 0.7 ± 0.3 g/min at 0 h to 1.1 ± 0.1 g/min after 6 h. The study identifies fatigue patterns in national elite cyclists. Peak sprint power stabilized after an initial impairment from 0 to 2 h, while TT power gradually declined over the 6 h simulated race, with increased differentiation in fatigue responses among athletes. [ABSTRACT FROM AUTHOR]

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 ˙ O 2 max ∼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. [ABSTRACT FROM AUTHOR]

Introduction: Male elite cyclists (average VO2‐max: 71 mL/min/kg, n = 18) completed 7 weeks of high‐intensity interval training (HIT) (3×/week; 4‐min and 30‐s intervals) during the competitive part of the season. The influence of a maintained or lowered total training volume combined with HIT was evaluated in a two‐group design. Weekly moderate‐intensity training was lowered by ~33% (~5 h) (LOW, n = 8) or maintained at normal volume (NOR, n = 10). Endurance performance and fatigue resistance were evaluated via 400 kcal time‐trials (~20 min) commenced either with or without prior completion of a 120‐min preload (including repeated 20‐s sprints to simulate physiologic demands during road races). Results: Time‐trial performance without preload was improved after the intervention (p = 0.006) with a 3% increase in LOW (p = 0.04) and a 2% increase in NOR (p = 0.07). Preloaded time‐trial was not significantly improved (p = 0.19). In the preload, average power during repeated sprinting increased by 6% in LOW (p < 0.01) and fatigue resistance in sprinting (start vs end of preload) was improved (p < 0.05) in both groups. Blood lactate during the preload was lowered (p < 0.001) solely in NOR. Measures of oxidative enzyme activity remained unchanged, whereas the glycolytic enzyme PFK increased by 22% for LOW (p = 0.02). Conclusion: The present study demonstrates that elite cyclists can benefit from intensified training during the competitive season both with maintained and lowered training volume at moderate intensity. In addition to benchmarking the effects of such training in ecological elite settings, the results also indicate how some performance and physiological parameters may interact with training volume. [ABSTRACT FROM AUTHOR]

Women's football is an intermittent sport characterized by frequent intense actions throughout the match. The high number of matches with limited recovery time played across a long competitive season underlines the importance of nutritional strategies to meet these large physical demands. In order to maximize sport performance and maintain good health, energy intake must be optimal. However, a considerable proportion of female elite football players does not have sufficient energy intake to match the energy expenditure, resulting in low energy availability that might have detrimental physiologic consequences and impair performance. Carbohydrates appear to be the primary fuel covering the total energy supply during match‐play, and female elite football players should aim to consume sufficient carbohydrates to meet the requirements of their training program and to optimize the replenishment of muscle glycogen stores between training bouts and matches. However, several macro‐ and micronutrients are important for ensuring sufficient energy and nutrients for performance optimization and for overall health status in female elite football players. The inadequacy of macro‐and micronutrients in the diet of these athletes may impair performance and training adaptations, and increase the risk of health disorders, compromising the player's professional career. In this topical review, we present knowledge and relevant nutritional recommendations for elite female football players for the benefit of sports nutritionists, dietitians, sports scientists, healthcare specialists, and applied researchers. We focus on dietary intake and cover the most pertinent topics in sports nutrition for the relevant physical demands in female elite football players as follows: energy intake, macronutrient and micronutrient requirements and optimal composition of the everyday diet, nutritional and hydration strategies to optimize performance and recovery, potential ergogenic effects of authorized relevant supplements, and future research considerations. [ABSTRACT FROM AUTHOR]

