BackgroundAs part of the growing lifestyle diversity in modern society, there is wide variation in the time of day individuals choose to exercise. Recent surveys in the US and Japan have reported that on weekdays, more people exercise in the evening, with fewer individuals exercising in the morning or afternoon. Exercise performed in the post-prandial state has little effect on accumulated fat oxidation over 24 h (24-h fat oxidation) when energy intake is matched to energy expenditure (energy-balanced condition). The present study explored the possibility that exercise increases 24-h fat oxidation only when performed in a post-absorptive state, i.e. before breakfast.MethodsIndirect calorimetry using a metabolic chamber was performed in 10 young, non-obese men over 24 h. Subjects remained sedentary (control) or performed 60-min exercise before breakfast (morning), after lunch (afternoon), or after dinner (evening) at 50% of VO2max. All trials were designed to be energy balanced over 24 h. Time course of energy and substrate balance relative to the start of calorimetry were estimated from the differences between input (meal consumption) and output (oxidation).FindingsFat oxidation over 24 h was increased only when exercise was performed before breakfast (control, 456 ± 61; morning, 717 ± 64; afternoon, 446 ± 57; and evening, 432 ± 44 kcal/day). Fat oxidation over 24 h was negatively correlated with the magnitude of the transient deficit in energy and carbohydrate.InterpretationUnder energy-balanced conditions, 24-h fat oxidation was increased by exercise only when performed before breakfast. Transient carbohydrate deficits, i.e., glycogen depletion, observed after morning exercise may have contributed to increased 24-h fat oxidation.
Exercise can improve sleep by reducing sleep latency and increasing slow-wave sleep (SWS). Some studies, however, report adverse effects of exercise on sleep architecture, possibly due to a wide variety of experimental conditions used. We examined the effect of exercise on quality of sleep using standardized exercise parameters and novel analytical methods. In a cross-over intervention study we examined the effect of 60 min of vigorous exercise at 60% $$\dot{V}{\text{O}}_{2}$$ V ˙ O 2 max on the metabolic state, assessed by core body temperature and indirect calorimetry, and on sleep quality during subsequent sleep, assessed by self-reported quality of sleep and polysomnography. In a novel approach, envelope analysis was performed to assess SWS stability. Exercise increased energy expenditure throughout the following sleep phase. The subjective assessment of sleep quality was not improved by exercise. Polysomnography revealed a shorter rapid eye movement latency and reduced time spent in SWS. Detailed analysis of the sleep electro-encephalogram showed significantly increased delta power in SWS (N3) together with increased SWS stability in early sleep phases, based on delta wave envelope analysis. Although vigorous exercise does not lead to a subjective improvement in sleep quality, sleep function is improved on the basis of its effect on objective EEG parameters.
Whole body fat oxidation increases during exercise. However, 24-h fat oxidation on a day with exercise often remains similar to that of sedentary day, when energy intake is increased to achieve an energy-balanced condition. The present study aimed to examine a possibility that time of the day when exercise is performed makes differences in 24-h fat oxidation. As a potential mechanism of exercise affecting 24-h fat oxidation, its relation to exercise-induced transient energy deficit was examined. Nine young male endurance athletes underwent three trials of indirect calorimetry using a metabolic chamber, in which they performed a session of 100 min of exercise before breakfast (AM), after lunch (PM), or two sessions of 50 min of exercise before breakfast and after lunch (AM/PM) at 65% of maximal oxygen uptake. Experimental meals were designed to achieve individual energy balance. Twenty-four-hour energy expenditure was similar among the trials, but 24-h fat oxidation was 1,142 ± 97, 809 ± 88, and 608 ± 46 kcal/24 h in descending order of its magnitude for AM, AM/PM, and PM, respectively (P < 0.05). Twenty-four-hour carbohydrate oxidation was 2,558 ± 110, 2,374 ± 114, and 2,062 ± 96 kcal/24 h for PM, AM/PM, and AM, respectively. In spite of energy-balanced condition over 24 h, exercise induced a transient energy deficit, the magnitude of which was negatively correlated with 24-h fat oxidation (r = -0.72, P < 0.01). Similarly, transient carbohydrate deficit after exercise was negatively correlated with 24-h fat oxidation (r = -0.40, P < 0.05). The time of the day when exercise is performed affects 24-h fat oxidation, and the transient energy/carbohydrate deficit after exercise is implied as a factor affecting 24-h fat oxidation.
