Key point: Optimal vascular function is critical for health, and endurance training (ET) has previously been shown to be an effective method of improving this. Sprint interval training (SIT) has been proposed as a time efficient alternative to ET but its effect on skeletal muscle microvasculature has not been studied and no direct comparison with ET has been made. ET and SIT in this study were equally effective at decreasing arterial stiffness and increasing skeletal muscle capillarisation and eNOS content. The main results suggest that both training modes improve skeletal muscle microvascular and macrovascular function, with SIT being a time efficient alternative. Abstract  Sprint interval training (SIT) has been proposed as a time efficient alternative to endurance training (ET) for increasing skeletal muscle oxidative capacity and improving certain cardiovascular functions. In this study we sought to make the first comparisons of the structural and endothelial enzymatic changes in skeletal muscle microvessels in response to ET and SIT. Sixteen young sedentary males (age 21 ± SEM 0.7 years, BMI 23.8 ± SEM 0.7 kg m⁻²) were randomly assigned to 6 weeks of ET (40–60 min cycling at ∼65%, 5 times per week) or SIT (4–6 Wingate tests, 3 times per week). Muscle biopsies were taken from the m. vastus lateralis before and following 60 min cycling at 65% to measure muscle microvascular endothelial eNOS content, eNOS serine¹¹⁷⁷ phosphorylation, NOX2 content and capillarisation using quantitative immunofluorescence microscopy. Whole body insulin sensitivity, arterial stiffness and blood pressure were also assessed. ET and SIT increased skeletal muscle microvascular eNOS content (ET 14%; P < 0.05, SIT 36%; P < 0.05), with a significantly greater increase observed following SIT (P < 0.05). Sixty minutes of moderate intensity exercise increased eNOS ser¹¹⁷⁷ phosphorylation in all instances (P < 0.05), but basal and post‐exercise eNOS ser¹¹⁷⁷ phosphorylation was lower following both training modes. All microscopy measures of skeletal muscle capillarisation (P < 0.05) were increased with SIT or ET, while neither endothelial nor sarcolemmal NOX2 was changed. Both training modes reduced aortic stiffness and increased whole body insulin sensitivity (P < 0.05). In conclusion, in sedentary males SIT and ET are effective in improving muscle microvascular density and eNOS protein content.

Key points: Increases in aerobic capacity and intramuscular triglyceride (IMTG) utilization are well‐described adaptations to endurance training (ET) and contribute to improvements in insulin sensitivity. Sprint interval training (SIT) also improves aerobic capacity and insulin sensitivity with a lower time commitment than ET. This study aimed to determine whether SIT also induces improvements in insulin sensitivity and net IMTG breakdown, and to investigate the underlying mechanisms. Six weeks of ET and SIT increased net IMTG breakdown during moderate‐intensity cycling, and improved insulin sensitivity. A greater concentration of lipid droplet‐associated proteins, perilipin 2 and perilipin 5, was observed following both training modes and contributes to the increases in net IMTG breakdown following training. The results suggest a novel mechanism for the training‐induced improvements in IMTG breakdown and insulin sensitivity, and clearly demonstrate that SIT is an alternative, time‐efficient training strategy that induces similar beneficial metabolic adaptations. Abstract  Intramuscular triglyceride (IMTG) utilization is enhanced by endurance training (ET) and is linked to improved insulin sensitivity. This study first investigated the hypothesis that ET‐induced increases in net IMTG breakdown and insulin sensitivity are related to increased expression of perilipin 2 (PLIN2) and perilipin 5 (PLIN5). Second, we hypothesized that sprint interval training (SIT) also promotes increases in IMTG utilization and insulin sensitivity. Sixteen sedentary males performed 6 weeks of either SIT (4–6, 30 s Wingate tests per session, 3 days week⁻¹) or ET (40–60 min moderate‐intensity cycling, 5 days week⁻¹). Training increased resting IMTG content (SIT 1.7‐fold, ET 2.4‐fold; P < 0.05), concomitant with parallel increases in PLIN2 (SIT 2.3‐fold, ET 2.8‐fold; P < 0.01) and PLIN5 expression (SIT 2.2‐fold, ET 3.1‐fold; P < 0.01). Pre‐training, 60 min cycling at ∼65% pre‐training decreased IMTG content in type I fibres (SIT 17 ± 10%, ET 15 ± 12%; P < 0.05). Following training, a significantly greater breakdown of IMTG in type I fibres occurred during exercise (SIT 27 ± 13%, ET 43 ± 6%; P < 0.05), with preferential breakdown of PLIN2‐ and particularly PLIN5‐associated lipid droplets. Training increased the Matsuda insulin sensitivity index (SIT 56 ± 15%, ET 29 ± 12%; main effect P < 0.05). No training × group interactions were observed for any variables. In conclusion, SIT and ET both increase net IMTG breakdown during exercise and increase in PLIN2 and PLIN5 protein expression. The data are consistent with the hypothesis that increases in PLIN2 and PLIN5 are related to the mechanisms that promote increased IMTG utilization during exercise and improve insulin sensitivity following 6 weeks of SIT and ET.

Within a controlled laboratory environment, high-intensity interval training (HIT) elicits similar cardiovascular and metabolic benefits as traditional moderate-intensity continuous training (MICT). It is currently unclear how HIT can be applied effectively in a real-world environment. To investigate the hypothesis that 10 weeks of HIT, performed in an instructor-led, group-based gym setting, elicits improvements in aerobic capacity (VO_2max), cardio-metabolic risk and psychological health which are comparable to MICT. Ninety physically inactive volunteers (42±11 y, 27.7±4.8 kg.m^-2) were randomly assigned to HIT or MICT group exercise classes. HIT consisted of repeated sprints (15–60 seconds, >90% HR_max) interspersed with periods of recovery cycling (≤25 min.session^-1, 3 sessions.week^-1). MICT participants performed continuous cycling (~70% HR_max, 30–45 min.session^-1, 5 sessions.week^-1). VO_2max, markers of cardio-metabolic risk, and psychological health were assessed pre and post-intervention. Mean weekly training time was 55±10 (HIT) and 128±44 min (MICT) (p<0.05), with greater adherence to HIT (83±14% vs. 61±15% prescribed sessions attended, respectively; p<0.05). HIT improved VO_2max, insulin sensitivity, reduced abdominal fat mass, and induced favourable changes in blood lipids (p<0.05). HIT also induced beneficial effects on health perceptions, positive and negative affect, and subjective vitality (p<0.05). No difference between HIT and MICT was seen for any of these variables. HIT performed in a real-world gym setting improves cardio-metabolic risk factors and psychological health in physically inactive adults. With a reduced time commitment and greater adherence than MICT, HIT offers a viable and effective exercise strategy to target the growing incidence of metabolic disease and psychological ill-being associated with physical inactivity.

Intramuscular triacylglycerol (IMTG) is both a dynamic fat-storage depot that can expand during periods of elevated lipid availability and a fatty acid source that can be utilized during periods of increased energy expenditure in active individuals. Although many studies have investigated the lifestyle determinants of IMTG content, the results are far from consistent, and studies attempting to unravel the mechanisms behind IMTG metabolism are in their infancy. The limited evidence available suggests that the enzymes responsible for skeletal muscle lipolysis and IMTG synthesis play an important role in determining the fate of fatty acids and therefore the concentration of lipid metabolites and insulin sensitivity of skeletal muscle. This review provides a summary of current knowledge on the effects of acute and chronic exercise as well as energy intake and macronutrient composition of the diet upon the metabolism of IMTG and the implications for metabolic health.