Casper Skovgaard

Concurrent speed endurance and resistance training improves performance, running economy and muscle NHE1 in moderately trained runners

The purpose of this study was to examine whether speed endurance training (SET, repeated 30-s sprints) and heavy resistance training (HRT, 80-90% of 1 repetition maximum) performed in succession are compatible and lead to performance improvements in moderately trained endurance runners. For an 8-wk intervention period (INT) 23 male runners [maximum oxygen uptake (V̇O(2max)) 59 ± 1 ml·min(-1)·kg(-1); values are means ± SE] either maintained their training (CON, n = 11) or performed high-intensity concurrent training (HICT, n = 12) consisting of two weekly sessions of SET followed by HRT and two weekly sessions of aerobic training with an average reduction in running distance of 42%. After 4 wk of HICT, performance was improved (P < 0.05) in a 10-km run (42:30 ± 1:07 vs. 44:11 ± 1:08 min:s) with no further improvement during the last 4 wk. Performance in a 1,500-m run (5:10 ± 0:05 vs. 5:27 ± 0:08 min:s) and in the Yo-Yo IR2 test (706 ± 97 vs. 491 ± 65 m) improved (P < 0.001) only following 8 wk of INT. In HICT, running economy (189 ± 4 vs. 195 ± 4 ml·kg(-1)·km(-1)), muscle content of NHE1 (35%) and dynamic muscle strength was augmented (P < 0.01) after compared with before INT, whereas V̇O(2max), muscle morphology, capillarization, content of muscle Na(+)/K(+) pump subunits, and MCT4 were unaltered. No changes were observed in CON. The present study demonstrates that SET and HRT, when performed in succession, lead to improvements in both short- and long-term running performance together with improved running economy as well as increased dynamic muscle strength and capacity for muscular H(+) transport in moderately trained endurance runners.

Combined speed endurance and endurance exercise amplify the exercise‐induced PGC‐1α and PDK4 mRNA response in trained human muscle

The aim of this study was to investigate the mRNA response related to mitochondrial biogenesis, metabolism, angiogenesis, and myogenesis in trained human skeletal muscle to speed endurance exercise (S), endurance exercise (E), and speed endurance followed by endurance exercise (S + E). Seventeen trained male subjects (maximum oxygen uptake (VO2‐max): 57.2 ± 3.7 (mean ± SD) mL·min−1·kg−1) performed S (6 × 30 sec all‐out), E (60 min ~60% VO2‐max), and S + E on a cycle ergometer on separate occasions. Muscle biopsies were obtained at rest and 1, 2, and 3 h after the speed endurance exercise (S and S + E) and at rest, 0, 1, and 2 h after exercise in E. In S and S + E, muscle peroxisome proliferator‐activated receptor‐γ coactivator‐1 (PGC‐1α) and pyruvate dehydrogenase kinase‐4 (PDK4) mRNA were higher (P < 0.05) 2 and 3 h after speed endurance exercise than at rest. Muscle PGC‐1α and PDK4 mRNA levels were higher (P < 0.05) after exercise in S + E than in S and E, and higher (P < 0.05) in S than in E after exercise. In S and S + E, muscle vascular endothelial growth factor mRNA was higher (P < 0.05) 1 (S only), 2 and 3 h after speed endurance exercise than at rest. In S + E, muscle regulatory factor‐4 and muscle heme oxygenase‐1 mRNA were higher (P < 0.05) 1, 2, and 3 h after speed endurance exercise than at rest. In S, muscle hexokinase II mRNA was higher (P < 0.05) 2 and 3 h after speed endurance exercise than at rest and higher (P < 0.05) than in E after exercise. These findings suggest that in trained subjects, speed endurance exercise provides a stimulus for muscle mitochondrial biogenesis, substrate regulation, and angiogenesis that is not evident with endurance exercise. These responses are reinforced when speed endurance exercise is followed by endurance exercise.

