Today, I would like to present some abstracts from the last Congress of the European College of Sports Science (Belgium, July 2012). In general, many studies, more than 2000 participants and a nice city (Bruges). What I have tried to do below is to group the most interesting studies into:
- · Physiology
- · hot methods & new equipment
- · Injury prevention
- · High intensity intermittent training
TRAINABILITY: A MATTER OF GENE VARIANTS?
Ring-Dimitriou et al
University of Salzburg
Beside exercise prescription single-nucleotide polymorphism (SNP) in genes important for mitochondria function such as PPARGC1A and PPARD have been reported to affect the change in anaerobic threshold in a retrospective study (Stefan et al., 2007). Therefore we prospectively investigated a 10-wk training response of men with SNP in these genes. Methods Genotyping (TaqMan, ABI7900HT) was performed in 838 sedentary males for SNP in PPARGC1A (rs8192678) and PPARD (rs2267668). After intervention (supervised 10 wks cycling, 3x 60 min, HR@70-90% VO2peak) n=28 remained for post tests (59±7 yrs, 27.6±4.1 kg/m² BMI, 36.3±6.9 ml/kg/min VO2peak). Subjects were assigned to wild type (WT=13), SNP1 (minor risk allele for PPARGC1A, WT for PPARD, n=6), and SNP2 (risk alleles for both genes, n=9). Trainability was determined as the relative change in work rate P@VT (point of optimal respiration), P@AT (anaerobic threshold), and P@RCP (respiratory compensation point) based on gas exchange analyses (ZAN680, nSpire Health, US) during incremental cycling (Ergoline, Schiller). Mean differences within and between groups were determined by ANOVA with p<0.05. The study was approved by the Salzburg Ethics Committee and funded by National Bank of Austria (J14156). Results Significant differences were found within WT in P@VT (99±21 vs. 122±19 W, p=.005) and @RCP (155±25 vs. 185±29 W, p=.009) only. P@RCP was significantly lowest in SNP1 compared to SNP2 and WT (%, 3±9 vs. 12±5 vs. 20±15; F=4.6, p=.02). VO2@VT and @RCP were significantly lower in SNP1 and SNP2 compared to WT (%, 2±10 vs. 4±13 vs. 18±15, F=3.6, p=.04, and 0±8 vs. 6±5 vs. 17±16 vs., F=4.8, p=.02, respectively). Discussion In line with the findings of Stefan et al. (2007), we found a diminished exercise effect at sub maximal performance level of untrained males with SNPs. The short-term response at these levels of >15% in WT was sufficient compared to other reports (Skinner et al., 2001) and could probably serve as trainability markers regarding to Vollaard et al. (2009). Although the power of our study is limited due to sample size and sex selection, our data indicate that the trainability of aerobic performance could be affected by gene variants.
REGULATION OF HUMAN MUSCLE STEM CELLS FOLLOWING EXERCISE
McMaster University, Canada
The role of muscle stem cells (satellite cells) in promoting muscle growth and adaptation in humans has largely been understudied. Nonetheless, excellent work has been reported by groups from around the world. The fact that a satellite cell response is triggered following an acute bout of exercise is generally accepted as fact. What remains a significant point of contention is whether or not satellite cells play a role in promoting growth in adulthood. Additionally, very little is known about the regulatory mechanisms that govern satellite cell function and fate. Over the last five years we and others have made a significant effort to reveal regulatory mechanisms that may govern satellite cell activation, proliferation and differentiation in humans. Modest progress has been made, however the regulatory mechanisms that drive the satellite cell response in humans are now being revealed. To date we have identified key roles for myostatin in
the activation of satellite cells following exercise and IL6 in the proliferation of satellite cells. We have also identified how these factors are affected by age in their ability to promote satellite cell activation and proliferation. Collectively, we are just beginning to appreciate the complex regulatory mechanisms that govern human satellite cell function.
