Higher-intensity aerobic training programmes, supplemented by resistance training, have been recommended and deemed safe for cardiac rehabilitation patients by many authorities. Based on research evidence, this may also provide superior outcomes for patients and should therefore be considered when developing an international consensus for exercise prescription in cardiac rehabilitation.

Purpose and methodsThis review presents established knowledge on the effects of physical activity (PA) on whole-body insulin sensitivity (SI) and summarises the findings of recent (2013–2016) studies.Discussion and conclusionsRecent studies provide further evidence to support the notion that regular PA reduces the risk of insulin resistance, metabolic syndrome and type 2 diabetes, and SI improves when individuals comply with exercise and/or PA guidelines. Many studies indicate a dose response, with higher energy expenditures and higher exercise intensities, including high intensity interval training (HIIT), producing greater benefits on whole-body SI, although these findings are not unanimous. Aerobic exercise interventions can improve SI without an associated increase in cardiorespiratory fitness as measured by maximal or peak oxygen consumption. Both aerobic and resistance exercise can induce improvements in glycaemic regulation, with some suggestions that exercise regimens including both may be more efficacious than either exercise mode alone. Some studies report exercise-induced benefits to SI that are independent of habitual diet and weight loss, while others indicate an association with fat reduction, hence the debate over the relative importance of PA and weight loss continues. During exercise, muscle contraction stimulated improvements in SI are associated with increases in AMPK activity, which deactivates TCB1D1, promoting GLUT4 translocation to the cell membrane and thereby increasing glucose uptake. Postexercise, increases in Akt deactivate TCB1D4 and thereby increase GLUT4 translocation to the cell membrane. The reduction in intramuscular saturated fatty acids and concomitant reductions in ceramides, but not diacylglycerols, provide a potential link between intramuscular lipid content and SI. Increased skeletal muscle capillarisation provides another independent adaptation through which SI is improved, as does enhanced β cell activity. Recent studies are combining exercise interventions with dietary and feeding manipulations to investigate the potential for augmenting the exercise-induced improvements in SI and glycaemic control.

It is presently unclear whether the reported ergogenic effect of a carbohydrate (CHO) mouth rinse on cycling time-trial performance is affected by the acute nutritional status of an individual. Hence, the aim of this study was to investigate the effect of a CHO mouth rinse on a 60-min simulated cycling time-trial performance commenced in a fed or fasted state. Twelve competitive male cyclists each completed 4 experimental trials using a double-blinded Latin square design. Two trials were commenced 2 h after a meal that contained 2.5 g·kg(-1) body mass of CHO (FED) and 2 after an overnight fast (FST). Prior to and after every 12.5% of total time during a performance ride, either a 10% maltodextrin (CHO) or a taste-matched placebo (PLB) solution was mouth rinsed for 10 s then immediately expectorated. There were significant main effects for both pre-ride nutritional status (FED vs. FST; p < 0.01) and CHO mouth rinse (CHO vs. PLB; p < 0.01) on power output with an interaction evident between the interventions (p < 0.05). The CHO mouth rinse improved mean power to a greater extent after an overnight fast (282 vs. 273 W, 3.4%; p < 0.01) compared with a fed state (286 vs. 281 W, 1.8%; p < 0.05). We concluded that a CHO mouth rinse improved performance to a greater extent in a fasted compared with a fed state; however, optimal performance was achieved in a fed state with the addition of a CHO mouth rinse.

This study was designed to investigate the effect of exercise intensity on cardiorespiratory fitness and coronary heart disease risk factors. Maximum oxygen consumption (Vo(2 max)), lipid, lipoprotein, and fibrinogen concentrations were measured in 64 previously sedentary men before random allocation to a nonexercise control group, a moderate-intensity exercise group (three 400-kcal sessions per week at 60% of Vo(2 max)), or a high-intensity exercise group (three 400-kcal sessions per week at 80% of Vo(2 max)). Subjects were instructed to maintain their normal dietary habits, and training heart rates were represcribed after monthly fitness tests. Forty-two men finished the study. After 24 wk, Vo(2 max) increased by 0.38 +/- 0.14 l/min in the moderate-intensity group and by 0.55 +/- 0.27 l/min in the high-intensity group. Repeated-measures analysis of variance identified a significant interaction between monthly Vo(2 max) score and exercise group (F = 3.37, P < 0.05), indicating that Vo(2 max) responded differently to moderate- and high-intensity exercise. Trend analysis showed that total cholesterol, low-density lipoprotein cholesterol, non-high-density lipoprotein cholesterol, and fibrinogen concentrations changed favorably across control, moderate-intensity, and high-intensity groups. However, significant changes in total cholesterol (-0.55 +/- 0.81 mmol/l), low-density lipoprotein cholesterol (-0.52 +/- 0.80 mmol/l), and non-high-density lipoprotein cholesterol (-0.54 +/- 0.86 mmol/l) were only observed in the high-intensity group (all P < 0.05 vs. controls). These data suggest that high-intensity training is more effective in improving cardiorespiratory fitness than moderate-intensity training of equal energy cost. These data also suggest that changes in coronary heart disease risk factors are influenced by exercise intensity.

