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 α₂-isoform 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-FXYD1 ratio was 27% higher ( P < 0.01) after the intervention period, and, in IN, the AB_FXYD1ser68 signal was 18% lower ( P < 0.05) after inactivity. The change in FXYD1ser68-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.

The present study examined muscle adaptations and alterations in work capacity in endurance-trained runners after a change from endurance to sprint training. Fifteen runners were assigned to either a sprint training (ST, n = 8) or a control (CON, n = 7) group. ST replaced their normal training by 30-s sprint runs three to four times a week, whereas CON continued the endurance training (∼45 km/wk). After the 4-wk sprint period, the expression of the muscle Na⁺-K⁺ pump α₁-subunit and Na⁺/H⁺-exchanger isoform 1 was 29 and 30% higher ( P < 0.05), respectively. Furthermore, plasma K⁺ concentration was reduced ( P < 0.05) during repeated intense running. In ST, performance in a 30-s sprint test, Yo-Yo intermittent recovery test, and two supramaximal exhaustive runs was improved ( P < 0.05) by 7, 19, 27, and 19%, respectively, after the sprint training period, whereas pulmonary maximum oxygen uptake and 10-k time were unchanged. No changes in CON were observed. The present data suggest a role of the Na⁺-K⁺ pump in the control of K⁺ homeostasis and in the development of fatigue during repeated high-intensity exercise. Furthermore, performance during intense exercise can be improved and endurance performance maintained even with a reduction in training volume if the intensity of training is very high.

The present study examined muscle adaptations and alterations in work capacity in endurance-trained runners as a result of a reduced amount of training combined with speed endurance training. For a 6- to 9-wk period, 17 runners were assigned to either a speed endurance group with a 25% reduction in the amount of training but including speed endurance training consisting of six to twelve 30-s sprint runs 3–4 times/wk (SET group n = 12) or a control group ( n = 5), which continued the endurance training (∼55 km/wk). For the SET group, the expression of the muscle Na⁺-K⁺pump α₂-subunit was 68% higher ( P < 0.05) and the plasma K⁺level was reduced ( P < 0.05) during repeated intense running after 9 wk. Performance in a 30-s sprint test and the first of the supramaximal exhaustive runs was improved ( P < 0.05) by 7% and 36%, respectively, after the speed endurance training period. In the SET group, maximal O₂uptake was unaltered, but the 3-km (3,000-m) time was reduced ( P < 0.05) from 10.4 ± 0.1 to 10.1 ± 0.1 min and the 10-km (10,000-m) time was improved from 37.3 ± 0.4 to 36.3 ± 0.4 min (means ± SE). Muscle protein expression and performance remained unaltered in the control group. The present data suggest that both short- and long-term exercise performances can be improved with a reduction in training volume if speed endurance training is performed and that the Na⁺-K⁺pump plays a role in the control of K⁺homeostasis and in the development of fatigue during repeated high-intensity exercise.

The effects of regular football training on glycemic control, body composition, and peak oxygen uptake (VO₂peak) were investigated in men with type 2 diabetes mellitus (T2DM). Twenty‐one middle‐aged men (49.8 ± 1.7 years ± SEM) with T2DM were divided into a football training group (FG; n = 12) and an inactive control group (CG; n = 9) during a 24‐week intervention period (IP). During a 1‐h football training session, the distance covered was 4.7 ± 0.2 km, mean heart rate (HR) was 83 ± 2% of HRmax, and blood lactate levels increased (P < 0.001) from 2.1 ± 0.3 to 8.2 ± 1.3 mmol/L. In FG, VO₂peak was 11% higher (P < 0.01), and total fat mass and android fat mass were 1.7 kg and 12.8% lower (P < 0.001), respectively, after IP. After IP, the reduction in plasma glucose was greater (P = 0.02) in FG than the increase in CG, and in FG, GLUT‐4 tended to be higher (P = 0.072) after IP. For glycosylated hemoglobin (HbA1), an overall time effect (P < 0.01) was detected after 24 weeks. After IP, the number of capillaries around type I fibers was 7% higher (P < 0.05) in FG and 5% lower (P < 0.05) in CG. Thus, in men with T2DM, regular football training improves VO₂peak, reduces fat mass, and may positively influence glycemic control.

Exercise is an effective strategy in the prevention and treatment of metabolic diseases. Alterations in the skeletal muscle proteome, including post-translational modifications, regulate its metabolic adaptations to exercise. Here, we examined the effect of high-intensity interval training (HIIT) on the proteome and acetylome of human skeletal muscle, revealing the response of 3168 proteins and 1263 lysine acetyl-sites on 464 acetylated proteins. We identified global protein adaptations to exercise training involved in metabolism, excitation-contraction coupling, and myofibrillar calcium sensitivity. Furthermore, HIIT increased the acetylation of mitochondrial proteins, particularly those of complex V. We also highlight the regulation of exercise-responsive histone acetyl-sites. These data demonstrate the plasticity of the skeletal muscle proteome and acetylome, providing insight into the regulation of contractile, metabolic and transcriptional processes within skeletal muscle. Herein, we provide a substantial hypothesis-generating resource to stimulate further mechanistic research investigating how exercise improves metabolic health.

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, β₁, 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. 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%), β₁ 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.