PERIPHERAL VISUAL PERCEPTION DURING EXERCISE: WHY WE CANNOT SEE
Vision is one of the most important sensory modalities in humans. The visual field is defined as the area perceived by the eyes while people fixate on a point, and is composed of the central and peripheral visual fields. Many sports require high-level visual perceptual skills under conditions of physiological stress. In sports such as football, players gather visual information from the periphery of the visual field to see other players and objects beyond the central visual field. Thus, peripheral visual perception may play an important role in sports performance. In recent years, increasing empirical evidence suggests that acute exercise affects peripheral visual perception. A behavioral study has shown that peripheral visual perception may be vulnerable to exercise as compared with central visual perception (Ando et al. 2008). The following study suggested that the detrimental effects of exercise on peripheral visual perception are not primarily ascribed to low visual resolution, but to the impaired top-down control of visual attention (Ando et al. 2012). During incremental exercise, peripheral visual perception was impaired when engaged at exercise at high workloads above the ventilatory threshold (Ando et al. 2005). Furthermore, high aerobic capacity attenuated the increase in peripheral visual reaction time during strenuous exercise, suggesting that oxygen availability play a role in peripheral visual perception (Ando et al. 2005). Peripheral visual perception was impaired to some extent during exercise under mild hypoxia relative to normoxia although the differences between normoxia and hypoxia failed to reach statistical significance (Ando et al. 2010). Further analysis demonstrated that decreases in cerebral oxygenation were closely associated with the impairment in peripheral visual perception during exercise (Ando et al. 2010). In contrast, peripheral visual perception was not impaired even during strenuous exercise under hyperoxia where oxygen availability was elevated (Ando et al. 2009). These findings suggest that a decrease in cerebral oxygenation is associated with impairment in peripheral visual perception during strenuous exercise. The decrease in cerebral oxygenation during exercise means that oxygen availability may be insufficient to meet metabolic demand. It is plausible that decreases in cerebral oxygenation have detrimental effects on visual perceptual performance during exercise.
COOLING AND RECOVERY FROM INTENSE EXERCISE – A SYSTEMATIC REVIEW OF STUDIES WITH TRAINED ATHLETES
Poppendieck et al.
Saarland University, Saarbrücken, Germany
Cooling after exercise has been suggested as a method to improve recovery during intensive training periods or competitions lasting several days to weeks. It has been investigated in various studies and has also found its way into practice. However, many existing studies include untrained subjects to induce a higher degree of muscle soreness and fatigue due to a reduced fitness level. It is not clear if the results of those studies can be transferred to trained athletes. Although recent review articles on the topic of cooling and recovery exist, none of those has focused especially on trained athletes [Halson, 2011; Leeder et al., 2011]. The purpose of this work was to fill this gap. Methods A literature search was conducted using the following databases: PubMed, ISI Web of Science, AMED and EMBASE. Inclusion criteria were: a) explicit analysis of trained subjects, b) cooling after exercise, c) performance measurement, d) existence of a control group or condition, e) performance evaluation at least 2 h after cooling to exclude potential precooling effects. In total, 14 studies with 153 subjects were located and analyzed. For all studies, the effect of cooling on performance was determined, and effect sizes (Hedges’ g) were calculated. In order to determine under which circumstances cooling may be most beneficial, several parameters of the study design were more closely examined. Regarding performance measurement, the best effects were found for endurance parameters (3 studies/30 subjects, 3.7%, g=0.35), while for jump (3/35, 3.4%, g=0.13), strength (10/113, 2.4%, g=0.12) and sprint performance (4/46, 2.7%, g=0.10), effects were smaller. The effects were most pronounced when performance was evaluated 48 h after exercise (7/71, 5.0%, g=0.34). With respect to the exercise which was used to induce fatigue, effects after strength training (4/39, 3.6%, g=0.18) were slightly larger than after endurance-type exercise (10/114, 2.2%, g=0.16). Cold water immersion (10/117, 2.9%, g=0.19) and cryogenic chambers (2/18, 3.8%, g=0.14) seemed to be more beneficial than cooling packs (2/18, 0.3%, g=0.00). Overall, the effects of cooling on recovery were rather small (2.8%, g=0.17). Under appropriate conditions, however, cooling after exercise may have relevant positive effects on performance recovery of trained athletes.
EFFECTS OF HYDROTHERAPY ON ADAPTATION FOLLOWING A SIMULATED CYCLING GRAND TOUR
Halson et al.
