Twelve active men completed two seven day blocks of prescribed exercise on a provided diet, supplemented either with acetylated and butyrylated high amylose maize starch or with low amylose maize starch as the control, separated by a two week washout.
On day eight they cycled for 90 minutes at around 60 percent, then ran a 5 km treadmill time trial, with indirect calorimetry, stable isotopes and blood, muscle and urine biomarkers.
The starch raised both faecal and circulating short chain fatty acids relative to the control, and several markers of intestinal barrier damage and permeability were lower. Respiratory exchange ratio during steady state was higher by 0.02 (95% CI 0.01 to 0.03, p<0.001).
Muscle glycogen depletion differed by 14 umol per kilogram per gram dry weight (95% CI -116 to 143, p=0.613). The 5 km time trial differed by 5 seconds (95% CI -44 to 54, p=0.816).
| Muscle glycogen depletion difference | 14 umol/kg/g dry wt, 95% CI -116 to 143, p=0.613 |
| 5 km time trial difference | 5 s, 95% CI -44 to 54, p=0.816 |
| Respiratory exchange ratio during steady state | +0.02, 95% CI 0.01 to 0.03, p<0.001 |
| Faecal and serum short chain fatty acids | increased with the modified starch |
Proposed by the authors This is the explanation the authors offer in their discussion. This study did not test it.
The premise the authors set out to test is that short chain fatty acids are the fuel colon cells run on, and that raising their availability should both protect the intestinal barrier and spare muscle glycogen.
Their Key Points confirm the delivery worked. The strategy increased colonic and systemic short chain fatty acid concentrations before and during exercise, and preserved intestinal barrier function.
For the half of the hypothesis that failed they offer no positive account. They report that increasing availability did not impact glucose turnover, alter protein expression in muscle or spare muscle glycogen.
Their own conclusion is that the effects were not sufficient to spare glycogen or increase performance, leaving the practical relevance unclear and underscoring the challenge of translating promising preclinical findings to humans.
Drawn from Key Points statement, full text paywalled.
The gut barrier half of the short chain fatty acid story survived a human test, and the glycogen sparing half, which came from animal work, did not. That contradicts the preclinical expectation rather than refining it.
Twelve young active men, seven days of an engineered starch, one temperate laboratory session.
The same delivery tested in hot conditions over a race length effort with gastrointestinal symptoms as the outcome would show whether the barrier finding is worth anything to an athlete.
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