Despite a fraction of the time commitment, run SIT induces similar body composition, VO(2max), and performance adaptations as ET, but with no effect on Q(max). These data suggest that adaptations with ET are of central origin primarily, whereas those with SIT are more peripheral

It is increasingly recognized that obesity is a risk factor for microvascular disease, involving both structural and functional changes in the microvasculature. This review aims to describe how obesity impacts the microvasculature of a variety of tissues, including visceral adipose tissue, skeletal muscle, heart, brain, kidneys, and lungs. These changes involve endothelial dysfunction, which in turn (i) impacts control of vascular tone, (ii) contributes to development of microvascular insulin resistance, (iii) alters secretion of paracrine factors like nitric oxide and endothelin, but (iv) also influences vascular structure and perivascular inflammation. In concert, these changes impair organ perfusion and organ function thereby contributing to altered release and clearance of neurohumoral factors, such as adipokines and inflammatory cytokines. Global microvascular dysfunction in obese subjects is therefore a common pathway that not only explains exercise-intolerance but also predisposes to development of chronic kidney disease, microvascular dementia, coronary microvascular angina, heart failure with preserved ejection fraction, chronic obstructive pulmonary disease, and pulmonary hypertension.

Six weeks (3 times/wk) of sprint-interval training (SIT) or continuous endurance training (CET) promote body-fat losses despite a substantially lower training volume with SIT. In an attempt to explain these findings, the authors quantified VO₂ during and after (24 h) sprint-interval exercise (SIE; 2 min exercise) vs. continuous endurance exercise (CEE; 30 min exercise). VO₂ was measured in male students (n = 8) 8 times over 24 hr under 3 treatments (SIE, CEE, and control [CTRL, no exercise]). Diet was controlled. VO₂ was 150% greater (p < .01) during CEE vs. SIE (87.6 ± 13.1 vs. 35.1 ± 4.4 L O₂; M ± SD). The observed small difference between average exercise heart rates with CEE (157 ± 10 beats/min) and SIE (149 ± 6 beats/min) approached significance (p = .06), as did the difference in peak heart rates during CEE (166 ± 10 beats/min) and SIE (173 ± 6 beats/min; p = .14). Total O₂ consumed over 8 hr with CEE (263.3 ± 30.2 L) was greater (p < .01) than both SIE (224.2 ± 15.3 L; p < .001) and CTRL (163.5 ± 16.1 L; p < .001). Total O₂ with SIE was also increased over CTRL (p < .001). At 24 hr, both exercise treatments were increased (p < .001) vs. CTRL (CEE = 500.2 ± 49.2; SIE = 498.0 ± 29.4; CTRL = 400.2 ± 44.6), but there was no difference between CEE and SIE (p = .99). Despite large differences in exercise VO₂, the protracted effects of SIE result in a similar total VO₂ over 24 hr vs. CEE, indicating that the significant body-fat losses observed previously with SIT are partially due to increases in metabolism postexercise.

Data on whether sprint interval training (SIT) (repeated supermaximal intensity, short-duration exercise) affects body composition are limited, and the data that are available suggest that men respond more favourably than do women. Moreover, most SIT data involve cycling exercise, and running may differ because of the larger muscle mass involved. Further, running is a more universal exercise type. This study assessed whether running SIT can alter body composition (air displacement plethysmography), waist circumference, maximal oxygen consumption, peak running speed, and (or) the blood lipid profile. Fifteen recreationally active women (age, 22.9 ± 3.6 years; height, 163.9 ± 5.1 cm; mass, 60.8 ± 5.2 kg) completed 6 weeks of running SIT (4 to 6, 30-s "all-out" sprints on a self-propelled treadmill separated by 4 min of rest performed 3 times per week). Training decreased body fat mass by 8.0% (15.1 ± 3.6 to 13.9 ± 3.4 kg, P = 0.002) and waist circumference by 3.5% (80.1 ± 4.2 to 77.3 ± 4.4 cm, P = 0.048), whereas it increased fat-free mass by 1.3% (45.7 ± 3.5 to 46.3 ± 2.9 kg, P = 0.05), maximal oxygen consumption by 8.7% (46 ± 5 to 50 ± 6 mL/(kg·min), P = 0.004), and peak running speed by 4.8% (16.6 ± 1.7 to 17.4 ± 1.4 km/h, P = 0.026). There were no differences in food intake assessed by 3-day food records (P > 0.329) or in blood lipids (P > 0.595), except for a slight decrease in high-density lipoprotein concentration (1.34 ± 0.28 to 1.24 ± 0.24 mmol/L, P = 0.034). Running SIT is a time-efficient strategy for decreasing body fat while increasing aerobic capacity, peak running speed, and fat-free mass in healthy young women.

Olver TD, Laughlin MH. Endurance, interval sprint, and resistance exercise training: impact on microvascular dysfunction in type 2 diabetes.