Post-activation potentiation (PAP) is induced by a voluntary conditioning contraction (CC), performed typically at a maximal or near-maximal intensity, and has consistently been shown to increase both peak force and rate of force development during subsequent twitch contractions. The proposed mechanisms underlying PAP are associated with phosphorylation of myosin regulatory light chains, increased recruitment of higher order motor units, and a possible change in pennation angle. If PAP could be induced by a CC in humans, and utilized during a subsequent explosive activity (e.g. jump or sprint), it could potentially enhance mechanical power and thus performance and/or the training stimulus of that activity. However, the CC might also induce fatigue, and it is the balance between PAP and fatigue that will determine the net effect on performance of a subsequent explosive activity. The PAP-fatigue relationship is affected by several variables including CC volume and intensity, recovery period following the CC, type of CC, type of subsequent activity, and subject characteristics. These variables have not been standardized across past research, and as a result, evidence of the effects of CC on performance of subsequent explosive activities is equivocal. In order to better inform and direct future research on this topic, this article will highlight and discuss the key variables that may be responsible for the contrasting results observed in the current literature. Future research should aim to better understand the effect of different conditions on the interaction between PAP and fatigue, with an aim of establishing the specific application (if any) of PAP to sport.

Field-based team sports, such as soccer, rugby and hockey are popular worldwide. There have been many studies that have investigated the physiology of these sports, especially soccer. However, some fitness components of these field-based team sports are poorly understood. In particular, repeated-sprint ability (RSA) is one area that has received relatively little research attention until recent times. Historically, it has been difficult to investigate the nature of RSA, because of the unpredictability of player movements performed during field-based team sports. However, with improvements in technology, time-motion analysis has allowed researchers to document the detailed movement patterns of team-sport athletes. Studies that have published time-motion analysis during competition, in general, have reported the mean distance and duration of sprints during field-based team sports to be between 10-20 m and 2-3 seconds, respectively. Unfortunately, the vast majority of these studies have not reported the specific movement patterns of RSA, which is proposed as an important fitness component of team sports. Furthermore, there have been few studies that have investigated the physiological requirements of one-off, short-duration sprinting and repeated sprints (<10 seconds duration) that is specific to field-based team sports. This review examines the limited data concerning the metabolic changes occurring during this type of exercise, such as energy system contribution, adenosine triphosphate depletion and resynthesis, phosphocreatine degradation and resynthesis, glycolysis and glycogenolysis, and purine nucleotide loss. Assessment of RSA, as a training and research tool, is also discussed.

The aim of this study was to examine the construct validity of selected field tests as indicators of match-related physical performance. During the competitive season, eighteen professional soccer players (age 26.2 +/- 4.5 yrs, mass 80.8 +/- 7.8 kg, and height 181.9 +/- 3.7 cm) completed an incremental running field test to exhaustion, a vertical-jump and a repeated-sprint ability (RSA) test. Match physical performance was quantified during official matches using a video-computerized, semi-automatic, match analysis image recognition system, (ProZone, Leeds, UK). The selected measures of match physical performance were: total distance covered (TD), high intensity running (HIR: > 14.4 km . h (-1)), very high intensity running (VHIR:> 19.8 km . h (-1)), sprinting (> 25.2 km . h (-1)) and top running speed. Significant correlations were found between peak speed reached during the incremental field test and TD (r = 0.58, R (2) = 0.34; p < 0.05), HIR (r = 0.65, R (2) = 0.42; p < 0.01) and VHIR (r = 0.64, R (2) = 0.41; p < 0.01). Significant correlations were also found between RSA mean time and VHIR (r = - 0.60, R (2) = 0.36; p < 0.01) and sprinting distance (r = - 0.65, R (2) = 0.42; p < 0.01). Significant differences were found between the best and worst group as defined by the median split technique for peak speed (TD = 12 011 +/- 747 m vs. 10 712 +/- 669, HIR = 3192 +/- 482 m vs. 2314 +/- 347 m, and VHIR = 1014 +/- 120 vs. 779 +/- 122 m, respectively; p < 0.05) and RSA mean time (VHIR = 974 +/- 162 m vs. 819 +/- 144 m, and sprinting = 235 +/- 56 vs. 164 +/- 58 m, respectively; p < 0.05). In conclusion, this study gives empirical support to the construct validity of RSA and incremental running tests as measures of match-related physical performance in top-level professional soccer players.

Short-duration sprints (<10 seconds), interspersed with brief recoveries (<60 seconds), are common during most team and racket sports. Therefore, the ability to recover and to reproduce performance in subsequent sprints is probably an important fitness requirement of athletes engaged in these disciplines, and has been termed repeated-sprint ability (RSA). This review (Part I) examines how fatigue manifests during repeated-sprint exercise (RSE), and discusses the potential underpinning muscular and neural mechanisms. A subsequent companion review to this article will explain a better understanding of the training interventions that could eventually improve RSA. Using laboratory and field-based protocols, performance analyses have consistently shown that fatigue during RSE typically manifests as a decline in maximal/mean sprint speed (i.e. running) or a decrease in peak power or total work (i.e. cycling) over sprint repetitions. A consistent result among these studies is that performance decrements (i.e. fatigue) during successive bouts are inversely correlated to initial sprint performance. To date, there is no doubt that the details of the task (e.g. changes in the nature of the work/recovery bouts) alter the time course/magnitude of fatigue development during RSE (i.e. task dependency) and potentially the contribution of the underlying mechanisms. At the muscle level, limitations in energy supply, which include energy available from phosphocreatine hydrolysis, anaerobic glycolysis and oxidative metabolism, and the intramuscular accumulation of metabolic by-products, such as hydrogen ions, emerge as key factors responsible for fatigue. Although not as extensively studied, the use of surface electromyography techniques has revealed that failure to fully activate the contracting musculature and/or changes in inter-muscle recruitment strategies (i.e. neural factors) are also associated with fatigue outcomes. Pending confirmatory research, other factors such as stiffness regulation, hypoglycaemia, muscle damage and hostile environments (e.g. heat, hypoxia) are also likely to compromise fatigue resistance during repeated-sprint protocols.