Dietary nitrate supplementation has been shown to reduce pulmonary O2 uptake during submaximal exercise and enhance exercise performance. However, the effects of nitrate supplementation on local metabolic and haemodynamic regulation in contracting human skeletal muscle remain unclear. To address this, eight healthy young male sedentary subjects were assigned in a randomized, double‐blind, crossover design to receive nitrate‐rich beetroot juice (NO3, 9 mmol) and placebo (PLA) 2.5 h prior to the completion of a double‐step knee‐extensor exercise protocol that included a transition from unloaded to moderate‐intensity exercise (MOD) followed immediately by a transition to intense exercise (HIGH). Compared with PLA, NO3 increased plasma levels of nitrate and nitrite. During MOD, leg V̇O2 and leg blood flow (LBF) were reduced to a similar extent (∼9%–15%) in NO3. During HIGH, leg V̇O2 was reduced by ∼6%–10% and LBF by ∼5%–9% (did not reach significance) in NO3. Leg V̇O2 kinetics was markedly faster in the transition from passive to MOD compared with the transition from MOD to HIGH both in NO3 and PLA with no difference between PLA and NO3. In NO3, a reduction in nitrate and nitrite concentration was detected between arterial and venous samples. No difference in the time to exhaustion was observed between conditions. In conclusion, elevation of plasma nitrate and nitrate reduces leg skeletal muscle V̇O2 and blood flow during exercise. However, nitrate supplementation does not enhance muscle V̇O2 kinetics during exercise, nor does it improve time to exhaustion when exercising with a small muscle mass. Key points: Dietary nitrate supplementation has been shown to reduce systemic O2 uptake during exercise and improve exercise performance.The effects of nitrate supplementation on local metabolism and blood flow regulation in contracting human skeletal muscle remain unclear.By using leg exercise engaging a small muscle mass, we show that O2 uptake and blood flow are similarly reduced in contracting skeletal muscle of humans during exercise.Despite slower V̇O2 kinetics in the transition from moderate to intense exercise, no effects of nitrate supplementation were observed for V̇O2 kinetics and time to exhaustion.Nitrate and nitrite concentrations are reduced across the exercising leg, suggesting that these ions are extracted from the arterial blood by contracting skeletal muscle. [ABSTRACT FROM AUTHOR]

Purpose: To evaluate the influence of warm-up exercise intensity and subsequent recovery on intense endurance performance, selected blood variables, and the oxygen-uptake (VO2) response. Methods: Twelve highly trained male cyclists (VO2max 72.4 ± 8.0 mL • min–1 • kg–1, incremental-test peak power output (iPPO) 432 ± 31 W; mean ± SD) performed 3 warm-up strategies lasting 20 min before a 4-min maximal-performance test (PT). Strategies consisted of moderate-intensity exercise (50%iPPO) followed by 6 min of recovery (MOD6) or progressive high-intensity exercise (10–100%iPPO and 2 × 20-s sprints) followed by recovery for 6 min (HI6) or 20 min (HI20). Results: Before PT venous pH was lower (P < .001) in HI6 (7.27 ± 0.05) than in HI20 (7.34 ± 0.04) and MOD6 (7.35 ± 0.03). At the same time, differences (P < .001) existed for venous lactate in HI6 (8.2 ± 2.0 mmol/L), HI20 (5.1 ± 1.7 mmol/L), and MOD6 (1.4 ± 0.4 mmol/L), as well as for venous bicarbonate in HI6 (19.3 ± 2.6 mmol/L), HI20 (22.6 ± 2.3 mmol/L), and MOD6 (26.0 ± 1.4 mmol/L). Mean power in PT in HI6 (402 ± 38 W) tended to be lower (P = .11) than in HI20 (409 ± 34 W) and was lower (P = .007) than in MOD6 (416 ± 32 W). Total VO2 (15–120 s in PT) was higher in HI6 (8.18 ± 0.86 L) than in HI20 (7.85 ± 0.82 L, P = .008) and MOD6 (7.90 ± 0.74 L, P = .012). Conclusions: Warm-up exercise including race-pace and sprint intervals combined with short recovery can reduce subsequent performance in a 4-min maximal test in highly trained cyclists. Thus, a reduced time at high exercise intensity, a reduced intensity in the warm-up, or an extension of the recovery period after an intense warm-up is advocated. [ABSTRACT FROM AUTHOR]

The present study examined if high intensity training (HIT) could increase the expression of oxidative enzymes in fast-twitch muscle fibers causing a faster oxygen uptake (...O2) response during intense (INT), but not moderate (MOD), exercise and reduce the ...O2 slow component and muscle metabolic perturbation during INT. Pulmonary ...O2 kinetics was determined in eight trained male cyclists (...O2-max: 59 ± 4 (means ± SD) mL min-1 kg-1) during MOD (205 ± 12 W ~65% ...O2-max) and INT (286 ± 17 W ~85% ...O2-max) exercise before and after a 7-week HIT period (30-sec sprints and 4-min intervals) with a 50% reduction in volume. Both before and after HIT the content in fast-twitch fibers of CS (P < 0.05) and COX-4 (P < 0.01) was lower, whereas PFK was higher (P < 0.001) than in slow-twitch fibers. Content of CS, COX-4, and PFK in homogenate and fast-twitch fibers was unchanged with HIT. Maximal activity µmol g DW-1 min-1) of CS (56 ± 8 post-HIT vs. 59 ± 10 pre-HIT), HAD (27 ± 6 vs. 29 ± 3) and PFK (340 ± 69 vs. 318 ± 105) and the capillary to fiber ratio (2.30 ± 0.16 vs. 2.38 ± 0.20) was unaltered following HIT. ...O2 kinetics was unchanged with HIT and the speed of the primary response did not differ between MOD and INT. Muscle creatine phosphate was lower (42 ± 15 vs. 66 ± 17 mmol kg DW-1) and muscle lactate was higher (40 ± 18 vs. 14 ± 5 mmol kg DW-1) at 6 min of INT (P < 0.05) after compared to before HIT. A period of intensified training with a volume reduction did not increase the content of oxidative enzymes in fast-twitch fibers, and did not change ...O2 kinetics. [ABSTRACT FROM AUTHOR]

