L Stewart-Hunt’s research while affiliated with University of Guelph and other places

Starch rich (S) feeds reduce insulin sensitivity in untrained horses when compared to high fat (F) feeds, but insulin sensitivity is not affected when S or F are fed during exercise training. The effects of S vs. F on training-associated alterations in skeletal muscle glucose metabolism are unknown. To determine the effects of dietary energy source on training-associated changes in insulin sensitivity, skeletal muscle GLUT4 protein and hexokinase (HK) and glycogen synthase (GS) activities in horses. After a baseline period on an all forage diet (Phase 1), horses were adapted to high starch (S) or high fat (F) diets (n = 7/group) for 6 weeks (Phase 2) and then completed 7 weeks of exercise training (Phase 3) on the same diets. To measure insulin sensitivity (SI), minimal model analysis of a frequently-sampled i.v. glucose tolerance test was performed at the end of each phase. Middle gluteal muscle biopsies to measure GLUT-4 protein content, muscle glycogen and HK and GS activities were taken before and after euglycaemic-hyperinsulinaemic clamps administered after each phase. Data were analysed by repeated measures ANOVA. In S, SI was 36% lower (P < 0.05) after Phase 2 when compared to Phase 1 but was unchanged in F. After Phase 3, SI was increased (P < 0.01) in S and F compared to Phase 2 and did not differ (P > 0.05) between diets. Middle gluteal muscle GLUT-4 protein and post clamp HK activity were increased (P < 0.05) in S after Phase 3, with higher (P < 0.01) GLUT4 in S than in F. GS activities were unchanged in both diets. Adaptation to S resulted in decreased SI mitigated by moderate physical conditioning. Increased GLUT-4 protein content and HK activity in S may have contributed to higher SI after training.

There is limited information about factors regulating glucose utilisation post exercise in horses. To determine the effects of a single bout of moderate intensity exercise on measures of insulin-mediated (IMGU) and noninsulin-mediated (NIMGU) glucose uptake during a hyperglycaemic clamp (HC). Hyperglycaemic clamps were administered in random order to 8 Standardbreds under 4 conditions: 1) rest, insulinopenia (R-L); 2) rest, hyperinsulinaemia (R-H); 3) post exercise (45 min at ∼ 50% VO2peak), insulinopenia (Ex-L) and 4) post exercise, hyperinsulinaemia (Ex-H). In the R-L and Ex-L trials, somatostatin was infused to suppress insulin secretion and induce insulinopenia. After 30 min, a 2 h HC was initiated with plasma glucose concentrations maintained at ∼ 10 mmol/l by variable glucose infusion. In R-H and Ex-H, regular insulin (1.0 mu/kg bwt/min) was also administered to induce physiological hyperinsulinaemia. Serum insulin and C-peptide concentrations were measured in samples obtained at 10 min intervals. Glucose uptake was calculated from mean glucose infusion rate (GIR) during the last 60 min of the HC. In all HCs C-peptide remained below baseline concentrations, evidence of suppression of insulin secretion by somatostatin. Overall, mean ± s.e. insulin concentrations during the final 60 min of the HC in R-L and Ex-L were 5.7 ± 1.1 and 6.9 ± 1.9 mu/l respectively, and corresponding values in R-H and Ex-H were 64.1 ± 11.1 and 61.2 ± 10.9 mu/l. Prior exercise affected IMGU but not NIMGU. Over the final 60 min of the HC, mean GIR was higher (P < 0.001) in Ex-H (5.6 ± 1.1 mg/kg bwt/min) than in R-H (3.3 ± 0.9 mg/kg bwt/min), whereas mean GIR did not differ (P = 0.26) between R-L (1.2 ± 0.3 mg/kg bwt/min) and Ex-L (1.8 ± 0.5 mg/kg bwt/min). A single bout of moderate intensity exercise increased glucose uptake during a hyperglycaemic clamp under hyperinsulinaemic conditions but not under somatostatin-induced insulinopenia.