AIS Performance Recovery (Canberra, Australia)
Although cold water immersion is beneficial for recovery between bouts of high-intensity exercise, it may impair long term performance by attenuating the stimuli responsible for adaptation to training. Here we report a comparison of effects of cold-water immersion and passive rest on performance over a 39-day training block. Methods Thirty-four male endurance-trained competitive cyclists were randomized to cold water immersion or control (no recovery) groups for a simulated cycling grand tour consisting of 7 d of baseline training, 21 d of intense training, and an 11-d taper. Criteria for completion of training and testing were satisfied by 10 cyclists in the cold-water immersion group (age, 20.2 ± 1.7 y; mass, 70.9 ± 6.5 kg; maximal aerobic power, 5.13 ± 0.21 W/kg) and 11 in the control group (19.8 ± 1.7 y; 68.9 ± 8.0 kg; 5.01 ± 0.41 W/kg). Cyclists completed two sets of performance tests each week: a combination cycling test consisting of 6-s sprints (MMP1s), a series of varying intervals, and a 10-min time trial on one day, and two 4-min bouts separated by 30 min of recovery (2xMMP4m) the next day. Cold-water immersion was performed 4 times per week for 15 min at 15°C following training and testing sessions. Uncertainty in mean differences between groups in the changes in mean performance power between tests following baseline and taper periods was estimated as 90% confidence limits and evaluated probabilistically in relation to a smallest important effect on mean power of 1%. Results Cyclists in the cold water group had an unclear change in overall 4-min power relative to control (2.7%, ±5.7%); however when subtracting the power in the first effort from the second effort, the cold water group showed a clear likely beneficial effect compared with control (3.0%, ±3.8%). The change in MMP1s in the cold water group also demonstrated a clear likely beneficial effect compared to control (4.4%, ±4.2%). Observed differences between groups for the 10-min time trial were trivial but the effect was unclear (-0.4%, ±4.3%). Discussion The primary objective of this study was to evaluate whether cold water immersion during a 3-wk phase of rigorous cycling training (simulating aspects of a Grand Tour) would impair cycling performance. In summary, data from this study do not support recent speculation that cold-water immersion is detrimental to adaptations to 3 weeks of increased training load in competitive cyclists.
INSULATIVE TROUSERS INCORPORATING ACTIVE HEATING REDUCE MUSCLE TEMPERATURE DECLINE FOLLOWING WARM UP AND IMPROVE SPRINT CYCLING PERFORMANCE
Faulkner et al.
Loughborough University, UK
Elevations in muscle temperature (Tm) have been shown to be important for enhancing maximal muscle power output during short duration, sprint based activities, hence the completion of a warm up prior to many exercise types. In many sporting competitions it is not uncommon for there to be delays between warm up completion and performance execution, during which time activity levels may be insufficient to maintain elevations in Tm. Excessive decline in Tm may lead to sub-optimal contractile conditions and impaired exercise performance. Therefore, the aim of the present study was to determine to what extent a delay between warm up and competition might influence Tm and performance and whether this may be attenuated using an insulated athletic trouser with optional heating. On three separate occasions, 11 male cyclists (24 ± 5yrs; 182.4 ± 7.6cm; 77.4 ± 10.0kg) completed a standardized 15 min intermittent sprint-based warm up on a cycle ergometer, followed by a 30 min passive recovery period before completing a 30 sec maximal sprint test. Tm of the vastus lateralis was measured at depths of 1, 2 and 3 cm prior to and following the warm up and immediately before the sprint test. Measures of absolute and relative peak power output were taken. During the recovery period subjects wore a tracksuit top and (in a balanced order) either i) a standard tracksuit ensemble (CONT), ii) a pair of insulated athletic trousers (INS) or iii) insulated athletics trouser with inbuilt electric heating elements around the thighs (HEAT). The warm up increased Tm at all depths by ~2.5°C, with no differences between conditions. Following the recovery period Tm declined in both CONT (1cm 36.3 ± 0.4°C; 2cm 36.6 ± 0.3°C; 3cm 36.9 ± 0.2°C) and INS (1cm 36.5 ± 0.6°C; 2cm 36.8 ± 0.4°C; 3cm 37.0 ± 0.3°C), whereas Tm for HEAT remained elevated at all depths compared to both INS and CONT (1cm 37.4 ± 0.3°C; 2cm 37.3 ± 0.2°C; 3cm 37.3 ± 0.2°C; p<0.01). Peak power output was higher in HEAT (20.9 ± 1.6 W/kg) than both CONT (19.2 ± 1.7 W/Kg; 9%, p<0.05) and INS (20.3 ± 2.3 W/Kg; 3%, p<0.05). Though insulated trousers alone were not effective, the use of an insulated athletic trouser with the addition of electric heating elements around the thighs was able to reduce the decline in Tm that is associated with forced periods of inactivity between warm up completion and competition. Furthermore, the prevention of the decline in Tm improved subsequent sprint performance compared to when passive heating is not used.
