The aim of this study was to objectively quantify ratings of perceived enjoyment using the Physical Activity Enjoyment Scale following high-intensity interval running versus moderate-intensity continuous running. Eight recreationally active men performed two running protocols consisting of high-intensity interval running (6 × 3 min at 90% VO(2max) interspersed with 6 × 3 min active recovery at 50% VO(2max) with a 7-min warm-up and cool down at 70% VO(2max)) or 50 min moderate-intensity continuous running at 70% VO(2max). Ratings of perceived enjoyment after exercise were higher (P < 0.05) following interval running compared with continuous running (88 ± 6 vs. 61 ± 12) despite higher (P < 0.05) ratings of perceived exertion (14 ± 1 vs. 13 ± 1). There was no difference (P < 0.05) in average heart rate (88 ± 3 vs. 87 ± 3% maximum heart rate), average VO(2) (71 ± 6 vs. 73 ± 4%VO(2max)), total VO(2) (162 ± 16 vs. 166 ± 27 L) or energy expenditure (811 ± 83 vs. 832 ± 136 kcal) between protocols. The greater enjoyment associated with high-intensity interval running may be relevant for improving exercise adherence, since running is a low-cost exercise intervention requiring no exercise equipment and similar relative exercise intensities have previously induced health benefits in patient populations.

No abstract

Deliberately training with reduced carbohydrate (CHO) availability to enhance endurance-training-induced metabolic adaptations of skeletal muscle (i.e. the ‘train low, compete high’ paradigm) is a hot topic within sport nutrition. Train-low studies involve periodically training (e.g., 30–50% of training sessions) with reduced CHO availability, where train-low models include twice per day training, fasted training, post-exercise CHO restriction and ‘sleep low, train low’. When compared with high CHO availability, data suggest that augmented cell signalling (73% of 11 studies), gene expression (75% of 12 studies) and training-induced increases in oxidative enzyme activity/protein content (78% of 9 studies) associated with ‘train low’ are especially apparent when training sessions are commenced within a specific range of muscle glycogen concentrations. Nonetheless, such muscle adaptations do not always translate to improved exercise performance (e.g. 37 and 63% of 11 studies show improvements or no change, respectively). Herein, we present our rationale for the glycogen threshold hypothesis, a window of muscle glycogen concentrations that simultaneously permits completion of required training workloads and activation of the molecular machinery regulating training adaptations. We also present the ‘fuel for the work required’ paradigm (representative of an amalgamation of train-low models) whereby CHO availability is adjusted in accordance with the demands of the upcoming training session(s). In order to strategically implement train-low sessions, our challenge now is to quantify the glycogen cost of habitual training sessions (so as to inform the attainment of any potential threshold) and ensure absolute training intensity is not compromised, while also creating a metabolic milieu conducive to facilitating the endurance phenotype.

