Gymnastik- och idrottshögskolan, GIH

The objective of this work was to investigate myonuclear permanence and transcriptional regulation as mechanisms for cellular muscle memory after strength training in humans. Twelve untrained men and women performed 10 weeks of unilateral elbow-flexor strength training followed by 16 weeks of de-training. Thereafter, 10 weeks' re-training was conducted with both arms: the previously trained arm and the contralateral untrained control arm. Muscle biopsies were taken from the trained arm before and after both training periods and from the control arm before and after re-training. Muscle biopsies were analysed for fibre cross-sectional area (fCSA), myonuclei and global transcriptomics (RNA sequencing). During the first training period, myonuclei increased in type 1 (13 ± 17%) and type 2 (33 ± 23%) fibres together with a 30 ± 43% non-significant increase in mixed fibre fCSA (P = 0.069). Following de-training, fCSA decreased in both fibre types, whereas myonuclei were maintained, resulting in 33% higher myonuclear number in previously trained vs. control muscle in type 2 fibres. Furthermore, in the previously trained muscle, three differentially expressed genes (DEGs; EGR1, MYL5 and COL1A1) were observed. Following re-training, the previously trained muscle showed larger type 2 fCSA compared to the control (P = 0.035). However, delta change in type 2 fCSA was not different between muscles. Gene expression was more dramatically changed in the control arm (1338 DEGs) than in the previously trained arm (822 DEGs). The sustained higher number of myonuclei in the previously trained muscle confirms myonuclear accretion and permanence in humans. Nevertheless, because of the unclear effect on the subsequent hypertrophy with re-training, the physiological benefit remains to be determined. KEY POINTS: Muscle memory is a cellular mechanism that describes the capacity of skeletal muscle fibres to respond differently to training stimuli if the stimuli have been previously encountered. This study overcomes past methodological limitations related to the choice of muscles and analytical procedures. We show that myonuclear number is increased after strength training and maintained during de-training. Increased myonuclear number and differentially expressed genes related to muscle performance and development in the previously trained muscle did not translate into a clearly superior responses during re-training. Because of the unclear effect on the subsequent hypertrophy and muscle strength gain with re-training, the physiological benefit remains to be determined.

Blood flow restriction (BFR) with low-load resistance exercise (RE) is often used as a surrogate to traditional high-load RE to stimulate muscular adaptations, such as hypertrophy and strength. However, it is not clear whether such adaptations are achieved through similar cellular and molecular processes. We compared changes in muscle function, morphology and signaling pathways between these differing training protocols. Twenty-one males and females (mean ± SD: 24.3 ± 3.1 years) experienced with resistance training (4.9 ± 2.6 years) performed nine weeks of resistance training (three times per week) with either high-loads (75-80% 1RM; HL-RT), or low-loads with BFR (30-40% 1RM; LL-BFR). Before and after the training intervention, resting muscle biopsies were collected, and quadricep cross-sectional area (CSA), muscular strength and power were measured. Approximately 5 days following the intervention, the same individuals performed an additional 'acute' exercise session under the same conditions, and serial muscle biopsies were collected to assess hypertrophic- and ribosomal-based signaling stimuli. Quadricep CSA increased with both LL-BFR (7.4±4.3%) and HL-RT (4.6±2.9%), with no significant differences between training groups (p=0.37). Muscular strength also increased in both training groups, but with superior gains in squat 1RM occurring with HL-RT (p<0.01). Acute phosphorylation of several key proteins involved in hypertrophy signaling pathways, and expression of ribosomal RNA transcription factors occurred to a similar degree with LL-BFR and HL-RT (all p>0.05 for between-group comparisons). Together, these findings validate low-load resistance training with continuous BFR as an effective alternative to traditional high-load resistance training for increasing muscle hypertrophy in trained individuals.

PURPOSE: This study compared the effects of heavy resisted sprint training (RST) versus unresisted sprint training (UST) on sprint performance among adolescent soccer players.

METHODS: Twenty-four male soccer players (age: 15.7 [0.5] y; body height: 175.7 [9.4] cm; body mass: 62.5 [9.2] kg) were randomly assigned to the RST group (n = 8), the UST group (n = 10), or the control group (n = 6). The UST group performed 8 × 20 m unresisted sprints twice weekly for 4 weeks, whereas the RST group performed 5 × 20-m heavy resisted sprints with a resistance set to maximize the horizontal power output. The control group performed only ordinary soccer training and match play. Magnitude-based decision and linear regression were used to analyze the data.