MONITORING BRAIN TEMPERATURE – A CRITICAL THRESHOLD THAT CONTROLS CENTRAL FATIGUE?
Stahn et al.
Center for Space Medicine, Charité (Berlin, Germany)
Hyperthermia has been suggested to control central fatigue by a threshold temperature (critical limiting temperature, CLT) and/or selective brain cooling, having a neuroprotective effect against lethal heat stress. Recently, however, the role of these mechanisms has been questioned (Marino 2011). Previous studies in this field have been limited to small sample sizes due to technical difficulties and inconveniences associated with core body temperature measurements such as rectal or esophageal recordings. In addition, present temperature monitoring technologies might not accurately reflect brain temperature, and specifically temperature in the hypothalamus where the center of thermoregulation is located. We therefore introduced a new non-invasive heatflux technology for determining core body temperature at the forehead (Gunga et al. 2009; Stahn et al. 2011). The aim of the present study was therefore to investigate whether there is a consistent CLT determined close to the hypothalamus during intense exercise in a large sample of young men and women with varying degrees of maximal aerobic capacity. A total of 64 young subjects (43 men, 21women) completed a graded maximal exercise until volitional exhaustion on a bicycle ergometer. In addition to oxygen uptake (breath-by-breath) core body temperature was continuously determined using a new non-invasive heatflux sensor (Double Sensor) positioned at the forehead. Average CBT at the time of exhaustion was 40.2 °C with men displaying slightly, but significantly higher CBT than women (40.3 vs. 39.9°C, P < 0.05). ANCOVA revealed that this difference could be attributed to higher maximal aerobic capacity in men. Comparing high and low fit subjects irrespective of gender demonstrated that CBT was significantly higher at submaximal (60% and 80% VO2max) and maximal exercise (40.6 vs. 39.7 °C, P < 0.001). In addition, CBT demonstrated a linear increase as a function of maximal aerobic capacity (r = 0.53; P < 0.001). While volitional exhaustion was reached around 40 °C irrespective of initial CBT and its rate of increase, suggesting a consistent CLT there was considerable variation in CBT between subjects. In addition this variation was characterized by a positive linear relationship between CBT during maximal exercise and maximal aerobic capacity. These data suggest that either subjects may adapt to higher levels of heat stress by increasing CLT or that neuroprotection from heat stress might not be the primary cause per se for the discontinuation of vigorous physical activity (Marino 2011).
EFFECTS OF THE FIFA 11+ INJURY PREVENTION PROGRAM ON NEUROMUSCULAR CONTROL, STRENGTH AND PERFORMANCE IN AMATEUR SOCCER PLAYERS: A RANDOMIZED CONTROLLED TRIAL
Impellizzeri et al.