Bartlett JD, Louhelainen J, Iqbal Z, Cochran AJ, Gibala MJ, Gregson W, Close GL, Drust B, Morton JP. Reduced carbohydrate availability enhances exercise-induced p53 signaling in human skeletal muscle: implications for mitochondrial biogenesis. Am J Physiol Regul Integr Comp Physiol 304: R450 -R458, 2013. First published January 30, 2013 doi:10.1152/ajpregu.00498.2012The mechanisms that regulate the enhanced skeletal muscle oxidative capacity observed when training with reduced carbohydrate (CHO) availability are currently unknown. The aim of the present study was to test the hypothesis that reduced CHO availability enhances p53 signaling and expression of genes associated with regulation of mitochondrial biogenesis and substrate utilization in human skeletal muscle. In a repeated-measures design, muscle biopsies (vastus lateralis) were obtained from eight active males before and after performing an acute bout of high-intensity interval running with either high (HIGH) or low CHO availability (LOW). Resting muscle glycogen (HIGH, 467 Ϯ 19; LOW, 103 Ϯ 9 mmol/kg dry wt) was greater in HIGH compared with LOW (P Ͻ 0.05). Phosphorylation (P-) of ACC Ser79 (HIGH, 1.4 Ϯ 0.4; LOW, 2.9 Ϯ 0.9) and p53 Ser15 (HIGH, 0.9 Ϯ 0.4; LOW, 2.6 Ϯ 0.8) was higher in LOW immediately postexercise and 3 h postexercise, respectively (P Ͻ 0.05). Before and 3 h postexercise, mRNA content of pyruvate dehydrogenase kinase 4, mitochondrial transcription factor A, cytochrome-c oxidase IV, and PGC-1␣ were greater in LOW compared with HIGH (P Ͻ 0.05), whereas carnitine palmitoyltransferase-1 showed a trend toward significance (P ϭ 0.09). However, only PGC-1␣ expression was increased by exercise (P Ͻ 0.05), where three-fold increases occurred independently of CHO availability. We conclude that the exerciseinduced increase in p53 phosphorylation is enhanced in conditions of reduced CHO availability, which may be related to upstream signaling through AMPK. Given the emergence of p53 as a molecular regulator of mitochondrial biogenesis, such nutritional modulation of contraction-induced p53 activation has implications for both athletic and clinical populations.AMPK; PGC-1␣; glycogen; high-intensity interval running SKELETAL MUSCLE MITOCHONDRIAL biogenesis is one of the most prominent adaptations induced by endurance exercise training (20). At a molecular level, mitochondrial adaptations to exercise are thought to be due to the cumulative effects of the transient increases in the transcripts of mRNA that encode the upregulation of mitochondrial proteins (37). In considering possible contractile induced stressors for activating the acute cell signaling pathways associated with regulation of mitochondrial biogenesis, reductions in carbohydrate (CHO) availability is now emerging as one of the most potent signals (41). For example, in healthy subjects, the acute exercise-induced activation of the signaling kinases AMPK (60, 62) and p38MAPK (8, 12) are greater when preexercise glycogen availability is low. Transcription of several metabolic related genes ...

The aim of the present study was to test the hypothesis that acute high-intensity interval (HIT) running induces greater activation of signaling pathways associated with mitochondrial biogenesis compared with moderate-intensity continuous (CONT) running matched for work done. In a repeated-measures design, 10 active men performed two running protocols consisting of HIT [6 × 3-min at 90% maximal oxygen consumption (Vo(2max)) interspersed with 3-min recovery periods at 50% Vo(2max) with a 7-min warm-up and cool-down period at 70% Vo(2max)] or CONT (50-min continuous running at 70% Vo(2max)). Both protocols were matched, therefore, for average intensity, duration, and distance run. Muscle biopsies (vastus lateralis) were obtained preexercise, postexercise, and 3 h postexercise. Muscle glycogen decreased (P < 0.05) similarly in HIT and CONT (116 ± 11 vs. 111 ± 17 mmol/kg dry wt, respectively). Phosphorylation (P-) of p38MAPK(Thr180/Tyr182) (1.9 ± 0.1- vs. 1.5 ± 0.2-fold) and AMPK(Thr172) (1.5 ± 0.3- vs. 1.5 ± 0.1-fold) increased immediately postexercise (P < 0.05) in HIT and CONT, respectively, and returned to basal levels at 3 h postexercise. P-p53(Ser15) (HIT, 2.7 ± 0.8-fold; CONT, 2.1 ± 0.8-fold), PGC-1α mRNA (HIT, 4.2 ± 1.7-fold; CONT, 4.5 ± 0.9-fold) and HSP72 mRNA (HIT, 4.4 ± 2-fold; CONT, 3.5 ± 1-fold) all increased 3 h postexercise (P < 0.05) although neither parameter increased (P > 0.05) immediately postexercise. There was no difference between trials for any of the above signaling or gene expression responses (P > 0.05). We provide novel data by demonstrating that acute HIT and CONT running (when matched for average intensity, duration, and work done) induces similar activation of molecular signaling pathways associated with regulation of mitochondrial biogenesis. Furthermore, this is the first report of contraction-induced p53 phosphorylation in human skeletal muscle, thus highlighting an additional pathway by which exercise may initiate mitochondrial biogenesis.