Literature DB >> 26156806

Physiological and molecular responses to an acute bout of reduced-exertion high-intensity interval training (REHIT).

R S Metcalfe1,2, F Koumanov3, J S Ruffino1, K A Stokes1, G D Holman3, D Thompson1, N B J Vollaard4.   

Abstract

PURPOSE: We have previously shown that 6 weeks of reduced-exertion high-intensity interval training (REHIT) improves VO2max in sedentary men and women and insulin sensitivity in men. Here, we present two studies examining the acute physiological and molecular responses to REHIT.
METHODS: In Study 1, five men and six women (age: 26 ± 7 year, BMI: 23 ± 3 kg m(-2), VO2max: 51 ± 11 ml kg(-1) min(-1)) performed a single 10-min REHIT cycling session (60 W and two 20-s 'all-out' sprints), with vastus lateralis biopsies taken before and 0, 30, and 180 min post-exercise for analysis of glycogen content, phosphorylation of AMPK, p38 MAPK and ACC, and gene expression of PGC1α and GLUT4. In Study 2, eight men (21 ± 2 year; 25 ± 4 kg·m(-2); 39 ± 10 ml kg(-1) min(-1)) performed three trials (REHIT, 30-min cycling at 50 % of VO2max, and a resting control condition) in a randomised cross-over design. Expired air, venous blood samples, and subjective measures of appetite and fatigue were collected before and 0, 15, 30, and 90 min post-exercise.
RESULTS: Acutely, REHIT was associated with a decrease in muscle glycogen, increased ACC phosphorylation, and activation of PGC1α. When compared to aerobic exercise, changes in VO2, RER, plasma volume, and plasma lactate and ghrelin were significantly more pronounced with REHIT, whereas plasma glucose, NEFAs, PYY, and measures of appetite were unaffected.
CONCLUSIONS: Collectively, these data demonstrate that REHIT is associated with a pronounced disturbance of physiological homeostasis and associated activation of signalling pathways, which together may help explain previously observed adaptations once considered exclusive to aerobic exercise.

Entities:  

Keywords:  AMPK; Energy balance; Exercise metabolism; Glycogen; HIT; Signalling pathways

Mesh:

Substances:

Year:  2015        PMID: 26156806     DOI: 10.1007/s00421-015-3217-6

Source DB:  PubMed          Journal:  Eur J Appl Physiol        ISSN: 1439-6319            Impact factor:   3.078


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