The role of exercise and hypoxia on glucose transport and regulation

Abstract

Muscle glucose transport activity increases with an acute bout of exercise, a process that is accomplished by the translocation of glucose transporters to the plasma membrane. This process remains intact in the skeletal muscle of individuals with insulin resistance and type 2 diabetes mellitus (T2DM). Exercise training is, therefore, an important cornerstone in the management of individuals with T2DM. However, the acute systemic glucose responses to carbohydrate ingestion are often augmented during the early recovery period from exercise, despite increased glucose uptake into skeletal muscle. Accordingly, the first aim of this review is to summarize the knowledge associated with insulin action and glucose uptake in skeletal muscle and apply these to explain the disparate responses between systemic and localized glucose responses post-exercise. Herein, the importance of muscle glycogen depletion and the key glucoregulatory hormones will be discussed. Glucose uptake can also be stimulated independently by hypoxia; therefore, hypoxic training presents as an emerging method for enhancing the effects of exercise on glucose regulation. Thus, the second aim of this review is to discuss the potential for systemic hypoxia to enhance the effects of exercise on glucose regulation.

Effects of exercise modality combined with moderate hypoxia on blood glucose regulation in adults with overweight

“…It is possible our time-points of analysis (i.e., pre-, immediately post-exercise, and 24 h post-exercise) may have missed the temporal resolution for observing alterations in these c-miRNAs with combined exercise and hypoxia. Furthermore, it is plausible the observed enhancement in plasma glucose responses with SIT were more confined to the translational level of protein regulation such that these improvements were mediated largely by increases in Akt-mediated skeletal muscle GLUT4 protein expression ( Camera et al, 2010 ; Soo et al, 2023 ). We also cannot rule out that the unchanged post-exercise responses observed in our selected c-mIRNAs may be due to the plasma and not the exosomal sample pool being analysed, with previous work highlighting differences in expression patterns of particular miRNAs following exercise between each sample pool ( D’Souza et al, 2018 ).…”

Protein Supplementation May Dampen Positive Effects of Exercise on Glucose Homeostasis: A Pilot Weight Loss Intervention

“…Increased gluconeogenesis coupled with insulin resistance may be a potential explanation as to why the PG (increased protein intake) showed smaller improvements in fasting plasma glucose and insulin resistance [41]. Although both groups experienced improvements in insulin resistance, the positive effects of exercise on insulin resistance may have masked the full extent of negative impacts on insulin resistance from high protein consumption [34,44]. One randomized control trial (RCT) found similar results, specifically that a whey protein supplement did not enhance the effects of resistance training on glycemic control in overweight older adults with T2D [45].…”

“…Additional evaluation should focus on how different types of protein supplementation may have different effects on glucose homeostasis (soy versus whey protein, for instance) [41]. Furthermore, many studies have shown timing of caloric intake pre-vs. post-exercise to have heterogenous effects on muscle protein breakdown and synthesis, which could, in turn, also influence glucose homeostasis [34,[66][67][68]. For instance, consuming a balanced meal following exercise may mitigate muscle protein breakdown early in the day [68], whereas others have found that ingesting protein every three hours was the best way to stimulate muscle protein synthesis [13,67].…”

“…A separate study highlighted how short-term high-protein diets improve prandial insulin secretion [32]. Furthermore, muscle contraction during exercise has been shown to improve glucose homeostasis via stimulation of the GLUT-4 glucose transporter, allowing for uptake of glucose from the bloodstream into the cell [34]. Such conflicting data for ways in which glucose homeostasis is worsened or enhanced via exercise and protein intake has created many questions.…”

Brain-Derived neurotrophic factor and inflammatory biomarkers are unaffected by acute and chronic intermittent hypoxic-hyperoxic exposure in geriatric patients: a randomized controlled trial

“…The neuroprotective effect of intermittent hypoxic exposure is thought to be related to the stabilization of hypoxia-inducible factor (HIF, especially HIF-1α) and the generation of reactive oxygen species (ROS) [ 48 , 49 ]. HIF-1α activates, among others, the transcription of genes responsible for angiogenesis [ 50 ], vasodilation [ 51 , 52 ], glucose transport, and glucose metabolism [ 53 , 54 ]. In this regard, especially cardiovascular and metabolic adaptations to intermittent hypoxia are assumed to protect against neurodegeneration (e.g.…”