Despite the known benefits of performing aerobic and resistance exercise independently, the metabolic effects of performing aerobic and resistance exercise in succession, remain unclear. Several studies suggest that the alteration of exercise sequence may influence carbohydrate and lipid oxidation and energy expenditure during exercise and in recovery. High intensity resistance exercise performed prior to a bout of aerobic exercise has been shown to augment fat oxidation during the subsequent bout of aerobic exercise. Changes in hormone and metabolite concentrations from prior resistance exercise could potentially influence substrate selection and energy expenditure in a subsequent bout of aerobic exercise. However, an exercise session whereby aerobic exercise is followed by a bout of resistance exercise has yet to be evaluated to determine the metabolic effects (specifically, the differences in substrate selection for energy provision) when exercise sequence is altered. It was hypothesized that when resistance exercise was performed prior to a bout of aerobic exercise, sympathetic nervous system activity would be elevated, leading to an increase in non-esterified fatty acid (NEFA) and glycerol concentrations and resultant increase in lipid oxidation during the aerobic portion of the exercise compared to the opposite sequence. It was also hypothesized that during recovery there would be an increased reliance on fat oxidation for energy provision with a resistance-aerobic exercise sequence compared to an aerobic-resistance exercise sequence. Additionally, the differences in metabolite concentrations and respiratory parameters between two identical bouts of aerobic exercise performed on separate days (~1 week apart) were measured and it was hypothesized that day-to-day variability would be non-significant (p>0.05). Plasma glucose, lactate, NEFA, glycerol, insulin, C-peptide, glucagon, epinephrine and norepinephrine concentrations in addition to oxygen consumption (VO2) and respiratory exchange ratio (RER) were measured in nine healthy, recreationally active males that participated in 3 different, randomized exercise trials (Trial A: aerobic exercise; Trial AR: aerobic exercise followed by a bout of resistance exercise; Trial RA: resistance exercise followed by an aerobic exercise bout). The aerobic exercise bout was performed at 60% VO2 max for 30 min while the resistance exercise bout consisted of 5 exercises (overhead squat, chest press, triceps extension, shoulder press, and dead-lift) performed for 3 sets of 8 repetitions at 70% 1-RM. Contrary to the primary hypothesis, NEFA concentrations and lipid oxidation rates were similar for the aerobic exercise bout of both the AR and RA trials. During recovery, lipid oxidation was elevated immediately post-exercise in the RA trial compared to the AR trial, however there were no differences between trials by 15 min post-exercise. Furthermore, only epinephrine, and not norepinephrine, concentrations were significantly higher after aerobic exercise in the RA trial compared to the AR trial. VO2 and energy expenditure values were similar for the duration of the 30 min recovery. These results suggest that while exercise sequence may influence carbohydrate and lipid oxidation immediately post exercise, substrate selection and utilization are similar during aerobic exercise bouts irrespective of the sequence in which aerobic and resistance exercise are performed. Thus, when resistance exercise is performed prior to aerobic exercise, compared to the opposite sequence, overall energy provision is not altered at the volume and intensity of exercise performed in this study.