RESULTS: The RST group improved sprint performances with moderate to large effect sizes (0.76-1.41) across all distances, both within and between groups (>92% beneficial effect likelihood). Conversely, there were no clear improvements in the UST and control groups. The RST evoked the largest improvements over short distances (6%-8%) and was strongly associated with increased maximum horizontal force capacities (r = .9). Players with a preintervention deficit in force capacity appeared to benefit the most from RST.

CONCLUSIONS: Four weeks of heavy RST led to superior improvements in short-sprint performance compared with UST among adolescent soccer players. Heavy RST, using a load individually selected to maximize horizontal power, is therefore highly recommended as a method to improve sprint acceleration in youth athletes.

Muscle disuse has rapid and debilitating effects on muscle mass and overall health, making it an important issue from both scientific and clinical perspectives. However, the myocellular adaptations to muscle disuse are not yet fully understood, particularly those related to the myonuclear permanence hypothesis. Therefore, in this study, we assessed fiber size, number of myonuclei, satellite cells, and capillaries in human gastrocnemius muscle after a period of immobilization following an Achilles tendon rupture. Six physically active patients (5M/1F, 43 {plus minus} 15 years) were recruited to participate after sustaining an acute unilateral Achilles tendon rupture. Muscle biopsies were obtained from the lateral part of the gastrocnemius before and after six weeks of immobilization using a plaster cast and orthosis. Muscle fiber characteristics were analyzed in tissue cross-sections and isolated single fibers using immunofluorescence and high-resolution microscopy. Immobilization did not change muscle fiber type composition nor cross-sectional area of type I or type II fibers, but muscle fiber volume tended to decline by 13% (p=0.077). After immobilization, the volume per myonucleus was significantly reduced by 20% (p=0.008). Myonuclei were not lost in response to immobilization but tended to increase in single fibers and type II fibers. No significant changes were observed for satellite cells or capillaries. Myonuclei were not lost in the gastrocnemius muscle after a prolonged period of immobilization, which may provide support to the myonuclear permanence hypothesis in human muscle. Capillaries remained stable throughout the immobilization period, whereas the response was variable for satellite cells, particularly in type II fibers.

INTRODUCTION: Human skeletal muscle is thought to have heightened sensitivity to exercise stimulus when it has been previously trained (i.e., it possesses "muscle memory"). We investigated whether basal and acute resistance exercise-induced gene expression and cell signaling events are influenced by previous strength training history.

METHODS: Accordingly, 19 training naïve women and men completed 10 weeks of unilateral leg strength training, followed by 20 weeks of detraining. Subsequently, an acute resistance exercise session was performed for both legs, with vastus lateralis biopsies taken at rest and 1 h after exercise in both legs (memory and control).

RESULTS: The phosphorylation of AMPK and eEF2 was higher in the memory leg than in the control leg at both time points. Post-exercise phosphorylation of 4E-BP1 was higher in the memory leg than in the control leg. The memory leg had lower basal mRNA levels of total PGC1α, and, unlike the control leg, exhibited increases in PGC1α-ex1a transcripts after exercise. In the genes related to myogenesis (SETD3, MYOD1, and MYOG), mRNA levels differed between the memory and the untrained leg; these effects were evident primarily in the male subjects. Expression of the novel gene SPRYD7 was lower in the memory leg at rest and decreased after exercise only in the control leg, but SPRYD7 protein levels were higher in the memory leg.

CONCLUSION: In conclusion, several key regulatory genes and proteins involved in muscular adaptations to resistance exercise are influenced by previous training history. Although the relevance and mechanistic explanation for these findings need further investigation, they support the view of a molecular muscle memory in response to training.

BACKGROUND: The effect of concurrent training on the development of maximal strength is unclear, especially in individuals with different training statuses.

OBJECTIVE: The aim of this systematic review and meta-analysis study was to compare the effect of concurrent resistance and endurance training with that of resistance training only on the development of maximal dynamic strength in untrained, moderately trained, and trained individuals.