Schulthess Clinic (Zurich, Switzerland)
To develop an injury prevention program that can be easily implemented in the everyday training routine (especially at amateur level), the FIFA Medical Assessment and Research Centre (F-MARC) has developed an advanced version of a previous prevention program: “The 11+”. A cluster randomized controlled trial has recently shown that “The 11+” is effective in reducing injuries (Soligard et al. 2008). “The 11+” is a warm-up routine designed for training some physical components: core stability, neuromuscular control and balance, eccentric training of the hamstrings, plyometric and agility. The aim of this study was to examine whether “The 11+” can improve neuromuscular control, strength and performance in amateur soccer players. Eighty-four male amateur players from 6 teams participated to this parallel, two groups, pre-post, randomized controlled trial. They were allocated to “The 11+”(n=42) and control (n=39) group using a restricted blocked randomization where each block corresponded to a team. The players had to complete the warm-up routines 3 times a week for 9 weeks. Outcome measures were: eccentric and concentric strength of flexors and extensors, star excursion balance test, time-to-stabilization, core-stability of the trunk, vertical jump, sprint, agility. Analysis was performed using mixed models and magnitude of inferences. No differences between groups were found in training load and training components (0.146 < p <0.680). Both groups completed an average of 2.1 sessions a week. After controlling for confounders and baseline values, possible worthwhile differences (47 to 72%) in favor of the 11+ group were found for flexors concentric strength at 60°/s (3.2%, 95% CI 0.6 to 5.9%; ANCOVA p level=0.046) and 180°/s (4.6%, 95%CI 1.0 to 8.3%;p=0.038), flexors eccentric strength (3.8%, 95%CI 1.4 to 6.2%;p=0.010), sprint (-0.9%, 95%CI -1.9 to 0.1%;p=0.123), agility (-1.1%, 95%CI -2.6 to 0.1%;p=0.265). Likely worthwhile differences (93-95%) in favor of “the 11+” group were found for Time-to-stabilization (-2.8%, 95%CI –4.4 to -1.2%;p=0.005) and core-stability (-8.9%, 95%CI -15 to -3%;p=0.012).The results of this study showed that nine weeks implementing “The 11+” as a routine warm-up can induce substantial improvement in neuromuscular control and possible worthwhile changes in flexors strength. Therefore, the 11+ not only can prevent injuries but can also induce positive effects on important physical components in amateur players.
High intensity intermittent training and health
Benefits of High Intensity Intermittent Training (HIIT) in Untrained and Diseased People
APPLICATION OF HIIT TO CLINICAL POPULATIONS AND EFFECT ON MARKERS OF DISEASE RISK
High-intensity interval training (HIT) can serve as an effective alternate to traditional endurance-based training, inducing similar or even superior physiological adaptations in healthy individuals and diseased populations, at least when compared on a matched-work basis. While less well studied, low-volume HIT can also stimulate physiological remodeling comparable to moderate-intensity continuous training despite a substantially lower time commitment and reduced total exercise volume (1). For example, as little as six sessions of HIT over 2 wk, totaling 15 min of “all out” cycle exercise within a total training time commitment of ~2 h, increases the maximal activity of mitochondrial enzymes and improves performance during tasks that rely heavily on aerobic energy provision. These data suggest that HIT may be a potent and time-efficient strategy to induce skeletal muscle metabolic adaptations that are linked to improved health. Many low-volume HIT studies have employed relatively extreme variable-load exercise interventions (e.g., repeated Wingate Tests) that may not be safe or well tolerated by certain individuals. Recent work has shown that short-term training using a more “practical” model of HIT (e.g., 10 x 1 min repeats at 90% maximal aerobic work capacity, interspersed by 1 min of recovery) increased muscle oxidative capacity and improved endurance performance (2). Low-volume HIT studies in persons who might be at risk for cardiometabolic disorders or patients with chronic disease are very limited. However, it was recently demonstrated that low-volume HIT was effective and well tolerated in people with type 2 diabetes (3). Two weeks of HIT reduced average 24-h blood glucose concentration and postprandial glucose excursions, measured via continuous glucose monitoring under standardized diet but otherwise free-living conditions. Given that “lack of time” is the most commonly cited barrier to regular exercise participation, it is tempting to speculate that low-volume HIT may represent a time-efficient alternative to traditional endurance training. While the preliminary evidence from small, short-term studies are intriguing, large-scale studies are clearly needed to resolve whether low-volume HIT is a realistic, time-efficient exercise alternative to improve health and reduce the risk of cardiometabolic disease.
