Preexercise High-Fat Meal Following Carbohydrate Loading Attenuates Glycogen Utilization During Endurance Exercise in Male Recreational Runners.

ABSTRACT: Iwayama, K, Tanabe, Y, Yajima, K, Tanji, F, Onishi, T, and Takahashi, H. Preexercise high-fat meal following carbohydrate loading attenuates glycogen utilization during endurance exercise in male recreational runners. J Strength Cond Res 37(3): 661-668, 2023-This study aimed to investigate whether one preexercise high-fat meal can increase glycogen conservation during endurance exercise, as compared with one preexercise high-carbohydrate meal. Ten young male recreational runners (22.0 ± 0.6 years; 171.3 ± 0.9 cm; 58.3 ± 1.9 kg; maximal oxygen uptake [V̇ o2 max], 62.0 ± 1.6 ml·kg -1 ·min -1 ) completed 2 exercise trials after high-carbohydrate loading: eating a high-carbohydrate (CHO; 7% protein, 13% fat, 80% carbohydrate) meal or eating a high-fat (FAT; 7% protein, 42% fat, 52% carbohydrate) meal 3.5 hours before exercise. The order of the 2 trials was randomized, and the interval between trials was at least 1 week. The experimental exercise consisted of running on a treadmill for 60 minutes at 95% of each subject's lactate threshold. Muscle and liver glycogen content were assessed using noninvasive carbon magnetic resonance spectroscopy before the experimental meal as well as before and after exercise; respiratory gases were measured continuously during exercise. The respiratory exchange ratio during exercise was statistically lower in the FAT trial than in the CHO trial ( p < 0.01). In addition, muscle ( p < 0.05) and liver ( p < 0.05) glycogen utilization during exercise was less in the FAT trial than in the CHO trial. Therefore, one high-fat meal following carbohydrate loading reduced muscle and liver glycogen use during the 60-minute exercise. These results suggest that this dietary approach may be applied as a strategy to optimize energy utilization during endurance exercise.

Diurnal variation in the glycogen content of the human liver using 13 C MRS.

Glycogen in tissues functions not only as carbohydrate reserves, but also as molecular sensors capable of activating signaling pathways in response to physical activity. While glycogen in the skeletal muscles is mainly a local energy substrate, glycogen in the liver serves as a glucose reserve to maintain normal blood glucose levels in the body, even during the sleep state. The aim of this study is to compare the diurnal variation of glycogen in the muscle and liver of human subjects under normal conditions. The glycogen content was measured in the muscle and liver of 10 young, healthy, male volunteers using 13 C MRS, a non-invasive technique. The subjects remained sedentary, and glycogen concentration was measured six times daily. Experimental meals were provided to achieve individual energy balance, estimated according to the energy requirement guideline for patients from Japan. The largest variation in muscle glycogen compared with 1 h after supper (20:00 on Day 1) was 3.1 ± 8.2 mmol/L (16:00 on Day 2). In the liver, however, the glycogen content decreased by 80.6 ± 40.4 mmol/L through the overnight fasting period (07:00 on Day 2). This study demonstrated that the glycogen content in the liver was significantly lower in the morning, while the glycogen content in the calf muscles underwent minimal diurnal variation. The overnight fast is a characteristic daily condition, in which liver glycogen content is low, whereas muscle glycogen content is relatively unaffected.

Anagliptin increases insulin-induced skeletal muscle glucose uptake via an NO-dependent mechanism in mice.

AIMS/HYPOTHESIS: Recently, incretin-related agents have been reported to attenuate insulin resistance in animal models, although the underlying mechanisms remain unclear. In this study, we investigated whether anagliptin, the dipeptidyl peptidase 4 (DPP-4) inhibitor, attenuates skeletal muscle insulin resistance through endothelial nitric oxide synthase (eNOS) activation in the endothelial cells. We used endothelium-specific Irs2-knockout (ETIrs2KO) mice, which show skeletal muscle insulin resistance resulting from a reduction of insulin-induced skeletal muscle capillary recruitment as a consequence of impaired eNOS activation. METHODS: In vivo, 8-week-old male ETIrs2KO mice were fed regular chow with or without 0.3% (wt/wt) DPP-4 inhibitor for 8 weeks to assess capillary recruitment and glucose uptake by the skeletal muscle. In vitro, human coronary arterial endothelial cells (HCAECs) were used to explore the effect of glucagon-like peptide 1 (GLP-1) on eNOS activity. RESULTS: Treatment with anagliptin ameliorated the impaired insulin-induced increase in capillary blood volume, interstitial insulin concentration and skeletal muscle glucose uptake in ETIrs2KO mice. This improvement in insulin-induced glucose uptake was almost completely abrogated by the GLP-1 receptor (GLP-1R) antagonist exendin-(9-39). Moreover, the increase in capillary blood volume with anagliptin treatment was also completely inhibited by the NOS inhibitor. GLP-1 augmented eNOS phosphorylation in HCAECs, with the effect completely disappearing after exposure to the protein kinase A (PKA) inhibitor H89. These data suggest that anagliptin treatment enhances insulin-induced capillary recruitment and interstitial insulin concentrations, resulting in improved skeletal muscle glucose uptake by directly acting on the endothelial cells via NO- and GLP-1-dependent mechanisms in vivo. CONCLUSIONS/INTERPRETATION: Anagliptin may be a promising agent to ameliorate skeletal muscle insulin resistance in obese patients with type 2 diabetes.

The effect of nocturnal blue light exposure from light-emitting diodes on wakefulness and energy metabolism the following morning.