METHODS: On the basis of the predetermined criteria, 27 studies that compared effects between concurrent and resistance training only on lower-body 1-repetition maximum (1RM) strength were included. The effect size (ES), calculated as the standardised difference in mean, was extracted from each study, pooled, and analysed with a random-effects model.

RESULTS: The 1RM for leg press and squat exercises was negatively affected by concurrent training in trained individuals (ES =  - 0.35, p < 0.01), but not in moderately trained ( - 0.20, p = 0.08) or untrained individuals (ES = 0.03, p = 0.87) as compared to resistance training only. A subgroup analysis revealed that the negative effect observed in trained individuals occurred only when resistance and endurance training were conducted within the same training session (ES same session =  - 0.66, p < 0.01 vs. ES different sessions =  - 0.10, p = 0.55).

CONCLUSION: This study demonstrated the novel and quantifiable effects of training status on lower-body strength development and shows that the addition of endurance training to a resistance training programme may have a negative impact on lower-body strength development in trained, but not in moderately trained or untrained individuals. This impairment seems to be more pronounced when training is performed within the same session than in different sessions. Trained individuals should therefore consider separating endurance from resistance training during periods where the development of dynamic maximal strength is prioritised.

The effects of concurrent strength and endurance training have been well studied in untrained and moderately-trained individuals. However, studies examining these effects in individuals with a long history of resistance training (RT) are lacking. Additionally, few studies have examined how strength and power are affected when different types of endurance training are added to an RT protocol. The purpose of the present study was to compare the effects of concurrent training incorporating either low-volume, high-intensity interval training (HIIT, 8-24 Tabata intervals at ~150% of VO2max) or high-volume, medium-intensity continuous endurance training (CT, 40-80 min at 70% of VO2max), on the strength and power of highly-trained individuals. Sixteen highly-trained ice-hockey and rugby players were divided into two groups that underwent either CT (n = 8) or HIIT (n = 8) in parallel with RT (2-6 sets of heavy parallel squats, > 80% of 1RM) during a 6-week period (3 sessions/wk). Parallel squat performance improved after both RT + CT and RT + HIIT (12 ± 8% and 14 ± 10% respectively, p < 0.01), with no difference between the groups. However, aerobic power (VO2max) only improved after RT + HIIT (4 ± 3%, p < 0.01). We conclude that strength gains can be obtained after both RT + CT and RT + HIIT in athletes with a prior history of RT. This indicates that the volume and/or intensity of the endurance training does not influence the magnitude of strength improvements during short periods of concurrent training, at least for highly-trained individuals when the endurance training is performed after RT. However, since VO2max improved only after RT + HIIT and this is a time efficient protocol, we recommend this type of concurrent endurance training.

Physical characteristics of elite male bandy players have not been studied for the last 30 years. Therefore, the purpose of this study was to evaluate the physical characteristics of elite male bandy players with respect to playing positions. A cross-sectional study was performed that included 25 male bandy players from one of the highest-ranked bandy leagues in the world. Body weight, length, isometric mid-thigh pull, countermovement jump, squat jump, unilateral long jump, bilateral long jump, 15- and 30-m sprint, 15-m flying sprint, and VO_2max were tested. Players were divided into forwards, midfielders, and defenders. Forwards had significantly (p = 0.012) higher relative VO_2max than defenders (59.8 ± 4.3 compared to 53.0 ± 5.6 mL/kg/min). No significant differences for any of the other measurements were observed between positions. This is the first study to present the physical characteristics between playing positions in off- and on-ice tests for male bandy players competing at the highest level. Today's bandy players are heavier and have lower relative VO_2max compared with players in the early 1990s. However, their work capacities have increased since their absolute VO_2max is higher. These results provide benchmark values that can serve as a foundation for strength and conditioning professionals when designing future training programs.