This study examined the ergogenic effects in a 6 min maximal performance test (PT) on 12 elite rowers: 6 open-weight (mean ± SD; 25 ± 1 years, and 92 ± 3 kg) and 6 light-weight (25 ± 3 years, and 73 ± 6 kg), following supplementation with caffeine (CAF), sodium bicarbonate (SB), and the combination of both, in a double-blind randomized placebo (PLA) controlled design. PT was executed on 4 occasions, on separate days within a week, and in a non-fasted state, with standardized training being performed the day before PT. Protocols were as follows: ( i) CAF, 3 mg/kg, 45 min prior to PT + calcium as SB-PLA; ( ii) SB, 0.3 g/kg, 75 min prior to PT + dextrose as CAF-PLA; ( iii) CAF + SB; and ( iv) PLA; CAF-PLA + SB-PLA. The total distance in the CAF (1878 ± 97 m) and CAF + SB (1877 ± 97 m) was longer than in the PLA (1865 ± 104 m; P < 0.05) and SB (1860 ± 96 m; P < 0.01). The mean power in CAF (400 ± 58 W) and CAF + SB (400 ± 58 W) was higher than the PLA (393 ± 61 W; P < 0.05) and SB (389 ± 57 W; P < 0.01). In CAF and CAF + SB, power was higher ( P < 0.05) relative to PLA in the last half (4-6 min) of PT. Trials with CAF were more effective in light-weight rowers (1.0% ± 0.8% improvement in distance; P < 0.05) than in open-weight rowers (0.3% ± 0.8%; P > 0.05). No difference between interventions was observed for readiness and stomach comfort before PT and perceived exertion during PT. This study demonstrates that caffeine ingestion does improve performance in elite rowing. In contrast sodium bicarbonate does not appear to be ergogenic, but it does not abolish the ergogenic effect of caffeine. [ABSTRACT FROM AUTHOR]

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In response to hypoxic breathing most studies report slower pulmonary oxygen uptake (VO2) kinetics at the onset of exercise, but it is not known if this relates to an actual slowing of the VO2 in the active muscles. The aim of the present study was to evaluate whether thigh VO2 is slowed at the onset of intense exercise during acute exposure to hypoxia. Six healthy male subjects (25.8 ± 1.4 yr, 79.8 ± 4.0 kg, means ± SE) performed intense (100 ± 6 watts) two-legged knee-extensor exercise for 2 min in normoxia (NOR) and hypoxia [fractional inspired oxygen concentration (FIO2) = 0.13; HYP]. Thigh VO2 was measured by frequent arterial and venous blood sampling and blood flow measurements. In arterial blood, oxygen content was reduced (P < 0.05) from 191 ± 5 ml O2/l in NOR to 180 ± 5 ml O2/l in HYP, and oxygen pressure was reduced (P < 0.001) from 111 ± 4 mmHg in NOR to 63 ± 4 mmHg in HYP. Thigh blood flow was the same in NOR and HYP, and thigh oxygen delivery was consequently reduced (P < 0.05) in HYP, but femoral arterial-venous oxygen difference and thigh VO2 were similar in NOR and HYP. In addition, muscle lactate release was the same in NOR and HYP, and muscle lactate accumulation during the first 25 s of exercise determined from muscle biopsy sampling was also similar (0.35 ± 0.07 and 0.36 ± 0.07 mmol kg dry wt-1 s-1 in NOR and HYP). Thus the increase in thigh VO2 was not attenuated at the onset of intense knee-extensor exercise despite a reduction in oxygen delivery and pressure. [ABSTRACT FROM AUTHOR]

The article offers information on the study conducted by the authors related to VO2 performance and kinetics in soccer players after inactivity and intense training. It states that 17 players from the Danish second division and one from first division who were not on any medication participated in the research. It mentions that after the last match they were either assigned to training cessation group or high-intensity training group for two weeks. It highlights that they completed running protocol on a motorized treadmill in which running speed was increased until exhaustion. It reports that the kinetics were unaffected in the group which underwent training.

