Effect of Acute High-intensity Interval Exercise on Whole-body Fat Oxidation and Subcutaneous Adipose Tissue Cell Signaling in Overweight Women

International Journal of Exercise Science 13(2): 554-566, 2020. Exercise-induced alterations in adipose tissue insulin and/or β-adrenergic signaling may contribute to increases in whole-body fat oxidation following acute exercise. Thus, we examined changes in insulin (Akt, AS160) and β-adrenergic (PKA) signaling proteins in subcutaneous adipose tissue and whole-body fat oxidation in overweight women following acute high-intensity interval exercise (HIIE). Overweight females completed two experimental sessions in a randomized order: 1) control (bed rest) and 2) HIIE (10 x 4 min running intervals at 90% HRmax, 2-min recovery). Subcutaneous abdominal adipose tissue biopsies were obtained from 10 participants before (pre-), immediately (0hr) after (post-), 2hr post-, and 4hr post-exercise. Plasma glucose and insulin levels were assessed in venous blood samples obtained at each biopsy time-point from a different group of 5 participants (BMI-matched to biopsy group). Fat oxidation rates were estimated using the respiratory exchange ratio (RER) in all participants using indirect calorimetry pre-, 2hr post-, and 4hr post-exercise. RER was decreased (p \u3c 0.05) at 2hr post-exercise after HIIE (0.77 ± 0.04) compared to control (0.84 ± 0.04). Despite higher plasma glucose (p \u3c 0.01) and insulin (p \u3c 0.05) levels at 0hr post-exercise versus control, no significant interaction effects were observed for Akt or AS160 phosphorylation (p \u3e 0.05). Phosphorylation of PKA substrates was unaltered in both conditions (p \u3e 0.05). Collectively, altered β-adrenergic and insulin signaling in subcutaneous adnominal adipose tissue does not appear to explain increased whole-body fat oxidation following acute HIIE

Satellite cell activity, without expansion, after nonhypertrophic stimuli

The purpose of the present studies was to determine the effect of various nonhypertrophic exercise stimuli on satellite cell (SC) pool activity in human skeletal muscle. Previously untrained men and women (men: 29 ± 9 yr and women: 29 ± 2 yr, n = 7 each) completed 6 wk of very low-volume high-intensity sprint interval training. In a separate study, recreationally active men ( n = 16) and women ( n = 3) completed 6 wk of either traditional moderate-intensity continuous exercise ( n = 9, 21 ± 4 yr) or low-volume sprint interval training ( n = 10, 21 ± 2 yr). Muscle biopsies were obtained from the vastus lateralis before and after training. The fiber type-specific SC response to training was determined, as was the activity of the SC pool using immunofluorescent microscopy of muscle cross sections. Training did not induce hypertrophy, as assessed by muscle cross-sectional area, nor did the SC pool expand in any group. However, there was an increase in the number of active SCs after each intervention. Specifically, the number of activated (Pax7+/MyoD+, P ≤ 0.05) and differentiating (Pax7−/MyoD+, P ≤ 0.05) SCs increased after each training intervention. Here, we report evidence of activated and cycling SCs that may or may not contribute to exercise-induced adaptations while the SC pool remains constant after three nonhypertrophic exercise training protocols

Fibre-Specific Responses to Endurance and Low Volume High Intensity Interval Training: Striking Similarities in Acute and Chronic Adaptation

The current study involved the completion of two distinct experiments. Experiment 1 compared fibre specific and whole muscle responses to acute bouts of either low-volume high-intensity interval training (LV-HIT) or moderate-intensity continuous endurance exercise (END) in a randomized crossover design. Experiment 2 examined the impact of a six-week training intervention (END or LV-HIT; 4 days/week), on whole body and skeletal muscle fibre specific markers of aerobic and anaerobic capacity. Six recreationally active men (Age: 20.7±3.8 yrs; VO2peak: 51.9±5.1 mL/kg/min) reported to the lab on two separate occasions for experiment 1. Following a muscle biopsy taken in a fasted state, participants completed an acute bout of each exercise protocol (LV-HIT: 8, 20-second intervals at ∼170% of VO2peak separated by 10 seconds of rest; END: 30 minutes at ∼65% of VO2peak), immediately followed by a muscle biopsy. Glycogen content of type I and IIA fibres was significantly (p<0.05) reduced, while p-ACC was significantly increased (p<0.05) following both protocols. Nineteen recreationally active males (n = 16) and females (n = 3) were VO2peak-matched and assigned to either the LV-HIT (n = 10; 21±2 yrs) or END (n = 9; 20.7±3.8 yrs) group for experiment 2. After 6 weeks, both training protocols induced comparable increases in aerobic capacity (END: Pre: 48.3±6.0, Mid: 51.8±6.0, Post: 55.0±6.3 mL/kg/min LV-HIT: Pre: 47.9±8.1, Mid: 50.4±7.4, Post: 54.7±7.6 mL/kg/min), fibre-type specific oxidative and glycolytic capacity, glycogen and IMTG stores, and whole-muscle capillary density. Interestingly, only LV-HIT induced greater improvements in anaerobic performance and estimated whole-muscle glycolytic capacity. These results suggest that 30 minutes of END exercise at ∼65% VO2peak or 4 minutes of LV-HIT at ∼170% VO2peak induce comparable changes in the intra-myocellular environment (glycogen content and signaling activation); correspondingly, training-induced adaptations resulting for these protocols, and other HIT and END protocols are strikingly similar