This study aimed to investigate the effect of intrasession exercise order of maximal effort flywheel resistance training (RT; 436 repetitions [rep]) and high-intensity interval training (HIIT, 2–438 rep of 20 second at 130% of Watt atV̇O2max [wV̇O2max]), on the development of maximal strength and power in elite team-sport athletes. A 7-week training intervention involving 2 training sessions per week of either HIIT followed by RT (HIIT + RT, n 5 8), RT followed by HIIT (RT + HIIT, n 5 8), or RTalone (RT, n 5 7) was conducted in 23 elite male bandy players (24.7 6 4.3 years). Power and work were continuously measured during the flywheel RT. Isometric squat strength (ISq), countermovement jump, squat jump, and V̇O2max were measured before and after the training period. Power output during training differed between the groups (p 5 0.013, h2p5 0.365) with RT producing more power than HIIT + RT (p 5 0.005). ISq improved following RT + HIIT (;80%, d 5 2.10, p 5 0.001) and following HIIT + RT(;40%, d 5 1.64, p 5 0.005), and RT alone (;70%, d 5 1.67, p 5 0.004). V̇O2max increased following RT + HIIT and HIIT + RT(;10%, d51.98, p50.001 resp. d52.08, p50.001). HIIT before RT reduced power output during RT in elite team-sport athletes but did not lead to blunted development of maximal strength or power after a 7-week training period. During longer training periods(.7-weeks), it may be advantageous to schedule RT before HIIT because the negative effect of HIIT + RT on training quality increased during the final weeks of training. In addition, the largest training effect on maximal strength was observed following RT +HIIT.

Kombinerad styrke- och konditionsträning är vardagsmat för elitidrottare och elitmotionärer. Men personer som tränar mycket är särskilt känsliga för den här träningsformen. Passens ordningsföljd och rätt mängd vila är därför viktigt för att maximera styrkeutvecklingen, visar ny forskning.

Isometric leg press (ILP) and countermovement jump (CMJ) are commonly used to obtain strength- and power-related variables with important implications for health maintenance and sports performance. To enable the identification of true changes in performance with these measurements, the reliability must be known. This study evaluates the between-session reliability of strength- and power-related measures obtained from ILP and CMJ. Thirteen female elite ice hockey players (21.5 ± 5.1 years; 66.3 ± 8.0 kg) performed three maximal ILPs and CMJs on two different occasions. Variables from the ILP (peak force and peak rate of force development) and CMJ (peak power, peak force, peak velocity, and peak jump height) were obtained. The results were reported using the best trial, an average of the two best trials, or an average of three trials. The intraclass correlation coefficient (ICC) and coefficient of variation (CV) were high (ICC > 0.97; CV < 5.2%) for all outcomes. The CV for the CMJ (1.5-3.2%) was lower than that for the ILP (3.4-5.2%). There were no differences between reporting the best trial, an average of the two best trials, or an average of the three trials for the outcomes. ILP and CMJ are highly reliable when examining strength- and power-related variables in elite female ice hockey players.

This study investigates how different recovery periods after high-intensity interval training (HIIT) affects strength and explosive performance during a power training (PT) session. Fifteen female elite ice hockey players (22.5 ± 5.2 years) performed PT, including 6 sets of 2 repetitions (reps) of isometric leg press (ILP) and 6 sets of 3 reps of countermovement jump (CMJ), following a rested state and 10 minutes, 6 hours, or 24 hours after HIIT (3 sets of 8 × 20 seconds at 115% of power output at maximal oxygen consumption on a cycle ergometer). Peak force (PF) and peak rate of force development (pRFD) were measured during the ILP. Peak jump height (PJH), concentric phase duration (ConDur), eccentric phase duration, total duration, peak power (PP), velocity at peak power (V@PP), and force at peak power were measured during CMJ. The following variables were significantly reduced when only a 10-minute recovery period was allowed between HIIT and PT: PF was reduced by 7% (p < 0.001), pRFD by 17% (p < 0.001), PJH by 4% (p < 0.001), ConDur by 4% (p = 0.018), PP by 2% (p = 0.016), and V@PP by 2% (p = 0.007). None of the measured variables were reduced when PT was performed 6 and 24 hours after HIIT. We conclude that strength and explosive performance of elite female ice hockey players is reduced 10 minutes after HIIT but not negatively affected if a rest period of at least 6 hours is provided between HIIT and PT.