Mammals have circadian clocks, which consist of the central clock in the suprachiasmatic nucleus and the peripheral clocks in the peripheral tissues. The effect of exercise on phase of peripheral clocks have been reported in rodents but not in humans. Continuous sampling is necessary to assess the phase of the circadian rhythm of peripheral clock gene expressions. It has been assumed that the expression of the genes in leukocyte may be “an accessible window to the multiorgan transcriptome.” The present study aimed to examine whether exercise affects the level and phase of clock gene expression in human leukocytes. Eleven young men participated in three trials, in which they performed a single bout of exercise at 60% V̇o2max for 1 h beginning either at 0700 (morning exercise) or 1600 (afternoon exercise) or no exercise (control). Blood samples were collected at 0600, 0900, 1200, 1500, 1800, 2100, and 2300 and at 0600 the next morning, to assess diurnal changes of clock gene expression in leukocytes. Brain and muscle ARNT-like protein 1 ( Bmal1) expression level increased after morning and afternoon exercise, and Cryptochrome 1 ( Cry1) expression level increased after morning exercise. Compared with control trial, acrophase of Bmal1 expression tended to be earlier in morning exercise trial and later in afternoon exercise trial. Acrophase of Cry1 expression was earlier in morning exercise trial but not affected by afternoon exercise. Circadian locomotor output cycles kaput ( Clock), Period 1–3 ( Per1–3), and Cry2 expression levels and those acrophases were not affected by exercise. The present results suggest a potential role of a single bout of exercise to modify peripheral clocks in humans. NEW & NOTEWORTHY The present study showed that a single bout of exercise affected peripheral clock gene expression in human leukocytes and the effect of exercise depended on when it was performed. Brain and muscle ARNT-like protein 1 ( Bmal1) expression was increased after exercises performed in the morning and afternoon. Cryptochrome 1 ( Cry1) expression was also increased after the morning exercise. The effect of exercise on acrophase of Bmal1 depended on the time of the exercise: advanced after morning exercise and delayed after afternoon exercise.
BackgroundExercise performed in a postprandial state does not increase 24-h fat oxidation of male and female subjects. Conversely, it has been shown in male subjects that exercise performed in a postabsorptive state increases 24-h fat oxidation compared with that in sedentary control and that with exercise trials performed after breakfast, lunch, or dinner. There is a paucity of study evaluating the effect of exercise performed in a postabsorptive state in female subjects.MethodNine young female subjects participated in indirect calorimetry measurement over 24-h using a room-size metabolic chamber in which subjects remained sedentary or performed 60 min exercise before breakfast at 50% of . Exercise was accompanied by an increase in energy intake to ensure that subjects were in a similar state of energy balance over 24 h for the two trials.FindingsCompared with the sedentary condition, exercise performed before breakfast increased 24-h fat oxidation (519 ± 37 vs. 400 ± 41 kcal/day). Time courses of relative energy balance differed between trials with transient negative energy balance observed before breakfast. The lowest values of relative energy balance observed during the 24-h calorimetry, i.e., transient energy deficit, were greater in exercise trials than in sedentary trials. The transient deficit in carbohydrate balance was also observed before breakfast, and magnitude of the deficit was greater in exercise trial compared to that of sedentary trial.InterpretationUnder energy-balanced conditions, exercise performed in a post-absorptive state increases 24-h fat oxidation in female subjects. The effect of exercise performed before breakfast can be attributed to nutritional state: a transient deficit in energy and carbohydrate at the end of exercise.
It is not clear whether or not recreational runners can recover aerobic fitness and performance within one week after marathon running. This study aimed to investigate the effects of running a marathon race on aerobic fitness and performance one week later. Eleven recreational runners (six men, five women) completed the race in 3 h 36 min 20 s ± 41 min 34 s (mean ± standard deviation). Before and 7 days after the race, they performed a treadmill running test. Perceived muscle soreness was assessed before the race and for the following 7 days. The magnitude of changes in the treadmill running test was considered possibly trivial for maximal oxygen uptake (V˙O2max) (mean difference −1.2 ml/kg/min; ±90% confidence limits 2 ml/kg/min), unclear for %V˙O2max at anaerobic threshold (AT) (−0.5; ±4.1%) and RE (0.2; ±3.5 ml/kg/km), and likely trivial for both velocity at AT and peak (−0.2; ±0.49 km/h and −0.3; ±0.28 km/h). Perceived muscle soreness increased until 3 days after the race, but there were no clear differences between the values before the race and 4–7 days after it. These results show that physiological capacity associated with marathon running performance is recovered within 7 days after a marathon run.
Running economy (RE), which is evaluated at an exercise intensity below the lactate threshold (LT), is recognized as the most important physiological variable for estimating running performance. However, middle-and long-distance athletes run above LT intensity during their competitive events. This study elucidates the relation between 1,500-m running performance and physiological variables, including RE measured at intensities below and above the LT. The study included 34 male distance runners (1,500-m velocity: 22.2 ± 0.8 km·h −1 , equivalent to race times of 4′03″2 ± 8″5). RE was calculated at four running velocities selected to provide intensities of 90%LT and 95%LT below LT (REbLT) and 105%LT and 110%LT above LT (REaLT). RE was determined from aerobic energy metabolism, calculated from oxygen uptake and the respiratory exchange ratio, combined with anaerobic energy metabolism, calculated from the change in blood lactate concentration. Results show that the 1,500-m velocity was not related to maximal oxygen uptake (V ・ O 2 max) or LT intensity (r = 0.19 and 0.10, respectively). This velocity correlated with both REaLT and REbLT, with the correlation coefficient being higher for REaLT (r = −0.65 and −0.71 vs −0.56 and −0.58). Furthermore, the coefficient of determination for 1,500-m velocity determined from V ・ O 2 max, LT intensity and REaLT was higher than that determined from V ・ O 2 max, LT intensity and REbLT (R 2 = 0.603 and 0.640 vs 0.415 and 0.543). These results suggest that RE measured at an intensity above LT intensity may be better than other physiological variables for estimating 1,500-m running performance.
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