Thomas P. Gunnarsson

Reduced volume and increased training intensity elevate muscle Na+-K+ pump α2-subunit expression as well as short- and long-term work capacity in humans

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 ( approximately 55 km/wk). For the SET group, the expression of the muscle Na(+)-K(+) pump alpha(2)-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 O(2) uptake 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.

Effect of 2-wk intensified training and inactivity on muscle Na+-K+ pump expression, phospholemman (FXYD1) phosphorylation, and performance in soccer players

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_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.

The 10-20-30 training concept improves performance and health profile in moderately trained runners

The effect of an alteration from regular endurance to interval (10-20-30) training on the health profile, muscular adaptations, maximum oxygen uptake (Vo(2max)), and performance of runners was examined. Eighteen moderately trained individuals (6 females and 12 males; Vo(2max): 52.2 ± 1.5 ml·kg(-1)·min(-1)) (means ± SE) were divided into a high-intensity training (10-20-30; 3 women and 7 men) and a control (CON; 3 women and 5 men) group. For a 7-wk intervention period the 10-20-30 replaced all training sessions with 10-20-30 training consisting of low-, moderate-, and high-speed running (<30%, <60%, and >90% of maximal intensity) for 30, 20, and 10 s, respectively, in three or four 5-min intervals interspersed by 2 min of recovery, reducing training volume by 54% (14.0 ± 0.9 vs. 30.4 ± 2.3 km/wk) while CON continued the normal training. After the intervention period Vo(2max) in 10-20-30 was 4% higher, and performance in a 1,500-m and a 5-km run improved (P < 0.05) by 21 and 48 s, respectively. In 10-20-30, systolic blood pressure was reduced (P < 0.05) by 5 ± 2 mmHg, and total and low-density lipoprotein (LDL) cholesterol was lowered (P < 0.05) by 0.5 ± 0.2 and 0.4 ± 0.1 mmol/l, respectively. No alterations were observed in CON. Muscle membrane proteins and enzyme activity did not change in either of the groups. The present study shows that interval training with short 10-s near-maximal bouts can improve performance and Vo(2max) despite a ∼50% reduction in training volume. In addition, the 10-20-30 training regime lowers resting systolic blood pressure and blood cholesterol, suggesting a beneficial effect on the health profile of already trained individuals.

V?O2 Kinetics and Performance in Soccer Players after Intense Training and Inactivity

PURPOSE The studys purpose was to examine the effects of a short-term period with intensified training or training cessation of trained soccer players on VO(2) kinetics at 75% maximal aerobic speed, oxidative enzymes, and performance in repeated high-intensity exercise. METHODS After the last match of the season, 18 elite soccer players were, for a 2-wk period, assigned to a high-intensity training group (n = 7) performing 10 training sessions mainly consisting of aerobic high-intensity training (8 × 2 min) and speed endurance training (10-12 × 30-s sprints) or a training cessation group (n = 11) that refrained from training. RESULTS For the training cessation group, VO(2) kinetics became slower (P < 0.05) with a larger time constant (τ = 21.5 ± 2.9 vs 23.8 ± 3.2 s (mean ± SD, before vs after)) and a larger mean response time (time delay + τ = 45.0 ± 1.8 vs 46.8 ± 2.2 s). The amount of muscle pyruvate dehydrogenase (17%, P < 0.01) and maximal activity of citrate synthase (12%) and 3-hydroxyacyl-CoA (18%, P < 0.05) were lowered. In addition, the fraction of slow twitch fibers (56% ± 18% vs 47% ± 15%, P < 0.05), Yo-Yo intermittent recovery level 2 test (845 ± 160 vs 654 ± 99 m), and the repeated sprint performance (33.41 ± 0.96 vs 34.11 ± 0.92 s, P < 0.01) were reduced. For the high-intensity training group, running economy was improved (P < 0.05), and the amount of pyruvate dehydrogenase (17%) and repeated sprint performance (33.44 ± 1.17 vs 32.81 ± 1.01 s) were enhanced (P < 0.05). CONCLUSIONS Inactivity slows VO(2) kinetics in association with a reduction of muscle oxidative capacity and repeated high-intensity running performance. In addition, intensified training of already well-trained athletes can improve mechanical efficiency and repeated sprint performance.

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 β(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.

Effect of intensified training on muscle ion kinetics, fatigue development, and repeated short-term performance in endurance-trained cyclists

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.