Effect of increased and maintained frequency of speed endurance training on performance and muscle adaptations in runners

The aim of the study was, in runners accustomed to speed endurance training (SET), to examine the effect of increased and maintained frequency of SET on performance and muscular adaptations. After familiarization (FAM) to SET, 18 male (n = 14) and female (n = 4) runners (V̇o2max: 57.3 ± 3.4 ml/min; means ± SD) completed 20 sessions of maintained low-frequency (LF; every fourth day; n = 7) or high-frequency (HF; every second day; n = 11) SET. Before FAM as well as before and after an intervention period (INT), subjects completed a series of running tests and a biopsy from m. vastus lateralis was collected. Ten-kilometer performance improved (P < 0.05) ~3.5% during FAM with no further change during INT. Time to exhaustion at 90% vV̇o2max was 15 and 22% longer (P < 0.05) during FAM and a further 12 and 16% longer (P < 0.05) during INT in HF and LF, respectively. During FAM, muscle expression of NHE1 and maximal activity of citrate synthase (CS) and phosphofructokinase (PFK) increased (P < 0.05), running economy (RE) improved (P < 0.05), and V̇o2max was unchanged. During INT, both HF and LF increased (P < 0.05) muscle expression of NKAβ1, whereas maximal activity of CS and PFK, RE, and V̇o2max were unchanged. Furthermore, during INT, muscle expression of FXYD1 and SERCA1, and FXYD1 activity increased (P < 0.05) in HF, while muscle expression of SERCA2 decreased (P < 0.05) in LF. Thus increased or maintained frequency of SET leads to further improvements in short-term exercise capacity, but not in 10-km running performance. The better short-term exercise capacity may be associated with elevated expression of muscle proteins related to Na+/K+ transportation and Ca2+ reuptake. NEW & NOTEWORTHY Ten speed endurance training (SET) sessions improved short-term exercise capacity and 10-km performance, which was followed by further improved short-term exercise capacity, but unchanged 10-km performance after 20 SET sessions performed with either high frequency (4 per 8 days) or continued low frequency (2 per 8 days) in trained runners. The further gain in short-term exercise capacity was associated with changes in muscle expression of proteins of importance for the development of fatigue.

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.

The effect of repeated periods of speed endurance training on performance, running economy, and muscle adaptations

The effect of repeated intense training interventions was investigated in eight trained male runners (maximum oxygen uptake [VO2‐max]: 59.3±3.2 mL/kg/min, mean±SD) who performed 10 speed endurance training (SET; repeated 30‐seconds “all‐out” bouts) and 10 aerobic moderate‐intensity training sessions during two 40‐day periods (P1 and P2) separated by ~80 days of habitual training. Before and after both P1 and P2, subjects completed an incremental test to exhaustion to determine VO2‐max and a repeated running test at 90% vVO2‐max to exhaustion (RRT) to determine short‐term endurance capacity. In addition, running economy (RE) was measured at 60% vVO2‐max (11.9±0.5 km/h) and v10‐km (14.3±0.9 km/h), a 10‐km track‐running test was performed, and a biopsy from m. vastus lateralis was collected. 10‐km performance and VO2‐max (mL/min) were the same prior to P1 and P2, whereas RE was better (P<.05) before P2 than before P1. During P1 and P2, 10‐km performance (2.9% and 2.3%), VO2‐max (2.1% and 2.6%), and RE (1.9% and 1.8% at 60% vVO2‐max; 1.6% and 2.0% at v10‐km) improved (P<.05) to the same extent, respectively. Performance in RRT was 20% better (P<.05) after compared to before P2, with no change in P1. No changes in muscle expression of Na+,K+‐ATPase α1, α2 and β1, NHE1, SERCA1 and SERCA2, actin, and CaMKII were found during neither P1 nor P2. Thus, the present study demonstrates that a second period of intense training leads to improved short‐term performance and further improved RE, whereas 10‐km performance and VO2‐max improve to the same extent as during the first period.