Endurance training is a powerful tool to improve both health and performance. Physical activity is now recognized as an effective treatment and prevention therapy for a wide range of diseases. One of the most profound adaptations to endurance training is increased mitochondrial function and content within the exercising muscles. Mitochondrial quality and quantity are closely related to several of the positive health effects reported after training. High mitochondrial content strongly correlates with muscle oxidative capacity and endurance performance. Even though it is well known that endurance training increases mitochondrial content, it is unclear which type of training is the most efficient to promote mitochondrial biogenesis. Therefore, the basis for current exercise recommendations relative to mitochondrial biogenesis is poor or absent. Thus, the main objective of this thesis was to evaluate the effect of different training strategies on mitochondrial biogenesis.

Recent developments in molecular methods have made it possible to study the initial adaptations to training through measurement of mRNA gene expression of exercise induced genes. One such gene is transcriptional coactivator peroxisome proliferator–activated receptor-γ coactivator-1α (PGC-1α). PGC-1α is a key regulator of mitochondrial biogenesis and the expression of PGC-1α can therefore be used as a marker of this process.

The first four studies presented in this thesis are acute exercise studies where two different exercise models were compared using a cross-over design. Muscle biopsies were obtained pre and post exercise and analysed for gene expression and glycogen, apart from study II. The final study was a long-term training study where muscle biopsies were obtained before and after the training period and analysed for mitochondrial enzyme activities and protein content.

Study I: The expression of PGC-1α and related genes were examined after 90 min of continuous and interval exercise in untrained subjects. The exercise protocols influenced the expression of genes involved in mitochondrial biogenesis and oxidative metabolism in a similar manner. Both interval and continuous exercise were potent training strategies for relatively sedentary individuals.

Study II: The expression of PGC-1α and related genes were examined after low-volume sprint interval (SIT) and high-volume interval (IE) exercise in highly trained cyclists. SIT induced a similar increase in PGC-1α expression as IE despite a much lower time commitment and work completed. Sprint interval exercise might, therefore, be a time efficient training strategy for highly trained individuals.

Study III: The expression of PGC-1α and related genes, as well as the activity of upstream proteins, were examined after concurrent (ER: cycling + leg press) and single-mode (E: cycling only) exercise in untrained subjects. PGC-1α expression doubled after ER compared with E. It was concluded that concurrent training might be beneficial for mitochondrial biogenesis in untrained individuals.

Study IV: The expression of PGC-1α and related genes were examined after exercise performed with low (LG) and normal (NG) muscle glycogen in well-trained cyclists. PGC-1α expression increased approximately three times more after LG compared with NG. This finding suggested that low glycogen exercise is a potent inducer of mitochondrial biogenesis in well-trained individuals.

Study V: Mitochondrial enzyme activity, protein content and endurance performance were examined after eight weeks of concurrent (ES: cycling + leg press) or single-mode (E: cycling only) training in cyclists. ES did not affect enzyme activity, protein content or endurance performance differently than E. The beneficial effect previously observed in untrained subjects did not translate to higher numbers of mitochondria in trained individuals.

In three of the studies, I, III, and IV, both glycogen and PGC-1α expression were measured after exercise. These data were then pooled and examined. The highest PGC-1α mRNA expression levels were identified when glycogen levels were low, and vice versa. This suggests that low glycogen might play an important role in the regulation of mitochondrial biogenesis also during interval and concurrent strength and endurance exercise.

In conclusion, key markers of mitochondrial biogenesis can be effectively up-regulated by interval, concurrent and low glycogen exercise. A possible explanation for this might be that though the exercise protocols are quite divergent in nature, they all have a pronounced effect on muscle glycogen and/or perturbation in energetic stress.

Introduction

It is well known that muscle strength increases in both the untrained and trained limb after a period of unilateral strength training. However, it is not known how this so called cross-education effect (CE-effect) is affected by a long period of detraining, and if there are any sex differences. Also, there are conflicting results regarding the effect of unilateral training on muscle mass in the untrained limb.

Aim

The primary objective was to study the CE-effect in men and women after a period of unilateral strength training and detraining. The secondary objective was to study if training one limb would affect the muscle mass of the homologous opposite limb.

Method

Sixteen untrained individuals, 9 females and 7 males, completed the study. The training intervention was 10 weeks (34 sessions) of unilateral strength training (leg press (LP) and leg extension (LE) exercise). 1RM and muscle thickness (vastus lateralis) were measured pre-, post- and 20 weeks post-training.