A systematic upregulation of nuclear and mitochondrial genes is not present in the initial post-exercise recovery period in human skeletal muscle

The purpose of the current investigation was to determine if an exercise-mediated upregulation of nuclear and mitochondrial-encoded genes targeted by the transcriptional co-activator peroxisome-proliferator-activated receptor gamma co-activator-1 alpha (PGC-1α) occurs in a systematic manner following different exercise intensities in humans. Ten recreationally active males (Age: 23 ±3 yrs; VO2peak: 41.8 ±6.6 mL/kg/min) completed two acute bouts of work-matched interval exercise at ~73% (LO) and ~100% (HI) of work rate at VO2peak in a randomized cross-over design. Muscle biopsies were taken before (Pre), immediately after (Post), and 3 hours into recovery (3hr) following each exercise bout. A main effect of time (pThe accepted manuscript in pdf format is listed with the files at the bottom of this page. The presentation of the authors' names and (or) special characters in the title of the manuscript may differ slightly between what is listed on this page and what is listed in the pdf file of the accepted manuscript; that in the pdf file of the accepted manuscript is what was submitted by the author

The impact of work-matched interval training on VO2peak and VO2 kinetics: diminishing returns with increasing intensity

High intensity interval training (HIIT) improves VO2peak and VO2 kinetics, however, it is unknown whether an optimal intensity of HIIT exists for eliciting improvements in these measures of whole body oxidative metabolism. The purpose of this study was to: 1) investigate the effect of interval intensity on training-induced adaptations in VO2peak and VO2 kinetics, and 2) examine the impact of interval intensity on the frequency of non-responders in VO2peak. 36 healthy men and women completed 3 weeks of cycle ergometer HIIT, consisting of intervals targeting 80% (LO), 115% (MID) or 150% (HI) of peak aerobic power. Total work performed per training session was matched across groups. A main effect of training (pThe accepted manuscript in pdf format is listed with the files at the bottom of this page. The presentation of the authors' names and (or) special characters in the title of the manuscript may differ slightly between what is listed on this page and what is listed in the pdf file of the accepted manuscript; that in the pdf file of the accepted manuscript is what was submitted by the author

An examination of resveratrol's mechanisms of action in human tissue: impact of a single dose in vivo and dose responses in skeletal muscle ex vivo.

The current study tested the hypothesis that a single, moderate dose of RSV would activate the AMPK/SIRT1 axis in human skeletal muscle and adipose tissue. Additionally, the effects of RSV on mitochondrial respiration in PmFBs were examined. Eight sedentary men (23.8±2.4 yrs; BMI: 32.7±7.1) reported to the lab on two occasions where they were provided a meal supplemented with 300 mg of RSV or a placebo. Blood samples, and a muscle biopsy were obtained in the fasted state and again, with the addition of an adipose tissue biopsy, two hours post-prandial. The effect of RSV on mitochondrial respiration was examined in PmFBs taken from muscle biopsies from an additional eight men (23.4±5.4 yrs; BMI: 24.4±2.8). No effect of RSV was observed on nuclear SIRT1 activity, acetylation of p53, or phosphorylation of AMPK, ACC or PKA in either skeletal muscle or adipose tissue. A decrease in post absorptive insulin levels was accompanied by elevated skeletal muscle phosphorylation of p38 MAPK, but no change in either skeletal muscle or adipose tissue insulin signalling. Mitochondrial respiration in PmFBs was rapidly inhibited by RSV at 100-300 uM depending on the substrate examined. These results question the efficacy of a single dose of RSV at altering skeletal muscle and adipose tissue AMPK/SIRT1 activity in humans and suggest that RSV mechanisms of action in humans may be associated with altered cellular energetics resulting from impaired mitochondrial ATP production

Incidence of Non-Response and Individual Patterns of Response Following Sprint Interval Training

The current study sought to explore the incidence of non-responders for maximal or submaximal performance following a variety of sprint interval training (SIT) protocols. Data from 63 young adults from 5 previously published studies were utilized in the current analysis. Non-responders were identified using 2 times the typical error (TE) of measurement for VO2peak (2 x TE = 1.74 mL/kg/min), lactate threshold (2 x TE = 15.7 W), or 500 kcal time to completion (TTC; 2 x TE = 306 secs) trial. TE was determined on separate groups of participants by calculating the test re-test variance for each outcome. The overall rate of non-responders for VO2peak across all participants studied was 22% (14/63) with 4 adverse responders observed. No non-responders for VO2peak were observed in studies where participants trained 4 times per week (n=18), while higher rates were observed in most studies requiring training 3 times per week (30-50%; n=45). A non-response rate of 44% (8/18) and 50% (11/22) was observed for the TTC test and lactate threshold, respectively. No significant correlations were observed between the changes in VO2peak and TTC (r = 0.014; p = 0.96) or lactate threshold (r = 0.17; p = 0.44). The current analysis demonstrates a significant incidence of non-responders for VO2peak and heterogeneity in the individual patterns of response following SIT. Additionally, these data support the importance of training dose and suggest that the incidence of non-response may mitigated by utilizing the optimal dose of SIT.The accepted manuscript in pdf format is listed with the files at the bottom of this page. The presentation of the authors' names and (or) special characters in the title of the manuscript may differ slightly between what is listed on this page and what is listed in the pdf file of the accepted manuscript; that in the pdf file of the accepted manuscript is what was submitted by the author