Effect of tapering after a period of high-volume sprint interval training on running performance and muscular adaptations in moderately trained runners

The effect of tapering following a period of high-volume sprint interval training (SIT) and a basic volume of aerobic training on performance and muscle adaptations in moderately trained runners was examined. Eleven (8 men, 3 women) runners [maximum oxygen uptake (V̇o2max): 56.8 ± 2.9 ml·min-1·kg-1; mean ± SD] conducted high-volume SIT (HV; 20 SIT sessions; 8-12 × 30 s all-out) for 40 days followed by 18 days of tapering (TAP; 4 SIT sessions; 4 × 30 s all-out). Before and after HV as well as midway through and at the end of TAP, the subjects completed a 10-km running test and a repeated running test at 90% of vV̇o2max to exhaustion (RRT). In addition, a biopsy from the vastus lateralis muscle was obtained at rest. Performance during RRT was better ( P < 0.01) at the end of TAP than before HV (6.8 ± 0.5 vs. 5.6 ± 0.5 min; means ± SE), and 10-km performance was 2.7% better ( P < 0.05) midway through (40.7 ± 0.7 min) and at the end of (40.7 ± 0.6 min) TAP than after HV (41.8 ± 0.9 min). The expression of muscle Na+-K+-ATPase (NKA)α1, NKAβ1, phospholemman (FXYD1), and sarcoplasmic reticulum calcium transport ATPase (SERCA1) increased ( P < 0.05) during HV and remained higher during TAP. In addition, oxygen uptake at 60% of vV̇o2max was lower ( P < 0.05) at the end of TAP than before and after HV. Thus short-duration exercise capacity and running economy were better than before the HV period together with higher expression of muscle proteins related to Na+/K+ transport and Ca2+ reuptake, while 10-km performance was not significantly improved by the combination of HV and tapering. NEW & NOTEWORTHY Short-duration performance became better after 18 days of tapering from ~6 wk of high-volume sprint interval training (SIT), whereas 10-km performance was not significantly affected by the combination of high-volume SIT and tapering. Higher expression of muscle NKAα1, NKAβ1, FXYD1, and SERCA1 may reflect faster Na+/K+ transport and Ca2+ reuptake that could explain the better short-duration performance. These results suggest that the type of competition should determine the duration of tapering to optimize performance.

Abundance of ClC-1 chloride channel in human skeletal muscle: Fibre type specific differences and effect of training

Cl- channel protein 1 (ClC-1) may be important for excitability and contractility in skeletal muscle, but ClC-1 abundance has not been examined in human muscle. The aim of the present study was to examine ClC-1 abundance in human skeletal muscle, including fiber type specific differences and the effect of exercise training. A commercially available antibody was tested with positive and negative control tissue, and it recognized specifically ClC-1 in the range from 100 to 150 kDa. Abundance of ClC-1 was 38% higher ( P < 0.01) in fast twitch Type IIa muscle fibers than in slow twitch Type I. Muscle ClC-1 abundance did not change with 4 wk of training consisting of 30 min cycling at 85% of maximal heart rate (HRmax) and 3 × 30-s all out sprints or during a 7-wk training period with 10-12 × 30 s uphill cycling and 4-5 × ~4 min cycling at 90%-95% of HRmax. ClC-1 abundance correlated negatively ( P < 0.01) with maximal oxygen consumption ( r = -0.552) and incremental exercise performance ( r = -0.546). In addition, trained cyclists had lower ( P < 0.01) ClC-1 abundance than lesser trained individuals. The present observations indicate that a low abundance of muscle ClC-1 may be beneficial for exercise performance, but the role of abundance and regulation of ClC-1 in skeletal muscle of humans with respect to exercise performance and trainability need to be elucidated. NEW & NOTEWORTHY Abundance of the Cl- channel protein 1 (ClC-1) chloride channel may be important for excitability and contractility in human skeletal muscle and may therefore have implications for fatigue development. In this study, we confirmed ClC-1 specificity for a commercially available antibody, and this study is first to our knowledge to determine ClC-1 protein abundance in human muscle by Western blotting. We observed that abundance of ClC-1 was higher in fast compared with slow twitch fibers and lower in trained individuals than in recreationally active.