The present study examined muscle adaptations and alterations in performance of highly trained soccer players with intensified training or training cessation. Eighteen elite soccer players were, for a 2-wk period, assigned to either a group that performed high-intensity training with a reduction in the amount of training (HI, n = 7), or an inactivity group without training (IN, n = 11). HI improved (P <0.05) performance of the 4th, 6th, and 10th sprint in a repeated 20-rn sprint test, and IN reduced (P < 0.05) performance in the 5th to the 10th sprints after the 2-wk intervention period. In addition, the Yo-Yo intermittent recovery level 2 test performance of IN was lowered from 845 ± 48 to 654 ± 30 m. In HI, the protein expression of the Na+-K+ pump α2-isoforrn was 15% higher (P < 0.05) after the intervention period, whereas no changes were observed in α1- and β1-isoform expression. In IN, Na+-K+ pump expression was not changed. In HI, the FXYD1ser68-to-FXYD1I ratio was 27% higher (P < 0.01) after the intervention period, and, in IN, the AB..FXYD1 ser68 signal was 18% lower (P < 0.05) after inactivity. The change in FXYD1-ser68-to-FXYD1 ratio was correlated (r2 = 0.35; P < 0.05) with change in performance in repeated sprint test. The present data suggest that short-term intensified training, even for trained soccer players, can increase muscle Na+-K+ pump α2-isoform expression, and that cessation of training for 2 wk does not affect the expression of Na+-K+ pump isoforms. Resting phosphorylation status of the Na+-K+ pump is changed by training and inactivity and may play a role in performance during repeated, intense exercise. [ABSTRACT FROM AUTHOR]

Purpose: To investigate metabolism and exercise economy during prolonged race simulation (>4 h) in a world-class, full-distance triathlete to help guide/adjust strategies for training, nutrition, hydration, and thermoregulation., Methods: Two experimental race-simulation days, designed to mimic the demands of a full-distance triathlon, were executed by a world-class male triathlete (MD; 25 y, body weight 82 kg, V˙O2max 6.2 L·min-1, blood lactate threshold ∼410 W, and 18 km · h-1 in cycling and running) who at the time ranked second in the world. Race simulation was performed 23 and 10 days prior to competing in Challenge Roth 2023, where MD won in a new world record/best time (7:24:40 h:min:s). Both test days lasted ∼4 to 5 hours with physiologic testing every ∼45 to 60 minutes in a "stationary" setting during cycling on a direct-mount trainer (∼320 W) and treadmill running (16 km · h-1), enabling gas exchange measurements (V˙O2 and respiratory exchange ratio) and other physiologic measurements of interest (ie, core temperature and heart rate). This was combined with "real activity" as repeated loops in an open-air field setting at expected race pace in swimming, biking, and running., Results: V˙O2 was maintained at ∼4.2 L·min-1, with carbohydrates being the dominant fuel for oxidation as respiratory exchange ratio values dropped from ∼1 at the start of cycling to ∼0.85 during running. Cycling economy was stable, whereas a slight impairment in running economy occurred over time., Conclusion: High aerobic energy turnover and stable exercise economy can be maintained in a world-class record-breaking triathlete for prolonged period of time (+4 h), showcasing the importance of both for success in competition.

During 6 min. all-out ergometer rowing (average power: 553 W) a maximum O2 uptake (VO2-max) of 6,93 l/min. was measured in a rower (age: 25 years, weight: 97 kg, height: 193 cm), who won a silver medal at the World championships. The VO2-max value is the highest measured by Team Denmark and is close to the upper human limit, which is underlined in this case report.