Increased insulin sensitivity occurs after a period of exercise training, but the mechanisms underlying this training-associated increase in insulin action have not been investigated. To examine the effects of short-term endurance training (7 consecutive days) and a subsequent period of inactivity (5 days) on whole body insulin sensitivity and GLUT-4 protein and the activities of glycogen synthase (GS) and hexokinase (HK) in skeletal muscle. It was hypothesised that training would increase insulin sensitivity in association with increased GLUT-4 protein and activities of GS and HK, but that these changes would be transient, returning to baseline after 5 days of inactivity. Seven mature Standardbred horses completed training consisting of 7 consecutive days of 45 min of treadmill exercise at a speed that elicited 55% of pretraining maximal aerobic capacity (VO2peak). Insulin sensitivity was determined by rate of glucose disposal (M) during the last 60 min of a 120 min euglycaemic-hyperinsulinaemic clamp (EHC) performed before (-2 days) and at 1 and 6 days following training. VO2peak was measured before (UT) and after (TR) training and the period of inactivity (IA). Training resulted in a 9% increase in mean VO2peak (P<0.05) that was maintained following inactivity (IA). Mean M values were more than 2-fold higher (P<0.05) in TR than in UT. Mean M was also higher (P<0.05) in IA when compared to UT. GLUT-4 protien abundancewas more than 10-fold higher in TR and IA (P<0.001) than in UT. Pre-EHC GS activity and GS fractional velocity were increased (P<0.05) in TR when compared to UT and IA. Pre-EHC HK activity was increased (P<0.05) in IA when compared to UT and TR. Muscle glycogen was 66% lower (P<0.05) in TR than in UT and IA. Short-term training resulted in increases in whole body insulin sensitivity, and GLUT-4 protein content and glycogen synthase activity in skeletal muscle. The enhancements in insulin sensitivity, GLUT-4 protein and glycogen synthase activity were still evident after 5 days of inactivity. Insulin resistance in equids has been associated with obesity and predisposition to laminitis. Regular physical activity may mitigate risk of these conditions via enhancement of insulin sensitivity and/or control of bodyweight.

No studies in horses have examined the effect of route of carbohydrate (glucose) administration on the rate of muscle glycogen storage following glycogen-depleting exercise. Glucose delivery from the gastrointestinal tract limits the rate of muscle glycogen storage following glycogen-depleting exercise. In a crossover design, 7 fit horses completed treadmill exercise (EX) on 3 occasions to deplete muscle glycogen by approximately 50%. After EX horses received: 1) i.v. glucose infusion (IV; 0.5 g/kg bwt/h for 6 h), 2) oral glucose boluses (OR; 1 g/kg bwt at 0, 2 and 4 h post EX) or 3) no glucose supplementation (CON). Blood samples for measurement of glucose and insulin concentrations were collected before EX and during the 6 h treatment period. Muscle biopsies for measurement of muscle glycogen content (GLY) and glycogen synthase (GS) activity were taken before and after exercise and at 3 and 6 h. Mean plasma glucose concentrations were significantly higher in IV and OR than in CON throughout treatment. The average serum insulin responses in IV and OR treatments were also significantly greater than in CON. After EX, GLY was not different among the 3 treatments. However, glycogen storage rates were significantly higher in IV than in CON and OR during the first 3 h and second 3 h of recovery, and GLY was significantly higher in IV than in OR and CON at 6 h of recovery. GS activity was significantly higher in IV than in OR and CON at 3 h of recovery. Muscle glycogen storage in horses during a 6 h period after exercise was enhanced by i.v. glucose administration (3 g/kg) but not by an equivalent glucose dose administered per os. While oral administration of glucose achieved a level of hyperglycaemia and hyperinsulinaemia that markedly accelerates glycogen storage in other species, the rate of glycogen storage following oral supplementation was not different to control conditions. Glucose supplementation via the i.v. route should be considered when rapid replenishment of muscle glycogen stores is desired.