OBJECTIVES: The control of sleep/wakefulness is associated with the regulation of energy metabolism. The present experiment was designed to assess the effect of nocturnal blue light exposure on the control of sleep/wakefulness and energy metabolism until next noon. METHODS: In a balanced cross-over design, nine young male subjects sitting in a room-size metabolic chamber were exposed either to blue LEDs or to no light for 2 h in the evening. Wavelength of monochromatic LEDs was 465 nm and its intensity was 12.1 µW/cm(2). RESULTS: During sleep, sleep architecture and alpha and delta power of EEG were similar in the two experimental conditions. However, the following morning, when subjects were instructed to stay awake in a sitting position, duration judged as sleep at stages 1 and 2 was longer for subjects who received than for those who received no light exposure. Energy metabolism during sleep was not affected by evening blue light exposure, but the next morning energy expenditure, oxygen consumption, carbon dioxide production and the thermic effect of breakfast were significantly lower in subjects who received blue light exposure than in those who received no light exposure. CONCLUSIONS: Exposure to low intensity blue light in the evening, which does not affect sleep architecture and energy metabolism during sleep, elicits drowsiness and suppression of energy metabolism the following morning.

Comparison of energy requirement estimation using activity record or accelerometer with doubly labeled water method in collegiate male sprinters.

BACKGROUND & AIMS: Track and field sprinters must obtain an optimal body composition to improve sprint performance. To successfully change body composition, it is important to evaluate the estimated energy requirements (EER) and fluctuations in total energy expenditure (TEE). However, methods to accurately evaluate the EER and TEE in sprinters have not been fully investigated. The aim of this study was to compare currently used methods with the doubly labeled water (DLW) method, which is currently the gold standard for evaluating EER and TEE. METHODS: Ten male collegiate sprinters participated in the study. We evaluated TEEDLW and compared it with the EER calculated using two equations used by the National Institute of Health and Nutrition (NIHN) and the Japan Institute of Sports Sciences (JISS). In addition, we evaluated the TEE from the activity record (AR) and triaxial accelerometer (ACC). RESULTS: TEEDLW (3172 ± 415 kcal/day) was not significantly different from EERNIHN (p = 0.076) or EERJISS (p = 0.967). In addition, there were no significant differences between TEEDLW and TEEAR (p = 0.218). However, two accelerometer-derived equations used to evaluate TEE were found to have underestimated (2783 ± 377 kcal/day, p < 0.001) and overestimated (3405 ± 369 kcal/day, p = 0.009) the TEE. CONCLUSION: Our results suggest that EERNIHN and EERJISS may be useful in evaluating the EER of collegiate male sprinters on a group basis, and AR may be more accurate than ACC in evaluating the TEE. These results may be helpful when considering nutritional support for male collegiate sprinters.

Exercise Timing Matters for Glycogen Metabolism and Accumulated Fat Oxidation over 24 h.

Due to increasingly diverse lifestyles, exercise timings vary between individuals: before breakfast, in the afternoon, or in the evening. The endocrine and autonomic nervous systems, which are associated with metabolic responses to exercise, show diurnal variations. Moreover, physiological responses to exercise differ depending on the timing of the exercise. The postabsorptive state is associated with greater fat oxidation during exercise compared to the postprandial state. The increase in energy expenditure persists during the post-exercise period, known as "Excess Post-exercise Oxygen Consumption". A 24 h evaluation of accumulated energy expenditure and substrate oxidation is required to discuss the role of exercise in weight control. Using a whole-room indirect calorimeter, researchers revealed that exercise performed during the postabsorptive state, but not during the postprandial state, increased accumulated fat oxidation over 24 h. The time course of the carbohydrate pool, as estimated by indirect calorimetry, suggests that glycogen depletion after postabsorptive exercise underlies an increase in accumulated fat oxidation over 24 h. Subsequent studies using 13C magnetic resonance spectroscopy confirmed that the variations in muscle and liver glycogen caused by postabsorptive or postprandial exercise were consistent with indirect calorimetry data. These findings suggest that postabsorptive exercise alone effectively increases 24 h fat oxidation.

Diurnal variations in muscle and liver glycogen differ depending on the timing of exercise.

It has been suggested that glycogen functions not only in carbohydrate energy storage, but also as molecular sensors capable of activating lipolysis. This study aimed to compare the variation in liver and muscle glycogen during the day due to different timing of exercise. Nine healthy young men participated in two trials in which they performed a single bout of exercise at 70% of their individual maximal oxygen uptake for 60 min in the post-absorptive (morning) or post-prandial (afternoon) state. Liver and muscles glycogen levels were measured using carbon magnetic resonance spectroscopy (13C MRS). Diurnal variations in liver and muscle glycogen compared to baseline levels were significantly different depending on the timing of exercise. The effect of the timing of exercise on glycogen fluctuation is known to be related to a variety of metabolic signals, and the results of this study will be useful for future research on energy metabolism.

Metabolic flexibility during sleep.

Known as metabolic flexibility, oxidized substrate is selected in response to changes in the nutritional state. Sleep imposes an extended duration of fasting, and oxidized substrates during sleep were assumed to progressively shift from carbohydrate to fat, thereby gradually decreasing the respiratory quotient (RQ). Contrary to this assumption, whole-room indirect calorimetry with improved time resolution revealed that RQ re-ascended prior to awakening, and nadir of RQ in non-obese young adults occurred earlier in women than men after bedtime. The transient decrease in RQ during sleep was blunted in metabolically inflexible men with smaller amplitude of diurnal rhythm in RQ. Similarly, the effect of 10 years difference in age on RQ became significant during sleep; the decrease in RQ during sleep was blunted in older subjects. Inter-individual difference in RQ become apparent during sleep, and it might serve as a window to gain insight into the early-stage pathogenesis of metabolic inflexibility.

Exercise improves the quality of slow-wave sleep by increasing slow-wave stability.

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% [Formula: see text]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.