Primary, Secondary, and Tertiary Effects of Carbohydrate Ingestion During Exercise

Abstract

The purpose of this current opinion paper is to describe the journey of ingested carbohydrate from 'mouth to mitochondria' culminating in energy production in skeletal muscles during exercise. This journey is conveniently described as primary, secondary, and tertiary events. The primary stage is detection of ingested carbohydrate by receptors in the oral cavity and on the tongue that activate reward and other centers in the brain leading to insulin secretion. After digestion, the secondary stage is the transport of monosaccharides from the small intestine into the systemic circulation. The passage of these monosaccharides is facilitated by the presence of various transport proteins. The intestinal mucosa has carbohydrate sensors that stimulate the release of two 'incretin' hormones (GIP and GLP-1) whose actions range from the secretion of insulin to appetite regulation. Most of the ingested carbohydrate is taken up by the liver resulting in a transient inhibition of hepatic glucose release in a dose-dependent manner. Nonetheless, the subsequent increased hepatic glucose (and lactate) output can increase exogenous carbohydrate oxidation rates by 40-50%. The recognition and successful distribution of carbohydrate to the brain and skeletal muscles to maintain carbohydrate oxidation as well as prevent hypoglycaemia underpins the mechanisms to improve exercise performance.

Fig. 1

Influence of carbohydrate ingestion on carbohydrate appearance in the systemic circulation. In the absence of carbohydrate ingestion, during prolonged moderate-intensity exercise, there is a decline in liver glycogen content due to the stimulation of glycogenolysis to maintain delivery rates of endogenous blood glucose into the systemic circulation. When large amounts of glucose are ingested during exercise, exogenous glucose appearance rates displace almost all hepatic glycogenolysis as the source of systemic glucose appearance, leading to an attenuation or prevention of liver glycogen depletion. When large amounts of glucose plus fructose are ingested during exercise, there is, as yet no evidence that this leads to net liver glycogen storage, but rather the additional carbohydrate that is available is released into the systemic circulation for oxidation. Data pooled from maximal rates observed [, –81].

Fig. 2

With increasing rates of glucose ingestion during prolonged moderate-intensity exercise, there is a progressive suppression of endogenous glucose appearance rates, which reach negligible rates when glucose is ingested at rates exceeding ~ 1.5 g⋅min⁻¹. This is more than offset by an increase in exogenous glucose appearance rates, and therefore, total glucose appearance rates also increase with glucose ingestion rates to a maximum rate of 1.2 g⋅min⁻¹

Fig. 3

Schematic to capture the proposed primary (1), secondary (2), and tertiary (3) effects of CHO (grey hexagon) ingestion during exercise. Solid arrow indicates the movement of CHO in the body. Dotted arrow indicates the proposed mechanism of action. Carbohydrate intake guidelines are specific to performance-related goals over the associated duration and at exercise intensities > 70% VO₂max