Intermittent-sprint exercise: performance and muscle adaptations in health and chronic disease

The aim of this thesis was to investigate the acute and chronic effects of high-intensity intermittent exercise, in the form of repeated-sprint exercise (RSE) and indoor football (futsal), on performance responses and skeletal muscle molecular adaptations in young, healthy and middle-aged, sedentary individuals. This was accomplished through four studies. Study I part I. Ten young, healthy adults (age 22.3 ± 4.1 years; height 174.4 ± 9 cm; mass 70.2 ± 11.6 kg; 7 males, 3 females) performed an incremental test, a Yo-Yo intermittent recovery test level 1 (Yo-Yo IR1), and one RSE trial. RSE comprised three sets of 5 x 4-s maximal sprints on a non-motorised treadmill, with 20 s of passive recovery between repetitions and 4.5 min of passive recovery between sets. After ten repeated-sprint training sessions, participants performed all tests again. During RSE, performance was determined by measuring acceleration, mean and peak power/velocity. Recovery heart rate (HR), HR variability, and finger-tip capillary lactate concentration ([Lac-]) were measured. Performance progressively decreased across the three sets of RSE, with the indices of repeated-sprint ability being impaired to a different extent before and after training. Training induced a significant increase (p < 0.05) in all indices of performance, particularly acceleration by 21.9, 14.7 and 15.2 % during sets 1, 2 and 3, respectively. Training significantly increased Yo-Yo IR1 performance by 8 % and decreased D[Lac-]/work ratio by 15.2, 15.5, and 9.4 % during sets 1, 2 and 3, respectively, and recovery HR during RSE. There were strong correlations between Yo-Yo IR1 performance and indices of RSE performance, especially acceleration post-training (r = 0.88, p = 0.004). Repeated-sprint training, comprising only 10 min of exercise overall, effectively improved performance during multiple-set RSE. This exercise model better reflects team-sport activities than single-set RSE. The rapid training-induced improvement in acceleration, quantified here for the first time, has wide applications for professional and recreational sport activities. Study I part II. Ten young, healthy adults (age 22.3 ± 4.1 years; height 174.4 ± 9 cm; mass 70.2 ± 11.6 kg; 7 males, 3 females) performed an RSE trial. After 4 weeks of repeated-sprint training (3 x wk.) participants repeated the RSE. A muscle biopsy was obtained at rest, immediately after, 1h and 4h after RSE, both pre- and post-training. Real time RT-PCR and western blotting were used to measure mRNA expression and protein abundance, respectively. Acute RSE increased the phosphorylation of Acetyl-CoA Carboxylase (ACC; 86 %; effect size (ES) ± confidence interval: 1.4 ± 0.8; p < 0.001) and Ca2+ calmodulin-dependent protein kinase II (CaMK II; 69 %; ES 0.7 ± 0.6). Peroxisome proliferator-activated receptor gamma co-activator 1alpha (PGC-1alpha 208 %; ES 1.5 ± 0.7; p < 0.001), and nuclear respiratory factor 1 (NRF1; 92 %, ES 0.7 ± 0.8) mRNA expression were increased following RSE. Four weeks of training increased PGC-1 protein abundance at rest (33 %, ES 0.9 ± 0.7). Both acute and chronic RSE, despite only 60 s and 12 min of exercise respectively, altered the molecular signalling associated with mitochondrial adaptations and PGC-1alpha mRNA expression in skeletal muscle. However, the small-to-moderate changes in resting PGC-1alpha protein abundance after training, together with the absence of changes in aerobic fitness, indicate that further research is required to understand the functional significance of PGC-1alpha in response to repeated-sprint exercise. Study II. Skeletal muscle protein signalling associated with mitochondrial biogenesis was assessed in response to a futsal game vs. work-matched, moderate-intensity continuous running exercise. Sixteen young, healthy men (age 21.4 ± 1.7 years; height 179.2 ± 6.0 cm; mass 74.8 ± 5.9 kg) performed an incremental exercise test. After 48 h, a resting muscle biopsy was performed. Then, after one week, participants were assigned to either a futsal group (FUT, n = 8) or a moderate-intensity running exercise group (MOD, n = 8). The FUT group performed a 2 x 20-min halves futsal game on a parquet indoor court. The MOD group performed moderate-intensity exercise on a treadmill with triaxial accelerometers used to match the work performed by the two groups. Immediately after exercise, all participants underwent another muscle biopsy. Protein signalling was assessed via western blotting. An acute FUT game was associated with increased ATF-2 phosphorylation (50 %, ES 0.59 ± 0.13, p = 0.001), while no change was detected in response to MOD (interaction time x training, p = 0.02). Both FUT and MOD increased ACC phosphorylation, by 119 and 75 %, respectively (main effect for time, p = 0.01). Similarly, both training interventions increased p38 MAPK phosphorylation by 85 and 36 % for FUT and MOD, respectively (main effect for time, p = 0.003). In conclusion, both FUT and MOD induced similar protein signalling responses in human skeletal muscle, which signifies that FUT may be used as an appropriate alternative to traditional aerobic exercise to promote mitochondrial biogenesis. Study III. The effects of FUT and MOD training on skeletal muscle and systemic adaptations associated with the reduction of diabetes risk factors were then assessed. Twenty middle-aged, sedentary men (age 44.2 ± 6.3 years; height 177.0 ± 0.1 cm; mass 91.6 ± 14.2 kg) were allocated to either FUT (n = 12) or MOD (n = 8) for 8 weeks, 3 times per week. Before and after the training interventions, participants underwent an oral glucose tolerance test (OGTT), a resting muscle biopsy, and an incremental exercise test. Plasma glucose and insulin concentration, and peripheral insulin sensitivity were measured in response to the OGTT. The abundance of selected proteins associated with mitochondrial biogenesis and glucose transport was measured at rest and analysed via western blotting. Blood lipids, HbA1c, blood pressure, anthropometry and self-reported dietary intake were also assessed. Peripheral insulin sensitivity was improved only in FUT (+31 %, ES 0.67 ± 0.53). Mitochondrial complex IV, subunit II (COXII) resting protein abundance was increased in FUT only (+16 %, ES 0.79 ± 0.24), while glucose transporter 4 (GLUT4) was equally increased in FUT and MOD (+45 %, ES 0.78 ± 0.57; and +44 %, ES 0.67 ± 0.57, respectively). Only FUT training resulted in a lowered plasma total cholesterol and triglycerides concentration (-8 %, ES 0.44 ± 0.24; and -32 %, ES 0.52 ± 0.3, respectively). No changes were detected for BMI, waist circumference, and self-reported dietary intake for either training intervention. These data suggest that FUT training may be employed as an effective exercise model to assist in the prevention of diabetes in middle-aged sedentary males. Conclusions. Acute RSE increased protein signalling associated with mitochondrial biogenesis and glucose metabolism. These increases were replicated in response to an acute game of futsal and were comparable to a work-matched, continuous running exercise. Chronic participation in RSE improved sprint performance in young adults, however it did not induce significant changes in the abundance of proteins associated with mitochondrial biogenesis. On the contrary, futsal training was effective in promoting molecular changes associated with mitochondrial biogenesis and glucose metabolism, and assisted in the reduction of diabetes risk factors in middle-aged men.