THE EFFECTS OF HIIT ON THE ABILITY TO OXIDIZE FAT IN HUMAN SKELETAL MUSCLE
University of Gelph
It is now well established that models of high intensity intermittent training (HIIT) produce robust increases in mitochondrial volume. Mitochondrial biogenesis occurs rapidly with this training model with increased mitochondrial protein content observed after as little as 3-4 training sessions in humans. The HIIT models ask subjects to perform short bouts of exercise anywhere from ~90% VO2max for 1-4 min to all out sprints at power outputs as high as 300% of what is needed to elicit VO2max for 30 sec. These workouts are usually completed every other day. The ability to exercise at high aerobic intensities (~90% VO2max) is not surprisingly drastically improved following HIIT. Interestingly, when subjects are asked to exercise at ~60-65% of the pre-training VO2max following HIIT, the reliance on fat as a fuel in also increased. This is similar to what is seen following the classical endurance training protocols where subjects exercise for 1-2 hours/day at ~60% VO2max, 5 times a week. These results demonstrate that the HIIT exercise stress is able to activate the molecular machinery to produce the many proteins needed to increase mitochondrial volume and capacity. Numerous studies have assessed these adaptations by directly measuring either the activity and/or the protein content of enzymes and intermediates involved in the major mitochondrial pathways, including citrate synthase from the TCA cycle, cyctochrome IV from the electron transport chain, betahydroxylacyl dehydrogenase from the beta-oxidation pathway, enzymes of the electron transport shuttle into the mitochondria, and pyruvate dehydrogenase or regulatory elements of this complex. An impressive aspect of these adaptations is how rapid they occur where increases have been shown after as little as 3 HIIT workouts. HIIT also increased the amount of mitochondrial and plasma membrane fat transport proteins in human skeletal muscle. Hormone sensitive lipase activity was increased by 13% and the use of intramuscular triacylglycerol was increased by 35% during 1 hour of submaximal exercise, but these changes were not significant. The important conclusion seems to be that the high intensity exercise bouts during HIIT maximally or near-maximally activate the aerobic system at the onset of exercise and also the various molecular signals that lead to increased production of mitochondrial fat-metabolizing proteins. This leads to rapid upregulation of the pathways that metabolize fat resulting in an increase in the capacity to oxidize fat during submaximal exercise following HIIT.
MOLECULAR MECHANISMS UNDERPINNING RAPID MITOCHONDRIAL ADAPTATIONS TO HIIT
University of Guelph, Guelph, Ontario
Contraction signals a plethora of genomic events designed to increase the efficiency by which muscle responds to future energetic challenges. Central to this improved metabolic regulation is an increase in mitochondrial content described by Holloszy 45 years ago. This mitochondrial biogenesis is linked to lower substrate phosphorylation, carbohydrate sparing and increased fat oxidation, all of which contribute to improved endurance performance. Furthermore, Dudley et al demonstrated in the 1980’s that the rate and magnitude of mitochondrial protein accumulation during training is proportional to the training intensity. Multiple breakthroughs were then made ~15-20 years ago establishing nuclear genomic expression as the critical link between contraction and improvements in glucose uptake which later led to similar nuclear/mitochondrial genomic links for exercise-induced mitochondrial biogenesis. Initial explorations into contraction/exercise-induced gene expression by Neufer, Wasserman and others were followed by an explosion in research into the regulation of contraction-induced gene expression by transcription factors and co-activators. Most notably, the discovery of the PPAR, NRF, and PGC1 family of transcriptional regulators (and others) drastically improved our understanding throughout the last ~15 years of exercise-induced transcriptional regulation of mitochondrial biogenesis. In the past ~5 years, these same questions have been applied to HIIT in human muscle. We now possess a detailed understanding that the fast increases in mitochondrial content in human muscle during HIIT are likely mediated by multiple transcriptional regulators. Several groups have demonstrated that HIIT activates a variety of signaling cascades sensing specific signals generated during exercise which then activate transcription factors (PPARs, NRFs, etc) that are likely co-ordinated by co-activators (eg. PGC1s). These transcriptional regulators also increase in content at a rapid rate which precedes increases in mitochondrial proteins. This process requires repeated exercise sessions in order to accumulate sufficient genomic messages (mRNA) to drive translation of mitochondrial proteins at a level that sustains a greater mitochondrial content. Future studies should examine if the balance between net transcriptional repression (RIP140, etc) and activation (PGC1 regulators, etc) determines 1) the rate of mitochondrial biogenesis and 2) the onset of plateaus in protein content and performance improvements during training, with no single factor being essential but rather all cooperating to maximize the rate of adaptation. It is now clear that HIIT invokes rapid improvements in muscle energy homeostasis via a coordinated expression of multiple transcriptional programs controlling substrate uptake and catabolism. These molecular responses underscore the impressive efficacy of HIIT as a tool to stimulate robust increases in endurance performance and metabolic health in humans.