An evaluation of low volume high-intensity intermittent training (HIIT) for health risk reduction in overweight and obese men - PubMed (original) (raw)

An evaluation of low volume high-intensity intermittent training (HIIT) for health risk reduction in overweight and obese men

Benjamin M Kelly et al. BMC Obes. 2017.

Abstract

ᅟ: Both sprint interval training (SIT) and high-intensity intermittent training (HIIT) have been described as time-efficient strategies for inducing favourable metabolic and cardiorespiratory adaptations in healthy and diseased participants.

Background: To date, little attention has been given to profiling the potential health benefits of HIIT or modified HIIT training within overweight and obese cohorts with particular focus on inflammation. Within this pilot trial, we tested the hypothesis that 6 sessions of HIIT performed over 2 weeks with 1-2 days' rest would improve aerobic capacity, glucose metabolism and inflammatory profile in an overweight and obese male cohort. Additionally, we profiled the potential health benefits of 4 HIIT sessions performed over the same period.

Methods: 18 overweight or obese males (BMI = 31.2 ± 3.6; V̇O2 = 30.3 ± 4.4 ml.kg.min-1) were studied before and 72 h after HIIT. Training sessions consisted of 10 x 1 min intervals at 90% HRpeak separated by 1 min recovery periods. Exercise was performed either 6 (group 1, n = 8) or 4 (group 2, n = 10) times over a 2 week period.

Results: After training no changes were detected from baseline for body composition, aerobic capacity, glucose metabolism or inflammatory profile (p > 0.05) in either group.

Conclusion: Both 6 and 4 sessions of HIIT performed over a 2-week period are ineffective in improving selected health markers within an overweight and obese cohort.

Trial registration: This trial reports data from human participants and was retrospectively registered on 22/02/2017 with the ISRCTN registry, trial number ISRCTN90672085.

Keywords: Exercise; Health; High-intensity intermittent training (HIIT); Inflammation; Obesity; Prevention.

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Figures

Fig. 1

Fig. 1

Schematic illustrating the experimental protocol. Visits 1, 2 and 3 took place before commencement of the HIIT. Visits 4-9 were spread over 2 weeks of training (i.e., 2 or 3 HIIT sessions per week with 24 - 72h between each session). Visits 10 took place 48 h after the last training session and visit 11 took place 72h after the last training session

Fig. 2

Fig. 2

Participants’ individual V̇O2peak responses to HIIT in group 1 (top panel) and group 2 (bottom panel)

Fig. 3

Fig. 3

Group 1 percentage change in body composition parameters pre and post 2 weeks of HIIT

Fig. 4

Fig. 4

Group 2 percentage change in body composition parameters pre and post 2 weeks of HIIT

Fig. 5

Fig. 5

Participants’ individual basal fasted glucose responses to HIIT in group 1 (top panel) and group 2 (bottom panel)

Fig. 6

Fig. 6

Participants’ individual insulin resistance (Matsuda Index) responses to HIIT in group 1 (top panel) and group 2 (bottom panel)

Fig. 7

Fig. 7

a Group 1 plasma glucose (a) and insulin (b) response to a 75 g OGTT pre and post 2 weeks of HIIT. (dashed line) represents pre-training. (solid line) represents post training. b Group 2 plasma glucose (a) and insulin (b) response to a 75 g OGTT pre and post 2 weeks of HIIT. (dashed line) represents pre-training. (solid line) represents post training

References

    1. DeFronzo RA, Tripathy D. Skeletal muscle insulin resistance is the primary defect in type 2 diabetes. Diabetes Care. 2009;32:S157–S163. doi: 10.2337/dc09-S302. - DOI - PMC - PubMed
    1. Thyfault JP, Krogh-Madsen R. Metabolic disruptions induced by reduced ambulatory activity in free-living humans. J Appl Physiol. 2011;116:231–239. - PubMed
    1. McArdle MA, Finucane OM, Connaughton RM, McMorrow AM, Roche HM. Mechanisms of obesity-induced inflammation and insulin resistance: Insights into the emerging role of nutritional strategies. Front Endocrinol. 2013;52:1–23. - PMC - PubMed
    1. Wellen KE, Hotamisligil GS. Inflammation, stress, and diabetes. J Clin Invest. 2005;115:1111–19. doi: 10.1172/JCI200525102. - DOI - PMC - PubMed
    1. Hotamisligil GS. Inflammation and metabolic disorders. Nature. 2006;444:860–867. doi: 10.1038/nature05485. - DOI - PubMed

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