An examination of resveratrol's mechanisms of action in human tissue: impact of a single dose in vivo and dose responses in skeletal muscle ex vivo.

The current study tested the hypothesis that a single, moderate dose of RSV would activate the AMPK/SIRT1 axis in human skeletal muscle and adipose tissue. Additionally, the effects of RSV on mitochondrial respiration in PmFBs were examined. Eight sedentary men (23.8±2.4 yrs; BMI: 32.7±7.1) reported to the lab on two occasions where they were provided a meal supplemented with 300 mg of RSV or a placebo. Blood samples, and a muscle biopsy were obtained in the fasted state and again, with the addition of an adipose tissue biopsy, two hours post-prandial. The effect of RSV on mitochondrial respiration was examined in PmFBs taken from muscle biopsies from an additional eight men (23.4±5.4 yrs; BMI: 24.4±2.8). No effect of RSV was observed on nuclear SIRT1 activity, acetylation of p53, or phosphorylation of AMPK, ACC or PKA in either skeletal muscle or adipose tissue. A decrease in post absorptive insulin levels was accompanied by elevated skeletal muscle phosphorylation of p38 MAPK, but no change in either skeletal muscle or adipose tissue insulin signalling. Mitochondrial respiration in PmFBs was rapidly inhibited by RSV at 100-300 uM depending on the substrate examined. These results question the efficacy of a single dose of RSV at altering skeletal muscle and adipose tissue AMPK/SIRT1 activity in humans and suggest that RSV mechanisms of action in humans may be associated with altered cellular energetics resulting from impaired mitochondrial ATP production

The impact of a 48-hour fast on SIRT1 and GCN5 in human skeletal muscle

The present study examined the impact of a 48 hour fast on the expression and activation status of SIRT1 and GCN5, and the relationship between SIRT1/GCN5 and the gene expression of PGC-1α, and the PGC-1α target PDK4, in the skeletal muscle of ten lean healthy men (age, 22.0 ± 1.5 years; VO2peak, 47.2 ± 6.7 mL/min/kg). Muscle biopsies and blood samples were collected 1 hour postprandial (Fed) and following 48 hours of fasting (Fasted). Plasma insulin (Fed, 80.8 ± 47.9 pmol/L; Fasted, not detected) and glucose (Fed, 4.36 ± 0.86; Fasted, 3.74 ± 0.25 mmol/L, p = 0.08) decreased, confirming participant adherence to fasting. Gene expression of PGC-1α decreased (pThe accepted manuscript in pdf format is listed with the files at the bottom of this page. The presentation of the authors' names and (or) special characters in the title of the manuscript may differ slightly between what is listed on this page and what is listed in the pdf file of the accepted manuscript; that in the pdf file of the accepted manuscript is what was submitted by the author

Cardiovascular and Cortisol Reactivity to Acute Mental Stress in Female Shift and Non-Shift Workers

High cardiovascular and cortisol reactivity to stressful tasks are predictors of increased future cardiovascular risk. Few studies have investigated the impact of shift work on cardiovascular reactivity, and none have examined cortisol reactivity. The purpose of this study was to compare cardiovascular and cortisol stress reactivity in female shift workers (SW) versus non-shift workers (NSW). Nineteen SW (40 ± 11 years) and 19 NSW (42 ± 11 years) participated. Heart rate, systolic blood pressure, and diastolic blood pressure (DBP) were measured at rest, and during each minute of a speech (5 min) and mental arithmetic (5 min) stress task. Serum cortisol was measured pre- and poststress task (immediately and 15 min post). Values are means ±  SD . Peak increases in DBP during the task did not differ between groups ( p  = .261), however, analyzed over time there was an interaction such that DBP increased significantly more in SW during the fifth minute of the speech task ( p  = .035). There were no group differences in heart rate or systolic blood pressure responses. The increase in cortisol also did not differ between groups (ΔSW: 5.5 ± 7.5 µg/dL, ΔNSW: 1.8 ± 2.9 µg/dL, p  = .165). However, when compared separately, the increase in cortisol from baseline to peak poststress was significant in SW ( p  = .013) but not in NSW ( p  = .125). In conclusion, these preliminary data suggest that shift work exposure may have a modest influence on cardiovascular and cortisol reactivity. Further research is necessary to fully characterize and explore the importance of stress reactivity in this population