Results

Strength (1RM) in the trained leg increased for both men and woman (LP: ~60%, LE ~20%, p<0.01), with no sex differences. However, only the men had a strength increase in the untrained leg (LP: 26%, LE: 10%, p<0.05) and the non-significant increase observed for the woman (LP: 10%, LE: 3%) was significantly smaller than the increase in the men (p<0.05). Muscle thickness increased similarly for both men and women (trained leg: ~14%, p<0.01; untrained leg: ~4%, p<0.05). The detraining period did not affect strength, but muscle thickness was reduced close to pre-training values in both men and women.

Conclusion

The results of the present study show that the CE-effect is larger in men than women, and that it is long lasting (at least 20 weeks). Further, strength training of one leg can increase the muscle mass of the homologous opposite leg.

Previously trained mouse muscles acquire strength and volume faster than naïve muscles; it has been suggested that this is related to increased myonuclear density. The present study aimed to determine whether a previously strength-trained leg (mem-leg) would respond better to a period of strength training than a previously untrained leg (con-leg). Nine men and 10 women performed unilateral strength training (T1) for 10 weeks, followed by 20 weeks of detraining (DT) and a 5-week bilateral retraining period (T2). Muscle biopsies were taken before and after each training period and analyzed for myonuclear number, fiber volume, and cross-sectional area (CSA). Ultrasound and one repetition of maximum leg extension were performed to determine muscle thickness (MT) and strength. CSA (~17%), MT (~10%), and strength (~20%) increased during T1 in the mem-leg. However, the myonuclear number and fiber volume did not change. MT and CSA returned to baseline values during DT, but strength remained elevated (~60%), supporting previous findings of a long-lasting motor learning effect. MT and strength increased similarly in the mem-leg and con-leg during T2, whereas CSA, fiber volume, and myonuclear number remained unaffected. In conclusion, training response during T2 did not differ between the mem-leg and con-leg. However, this does not discount the existence of human muscle memory since no increase in the number of myonuclei was detected during T1 and no clear detraining effect was observed for cell size during DT; thus, the present data did not allow for a rigorous test of the muscle memory hypothesis.

The molecular signaling of mitochondrial biogenesis is enhanced when resistance exercise is added to a bout of endurance exercise. The purpose of the present study was to examine if this mode of concurrent training translates into increased mitochondrial content and improved endurance performance. Moderately trained cyclists performed 8 weeks (two sessions per week) of endurance training only (E, n = 10; 60-min cycling) or endurance training followed by strength training (ES, n = 9; 60-min cycling + leg press). Muscle biopsies were obtained before and after the training period and analyzed for enzyme activities and protein content. Only the ES group increased in leg strength (+19%, P < 0.01), sprint peak power (+5%, P < 0.05), and short-term endurance (+9%, P < 0.01). In contrast, only the E group increased in muscle citrate synthase activity (+11%, P = 0.06), lactate threshold intensity (+3%, P < 0.05), and long-term endurance performance (+4%, P < 0.05). Content of mitochondrial proteins and cycling economy was not affected by training. Contrary to our hypothesis, the results demonstrate that concurrent training does not enhance muscle aerobic capacity and endurance performance in cyclists.

Recent studies suggest that carbohydrate restriction can improve the training-induced adaptation of muscle oxidative capacity. However, the importance of low muscle glycogen on the molecular signaling of mitochondrial biogenesis remains unclear. Here, we compare the effects of exercise with low (LG) and normal (NG) glycogen on different molecular factors involved in the regulation of mitochondrial biogenesis. Ten highly trained cyclists (VO(2max) 65 ± 1 ml/kg/min, W (max) 387 ± 8 W) exercised for 60 min at approximately 64 % VO(2max) with either low [166 ± 21 mmol/kg dry weight (dw)] or normal (478 ± 33 mmol/kg dw) muscle glycogen levels achieved by prior exercise/diet intervention. Muscle biopsies were taken before, and 3 h after, exercise. The mRNA of peroxisome proliferator-activated receptor-γ coactivator-1 was enhanced to a greater extent when exercise was performed with low compared with normal glycogen levels (8.1-fold vs. 2.5-fold increase). Cytochrome c oxidase subunit I and pyruvate dehydrogenase kinase isozyme 4 mRNA were increased after LG (1.3- and 114-fold increase, respectively), but not after NG. Phosphorylation of AMP-activated protein kinase, p38 mitogen-activated protein kinases and acetyl-CoA carboxylase was not changed 3 h post-exercise. Mitochondrial reactive oxygen species production and glutathione oxidative status tended to be reduced 3 h post-exercise. We conclude that exercise with low glycogen levels amplifies the expression of the major genetic marker for mitochondrial biogenesis in highly trained cyclists. The results suggest that low glycogen exercise may be beneficial for improving muscle oxidative capacity.

