Physical activity has been shown to improve insulin sensitivity in subjects with insulin resistance, but the effect of athletic conditioning on subjects with normal insulin sensitivity has received less scrutiny. Because strenuous exercise can be limited by the availability of substrates, it is reasonable to hypothesize that conditioning would increase the capacity for muscle uptake of substrates like glucose and to the extent that improvement in this process would include upregulation of the portions of the glucose uptake pathway in muscle, this increased capacity would also be reflected in insulin sensitivity. Therefore, we tested the hypothesis that conditioning for endurance exercise would result in increased insulin sensitivity using elite racing sled dogs.
A frequent-sampled intravenous glucose tolerance test was performed on these dogs before and after a full 7-month season of conditioning in preparation for a 1600-km race.
Compared with the results in unconditioned dogs, conditioned dogs rapidly cleared the intravenous glucose bolus through increases in both glucose mediated (7.6%·min−1 ± 3.4%·min−1 vs 3.0%·min−1 ± 2.2%·min−1, P = 0.008) and insulin-mediated (36.3 ± 18.4 × 10−4 L·min−1·mU−1 vs 11.5 ± 8.0 × 10−4 L·min−1·mU−1, P = 0.007) mechanisms. The more modest increase in serum insulin after the intravenous glucose bolus in conditioned dogs failed to suppress lipolysis and serum concentrations of nonesterified fatty acids remained constant in the conditioned dogs throughout the 4-h test.
These results, in particular the increase in insulin-independent peripheral uptake of glucose, describe novel alterations in metabolism induced by athletic conditioning that arguably result in near-continuous provision of oxidizable substrates to peripheral muscle in support of sustained muscular work typical of these dogs.
1Department of Physiological Sciences, Center for Veterinary Health Sciences, Oklahoma State University, Stillwater, OK; and
2Department of Large Animal Clinical Sciences, College of Veterinary Medicine, Michigan State University, East Lansing, MI
Address for correspondence: Michael S. Davis, D.V.M., Ph.D., 264 McElroy Hall, Stillwater, OK 74078; E-mail: Michael.email@example.com.
Submitted for publication April 2018.
Accepted for publication July 2018.