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Aging in humans is associated with a loss in neuromuscular function and performance. This is related, in part, to the reduction in muscular strength and power caused by a loss of skeletal muscle mass (sarcopenia) and changes in muscle architecture. Due to these changes, the force-velocity (f-v) relationship of human muscles alters with age. This change has functional implications such as slower walking speeds. Different methods to reverse these changes have been investigated, including traditional resistance training, power training and eccentric (or eccentrically-biased) resistance training. This review will summarise the changes of the f-v relationship with age, the functional implications of these changes and the various methods to reverse or at least partly ameliorate these changes.

Using a motorized treadmill the study investigated the effects of the ingestion of 3 g of caffeinated coffee on: the time taken to run 1500 m; the selected speed with which athletes completed a 1-min 'finishing burst' at the end of a high-intensity run; and respiratory factors, perceived exertion and blood lactate levels during a high intensity 1500-m run. In all testing protocols decaffeinated coffee (3 g) was used as a placebo and a double-blind experimental design was used throughout. The participants in the study were middle distance athletes of club, county and national standard. The results showed that ingestion of caffeinated coffee: decreases the time taken to run 1500 m (P < 0.005); increases the speed of the 'finishing burst' (P < 0.005); and increases Vo2 during the high-intensity 1500-m run (P < 0.025). The study concluded that under these laboratory conditions, the ingestion of caffeinated coffee could enhance the performance of sustained high-intensity exercise. Keywords: Caffeine, ergogenic acid, Vo2, blood lactate Caffeine has long been considered as a substance capable of enhancing performance or physiological functions1 and as a result of its reported ergogenic effects, the International Olympic Committee (IOC) have banned the use of high levels of caffeine. However, since caffeine is commonly found in many foods that are taken as part of the 'normal' diet, when testing for the drug the banned level is set above 15 ig ml-1 urine which is reported to represent the ingestion of 500-600 mg of caffeine (five to six cups of coffee) in a 1-2 h period2. Therefore in practical terms this dosage is only likely to be exceeded through the use of tablets, injections, suppositories or the deliberate ingestion of large amounts3. medulla increasing the secretion of catecholamines; the release of calcium ions from the sarcoplasmic reticulum; and the oxidation of free fatty acids which would produce a glycogen-sparing effect during prolonged exercise.Research into the effects of caffeine has tended to concentrate upon endurance activities such as marathon running or prolonged cyclingI7, with other investigations studying its effects upon maximal strength and power8 9. However, relatively little research has looked at the effects of caffeine upon high-intensity prolonged exercise, where the relative importance of the different physiological parameters required to produce a high level of performance and the physiological causes of fatigue can differ from those of endurance and short-term high-intensity exercise.The aim of this investigation was therefore to study the effect(s) of low doses of caffeine (approximately equivalent to the amount found in two strong cups of coffee) on a number of factors during prolonged high-intensity exercise. The study utilized doses of caffeine that would realistically be ingested by a sports performer before exercise as part of their 'normal' dietary habits without contravening the doping control regulations. Materials and methods

We determined the effects of "periodized nutrition" on skeletal muscle and whole body responses to a bout of prolonged exercise the following morning. Seven cyclists completed two trials receiving isoenergetic diets differing in the timing of ingestion: they consumed either 8 g/kg body mass (BM) of carbohydrate (CHO) before undertaking an evening session of high-intensity training (HIT) and slept without eating (FASTED), or consumed 4 g/kg BM of CHO before HIT, then 4 g/kg BM of CHO before sleeping (FED). The next morning subjects completed 2 h of cycling (120SS) while overnight fasted. Muscle biopsies were taken on day 1 (D1) before and 2 h after HIT and on day 2 (D2) pre-, post-, and 4 h after 120SS. Muscle [glycogen] was higher in FED at all times post-HIT (P < 0.001). The cycling bouts increased PGC1α mRNA and PDK4 mRNA (P < 0.01) in both trials, with PDK4 mRNA being elevated to a greater extent in FASTED (P < 0.05). Resting phosphorylation of AMPK(Thr172), p38MAPK(Thr180/Tyr182), and p-ACC(Ser79) (D2) was greater in FASTED (P < 0.05). Fat oxidation during 120SS was higher in FASTED (P = 0.01), coinciding with increases in ACC(Ser79) and CPT1 as well as mRNA expression of CD36 and FABP3 (P < 0.05). Methylation on the gene promoter for COX4I1 and FABP3 increased 4 h after 120SS in both trials, whereas methylation of the PPARδ promoter increased only in FASTED. We provide evidence for shifts in DNA methylation that correspond with inverse changes in transcription for metabolically adaptive genes, although delaying postexercise feeding failed to augment markers of mitochondrial biogenesis.