Is Oxygen Consumption and Oxygen Delivery During Leg Exercise Compromised in Type II Diabetes?

Pak, Melissa; Moynes, Jaclyn; Poitras, Veronica J.; Tschakovsky, Michael E.

doi:10.1249/01.mss.0000384301.18771.9d

Cited by 2 publications

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“…Their impact on VO 2peak emerges from correlations studies in subjects with T2DM [ 62 ] that are consistent with reduced muscle blood flow during exercise [ 63 ] and increased peripheral vascular resistance [ 64 ]. Slowed microvascular blood flow kinetics were reported in T2DM both at the beginning of exercise [ 65 , 66 ] and during the steady-state [ 67 , 68 ], with some heterogeneity among the studies. A slowed rate of adjustment of peripheral vascular resistance at the beginning of exercise could explain the slowed VO 2 kinetics frequently observed in this population.…”

Section: Determinants Of Reduced Exercise Capacity In Type 2 Diabetesmentioning

confidence: 99%

Type 2 diabetes and reduced exercise tolerance: a review of the literature through an integrated physiology approach

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Pugliese

Sciuto

et al. 2020

Cardiovasc Diabetol

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The association between type 2 diabetes mellitus (T2DM) and heart failure (HF) is well established. Early in the course of the diabetic disease, some degree of impaired exercise capacity (a powerful marker of health status with prognostic value) can be frequently highlighted in otherwise asymptomatic T2DM subjects. However, the literature is quite heterogeneous, and the underlying pathophysiologic mechanisms are far from clear. Imaging-cardiopulmonary exercise testing (CPET) is a non-invasive, provocative test providing a multi-variable assessment of pulmonary, cardiovascular, muscular, and cellular oxidative systems during exercise, capable of offering unique integrated pathophysiological information. With this review we aimed at defying the cardiorespiratory alterations revealed through imaging-CPET that appear specific of T2DM subjects without overt cardiovascular or pulmonary disease. In synthesis, there is compelling evidence indicating a reduction of peak workload, peak oxygen assumption, oxygen pulse, as well as ventilatory efficiency. On the contrary, evidence remains inconclusive about reduced peripheral oxygen extraction, impaired heart rate adjustment, and lower anaerobic threshold, compared to non-diabetic subjects. Based on the multiparametric evaluation provided by imaging-CPET, a dissection and a hierarchy of the underlying mechanisms can be obtained. Here we propose four possible integrated pathophysiological mechanisms, namely myocardiogenic, myogenic, vasculogenic and neurogenic. While each hypothesis alone can potentially explain the majority of the CPET alterations observed, seemingly different combinations exist in any given subject. Finally, a discussion on the effects-and on the physiological mechanisms-of physical activity and exercise training on oxygen uptake in T2DM subjects is also offered. The understanding of the early alterations in the cardiopulmonary response that are specific of T2DM would allow the early identification of those at a higher risk of developing HF and possibly help to understand the pathophysiological link between T2DM and HF.

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Section: Determinants Of Reduced Exercise Capacity In Type 2 Diabetesmentioning

confidence: 99%

Type 2 diabetes and reduced exercise tolerance: a review of the literature through an integrated physiology approach

Nesti

Pugliese

Sciuto

et al. 2020

Cardiovasc Diabetol

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Exercise intolerance in Type 2 diabetes: is there a cardiovascular contribution?

Poitras

Hudson

Tschakovsky

2018

Journal of Applied Physiology

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Physical activity is critically important for Type 2 diabetes management, yet adherence levels are poor. This might be partly due to disproportionate exercise intolerance. Submaximal exercise tolerance is highly sensitive to muscle oxygenation; impairments in exercising muscle oxygen delivery may contribute to exercise intolerance in Type 2 diabetes since there is considerable evidence for the existence of both cardiac and peripheral vascular dysfunction. While uncompromised cardiac output during submaximal exercise is consistently observed in Type 2 diabetes, it remains to be determined whether an elevated cardiac sympathetic afferent reflex could sympathetically restrain exercising muscle blood flow. Furthermore, while deficits in endothelial function are common in Type 2 diabetes and are often cited as impairing exercising muscle oxygen delivery, no direct evidence in exercise exists, and there are several other vasoregulatory mechanisms whose dysfunction could contribute. Finally, while there are findings of impaired oxygen delivery, conflicting evidence also exists. A definitive conclusion that Type 2 diabetes compromises exercising muscle oxygen delivery remains premature. We review these potentially dysfunctional mechanisms in terms of how they could impair oxygen delivery in exercise, evaluate the current literature on whether an oxygen delivery deficit is actually manifest, and correspondingly identify key directions for future research.

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Is Oxygen Consumption and Oxygen Delivery During Leg Exercise Compromised in Type II Diabetes?

Cited by 2 publications

References 0 publications

Type 2 diabetes and reduced exercise tolerance: a review of the literature through an integrated physiology approach

Type 2 diabetes and reduced exercise tolerance: a review of the literature through an integrated physiology approach

Exercise intolerance in Type 2 diabetes: is there a cardiovascular contribution?

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