Effect of whey protein- and carbohydrate-enriched diet on glycogen resynthesis during the first 48 h after a soccer game

The effect of a whey protein‐ and carbohydrate (CHO)‐enriched diet on the rate of muscle glycogen resynthesis after a soccer match was examined. Sixteen elite soccer players were randomly assigned to a group ingesting a diet rich in carbohydrates and whey protein [CHO, protein, and fat content was 71, 21, and 8E%, respectively; high content of carbohydrates and whey protein (HCP), n = 9] or a group ingesting a normal diet (55, 18, and 26E%; control [CON], n = 7) during a 48‐h recovery period after a soccer match. CON and three additional players carried out a 90‐ and 60‐min simulated match without body contacts (SIM90 and SIM60). Muscle glycogen was lowered (P < 0.05) by 54, 48, 53, and 38% after the matches in CON, HCP, SIM90, and SIM60, respectively. Glycogen resynthesis during the first 48 h after the match was not different between CON and HCP, whereas glycogen resynthesis was slower (P < 0.05) during the first 24 h after SIM60 than SIM90 (2.88 ± 0.84 vs 4.32 ± 0.54 mmol/kg dw/h). In HCP, glycogen content in type II muscle fibers was still lowered 48 h after the match. In conclusion, glycogen resynthesis 48 h after a soccer match is not elevated by ingestion of a HCP diet. Furthermore, glycogen resynthesis does not appear to be impaired by body contacts during a match.

Impact of adrenaline and metabolic stress on exercise-induced intracellular signaling and PGC-1α mRNA response in human skeletal muscle.

This study tested the hypothesis that elevated plasma adrenaline or metabolic stress enhances exercise‐induced PGC‐1α mRNA and intracellular signaling in human muscle. Trained (VO2‐max: 53.8 ± 1.8 mL min−1 kg−1) male subjects completed four different exercise protocols (work load of the legs was matched): C – cycling at 171 ± 6 W for 60 min (control); A – cycling at 171 ± 6 W for 60 min, with addition of intermittent arm exercise (98 ± 4 W). DS – cycling at 171 ± 6 W interspersed by 30 sec sprints (513 ± 19 W) every 10 min (distributed sprints); and CS – cycling at 171 ± 6 W for 40 min followed by 20 min of six 30 sec sprints (clustered sprints). Sprints were followed by 3:24 min:sec at 111 ± 4 W. A biopsy was obtained from m. vastus lateralis at rest and immediately, and 2 and 5 h after exercise. Muscle PGC‐1α mRNA content was elevated (P < 0.05) three‐ to sixfold 2 h after exercise relative to rest in C, A, and DS, with no differences between protocols. AMPK and p38 phosphorylation was higher (P < 0.05) immediately after exercise than at rest in all protocols, and 1.3‐ to 2‐fold higher (P < 0.05) in CS than in the other protocols. CREB phosphorylation was higher (P < 0.05) 2 and 5 h after exercise than at rest in all protocols, and higher (P < 0.05) in DS than CS 2 h after exercise. This suggests that neither plasma adrenaline nor muscle metabolic stress determines the magnitude of PGC‐1α mRNA response in human muscle. Furthermore, higher exercise‐induced changes in AMPK, p38, and CREB phosphorylation are not associated with differences in the PGC‐1α mRNA response.

10-20-30 training increases performance and lowers blood pressure and VEGF in runners.

The present study examined the effect of training by the 10‐20‐30 concept on performance, blood pressure (BP), and skeletal muscle angiogenesis as well as the feasibility of completing high‐intensity interval training in local running communities. One hundred sixty recreational runners were divided into either a control group (CON; n = 28), or a 10‐20‐30 training group (10‐20‐30; n = 132) replacing two of three weekly training sessions with 10‐20‐30 training for 8 weeks and performance of a 5‐km run (5‐K) and BP was measured. VO2max was measured and resting muscle biopsies were taken in a subgroup of runners (n = 18). 10‐20‐30 improved 5‐K time (38 s) and lowered systolic BP (2 ± 1 mmHg). For hypertensive subjects in 10‐20‐30 (n = 30), systolic and diastolic BP was lowered by 5 ± 4 and 3 ± 2 mmHg, respectively, which was a greater reduction than in the non‐hypertensive subjects (n = 102). 10‐20‐30 increased VO2max but did not influence muscle fiber area, distribution or capillarization, whereas the expression of the pro‐angiogenic vascular endothelial growth factor (VEGF) was lowered by 22%. No changes were observed in CON. These results suggest that 10‐20‐30 training is an effective and easily implemented training intervention improving endurance performance, VO2max and lowering BP in recreational runners, but does not affect muscle morphology and reduces muscle VEGF.

Unchanged content of oxidative enzymes in fast-twitch muscle fibers and V˙O2 kinetics after intensified training in trained cyclists.

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 ( V˙O2 ) response during intense (INT), but not moderate (MOD), exercise and reduce the V˙O2 slow component and muscle metabolic perturbation during INT. Pulmonary V˙O2 kinetics was determined in eight trained male cyclists ( V˙O2 ‐max: 59 ± 4 (means ± SD) mL min−1 kg−1) during MOD (205 ± 12 W ~65% V˙O2 ‐max) and INT (286 ± 17 W ~85% V˙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. V˙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 V˙O2 kinetics.