Vigorous running suppresses plasma acylated ghrelin concentrations but the limited literature on cycling suggests that acylated ghrelin is unchanged, perhaps because body mass is supported during cycling. It is important from a research and applied perspective to determine whether acylated ghrelin and hunger responses are exercise-mode specific. This study sought to examine this. Eleven recreationally active males fasted overnight and completed three 4-h trials: control, running, and cycling, in a random order. Participants rested throughout the control trial and ran or cycled at 70% of mode-specific maximal oxygen uptake for the first hour during exercise trials, resting thereafter. Hunger was measured every 0.5 h using visual analogue scales. Eight venous blood samples were collected to determine acylated ghrelin concentrations and a standardised meal was consumed at 3 h. Compared with the control trial, acylated ghrelin concentrations were suppressed to a similar extent at 0.5 and 1 h during the running (p < 0.005) and cycling (p < 0.001) trials. Area under the curve values for ghrelin concentration over time were lower during exercise trials versus control (Control: 606 ± 379; Running: 455 ± 356; Cycling: 448 ± 315 pg·mL(-1)·4 h(-1); mean ± SD, p < 0.05). Hunger values did not differ significantly between trials but an interaction effect (p < 0.05) indicated a tendency for hunger to be suppressed during exercise. Thus, at similar relative exercise intensities, plasma acylated ghrelin concentrations are suppressed to a similar extent during running and cycling.
"Following REHIT systemic concentrations of acylated ghrelin were reduced by >50% in the immediate post-exercise period, with little or no change observed following a bout of continuous cycling at a moderate intensity. This is consistent with other HIT studies (Sim et al. 2013; Deighton et al. 2013) and fits with previous research which highlights the key effect of relative exercise intensity on modulating the response of acylated ghrelin to aerobic exercise, with suppression occurring at higher (≥70% V̇ O2max) but not lower (≤50% V̇ O2max) exercise intensities (King et al. 2010; Ueda et al. 2009; Broom et al. 2007; Broom et al. 2009; Wasse et al. 2013). Conversely, circulating levels of total PYY appear to be unaffected by REHIT. "
[Show abstract][Hide abstract] ABSTRACT: Purpose
We have previously shown that 6 weeks of reduced-exertion high-intensity interval training (REHIT) improves V˙O2max in sedentary men and women and insulin sensitivity in men. Here, we present two studies examining the acute physiological and molecular responses to REHIT.
In Study 1, five men and six women (age: 26 ± 7 year, BMI: 23 ± 3 kg m−2, V˙O2max: 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 V˙O2max, 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.
Acutely, REHIT was associated with a decrease in muscle glycogen, increased ACC phosphorylation, and activation of PGC1α. When compared to aerobic exercise, changes in V˙O2, 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.
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.
[Show abstract][Hide abstract] ABSTRACT: The present study determined the changes in appetite and appetite-regulating gut hormones during and following bouts of both rope skipping exercise (weight-bearing) and bicycle ergometer exercise (non-weight-bearing). After a 12-h fast, 15 young men (mean±SD, age 24.4±1.7yrs, maximal oxygen uptake 47.0±6.5mL/kg/min) participated in three 160min trials: (1) rope skipping exercise (295±40kcal, 3 sets×10min with 5-min interval, then rested for 120min); (2) bicycle ergometer exercise (288±36kcal, 3 sets×10min with 5-min interval, then rested for 120min); (3) control (rested for 160min). Ratings of perceived hunger and acylated ghrelin were suppressed and total peptide YY (PYY) were increased during and immediately after exercise in both exercise trials, but glucagon liked peptide-1 was not changed. Furthermore, suppressed hunger during rope skipping exercise was greater than that during bicycle ergometer exercise, but there were no differences in acylated ghrelin and total PYY. These results indicate that weight-bearing exercise has a greater exercise-induced appetite suppressive effect compared with non-weight-bearing exercise, and both forms of exercise lowered acylated ghrelin and increased total PYY, but the changes did not differ significantly between exercise modes.
[Show abstract][Hide abstract] ABSTRACT: Since its discovery in 1999, ghrelin has been implicated in a multiplicity of physiological activities. Most notably, ghrelin has an important influence on energy metabolism and after the identification of its potent appetite stimulating effects ghrelin has been termed the 'hunger hormone.' Exercise is a stimulus which has a significant impact on energy homeostasis and consequently a substantial body of research has investigated the interaction between exercise and ghrelin. This narrative review provides an overview of research relating to the acute and chronic effects of exercise on circulating ghrelin (acylated, unacylated and total). To enhance study comparability, the scope of this review is limited to research undertaken in adult humans and consequently studies involving children and animals are not discussed. Although there is significant ambiguity within much of the early research, our review suggests that acute exercise transiently interferes with the production of acylated ghrelin. Furthermore, the consensus of evidence indicates that exercise training does not influence circulating ghrelin independent of weight loss. Additional research is needed to verify and extend the available literature, particularly by uncovering the mechanisms governing acute exercise-related changes and characterising responses in other populations such as females, older adults, and the obese.
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