Hamilton Marc T, Hamilton Deborah G, Zderic Theodore W
Department of Health and Human Performance, University of Houston, Houston, TX, United States.
Department of Biology and Biochemistry, University of Houston, Houston, TX, United States.
Front Endocrinol (Lausanne). 2025 Jul 4;16:1601474. doi: 10.3389/fendo.2025.1601474. eCollection 2025.
Herein, we describe overlooked/misunderstood physiological processes (beyond contraction-induced skeletal muscle insulin sensitivity that is already well appreciated) that either oppose or enhance glucose tolerance during distinct types of acute physical activity. This includes multiple mechanisms both within and outside of muscle. We describe the processes and physiological principles to help explain why postprandial glucose tolerance is often not improved after acute bouts of exercise, or when interrupting prolonged sitting with either brief physical activity breaks or more prolonged standing. We also describe results from a specialized type of soleus muscle activity that is specifically well-geared to amplify and sustain oxidative muscle metabolism for long periods of time when sitting, with evidence that this has meaningful positive effects on systemic glucose and lipid regulation. Methods capable of elevating oxidative muscle metabolism could be advantageous to complement other lifestyle and pharmacological approaches whose mechanisms of action are limited to non-oxidative metabolic pathways. There is much potential need for inducing more oxidative muscle metabolism, because the entire musculature normally accounts for only about 15% of the oxidative metabolism of glucose when sitting inactive, despite being the body's largest lean tissue mass. A clear understanding of the multiple integrative processes that either tend to attenuate or amplify blood glucose excursions in the postprandial period is significant, given the strong influence of glucose tolerance on healthy aging and prevention of multiple chronic diseases.
在此，我们描述了一些被忽视/误解的生理过程（除了已经得到充分认识的收缩诱导的骨骼肌胰岛素敏感性之外），这些过程在不同类型的急性体育活动中，要么对抗要么增强葡萄糖耐量。这包括肌肉内外的多种机制。我们描述这些过程和生理原理，以帮助解释为什么急性运动后餐后葡萄糖耐量往往没有改善，或者当用短暂的身体活动休息或更长时间的站立来打断长时间坐着时，餐后葡萄糖耐量也没有改善。我们还描述了一种特殊类型的比目鱼肌活动的结果，这种活动特别适合在坐着时长时间放大和维持氧化肌肉代谢，有证据表明这对全身葡萄糖和脂质调节有显著的积极影响。能够提高氧化肌肉代谢的方法可能有利于补充其他生活方式和药理学方法，因为这些方法的作用机制仅限于非氧化代谢途径。诱导更多氧化肌肉代谢有很大的潜在需求，因为当坐着不动时，尽管肌肉是身体最大的瘦组织群，但整个肌肉组织通常仅占葡萄糖氧化代谢的约15%。鉴于葡萄糖耐量对健康衰老和多种慢性疾病预防的强烈影响，清楚地了解在餐后阶段倾向于减弱或放大血糖波动的多个整合过程具有重要意义。
