Exercising for Insulin Sensitivity - Is There a Mechanistic Relationship With Quantitative Changes in Skeletal Muscle Mass?

Jasmine Paquin,Jean-Christophe Lagacé,Martin Brochu,Isabelle J. Dionne

doi:10.3389/fphys.2021.656909

Abstract

Skeletal muscle (SM) tissue has been repetitively shown to play a major role in whole-body glucose homeostasis and overall metabolic health. Hence, SM hypertrophy through resistance training (RT) has been suggested to be favorable to glucose homeostasis in different populations, from young healthy to type 2 diabetic (T2D) individuals. While RT has been shown to contribute to improved metabolic health, including insulin sensitivity surrogates, in multiple studies, a universal understanding of a mechanistic explanation is currently lacking. Furthermore, exercised-improved glucose homeostasis and quantitative changes of SM mass have been hypothesized to be concurrent but not necessarily causally associated. With a straightforward focus on exercise interventions, this narrative review aims to highlight the current level of evidence of the impact of SM hypertrophy on glucose homeostasis, as well various mechanisms that are likely to explain those effects. These mechanistic insights could provide a strengthened rationale for future research assessing alternative RT strategies to the current classical modalities, such as low-load, high repetition RT or high-volume circuit-style RT, in metabolically impaired populations.

Highlights

Skeletal muscle (SM) is the most important component of fat-free mass (FFM) and plays a key role in overall metabolic health
The findings from this study suggest SM hypertrophy may FFM and FM changes
The mechanisms underlying a relationship between SM hypertrophy and whole-body glucose homeostasis have not been demonstrated without doubt

Summary

INTRODUCTION

Skeletal muscle (SM) is the most important component of fat-free mass (FFM) and plays a key role in overall metabolic health. Protein kinase B (PKB); AMPK, AMP-activated protein kinase; AT, aerobic training; ATP, adenosine triphosphate; Avg, average; AUC, area under the curve; BMI, body mass index (kg/m2); BC, body composition; BF, body fat; C, citrate synthase; COX, cytochrome oxidase; CSA, cross-sectional area; eNOSser1177, endothelial nitric oxide synthase at phosphorylation site 1177; F-glucose, fasting glucose; F-insulin, fasting insulin; FFM, fat-free mass; FFMI, fat-free mass index (kg/m2); FM, fat mass; GIR, glucose infusion rate; GLUT4, glucose transporter type 4; GS, glycogen synthase; GT, glucose tolerance; GU, glucose uptake; HOMA-IR, homeostatic model assessment for insulin resistance; HAD, 3-hydroxyacyl-CoA dehydrogenase; IMTG, intramuscular triglycerides; IRS-1, insulin receptor substrate-1; LDH, lactate dehydrogenase; M, hyperinsulinemic-euglycemic clamp-derived insulin sensitivity; OGTT, oral glucose tolerance test; PGC-1α, peroxisome proliferator-activated receptor gamma coactivator 1-alpha; PI 3-k, phosphatidylinositol 3-kinases; REPS, repetitions; RM, maximal repetition; RT, resistance training; SLIVGTT, stable-label iv glucose tolerance test; SM, skeletal muscle; T2D, Type 2 diabetes. The current body of evidence suggests that even if the importance of AT and RT in glucose metabolism is no longer to be proven regarding IMTG metabolism, it has yet to be confirmed whether quantitative changes in SM mass further drives those adaptations in other populations, such as individuals with metabolic impairments

A Perspective Approach on the Optimal Strategy

Findings

CONCLUSION