High-intensity exercise can result in up to a 1,000-fold increase in the rate of ATP demand compared to that at rest (Newsholme et al., 1983). To sustain muscle contraction, ATP needs to be regenerated at a rate complementary to ATP demand. Three energy systems function to replenish ATP in muscle: (1) Phosphagen, (2) Glycolytic, and (3) Mitochondrial Respiration. The three systems differ in the substrates used, products, maximal rate of ATP regeneration, capacity of ATP regeneration, and their associated contributions to fatigue. In this exercise context, fatigue is best defined as a decreasing force production during muscle contraction despite constant or increasing effort. The replenishment of ATP during intense exercise is the result of a coordinated metabolic response in which all energy systems contribute to different degrees based on an interaction between the intensity and duration of the exercise, and consequently the proportional contribution of the different skeletal muscle motor units. Such relative contributions also determine to a large extent the involvement of specific metabolic and central nervous system events that contribute to fatigue. The purpose of this paper is to provide a contemporary explanation of the muscle metabolic response to different exercise intensities and durations, with emphasis given to recent improvements in understanding and research methodology.

Sports scientists and strength and conditioning professionals spend the majority of the competition season trying to ensure that their athletes' training and recovery strategies are appropriate to ensure optimal performance on competition day. However, there is an additional window on the day of competition where performance can be acutely enhanced with a number of preconditioning strategies. These strategies include appropriately designed warm-up, passive heat maintenance, postactivation potentiation, remote ischemic preconditioning, and, more recently, prior exercise and hormonal priming. The aim of this review was to explore the potential practical use of these strategies and propose a theoretical timeline outlining how they may be incorporated into athlete's precompetition routine to enhance performance. For the purpose of this review the discussion is confined to strategies that may enhance performance of short-duration, high-intensity sports (eg, sprinting, jumping, throwing).

BackgroundThe current recommendations for resistance training (RT) frequency range from 2 to 5 days per week (days week− 1) depending on the subjects’ training status. However, the relationship between RT frequency and muscular strength remains controversial with reported variances existing across different population groups. We conducted a meta-analysis that (1) quantified the effects of low (LF; 1 day week− 1), medium (MF; 2 days week− 1), or high (HF; ≥ 3 days week− 1) RT frequency on muscular strength per exercise; (2) examined the effects of different RT frequency on one repetition maximum (1RM) strength gain profiles (multi-joint exercises and single joint exercises); (3) examined the effects of different RT frequency on 1RM strength gain when RT volume is equated; and (4) examined the effects of different RT frequency on 1RM strength gains on upper and lower body.MethodsComputerised searches were performed using the terms ‘strength training frequency’, ‘resistance training frequency’, ‘training frequency’, and ‘weekly training frequency’. After review, 12 studies were deemed suitable according to pre-set eligibility criteria. Primary data were pooled using a random-effects model. Outcomes analysed for main effects were pre- to post strength change with volume-equated studies that combined multi-joint and isolation exercise; isolation-only exercise and untrained subjects only. Heterogeneity between studies was assessed using I2 and Cochran’s Q statistics with funnel plots used to assess publication bias and sensitivity analyses calculated for subgroups.ResultsPre- versus post-training strength analysis comprised of 74 treatment groups from 12 studies. For combined multi-joint and isolation exercises, there was a trend towards higher RT frequency compared with lower frequency [mean effect size (ES) 0.09 (95% CI − 0.06–0.24)] however not significant (p = 0.25). Volume-equated pre- to post-intervention strength gain was similar when LF was compared to HF [mean ES 0.03 (95% CI − 0.20–0.27); p = 0.78]. Upper body pre- to post-intervention strength gain was greater when HF was compared with LF [mean ES 0.48 (95% CI 0.20–0.76)] with significant differences between frequencies (p < 0.01). Upper body pre- to post-intervention strength gain was similar when MF was compared with LF (ES 0.12; 95% CI − 0.22–0.47); p = 0.48]. There was no significant difference in lower body mean ES between HF and LF [mean ES 0.21(95% CI − 0.55–0.13); p = 0.22]. There was a trend towards a difference in mean ES between MF and HF [mean ES 0.41(95% CI − 0.26–1.09); however, the effect was not significant (p = 0.23).ConclusionsThe existing data does not provide a strong correlation between increased weekly training frequency (HF) and maximal strength gain in upper and lower body resistance exercises for a mixed population group. When RT is volume-equated for combined multi-joint and isolation exercises, there is no significant effect of RT frequency on muscular strength gain. More investigations are required to explore the effects of varyin...

ObjectivesNational dietary guidelines were introduced in 1977 and 1983, by the USA and UK governments, respectively, with the ambition of reducing coronary heart disease (CHD) mortality by reducing dietary fat intake. A recent systematic review and meta-analysis by the present authors, examining the randomised controlled trial (RCT) evidence available to the dietary committees during those time periods, found no support for the recommendations to restrict dietary fat. The present investigation extends our work by re-examining the totality of RCT evidence relating to the current dietary fat guidelines.MethodsA systematic review and meta-analysis of RCTs currently available, which examined the relationship between dietary fat, serum cholesterol and the development of CHD, was undertaken.ResultsThe systematic review included 62 421 participants in 10 dietary trials: 7 secondary prevention studies, 1 primary prevention and 2 combined. The death rates for all-cause mortality were 6.45% and 6.06% in the intervention and control groups, respectively. The risk ratio (RR) from meta-analysis was 0.991 (95% CI 0.935 to 1.051). The death rates for CHD mortality were 2.16% and 1.80% in the intervention and control groups, respectively. The RR was 0.976 (95% CI 0.878 to 1.084). Mean serum cholesterol levels decreased in all intervention groups and all but one control group. The reductions in mean serum cholesterol levels were significantly greater in the intervention groups; this did not result in significant differences in CHD or all-cause mortality.ConclusionsThe current available evidence found no significant difference in all-cause mortality or CHD mortality, resulting from the dietary fat interventions. RCT evidence currently available does not support the current dietary fat guidelines. The evidence per se lacks generalisability for population-wide guidelines.