Obesity is a major global health issue and a primary risk factor for metabolic-related disorders. While physical inactivity is one of the main contributors to obesity, it is a modifiable risk factor with exercise training as an established non-pharmacological treatment to prevent the onset of metabolic-related disorders, including obesity. Exposure to hypoxia via normobaric hypoxia (simulated altitude via reduced inspired oxygen fraction), termed hypoxic conditioning, in combination with exercise has been increasingly shown in the last decade to enhance blood glucose regulation and decrease the body mass index, providing a feasible strategy to treat obesity. However, there is no current consensus in the literature regarding the optimal combination of exercise variables such as the mode, duration, and intensity of exercise, as well as the level of hypoxia to maximize fat loss and overall body compositional changes with hypoxic conditioning. In this narrative review, we discuss the effects of such diverse exercise and hypoxic variables on the systematic and myocellular mechanisms, along with physiological responses, implicated in the development of obesity. These include markers of appetite regulation and inflammation, body conformational changes, and blood glucose regulation. As such, we consolidate findings from human studies to provide greater clarity for implementing hypoxic conditioning with exercise as a safe, practical, and effective treatment strategy for obesity.
Purpose: This study aimed to investigate the combined effects of moderate hypoxia with three different exercise modes on glucose regulation in healthy overweight adults. Methods: Thirteen overweight males (age: 31 ± 4 years; body fat 26.3 ± 3.2%) completed three exercise trials in a randomized crossover design involving 60 min cycling exercise at 90% lactate threshold (LOW), sprint interval training (20 × 4 s all-out; SIT) and lower limb functional bodyweight exercises (8 sets of 4 × 20 s; FEX) under moderate hypoxia (FiO2 = 16.5%). Post-exercise oral glucose tolerance test (OGTT) was performed following each trial. Heart rate, oxygen saturation (SpO2), physical activity enjoyment scale (PACES), and perceptual measures were recorded during each exercise session. Venous blood was collected pre-, immediately post-, and 24 h post-exercise and analysed for plasma glucose and insulin, incremental area under curve (iAUC), and circulating microRNA expression (c-miRs-486-5p, -126-5p, and -21-5p). Interstitial glucose concentrations were measured using continuous glucose monitoring (CGM). Results: Post-exercise OGTT iAUC for plasma glucose and insulin concentration were lower in SIT and LOW vs. control (p < 0.05) while post-exercise interstitial glucose iAUC and c-miRs were not different between exercise modes. Heart rate was greater in SIT vs. LOW and FEX, and FEX vs. LOW (p < 0.05), SpO2 was lower in SIT, while PACES was not different between exercise modes. Perceptual measures were greater in SIT vs. LOW and FEX. Conclusion: Acute SIT and LOW under moderate hypoxia improved post-exercise plasma insulin compared to FEX exercises. Considering SIT was also time-efficient, well tolerated, and enjoyable for participants, this may be the preferred exercise modality for improving glucose regulation in adult males with overweight when combined with moderate hypoxia.
We determined the effects of "periodized nutrition" on skeletal muscle and whole body responses to a bout of prolonged exercise the following morning. Seven cyclists completed two trials receiving isoenergetic diets differing in the timing of ingestion: they consumed either 8 g/kg body mass (BM) of carbohydrate (CHO) before undertaking an evening session of high-intensity training (HIT) and slept without eating (FASTED), or consumed 4 g/kg BM of CHO before HIT, then 4 g/kg BM of CHO before sleeping (FED). The next morning subjects completed 2 h of cycling (120SS) while overnight fasted. Muscle biopsies were taken on day 1 (D1) before and 2 h after HIT and on day 2 (D2) pre-, post-, and 4 h after 120SS. Muscle [glycogen] was higher in FED at all times post-HIT (P < 0.001). The cycling bouts increased PGC1α mRNA and PDK4 mRNA (P < 0.01) in both trials, with PDK4 mRNA being elevated to a greater extent in FASTED (P < 0.05). Resting phosphorylation of AMPK(Thr172), p38MAPK(Thr180/Tyr182), and p-ACC(Ser79) (D2) was greater in FASTED (P < 0.05). Fat oxidation during 120SS was higher in FASTED (P = 0.01), coinciding with increases in ACC(Ser79) and CPT1 as well as mRNA expression of CD36 and FABP3 (P < 0.05). Methylation on the gene promoter for COX4I1 and FABP3 increased 4 h after 120SS in both trials, whereas methylation of the PPARδ promoter increased only in FASTED. We provide evidence for shifts in DNA methylation that correspond with inverse changes in transcription for metabolically adaptive genes, although delaying postexercise feeding failed to augment markers of mitochondrial biogenesis.