Despite the known benefits of performing aerobic and resistance exercise independently, the metabolic effects of performing aerobic and resistance exercise in succession, remain unclear. Several studies suggest that the alteration of exercise sequence may influence carbohydrate and lipid oxidation and energy expenditure during exercise and in recovery. High intensity resistance exercise performed prior to a bout of aerobic exercise has been shown to augment fat oxidation during the subsequent bout of aerobic exercise. Changes in hormone and metabolite concentrations from prior resistance exercise could potentially influence substrate selection and energy expenditure in a subsequent bout of aerobic exercise. However, an exercise session whereby aerobic exercise is followed by a bout of resistance exercise has yet to be evaluated to determine the metabolic effects (specifically, the differences in substrate selection for energy provision) when exercise sequence is altered. It was hypothesized that when resistance exercise was performed prior to a bout of aerobic exercise, sympathetic nervous system activity would be elevated, leading to an increase in non-esterified fatty acid (NEFA) and glycerol concentrations and resultant increase in lipid oxidation during the aerobic portion of the exercise compared to the opposite sequence. It was also hypothesized that during recovery there would be an increased reliance on fat oxidation for energy provision with a resistance-aerobic exercise sequence compared to an aerobic-resistance exercise sequence. Additionally, the differences in metabolite concentrations and respiratory parameters between two identical bouts of aerobic exercise performed on separate days (~1 week apart) were measured and it was hypothesized that day-to-day variability would be non-significant (p>0.05). Plasma glucose, lactate, NEFA, glycerol, insulin, C-peptide, glucagon, epinephrine and norepinephrine concentrations in addition to oxygen consumption (VO2) and respiratory exchange ratio (RER) were measured in nine healthy, recreationally active males that participated in 3 different, randomized exercise trials (Trial A: aerobic exercise; Trial AR: aerobic exercise followed by a bout of resistance exercise; Trial RA: resistance exercise followed by an aerobic exercise bout). The aerobic exercise bout was performed at 60% VO2 max for 30 min while the resistance exercise bout consisted of 5 exercises (overhead squat, chest press, triceps extension, shoulder press, and dead-lift) performed for 3 sets of 8 repetitions at 70% 1-RM. Contrary to the primary hypothesis, NEFA concentrations and lipid oxidation rates were similar for the aerobic exercise bout of both the AR and RA trials. During recovery, lipid oxidation was elevated immediately post-exercise in the RA trial compared to the AR trial, however there were no differences between trials by 15 min post-exercise. Furthermore, only epinephrine, and not norepinephrine, concentrations were significantly higher after aerobic exercise in the RA trial compared to the AR trial. VO2 and energy expenditure values were similar for the duration of the 30 min recovery. These results suggest that while exercise sequence may influence carbohydrate and lipid oxidation immediately post exercise, substrate selection and utilization are similar during aerobic exercise bouts irrespective of the sequence in which aerobic and resistance exercise are performed. Thus, when resistance exercise is performed prior to aerobic exercise, compared to the opposite sequence, overall energy provision is not altered at the volume and intensity of exercise performed in this study.

Insulin resistance (IR), T2DM, and obesity together form a cluster of interrelated metabolic challenges that may be linked by metabolic inflexibility. Metabolic inflexibility is characterized by the resistance to switching substrate oxidation preference based on substrate availability and can be measured in either fasted or insulin-stimulated conditions. As the largest site for glucose disposal and a primary tissue influencing regulation of blood glucose concentrations, skeletal muscle likely plays a central role in regulating substrate oxidation preference based on substrate availability. Skeletal muscle lipotoxicity caused by an impaired regulation of fat uptake and oxidation is postulated to disrupt insulin signaling and lead to skeletal muscle IR. High dietary saturated fat intake results in reduced basal fat oxidation and a resistance to switching to carbohydrate oxidation during insulin-stimulated conditions in susceptible individuals. This metabolic inflexibility may lead to an accumulation of intramyocellular species that impair insulin signaling. Endurance exercise training improves the capacity for fat oxidation in metabolically inflexible individuals. However, relatively little is known about how endurance exercise training influences substrate oxidation preference when paired with a high fat diet (HFD). Therefore, the purpose of this study was to determine the effects of a HFD on substrate metabolism in skeletal muscle of sedentary and endurance trained (ET) males. Healthy, sedentary (n=17) and ET (n=7) males first consumed a 