Dataset Information

Energy compensation after sprint- and high-intensity interval training.

ABSTRACT:

Background

Many individuals lose less weight than expected in response to exercise interventions when considering the increased energy expenditure of exercise (ExEE). This is due to energy compensation in response to ExEE, which may include increases in energy intake (EI) and decreases in non-exercise physical activity (NEPA). We examined the degree of energy compensation in healthy young men and women in response to interval training.

Methods

Data were examined from a prior study in which 24 participants (mean age, BMI, & VO2max = 28 yrs, 27.7 kg•m-2, and 32 mL?kg-1?min-1) completed either 4 weeks of sprint-interval training or high-intensity interval training. Energy compensation was calculated from changes in body composition (air displacement plethysmography) and exercise energy expenditure was calculated from mean heart rate based on the heart rate-VO2 relationship. Differences between high (? 100%) and low (< 100%) levels of energy compensation were assessed. Linear regressions were utilized to determine associations between energy compensation and ?VO2max, ?EI, ?NEPA, and ?resting metabolic rate.

Results

Very large individual differences in energy compensation were noted. In comparison to individuals with low levels of compensation, individuals with high levels of energy compensation gained fat mass, lost fat-free mass, and had lower change scores for VO2max and NEPA. Linear regression results indicated that lower levels of energy compensation were associated with increases in ?VO2max (p < 0.001) and ?NEPA (p < 0.001).

Conclusions

Considerable variation exists in response to short-term, low dose interval training. In agreement with prior work, increases in ?VO2max and ?NEPA were associated with lower energy compensation. Future studies should focus on identifying if a dose-response relationship for energy compensation exists in response to interval training, and what underlying mechanisms and participant traits contribute to the large variation between individuals.

SUBMITTER: Schubert MM

PROVIDER: S-EPMC5731706 | biostudies-literature | 2017

REPOSITORIES: biostudies-literature

ACCESS DATA

Publications

Energy compensation after sprint- and high-intensity interval training.

Schubert Matthew M MM Palumbo Elyse E Seay Rebekah F RF Spain Katie K KK Clarke Holly E HE

PloS one 20171215 12

<h4>Background</h4>Many individuals lose less weight than expected in response to exercise interventions when considering the increased energy expenditure of exercise (ExEE). This is due to energy compensation in response to ExEE, which may include increases in energy intake (EI) and decreases in non-exercise physical activity (NEPA). We examined the degree of energy compensation in healthy young men and women in response to interval training.<h4>Methods</h4>Data were examined from a prior study ...[more]

PMID: 29244836

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Project description:Poststroke guidelines recommend moderate-intensity, continuous aerobic training (MCT) to improve aerobic capacity and mobility after stroke. High-intensity interval training (HIT) has been shown to be more effective than MCT among healthy adults and people with heart disease. However, HIT and MCT have not been compared previously among people with stroke.The purpose of this study was to assess the feasibility and justification for a definitive randomized controlled trial (RCT) comparing HIT and MCT in people with chronic stroke.A preliminary RCT was conducted.The study was conducted in a cardiovascular stress laboratory and a rehabilitation research laboratory.Ambulatory people at least 6 months poststroke participated.Both groups trained 25 minutes, 3 times per week, for 4 weeks. The HIT strategy involved 30-second bursts at maximum-tolerated treadmill speed alternated with 30- to 60-second rest periods. The MCT strategy involved continuous treadmill walking at 45% to 50% of heart rate reserve.Measurements included recruitment and attendance statistics, qualitative HIT acceptability, adverse events, and the following blinded outcome variables: peak oxygen uptake, ventilatory threshold, metabolic cost of gait, fractional utilization, fastest treadmill speed, 10-Meter Walk Test, and Six-Minute Walk Test.During the 8-month recruitment period, 26 participants consented to participate. Eighteen participants were enrolled and randomly assigned to either the HIT group (n=13) or the MCT group (n=5). Eleven out of the 13 HIT group participants attended all sessions. Participants reported that HIT was acceptable and no serious adverse events occurred. Standardized effect size estimates between groups were moderate to very large for most outcome measures. Only 30% of treadmill speed gains in the HIT group translated into overground gait speed improvement.The study was not designed to definitively test safety or efficacy.Although further protocol optimization is needed to improve overground translation of treadmill gains, a definitive RCT comparing HIT and MCT appears to be feasible and warranted.

Project description:Hyperbaric Oxygen (HBO2) has been proposed as a pre-conditioning method to enhance exercise performance. Most prior studies testing this effect have been limited by inadequate methodologies. Its potential efficacy and mechanism of action remain unknown. We hypothesized that HBO2 could enhance aerobic capacity by inducing mitochondrial biogenesis via redox signaling in skeletal muscle. HBO2 was administered in combination with high-intensity interval training (HIIT), a potent redox stimulus known to induce mitochondrial biogenesis. Aerobic capacity was tested during acute hypobaric hypoxia seeking to shift the limiting site of whole body V̇O2 from convection to diffusion, more closely isolating any effect of improved oxidative capacity. Healthy volunteers were screened with sea-level (SL) V̇O2peak testing. Seventeen subjects were enrolled (10 men, 7 women, ages 26.5±1.3 years, BMI 24.6±0.6 kg m-2, V̇O2peak SL = 43.4±2.1). Each completed 6 HIIT sessions over 2 weeks randomized to breathing normobaric air, "HIIT+Air" (PiO2 = 0.21 ATM) or HBO2 (PiO2 = 1.4 ATM) during training, "HIIT+HBO2" group. Training workloads were individualized based on V̇O2peak SL test. Vastus Lateralis (VL) muscle biopsies were performed before and after HIIT in both groups. Baseline and post-training V̇O2peak tests were conducted in a hypobaric chamber at PiO2 = 0.12 ATM. HIIT significantly increased V̇O2peak in both groups: HIIT+HBO2 31.4±1.5 to 35.2±1.2 ml kg-1·min-1 and HIIT+Air 29.0±3.1 to 33.2±2.5 ml kg-1·min-1 (p = 0.005) without an additional effect of HBO2 (p = 0.9 for interaction of HIIT x HBO2). Subjects randomized to HIIT+HBO2 displayed higher skeletal muscle mRNA levels of PPARGC1A, a regulator of mitochondrial biogenesis, and HK2 and SLC2A4, regulators of glucose utilization and storage. All other tested markers of mitochondrial biogenesis showed no additional effect of HBO2 to HIIT. When combined with HIIT, short-term modest HBO2 (1.4 ATA) has does not increase whole-body V̇O2peak during acute hypobaric hypoxia. (ClinicalTrials.gov Identifier: NCT02356900; https://clinicaltrials.gov/ct2/show/NCT02356900).

Dataset Information

Energy compensation after sprint- and high-intensity interval training.

Background

Methods

Results

Conclusions

Publications

Energy compensation after sprint- and high-intensity interval training.

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