The effects of intensified training in combination with a reduced training volume on muscle ion kinetics, transporters, and work capacity were examined. Eight well-trained cyclists replaced their regular training with speed-endurance training (12 × 30 s sprints) 2-3 times per week and aerobic high-intensity training (4-5 × 3-4 min at 90-100% of maximal heart rate) 1-2 times per week for 7 wk and reduced training volume by 70% (intervention period; IP). The duration of an intense exhaustive cycling bout (EX2; 368 ± 6 W), performed 2.5 min after a 2-min intense cycle bout (EX1), was longer (P < 0.05) after than before IP (4:16 ± 0:34 vs. 3:37 ± 0:28 min:s), and mean and peak power during a repeated sprint test improved (P < 0.05) by 4% and 3%, respectively. Femoral venous K(+) concentration in recovery from EX1 and EX2 was lowered (P < 0.05) after compared with before IP, whereas muscle interstitial K(+) concentration and net muscle K(+) release during exercise was unaltered. No changes in muscle lactate and H(+) release during and after EX1 and EX2 were observed, but the in vivo buffer capacity was higher (P < 0.05) after IP. Expression of the ATP-sensitive K(+) (KATP) channel (Kir6.2) decreased by IP, with no change in the strong inward rectifying K(+) channel (Kir2.1), muscle Na(+)-K(+) pump subunits, monocarboxylate transporters 1 and 4 (MCT1 and MCT4), and Na(+)/H(+) exchanger 1 (NHE1). In conclusion, 7 wk of intensified training with a reduced training volume improved performance during repeated intense exercise, which was associated with a greater muscle reuptake of K(+) and muscle buffer capacity but not with the amount of muscle ion transporters.

The present study examined whether a marked reduction in oxygen delivery, unlike findings in moderate-intensity exercise, would slow leg oxygen uptake (Vo2) kinetics during intense exercise (86 ± 3% of incremental test peak power). Seven healthy males (26 ± 1 years, means ± SE) performed one-legged knee-extensor exercise (60 ± 3 W) for 4 min in a control setting (CON) and with arterial infusion of N(G)-monomethyl-l-arginine and indomethacin in the working leg to reduce blood flow by inhibiting formation of nitric oxide and prostanoids (double blockade; DB). In DB leg blood flow (LBF) and oxygen delivery during the first minute of exercise were 25-50% lower (P < 0.01) compared with CON (LBF after 10 s: 1.1 ± 0.2 vs. 2.5 ± 0.3 l/min and 45 s: 2.7 ± 0.2 vs. 3.8 ± 0.4 l/min) and 15% lower (P < 0.05) after 2 min of exercise. Leg Vo2 in DB was attenuated (P < 0.05) during the first 2 min of exercise (10 s: 161 ± 26 vs. 288 ± 34 ml/min and 45 s: 459 ± 48 vs. 566 ± 81 ml/min) despite a higher (P < 0.01) oxygen extraction in DB. Net leg lactate release was the same in DB and CON. The present study shows that a marked reduction in oxygen delivery can limit the rise in Vo2 during the initial part of intense exercise. This is in contrast to previous observations during moderate-intensity exercise using the same DB procedure, which suggests that fast-twitch muscle fibers are more sensitive to a reduction in oxygen delivery than slow-twitch fibers.

The present study examined muscle adaptations and alterations in performance of highly trained soccer players with intensified training or training cessation. Eighteen elite soccer players were, for a 2-wk period, assigned to either a group that performed high-intensity training with a reduction in the amount of training (HI, n = 7), or an inactivity group without training (IN, n = 11). HI improved (P < 0.05) performance of the 4th, 6th, and 10th sprint in a repeated 20-m sprint test, and IN reduced (P < 0.05) performance in the 5th to the 10th sprints after the 2-wk intervention period. In addition, the Yo-Yo intermittent recovery level 2 test performance of IN was lowered from 845 +/- 48 to 654 +/- 30 m. In HI, the protein expression of the Na(+)-K(+) pump alpha(2)-isoform was 15% higher (P < 0.05) after the intervention period, whereas no changes were observed in alpha(1)- and beta(1)-isoform expression. In IN, Na(+)-K(+) pump expression was not changed. In HI, the FXYD1ser68-to-FXYD1 ratio was 27% higher (P < 0.01) after the intervention period, and, in IN, the AB&#95;FXYD1ser68 signal was 18% lower (P < 0.05) after inactivity. The change in FXYD1ser68-to-FXYD1 ratio was correlated (r(2) = 0.35; P < 0.05) with change in performance in repeated sprint test. The present data suggest that short-term intensified training, even for trained soccer players, can increase muscle Na(+)-K(+) pump alpha(2)-isoform expression, and that cessation of training for 2 wk does not affect the expression of Na(+)-K(+) pump isoforms. Resting phosphorylation status of the Na(+)-K(+) pump is changed by training and inactivity and may play a role in performance during repeated, intense exercise.