10-day moderate carbohydrate diet (55% carbohydrate, 30% total fat, <10% saturated fat) isocaloric to their individual energy requirements and then underwent a 4- hour high fat challenge testing session. During the session, they consumed a high fat meal (820 kcals; 25% carbohydrate, 63% total fat [26% saturated fat]), and skeletal muscle biopsies were taken in the fasted and 4-hour postprandial conditions. Participants then consumed a 5-day HFD (30% carbohydrate, 55% total fat, 25% saturated fat) and repeated the high fat challenge testing session. Substrate oxidation measures were performed on the collected skeletal muscle tissue, and the meal effect, defined as the percent change from the fasting to 4- hour postprandial condition, for each measure was calculated. There was a HFD by physical activity group interaction on meal effect for metabolic flexibility (P<0.05) and a HFD effect on meal effect for glucose oxidation (P<0.05). Meal effects for metabolic flexibility and glucose oxidation were maintained in the ET (20 ± 4% to 41 ± 21% and 128 ± 92% and 41 ± 15%, respectively; both P>0.05) but decreased in the sedentary (34 ± 7% to 4 ± 5% and 78 ± 26% to -21 ± 6%, respectively; both P<0.01) group. There were trends toward HFD effects on reductions in meal effects for total (P=0.062) and incomplete (P=0.075) fat oxidation, which were driven primarily by an increase in fasting total (12.1 ± 2.6 nmol/mg protein/h to 18.5 ± 2.3 nmol/mg protein/h; P<0.01) and incomplete (11.5 ± 2.5 nmol/mg protein/h to 17.6 ± 2.3 nmol/mg protein/h; P<0.01) fat oxidation in the ET group as a result of the HFD. Fasting total and incomplete fat oxidation did not change in the sedentary group (7.3 ± 0.8 nmol/mg protein/h to 7.8 ± 0.8 nmol/mg protein/h and 6.8 ± 0.7 nmol/mg protein/h to 7.2 ± 0.8 nmol/mg protein/h, respectively; both P>0.05). Overall, these findings suggest the ET state attenuates deleterious effects of a short-term HFD on reduced metabolic flexibility and insulin-stimulated glucose oxidation. In addition, a HFD-induced reduction in fat oxidation during the fasted-to-fed transition may be caused by differing mechanisms in sedentary and ET individuals. These findings provide a basis for future work targeting the elucidation of potential mechanistic differences in substrate oxidation preference between sedentary and ET individuals. / Ph. D. / Type 2 diabetes (T2DM) is a commonly occurring disease worldwide, and treatment of the disease is considerably burdensome for individuals and societies. T2DM is closely related to insulin resistance (IR) and obesity, and in each of these conditions, the characteristic of metabolic inflexibility has been observed. Metabolic inflexibility is a reduced ability to adjust fat or carbohydrate utilization for energy based on the availability of each of these macronutrients. Skeletal muscle may be an important tissue in the regulation of macronutrient utilization since it plays a key role in blood glucose regulation. High dietary saturated fat intake may lead to metabolic inflexibility in skeletal muscle in susceptible individuals. This metabolic inflexibility may result in increased storage of fat within skeletal muscle, which is hypothesized to disrupt insulin signaling. This disruption can lead to IR. Endurance exercise training improves metabolic flexibility. However, little is known about how endurance exercise training influences macronutrient utilization when paired with a high fat diet (HFD). Therefore, the purpose of this study was to determine the effects of a HFD on macronutrient utilization in skeletal muscle of sedentary and endurance trained (ET) males. Seventeen healthy, sedentary males and seven ET males first consumed a 10-day moderate-carbohydrate diet that was provided by the study investigators and designed to keep each participant weight stable. Participants then underwent a high fat challenge testing session in which they consumed a high fat meal and had skeletal muscle biopsies taken both before and after the meal. Participants then consumed a 5-day HFD, also designed to keep them weight stable, and repeated the high fat challenge testing session. Macronutrient utilization measures were performed on the collected skeletal muscle samples. Overall, metabolic flexibility was reduced in the sedentary group but was maintained in the ET group, which suggests that ET individuals may be protected against developing a HFD-induced metabolic inflexibility in skeletal muscle and its associated downstream negative effects on insulin signaling. In addition, fat utilization during the high fat challenge meal decreased in both sedentary and ET individuals as a result of the HFD. However, fat utilization in the fasted state was higher in ET individuals after the HFD compared with baseline, but fat utilization was the same in sedentary individuals before and after the HFD. This suggests there may be differences between sedentary and ET individuals in the mechanisms involved in the adjustment of fat utilization to dietary fat intake. Further research is needed to understand these differences, as they may play important roles in understanding how IR and T2DM develop.

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