Introduction: the current textbook model suggests that the myonuclear domain size is constant for muscle fibers in both their atrophic and hypertrophic state. However, recent animal studies show that myonuclear content is maintained after atrophy leading to a decreased myonuclear domain size (Gundersen et al. J Physiol. 2008 Jun 1;586(11):2675-81). This remains to be investigated in human skeletal muscle and the aim of the present study was therefore to study the effect of grave atrophy on myonuclear content and domain size in the vastus medialis muscle.

Materials and Methods: biopsies were obtained from vastus medialis on a 22 year old female patient before and 6 weeks after an anterior cruciate ligament reconstructionand meniscus repair surgery. Histochemical analyses were done to analyze fiber cross sectional area (CSA), fiber type composition and number of myonuclei per fiber.

Results: the CSA of type II muscle fibers decreased by 35% (from 4297±55 to 2807±64 µm²) whereas the number of myonuclei per fiber remained stable (3.4±0.4 and 3.9±0.5, pre and post respectively). The nuclear domain size was thereby decreased by ~40% (from 1255 to 722 µm²). There were only minor changes in type I muscle fiber CSA, myonuclei content and domain size.

Conclusion: in line with previous findings from animal studies, the present case study shows that the number of myonuclei per fiber is maintained and the domain size is reduced in human skeletal muscle after immobilization induced atrophy.

Många som vill öka sin muskelmassa och styrka undviker uthållighetsträning. En vanlig åsikt är nämligen att man inte bör kombinera styrke ochuthållighetsträning. Den uppfattningen har däremot inget stöd i den senaste forskningen.

Det finns många uppfattningar om hur man bäst förbättrar konditionen. Ofta förlitar idrottare sig mer på beprövad erfarenhet än på vetenskapen. Men under de senaste åren har idrottsforskningen, med hjälp av molekylärbiologisk teknik, gjort framsteg i hur man kan effektivisera sin träning genom kosten och sättet att träna.

Little is known about the effect of training on genetic markers for mitochondrial biogenesis in elite athletes. We tested the hypothesis that low-volume sprint interval exercise (SIE) would be as effective as high-volume interval exercise (IE). Ten male cyclists competing on national elite level (W (max) 403 ± 13 W, VO(2peak) 68 ± 1 mL kg(-1) min(-1)) performed two interval exercise protocols: 7 × 30-s "all-out" bouts (SIE) and 3 × 20-min bouts at ~87% of VO(2peak) (IE). During IE, the work was eightfold larger (1,095 ± 43 vs. 135 ± 5 kJ) and the exercise duration 17 times longer (60 vs. 3.5 min) than during SIE. Muscle samples were taken before and 3 h after exercise. The mRNA of upstream markers of mitochondrial biogenesis [peroxisome proliferator-activated receptor-γ coactivator-1 (PGC-1α), PGC-1α-related coactivator (PRC) and peroxisome proliferator-activated receptor δ (PPARδ)] increased to the same extent after SIE and IE (6-, 1.5- and 1.5-fold increase, respectively). Of the downstream targets of PGC-1α, mitochondrial transcription factor A (Tfam) increased only after SIE and was significantly different from that after IE (P < 0.05), whereas others increased to the same extent (pyruvate dehydrogenase kinase, PDK4) or was unchanged (nuclear respiratory factor 2, NRF2). We conclude that upstream genetic markers of mitochondrial biogenesis increase in a similar way in elite athletes after one exercise session of SIE and IE. However, since the volume and duration of work was considerably lower during SIE and since Tfam, the downstream target of PGC-1α, increased only after SIE, we conclude that SIE might be a time-efficient training strategy for highly trained individuals.

