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Exercise training increases mitochondrial content in active skeletal muscle. Previous work suggests that mitochondrial-related genes respond favorably to exercise in cold environments. However, the impact of localized tissue cooling is unknown. The purpose is to determine the impact of local muscle cooling during endurance exercise on human skeletal muscle mitochondrial-related gene expression. Twelve subjects (age 28±6 y) cycled at 65% Wpeak. One leg was cooled (C) for 30 minutes before and during exercise with a thermal wrap while the other leg was wrapped but not cooled, room temperature (RT). Muscle biopsies were taken from each VL before and 4 hours post-exercise for the analysis of gene expression. Muscle temperature was lower in C (29.2±0.7°C) than RT (34.1±0.3°C) after pre-cooling for 30 minutes before exercise (p<0.001) and remained lower after exercise in C (36.9±0.5) than RT (38.4±0.2, p<0.001). PGC-1α and NRF1 mRNA expression were lower in C (p=0.012 and p=0.045, respectively) than RT at 4-h post. There were no temperature related differences in other genes (p>0.05). These data suggest that local cooling has an inhibitory effect on exercise-induced PGC-1α and NRF1 expression in human skeletal muscle. Those considering using local cooling during exercise should consider other systemic cooling options. Novelty Bullets • Local cooling has an inhibitory effect on exercise-induced PGC-1α and NRF1 expression in human skeletal muscle. • Local cooling may lead to a less robust exercise stimulus compared to standard conditions.

Although the hallmark of obesity is the expansion of adipose tissue, not all adipose tissue expansion is the same. Expansion of healthy adipose tissue is accompanied by adequate capillary angiogenesis and mitochondria-centered metabolic integrity, whereas expansion of unhealthy adipose tissue is associated with capillary and mitochondrial derangement, resulting in deposition of immune cells (M1-stage macrophages) and excess production of pro-inflammatory cytokines. Accumulation of these dysfunctional adipose tissues has been linked to the development of obesity comorbidities, such as type 2 diabetes, hypertension, dyslipidemia, and cardiovascular disease, which are leading causes of human mortality and morbidity in modern society. Mechanistically, vascular rarefaction and mitochondrial incompetency (for example, low mitochondrial content, fragmented mitochondria, defective mitochondrial respiratory function, and excess production of mitochondrial reactive oxygen species) are frequently observed in adipose tissue of obese patients. Recent studies have demonstrated that exercise is a potent behavioral intervention for preventing and reducing obesity and other metabolic diseases. However, our understanding of potential cellular mechanisms of exercise, which promote healthy adipose tissue expansion, is at the beginning stage. In this review, we hypothesize that exercise can induce unique physiological stimuli that can alter angiogenesis and mitochondrial remodeling in adipose tissues and ultimately promote the development and progression of healthy adipogenesis. We summarize recent reports on how regular exercise can impose differential processes that lead to the formation of either healthy or unhealthy adipose tissue and discuss key knowledge gaps that warrant future research.

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There has been recent debate on the potential difference in physiological response between exposure to simulated altitude (normobaric hypoxia) and terrestrial altitude (hypobaric hypoxia). Purpose: To determine the difference in the physiological response to normobaric and hypobaric hypoxia during exercise. Methods: Eight recreationally active subjects (27 ¡ 5 years old, 73.1 ¡ 7.4 kg body weight, 170.6 ¡ 6.7 cm height, and 19.3 ¡ 9.2% body fat) completed incremental cycling exercise to volitional fatigue in three separate environments: normobaric normoxia (NN; 350 m), normobaric hypoxia (NH; simulated 3094 m), and hypobaric hypoxia (HH; 3094 m). Heart rate, blood oxygen saturation, and muscle tissue oxygenation were measured at rest and continuously throughout the exercise trials. Results: Blood oxygen saturation (SpO2) was ,10% higher in NN compared to the two hypoxic conditions (p , 0.001) at rest and all exercise stages, with no difference between NH and HH (p. 0.05). Heart rate was higher at rest in HH (98 ¡ 13 bpm) compared to NN (83 ¡ 15 bpm, p 5 0.011) and NH (84 ¡ 14 bpm, p 5 0.001) which persisted until 165 watts at which point no difference was observed (p. 0.05). Muscle tissue oxygenation was 17% higher in HH compared to NN and 19% higher than NH throughout exposure (p , 0.05). Conclusion: These data indicate that the hypoxic stresses resulting from normobaric and hypobaric hypoxia are not the same and that hypobaric hypoxia may not result in hypoxia at the level of the tissue.

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