The Effects of Different Modalities of an Acute Energy Deficit on Sleep and Next Morning Appetitive and Compensatory Behavior in Healthy Young Adults: The EDIES Protocol.

Sleep is bi-directionally linked to energy balance. This crossover study design will evaluate the acute effect of a moderate energy deficit (500 kcal) induced by diet, exercise, or mixed (-250 kcal by diet and 250 kcal by exercise) on sleep and the next morning's appetitive responses. The study sample comprises 24 healthy young adults. The experimental measurements will be conducted in a naturalistic, momentary manner and partly assessed by the participants. The participants will undergo a run-in period in order to stabilize their sleep schedules and provide them with training on the study protocol and measurements. Indirect calorimetry will be used to determine their resting metabolic rate and peak oxygen consumption (VO2 peak). Then, they will take part in a control session (CTL), followed by three energy deficit sessions in random order: a diet-induced energy deficit session (DED), an exercise-induced energy deficit session (EED), and a mixed energy deficit session (MED). All experimental sessions will be separated by a one-week washout. The participants' sleep will be monitored by ambulatory polysomnography, and the next morning's appetitive response will be evaluated via ad libitum food intake, appetite sensations, and food reward, measured by a food liking and wanting computerized test.

Effects of acute nitric oxide precursor intake on peripheral and central fatigue during knee extensions in healthy men.

NEW FINDINGS: What is the central question of this study? What is the effect of acute NO precursor intake on vascular function, muscle and cerebral oxygenation and peripheral and central neuromuscular fatigue during knee-extension exercise? What is the main finding and its importance? Acute NO precursor ingestion increases the plasma concentrations of NO precursors (nitrate, arginine and citrulline) and enhances post-ischaemic vasodilatation, but has no significant effect on muscle and cerebral oxygenation, peripheral and central mechanisms of neuromuscular fatigue and, consequently, does not improve exercise performance. ABSTRACT: Nitric oxide (NO) plays an important role in matching blood flow to oxygen demand in the brain and contracting muscles during exercise. Previous studies have shown that increasing NO bioavailability can improve muscle function. The aim of this study was to assess the effect of acute NO precursor intake on muscle and cerebral oxygenation and on peripheral and central neuromuscular fatigue during exercise. In four experimental sessions, 15 healthy men performed a thigh ischaemia-reperfusion test followed by submaximal isometric knee extensions (5 s on-4 s off; 45% of maximal voluntary contraction) until task failure. In each session, subjects drank a nitrate-rich beetroot juice containing 520 mg nitrate (N), N and citrulline (6 g; N+C), N and arginine (6 g; N+A) or a placebo (PLA). Prefrontal cortex and quadriceps near-infrared spectroscopy parameters were monitored continuously. Transcranial magnetic stimulation and femoral nerve electrical stimulation were used to assess central and peripheral determinants of fatigue. The post-ischaemic increase in thigh blood total haemoglobin concentration was larger in N (10.1 ± 3.7 mmol) and N+C (10.9 ± 3.3 mmol) compared with PLA (8.2 ± 2.7 mmol; P < 0.05). Nitric oxide precursors had no significant effect on muscle and cerebral oxygenation or on peripheral and central mechanisms of neuromuscular fatigue during exercise. The total number of knee extensions did not differ between sessions (N, 71.9 ± 33.2; N+A, 73.3 ± 39.4; N+C, 74.6 ± 34.0; PLA, 71.8 ± 39.9; P > 0.05). In contrast to the post-ischaemic hyperaemic response, NO bioavailability in healthy subjects might not be the limiting factor for tissue perfusion and oxygenation during submaximal knee extensions to task failure.

Effects of Acute Salbutamol Intake on Peripheral and Central Fatigue in Trained Men.

PURPOSE: Ergogenic effect in physically active subjects has been reported after acute salbutamol (SAL) intake. ß2-Agonists have potential stimulant effects within the central nervous system that could be involved in this ergogenic effect. We hypothesized that acute SAL intake would induce changes in cerebral responses during exercise, with significant improvement in cerebral oxygenation and voluntary activation (VA) contributing to an increase in muscle performance. METHODS: Fourteen trained male subjects (25 ± 5 yr) performed repeated isometric knee extensions until task failure (TF) after 4 mg (oral) SAL, 800 µg (inhaled) SAL, or placebo intake. VA, corticospinal excitability, and inhibition assessed by transcranial magnetic stimulation and changes in hemoglobin concentrations assessed by near-infrared spectroscopy were measured before and during the fatiguing task. RESULTS: SAL had no significant effect both at rest and during exercise on prefrontal cortex oxygenation (e.g., changes in oxyhemoglobin concentration at TF: 11.4 ± 11.1 (4 mg SAL) vs 10.4 ± 10.6 (800 µg SAL) vs 10.8 ± 8.1 µmol (placebo); P = 0.314) and neuromuscular function (e.g., VA measured by TMS at TF: 90.2% ± 6.6% vs 92.6% ± 5.0% vs 90.1% ± 7.0%; P = 0.760). SAL had no effect on the number of contractions until TF (95 ± 51 vs 100 ± 52 vs 93 ± 47; P = 0.629). CONCLUSIONS: These results indicate that acute SAL intake had no effect on central and peripheral mechanisms of neuromuscular fatigue and did not improve quadriceps endurance.

Ventilatory oscillations at exercise: effects of hyperoxia, hypercapnia, and acetazolamide.

Periodic breathing has been found in patients with heart failure and sleep apneas, and in healthy subjects in hypoxia, during sleep and wakefulness, at rest and, recently, at exercise. To unravel the cardiorespiratory parameters liable to modulate the amplitude and period of ventilatory oscillations, 26 healthy subjects were tested under physiological (exercise) and environmental (hypoxia, hyperoxia, hyperoxic hypercapnia) stresses, and under acetazolamide (ACZ) treatment. A fast Fourier transform spectral analysis of breath-by-breath ventilation (V˙E) evidenced an increase in V˙E peak power under hypercapnia (vs. normoxia and hyperoxia, P < 0.001) and a decrease under ACZ (vs. placebo, P < 0.001), whereas it was not modified in hyperoxia. V˙E period was shortened by exercise in all conditions (vs. rest, P < 0.01) and by hypercapnia (vs. normoxia, P < 0.05) but remained unchanged under ACZ (vs. placebo). V˙E peak power was positively related to cardiac output (Q˙c) and V˙E in hyperoxia (P < 0.01), in hypercapnia (P < 0.001) and under ACZ (P < 0.001). V˙E period was negatively related to Q˙c and V˙E in hyperoxia (P < 0.01 and P < 0.001, respectively), in hypercapnia (P < 0.05 and P < 0.01, respectively) and under ACZ (P < 0.05 and P < 0.01, respectively). Total respiratory cycle time was the main factor responsible for changes in V˙E period. In conclusion, exercise, hypoxia, and hypercapnia increase ventilatory oscillations by increasing Q˙c and V˙E, whereas ACZ decreases ventilatory instability in part by a contrasting action on O2 and CO2 sensing. An intrinsic oscillator might modulate ventilation through a complex system where peripheral chemoreflex would play a key role.