Combining endurance and strength training (concurrent training) may change the adaptation compared with single mode training. However, the site of interaction and the mechanisms are unclear. We have investigated the hypothesis that molecular signaling of mitochondrial biogenesis after endurance exercise is impaired by resistance exercise. Ten healthy subjects performed either only endurance exercise (E: 1h cycling at ~65% of VO(2max)) or endurance exercise followed by resistance exercise (ER: 1h cycling + 6 sets of leg press at 70-80% of 1 repetition maximum) in a randomized cross-over design. Muscle biopsies were obtained before and after exercise (1 and 3h Post cycling). The mRNA of genes related to mitochondrial biogenesis (PGC-1α, PRC) and substrate regulation (PDK4) increased after both E and ER, but the mRNA levels were about 2-fold higher after ER (P<0.01). Phosphorylation of proteins involved in the signaling cascade of protein synthesis (mTOR, S6K1 and eEF2) was altered after ER but not after E. Moreover, ER induced a larger increase in mRNA of genes associated with positive mTOR signaling (cMyc and Rheb). Phosphorylation of AMPK, ACC and Akt increased similarly at 1h Post (P<0.01) after both types of exercise. Contrary to our hypothesis, the results demonstrate that resistance exercise, performed after endurance exercise, amplifies the adaptive signaling response of mitochondrial biogenesis compared with single-mode endurance exercise. The mechanism may relate to a crosstalk between signaling pathways mediated by mTOR. The results suggest that concurrent training may be beneficial for the adaptation of muscle oxidative capacity.

PURPOSE: There is a debate whether interval or traditional endurance training is the most effective stimulus of mitochondrial biogenesis. Here, we compared the effects of acute interval exercise (IE) or continuous exercise (CE) on the muscle messenger RNA (mRNA) content for several genes involved in mitochondrial biogenesis and lipid metabolism. METHODS: Nine sedentary subjects cycled for 90 min with two protocols: CE (at 67% VO2max) and IE (12 s at 120% and 18 s at 20% of VO2max). The duration of exercise and work performed with CE and IE was identical. Muscle biopsies were taken before and 3 h after exercise. RESULTS: There were no significant differences between the two exercise protocols in the increases in VO2 and HR, the reduction in muscle glycogen (35%-40% with both protocols) or the changes in blood metabolites (lactate, glucose, and fatty acids). The mRNA content for major regulators of mitochondrial biogenesis [peroxisome proliferator-activated receptor (PPAR) gamma coactivator 1alpha (PGC-1alpha), PGC-1-related coactivator, PPARbeta/delta] and of lipid metabolism [pyruvate dehydrogenase kinase isozyme 4 (PDK4)] increased after exercise, but there was no significant difference between IE and CE. However, the mRNA content for several downstream targets of PGC-1alpha increased significantly only after CE, and mRNA content for nuclear respiratory factor 2 was significantly higher after CE (P < 0.025 vs IE). CONCLUSIONS: The present findings demonstrate that, when the duration of exercise and work performed is the same, IE and CE influence the transcription of genes involved in oxidative metabolism in a similar manner.

BACKGROUND: The effects of flywheel resistance training (FRT) on youth are relatively unknown. The aim of this study was to compare the effects of autoregulated FRT with traditional strength training (TST) on jumping, running performance and resistance training load progression in youth athletes. Thirty youth athletes (11.8 ± 0.9 yr) were matched for peak height velocity (PHV) status and block-randomised into two groups: FRT (n = 15, PHV -0.8 ± 1.6) and TST (n = 15, PHV -0.8 ± 1.5). Twelve resistance training sessions over a six-week intervention with flywheel or barbell squats were performed using autoregulated load prescription. Squat jump (SJ); countermovement jump (CMJ); and 10 m, 20 m and 30 m sprints were assessed pre- and post-intervention. The external load increased similarly for FRT and TST (z = 3.8, p = 0.06). SJ increased for both groups (p < 0.05) but running performance was unaffected (p > 0.05).

CONCLUSIONS: FRT resulted in similar load progression and motor skill development in youth athletes as TST, but the perceived exertion was less. Autoregulation is a practical method for adjusting training load during FRT and should be considered as an alternative to autoregulated TST.