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Effects of intermittent hypoxic training (IHT) are still controversial and detraining effects remain uninvestigated. Therefore, we investigated (a) whether IHT improves aerobic capacity; (b) whether aerobic detraining occurs post-IHT; and (c) whether intermittent hypoxic exposure (IHE) at rest reduces a possible aerobic detraining post-IHT. Twenty eight runners (21 men/7 women; 36 ± 2 years; maximal oxygen uptake [V[Combining Dot Above]O2max] 55.4 ± 1.3 ml·kg·min) participated in a single-blinded placebo-controlled trial. Twice a week, 1 group performed 6 weeks of IHT (n = 11), followed by 4 weeks of IHE (n = 11) at rest (IHT+IHE group). Another group performed 6 weeks of IHT (n = 10), followed by 4 weeks of normoxic exposure (NE, n = 9) at rest (IHT+NE group). A control group performed 6 weeks of normoxic training (NT, n = 7), followed by 4 weeks of NE (n = 6) at rest (NT+NE group). Hematological and submaximal/maximal aerobic measurements were conducted in normoxia at pretraining, posttraining, and postexposure. Hemoglobin concentration did not change, but lactate threshold and running economy improved in all groups at posttraining (p ≤ 0.05 vs. pretraining). Ventilatory threshold, respiratory compensation point, and V[Combining Dot Above]O2max increased after IHT (IHT+IHE group: 7.3, 5.4, and 9.2%, respectively; IHT+NE group: 10.7, 7.5, and 4.8%; p ≤ 0.05 vs. pretraining), but not after NT (-1.1, -1.0, and -3.8%; p > 0.05 vs. pretraining). Such IHT-induced adaptations were maintained at postexposure (p > 0.05 vs. postexposure). In conclusion, IHT induced further aerobic improvements than NT. These additional IHT adaptations were maintained for 4 weeks post-IHT, regardless of IHE.

ObjectivesTo investigate whether the muscle strength decrease that follows anterior cruciate ligament (ACL) reconstruction would lead to different cardiorespiratory adjustments during dynamic exercise. MethodEighteen active male subjects were submitted to isokinetic evaluation of knee flexor and extensor muscles four months after ACL surgery. Thigh circumference was also measured and an incremental unilateral cardiopulmonary exercise test was performed separately for both involved and uninvolved lower limbs in order to compare heart rate, oxygen consumption, minute ventilation, and ventilatory pattern (breath rate, tidal volume, inspiratory time, expiratory time, tidal volume/inspiratory time) at three different workloads (moderate, anaerobic threshold, and maximal). ResultsThere was a significant difference between isokinetic extensor peak torque measured in the involved (116.5±29.1 Nm) and uninvolved (220.8±40.4 Nm) limbs, p=0.000. Isokinetic flexor peak torque was also lower in the involved limb than in the uninvolved limb (107.8±15.4 and 132.5±26.3 Nm, p=0.004, respectively). Lower values were also found in involved thigh circumference as compared with uninvolved limb (46.9±4.3 and 48.5±3.9 cm, p=0.005, respectively). No differences were found between the lower limbs in any of the variables of the incremental cardiopulmonary tests at all exercise intensities. ConclusionsOur findings indicate that, four months after ACL surgery, there is a significant deficit in isokinetic strength in the involved limb, but these differences in muscle strength requirement do not produce differences in the cardiorespiratory adjustments to exercise. Based on the hypotheses from the literature which explain the differences in the physiological responses to exercise for different muscle masses, we can deduce that, after 4 months of a rehabilitation program after an ACL reconstruction, individuals probably do not present differences in muscle oxidative and peripheral perfusion capacities that could elicit higher levels of peripheral cardiorepiratory stimulus during exercise.

Factors linked to modern lifestyles, such as physical inactivity, Western diet, and poor sleep quality have been identified as key contributors to the positive energy balance (PEB). PEB rises adipose tissue hypertrophy and dysfunction over the years, affecting cells and tissues that are metabolically critical for energy homeostasis regulation, especially skeletal muscle, hypothalamic-pituitary-adrenal axis, and gut microbiota. It is known that the interaction among lifestyle factors and tissue metabolic dysfunction increases low-grade chronic systemic inflammation, leading to insulin resistance and other adverse metabolic disorders. Although immunometabolic mechanisms are widely discussed in obesity, neuroimmunoendocrine pathways have gained notoriety, as a link to neuroinflammation and central nervous system disorders. Hypothalamic inflammation has been associated with food intake dysregulation, which comprises homeostatic and non-homeostatic mechanisms, promoting eating behavior changes related to the obesity prevalence. The purpose of this review is to provide an updated and integrated perspective on the effects of Western diet, sleep debt, and physical exercise on the regulation of energy homeostasis and low-grade chronic systemic inflammation. Subsequently, we discuss the intersection between systemic inflammation and neuroinflammation and how it can contribute to energy imbalance, favoring obesity. Finally, we propose a model of interactions between systemic inflammation and neuroinflammation, providing new insights into preventive and therapeutic targets for obesity.

Increased ventilatory response to the metabolic demand ("ventilatory inefficiency") is commonly found during dynamic exercise in patients with chronic obstructive pulmonary disease (COPD). However, the role of enhanced muscle ergoreflex activity on this phenomenon is yet unknown. Ten non-hypoxaemic patients with varying degrees of disease severity (median and range of post-bronchodilator FEV(1) = 37.5 (27 to 70%) predicted) and 7 age- and gender-matched controls were studied. Subjects were submitted to wrist flexion tests to the limit of tolerance (Tlim) with and without post-exercise regional circulatory occlusion (PE-RCO) for 3 min. The muscle ergoreflex activity was quantified as the difference in ventilation between PE-RCO and control recovery periods corrected for the resting values (ergoreflex Delta). In addition, the area under the ventilatory curve in the recovery period was calculated in both conditions. We found that Tlim and the physiological stress associated with localized exercise did not differ between patients and controls. However, patients had increased ventilatory response to a given metabolic demand (VCO(2)), either at rest or during exercise (P < 0.05). There were no significant differences in ergoreflex Delta in patients and controls (-2.2 to 2.4 (0.2) vs. -0.6 to 1.8 (0.3) l/min, respectively). In addition, the area under the ventilatory curve in the recovery period did not differ between control and PE-RCO tests in patients and healthy subjects (P > 0.05). We conclude that increased muscle ergoreflex activity did not contribute to an excessive ventilatory response to exercise in patients with COPD-at least in non-hypoxaemic and non-cachetic subjects.