Any exercise mediated changes in mitochondrial content, and results from overexpression/knock out models have not yielded the expected results (please see [27,28] for a detailed review of this controversy). The 1317923 present results further highlight the need for future work examining the implications of altered whole muscle SIRT1 in humans, and the role of SIRT1 protein content in determining skeletal muscle mitochondrial content in vivo.VO2peak and Submaximal Exercise PerformanceThis study represents one of the first attempts to examine the impact of altered interval intensity and volume on aerobic fitness and submaximal exercise performance. Importantly, while intervention with intervals at both 70 and 100 of peak aerobic power improved aerobic capacity and exercise performance, these improvements were greater following HI than LO (Figure 3). These results agree with previous reports demonstrating that improvements in VO2peak following steady-state endurance training (ET) occur in an intensity dependent fashion [29]. This apparent intensity effect on increases in VO2peak may help explain why improvements in VO2peak following HIT are sometimes equivalent [5] or Title Loaded From File superior [30,31] to those observed following ET despite the significantly lower exercise volume typically associated with HIT. It is important to note that the lesser aerobic adaptations observed 18204824 in LO group of the present study may also be attributable to a lower total training volume. At present, we are unable to comment with certainty on the respective contribution of intensity and training volume on the aerobic adaptations observed in the present study. However, given the clinical relevance of VO2peak [32], and despite the possible psychological [7] and safety [33] concerns associated with high intensity exercise, these results highlight the importance of continuing to promote high intensity and volume when HIT is prescribed to overweight and obese populations.Title Loaded From File cardiovascular Adaptation to HITClassically, changes in VO2peak have been linked to improvements in stroke volume (SV), cardiac output (CO), and the ability of the cardiovascular systems ability to deliver O2 [34]. Consistent with this view, several recent reports have demonstrated concomitant increases in SV and VO2peak following training [35] and intensity dependent increases in SV [31]. While we did not measure SV or CO in the current study, the observed increase in peak O2 pulse (Figure 4) suggests that the greater improvement in VO2peak observed in the HI group was the result of greater cardiovascular adaptations. Coupled with the similar increases in skeletal muscle oxidative capacity in both groups (Figure 1), previous observations that oxidative capacity and capillary density increase in concert [36], and reports that changes in peak O2 pulse are strongly correlated with increases in SV [37,38], our data seem to suggest that increases in SV following HIT are dependent on both intensity and training volume. While this is an attractive explanation for our results, further studies confirming an intensity dependent increase in SV following interval training, the mechanism(s) underlying this effect, and the minimal intensity required to increase cardiovascular function are needed.Interval Training in Overweight/Obese MenSystemic InflammationChronic low-grade inflammation is a hallmark of obesity and may contribute to a number of diseases such as type 2 diabetes and metabolic syndrome [39]. While previous exercise inter.Any exercise mediated changes in mitochondrial content, and results from overexpression/knock out models have not yielded the expected results (please see [27,28] for a detailed review of this controversy). The 1317923 present results further highlight the need for future work examining the implications of altered whole muscle SIRT1 in humans, and the role of SIRT1 protein content in determining skeletal muscle mitochondrial content in vivo.VO2peak and Submaximal Exercise PerformanceThis study represents one of the first attempts to examine the impact of altered interval intensity and volume on aerobic fitness and submaximal exercise performance. Importantly, while intervention with intervals at both 70 and 100 of peak aerobic power improved aerobic capacity and exercise performance, these improvements were greater following HI than LO (Figure 3). These results agree with previous reports demonstrating that improvements in VO2peak following steady-state endurance training (ET) occur in an intensity dependent fashion [29]. This apparent intensity effect on increases in VO2peak may help explain why improvements in VO2peak following HIT are sometimes equivalent [5] or superior [30,31] to those observed following ET despite the significantly lower exercise volume typically associated with HIT. It is important to note that the lesser aerobic adaptations observed 18204824 in LO group of the present study may also be attributable to a lower total training volume. At present, we are unable to comment with certainty on the respective contribution of intensity and training volume on the aerobic adaptations observed in the present study. However, given the clinical relevance of VO2peak [32], and despite the possible psychological [7] and safety [33] concerns associated with high intensity exercise, these results highlight the importance of continuing to promote high intensity and volume when HIT is prescribed to overweight and obese populations.Cardiovascular Adaptation to HITClassically, changes in VO2peak have been linked to improvements in stroke volume (SV), cardiac output (CO), and the ability of the cardiovascular systems ability to deliver O2 [34]. Consistent with this view, several recent reports have demonstrated concomitant increases in SV and VO2peak following training [35] and intensity dependent increases in SV [31]. While we did not measure SV or CO in the current study, the observed increase in peak O2 pulse (Figure 4) suggests that the greater improvement in VO2peak observed in the HI group was the result of greater cardiovascular adaptations. Coupled with the similar increases in skeletal muscle oxidative capacity in both groups (Figure 1), previous observations that oxidative capacity and capillary density increase in concert [36], and reports that changes in peak O2 pulse are strongly correlated with increases in SV [37,38], our data seem to suggest that increases in SV following HIT are dependent on both intensity and training volume. While this is an attractive explanation for our results, further studies confirming an intensity dependent increase in SV following interval training, the mechanism(s) underlying this effect, and the minimal intensity required to increase cardiovascular function are needed.Interval Training in Overweight/Obese MenSystemic InflammationChronic low-grade inflammation is a hallmark of obesity and may contribute to a number of diseases such as type 2 diabetes and metabolic syndrome [39]. While previous exercise inter.
