Sprinting towards a time‐efficient strategy for microvascular remodelling in humans

In this issue of The Journal of Physiology, Cocks et al. (2013) present novel data regarding the human skeletal muscle microvascular response to traditional moderate-intensity continuous training (ET) and to sprint interval training (SIT), which is characterized by brief intermittent bursts of ‘all-out’ exercise. [In this Perspective, we use the term ‘SIT’ in order to be consistent with the paper by Cocks et al. (2013) as well as some of our previous work. The term high-intensity interval training (abbreviated ‘HIT’ or ‘HIIT’) is also widely used, and an effort to standardize nomenclature used to describe various interval training protocols is desirable for the future.] Sprint interval training is a potent and time-efficient stimulus to induce physiological remodelling similar to ET, which may be linked to reduced cardiometabolic disease risk (Gibala et al. 2012; Kessler et al. 2012); however, we know considerably more about the skeletal muscle metabolic and macrovascular adaptations to low-volume SIT than we do about the concomitant microvascular level responses. Previous examinations of cardiovascular remodelling in this regard have mainly employed animal models (Laughlin & Roseguini, 2008) or used human assessment techniques that do not permit determination of skeletal muscle capillary-specific changes (Gibala et al. 2012). The study by Cocks et al. (2013) is the first to provide a ‘glimpse’ inside the capillaries of human skeletal muscle and assess the adaptive response to two very distinct training protocols that differ markedly in terms of total exercise volume and time commitment. Sprint interval training appears to be a time-efficient alternative to ET training for improvement of capillary-specific markers of endothelial structure and function. Cocks et al. (2013) applied a new technique that permitted the investigators to probe the endothelial nitric oxide synthase (eNOS) and NADPH oxidase (NOX2) content and eNOS serine phosphorylation localized to the capillary endothelial layer within the exercised vastus lateralis muscle. Six weeks of either SIT or ET increased eNOS content and skeletal muscle capillary density, whereas endothelial and sarcolemmal NOX2 content remained unchanged. Acute exercise increased eNOS serine phosphorylation, but basal and postexercise eNOS serine phosphorylation was lower after both training modes. The impact of this work is increased by the robust experimental design, which included well-documented dietary and activity controls and included both resting and postexercise biopsies before and after training, as well as an assessment of the systemic impact of the training programmes. Cocks et al. (2013) confirmed that low-volume SIT is a time-efficient strategy to increase whole-body aerobic capacity, increase insulin sensitivity and reduce arterial stiffness, to an extent that was similar to that induced by ET. The SIT model employed by Cocks et al. (2013) was the Wingate test, which consists of 30 s of cycling at a maximal effort against a standardized resistance that is relative to body mass. Subjects completed four to six Wingate tests per training session, interspersed with 4.5 min of recovery (light cycling), for a total of only 2–3 min of very intense exercise spread over a period of ∼15–30 min. Wingate tests require a specialized cycle ergometer, and the all-out effort necessitates an extremely high level of subject motivation. Therefore, it may not be safe or practical to implement this form of training in the general population. Recent studies suggest that modified interval training protocols induce physiological adaptations similar to Wingate-based SIT and ET and may be more suitable for deconditioned individuals (Gibala et al. 2012). For example, Little et al. (2011) used a protocol that consisted of 10 bouts of 60 s of cycling at an intensity that elicited ∼90% of maximal heart rate interspersed with 60 s of recovery, and showed improvements in mean 24 h blood glucose concentration and glucose transport capacity in people with type 2 diabetes after only six sessions of training over a 2 week period. While still a demanding form of exercise, the absolute work intensity associated with this type of protocol is, nonetheless, much lower than that required during an all-out Wingate test, although the cardiovascular adaptations remain to be determined. The study by Cocks et al. (2013) provides valuable new information regarding the basic microvascular responses to SIT and ET, but also stimulates several potential areas for continued investigation. Most prior work in this field has assessed vasodilatory capacity in humans at the level of the conduit vessels and the resistance arterioles, and it is possible that the microvascular changes observed in the study by Cocks et al. (2013) might not be mirrored throughout the macrovascular tree. Laughlin and colleagues have amassed considerable data based on animal models to support the hypothesis that exercise training stimulates a process of vascular remodelling, which follows the pattern of initial functional changes that diminish with the establishment of structural changes (Laughlin & Roseguini, 2008). The time course for these changes may be dependent on numerous factors, including the initial baseline structure and function of the blood vessel, the intensity and duration of the exercise stimulus applied to the skeletal muscle vascular bed and the branching order and calibre of the vessel. While the results of Cocks et al. (2013) provide novel information regarding the process of exercise-induced cellular remodelling at the capillary level in humans, the precise time course for those changes and potential adaptations at the arteriolar or conduit artery level remain to be determined. It would also be interesting to see the application of this technique in different populations, including those with compromised endothelial function. In order to match these results with the body of knowledge from functional assessments of vascular function, paired measures of microvascular and macrovascular assessments would also be valuable. This novel immunohistochemical technique may now also be used to examine the potential influence of muscle fibre type in determining microvascular adaptations to training. The data of Cocks et al. (2013) suggest that we can ‘HIT’ the capillaries with high intensity intervals and induce impressive changes in microvascular structure and function, especially when considered in light of the relatively low volume of the SIT training stimulus.

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