The molecular mechanisms underlying the response to exercise and inactivity are not fully understood. We propose an innovative approach to profile the skeletal muscle transcriptome to exercise and inactivity using 66 published datasets. Data collected from human studies of aerobic and resistance exercise, including acute and chronic exercise training, were integrated using meta-analysis methods (www.metamex.eu). Here we use gene ontology and pathway analyses to reveal selective pathways activated by inactivity, aerobic versus resistance and acute versus chronic exercise training. We identify NR4A3 as one of the most exercise-and inactivity-responsive genes, and establish a role for this nuclear receptor in mediating the metabolic responses to exercise-like stimuli in vitro. The meta-analysis (MetaMEx) also highlights the differential response to exercise in individuals with metabolic impairments. MetaMEx provides the most extensive dataset of skeletal muscle transcriptional responses to different modes of exercise and an online interface to readily interrogate the database.

Three studies involving 108 football players were conducted to examine the reliability of a repeated-shuttle-sprint ability (RSSA) test and its ability to differentiate between players of various competitive levels and playing positions. Study 1: Short-term reliability was determined in 22 professional players completing the RSSA test (6 x 40-m sprints with 20 s of recovery between sprints) on two separate occasions. Study 2: Long-term reliability (seasonal changes) was examined in 31 professional players completing the RSSA test four times (during the preseason period, at the start, middle and end of the competitive season). Study 3: 108 players were divided and compared according to competitive level or playing position. Standard error of measurement values expressed as coefficient of variation for RSSA mean time and best time were 0.8 and 1.3 % (short-term reliability) and 0.9 and 1.2 % (long-term reliability), respectively. The smallest worthwhile changes were 0.5 % for both mean and best time. Professional players showed better RSSA performance than amateur players, and defenders displayed the lowest RSSA performance. In conclusion, the RSSA test showed adequate construct validity but only RSSA mean time showed sufficient reliability to detect large training-induced changes but not small important differences.

Limited information exists about the movement patterns of field-hockey players, especially during elite competition. Time-motion analysis was used to document the movement patterns during an international field-hockey game. In addition, the movement patterns of repeated-sprint activity were investigated, as repeated-sprint ability is considered to be an important fitness component of team-sport performance. Fourteen members of the Australian men's field-hockey team (age 26+/-3 years, body mass 76.7+/-5.6 kg, VO2max 57.9+/-3.6 ml.kg(-1).min(-1); mean+/-s) were filmed during an international game and their movement patterns were analysed. The majority of the total player game time was spent in the low-intensity motions of walking, jogging and standing (46.5+/-8.1, 40.5+/-7.0 and 7.4+/-0.9%, respectively). In comparison, the proportions of time spent in striding and sprinting were 4.1+/-1.1 and 1.5+/-0.6%, respectively. Our criteria for 'repeated-sprint' activity (defined as a minimum of three sprints, with mean recovery duration between sprints of less than 21 s) was met on 17 occasions during the game (total for all players), with a mean 4+/-1 sprints per bout. On average, 95% of the recovery during the repeated-sprint bouts was of an active nature. In summary, the results suggest that the motion activities of an elite field-hockey competition are similar to those of elite soccer, rugby and Australian Rules football. In addition, the investigation of repeated-sprint activity during competition has provided additional information about the unique physiological demands of elite field-hockey performance.

Low-volume, high-intensity interval training (HIT) increases skeletal muscle mitochondrial capacity, yet little is known regarding potential mechanisms promoting this adaptive response. Our purpose was to examine molecular processes involved in mitochondrial biogenesis in human skeletal muscle in response to an acute bout of HIT. Eight healthy men performed 4 × 30-s bursts of all-out maximal intensity cycling interspersed with 4 min of rest. Muscle biopsy samples (vastus lateralis) were obtained immediately before and after exercise, and after 3 and 24 h of recovery. At rest, the majority of peroxisome proliferator-activated receptor γ coactivator (PGC)-1α, a master regulator of mitochondrial biogenesis, was detected in cytosolic fractions. Exercise activated p38 MAPK and AMPK in the cytosol. Nuclear PGC-1α protein increased 3 h into recovery from exercise, a time point that coincided with increased mRNA expression of mitochondrial genes. This was followed by an increase in mitochondrial protein content and enzyme activity after 24 h of recovery. These findings support the hypothesis that an acute bout of low-volume HIT activates mitochondrial biogenesis through a mechanism involving increased nuclear abundance of PGC-1α.