Long-term maintenance of weight loss requires sustained energy balance at the reduced body weight. This could be attained by coupling low total daily energy intake (TDEI) with low total daily energy expenditure (TDEE; low energy flux), or by pairing high TDEI with high TDEE (high energy flux). Within an environment characterized by high energy dense food and a lack of need for movement, it may be particularly difficult for weight-reduced individuals to maintain energy balance in a low flux state. Most of these individuals will increase body mass due to an inability to sustain the necessary level of food restriction. This increase in TDEI may lead to the re-establishment of high energy flux at or near the original body weight. We propose that following weight loss, increasing physical activity can effectively re-establish a state of high energy flux without significant weight regain. Although the effect of extremely high levels of physical activity on TDEE may be constrained by compensatory reductions in non-activity energy expenditure, moderate increases following weight loss may elevate energy flux and encourage physiological adaptations favorable to weight loss maintenance, including better appetite regulation. It may be time to recognize that few individuals are able to re-establish energy balance at a lower body weight without permanent increases in physical activity. Accordingly, there is an urgent need for more research to better understand the role of energy flux in long-term weight maintenance.

Hypoxia impairs aerobic performance by accelerating fatiguing processes. These processes may originate from sites either distal (peripheral) or proximal (central) to the neuromuscular junction, though these are not mutually exclusive. Peripheral mechanisms include decrements in muscle glycogen or fluctuations in intramuscular metabolites, whereas central responses commonly refer to reductions in central motor drive elicited by alterations in blood glucose and neurotransmitter concentrations as well as arterial hypoxemia. Hypoxia may accelerate both peripheral and central pathways of fatigue, with the level of hypoxia strongly dictating the degree and primary locus of impairment. As more people journey to hypoxic settings for work and recreation, developing strategies to improve work capacity in these environments becomes increasingly relevant. Given that sea level performance improves with nutritional interventions such as carbohydrate (CHO) ingestion, a similar strategy may prove effective in delaying fatigue in hypoxia, particularly considering how the metabolic pathways enhanced with CHO supplementation overlap the fatiguing pathways upregulated in hypoxia. Many questions regarding the relationship between CHO, hypoxia, and fatigue remain unanswered, including specifics on when to ingest, what to ingest, and how varying altitudes influence supplementation effectiveness. Therefore, the purpose of this narrative review is to examine the peripheral and central mechanisms contributing to fatigue during aerobic exercise at varying degrees of hypoxia and to assess the role of CHO ingestion in attenuating fatigue onset.

When competing in road races, runners enter starting corrals long before the starting gun triggers. Athletes consequently must complete warm up routines well in advance of race commencement. To optimize performance readiness warm up intensity may need altered to account for the prolonged time between warm up and performance. This study tested the effectiveness of various warm up intensities on 1600 m run performance given a 20 min separation between warm up and time trial, and assessed the physiological bases for performance outcomes. In a randomized, crossover design, 14 athletic men and women [(age (mean ± SEM) = 22 ± 1 y; V·O₂peak = 50.3 ± 2.5 ml·kg⁻¹·min⁻¹] completed three warm up routines (light-, moderate-, or high-intensity warm up), rested for 20 min, and ran a 1600 m time trial. Warm up procedures were evaluated for their influence on performance, blood lactate, V·O₂, and alterations to neuromuscular function. Time trial performance was significantly faster ( P < 0.03) following a moderate-intensity warm up (6:12 ± 18 min:s·1600 m⁻¹) compared to a light-intensity warm up (6:30 ± 18 min:s·1600 m⁻¹). Performance following the high-intensity warm up (6:18 ± 24 min:s·1600 m⁻¹) fell between the light and moderate conditions. When stratified based on starting lactate concentrations, 1600 m performance was optimized when pre-time trial lactate was 2.0–4.9 mmol·l⁻¹. When a prolonged rest separates warm up exercise from time trial performance, warming up remains efficacious. Optimal warm up intensity may be identified using starting lactate as a gauge for performance readiness.

A healthy body mass contributes to a positive quality of life, and for overweight/obese individuals, weight loss of even modest proportions improves health-related outcomes. A novel approach to promoting body mass regulation is to pair exercise with high altitude, thereby upregulating metabolic processes and increasing caloric expenditure. As an added measure of body mass regulation, data suggest that high altitude stimulates the production of the appetite-suppressing hormone leptin. Issues arise, however, given that high altitude compromises aerobic exercise capacity. Whereas exercising at high altitude may compromise exercise intensity and duration, recovering at high altitude retains the integrity of exercise while still potentially conferring the benefits of the low oxygen environment on energy expenditure and energy intake. The purpose of this study was to perform a proof-of-concept pilot test on whether post-exercise exposure to a simulated high altitude influenced acute energy balance. Twelve healthy men and women ran for 30 min at a moderate intensity on two separate occasions. Following exercise, participants recovered for 30 min while breathing either sea level air or low oxygen air simulating high altitude (equivalent to 4500 m elevation). Blood samples and hunger ratings were collected pre-exercise and post-recovery. Heart rate was recorded throughout exercise and recovery and used to calculate caloric expenditure. Post-exercise energy expenditure was significantly higher (p = 0.03) following high altitude recovery (139 ± 15 kcal) compared to sea-level recovery (98 ± 11 kcal). Participants reported a lower desire to eat when they recovered in the high altitude environment (p = 0.01), though post-recovery leptin concentrations were similar between the two conditions. Post-exercise exposure to a simulated high altitude environment represents a promising method for increasing daily caloric expenditure and lowering appetite. Given the pilot nature of this study, future research is needed to address the question of high altitude recovery on a larger sample over a longer time period and with robust measures of caloric expenditure.

Objective: The purpose of this study was to investigate the effects of “train-high sleep-low” (THSL) dietary periodization on ventilatory strategies during cycling exercise at submaximal and maximal intensities. Method: In a randomized crossover design, 8 trained men [age (mean ± SEM) = 28 ± 1 y; peak oxygen uptake = 56.8 ± 2.4 mL kg⁻¹ min⁻¹] completed two glycogen-depleting protocols on a cycle ergometer on separate days, with the cycling followed by a low carbohydrate (CHO) meal and beverages containing either no additional CHO (THSL) or beverages containing 1.2 g kg⁻¹ CHO [traditional CHO replacement (TRAD)]. The following morning, participants completed 4 minutes of cycling below (Stage 1), at (Stage 2), and above (Stage 3) gas exchange threshold, followed by a 5-km time trial. Results: Timetrial performance was significantly faster in TRAD compared to THSL (8.7 ± 0.3 minutes and 9.0 ± 0.3 minutes, respectively; p = 0.02). No differences in ventilation, tidal volume, or carbon dioxide production occurred between conditions at any exercise intensity (p > 0.05). During Stage 1, oxygen uptake was 37.9 ± 1.5 mL kg⁻¹ min⁻¹ in the TRAD condition and 39.6 ± 1.8 mL kg⁻¹ min⁻¹ in THSL (p = 0.05). During Stage 2, VO2 was 44.6 ± 1.7 mL kg⁻¹ min⁻¹ in the TRAD condition and 47.0 ± 1.9 mL kg⁻¹ min⁻¹ in THSL (p = 0.07). No change in operating lung volume was detected between dietary conditions (p > 0.05). Conclusions: THSL impairs performance following the dietary intervention, but this occurs with no alteration of ventilatory measures.