Sprint interval training in older adults: recovery, acute effects, and training adaptations

Rationale & Introduction: Human ageing is presently characterised by an unavoidable biological ageing process following maturation, which occurs in the 2nd decade of life. Consequently, a decline in overall human functioning is observed. However, this process can be skewed to decelerate the ageing process and increase human functioning with the adoption of lifestyle changes. The focus of this thesis was to analyse the relevance of physical activity and its effects on markers of physical functioning and investigate the physiological and practical efficacy of high-intensity interval training (HIIT), and more specifically sprint interval training (SIT) as a method of improving physical functioning in ageing cohorts. Studies Overview: A systematic review meta-analysis was conducted with a focus on the physiological outcomes of HIIT interventions in older people. Study one investigated the peak power output recovery following 3 and 5 days of rest following SIT. Study two compared the physiological, psychological, and perceptive responses to SIT in three distinct modes: static sprinting, cycle ergometry, and box stepping. Study three investigated the effects of an 8 week SIT intervention in older adults on aerobic capacity, hemodynamics, and muscle power. Results: Systematic review meta-analysis) HIIT interventions were found to have a positive effect on aerobic capacity (standard difference in means [SDM] = 0.74)), muscle power (SDM = 1.13), muscle strength (SDM = 0.19), and lean body mass (SDM = 0.17), and a negative effect on body fat (SDM = -0.30). Study 1) The findings suggest that older individuals recover similarly between 3 and 5 five days of rest following SIT with a small effect (p = 0.702, n2p = 0.022). Study 2) The findings of study two indicate that static sprinting and the cycle ergometer modes are likely more suitable to providing the physiological stimulus required to instigate adaptations to SIT. A medium effect of exercise mode for peak oxygen uptake (VȮ̇̇̇2peak) was observed (n2=0.213, p=0.091), a large effect was observed for peak blood lactate (BLapeak) between exercise modes (n2=0.712, p<0.001), a large effect was observed for peak rating of perceived exertion (RPE) between exercise modes (n2=0.390, p=0.007), and a medium effect was observed for the PACES (Physical Activity Enjoyment Scale) total between exercise modes (n2=0.255, p=0.052). Study 3) The results of study three suggest that SIT is effective at improving aerobic capacity, hemodynamic function, and muscle power. There was a small effect of time on body mass index (BMI; p=0.210, n2=0.122), a small effect of time on systolic blood pressure (p=0.111, n2=0.167), a medium effect of time on diastolic blood pressure (p=0.027, n2=0.260), a large effect of time on mean arterial pressure (p=0.027, n2=0.260), no effect of time on resting heart rate (p=0.578, n2=0.045), a medium effect of time on peak heart rate (HRpeak; p=0.032, n2=0.250), no effect of time on postural sway (p=0.258, n2=0.107), a large effect of time on muscle power measured by the Herbert 6s peak power output (PPO) test (p=0.018, n2=0.517), a large effect of time on countermovement jump power (p=0.008, n2=0.332), a large effect of time on countermovement jump height (p=0.004, n2=0.370), a small effect of time on V̇̇O2max (p=0.017, n2=0.137), no effect of time on O2 pulse (p=0.289, n2=0.009), a medium effect of time on the anaerobic threshold (AT) as a percentage of V̇̇O2max (AT % @ V̇̇O2max) (p=0.035, n2=0.243), and a medium effect of time on power at V̇̇O2max (p=0.010, n2=0.292). Conclusion: The systematic review meta-analysis observed increased aerobic capacity, muscle power, muscle strength, lean body mass, and decreased fat mass with HIIT in older adults. However, the low number of studies reduces the reliability of findings. Peak power output recovery in older adults is similar at 3- and 5-days following SIT. SIT performed as different exercise modes (static sprinting, cycle ergometer, box stepping) result in different physiological, psychological, and perceptive responses. Static sprinting SIT performed twice a week over 8 weeks improves aerobic capacity, muscle power, and hemodynamic function in already physically active older adults

Aerobically trained older adults show impaired resting, but preserved exercise-induced circulating progenitor cell count, which was not improved by sprint interval training

Older adults exhibit a reduced number and function of CD34 + circulating progenitor cells (CPC), a known risk factor for cardiovascular disease. Exercise promotes the mobilisation of CPCs from bone marrow, so whether ageing per se or physical inactivity in older age reduces CPCs is unknown. Thus, this study examined the effect of age on resting and exercise-induced changes in CPCs in aerobically trained adults and the effect of 8 weeks of sprint interval training (SIT) on resting and exercise-induced CPCs in older adults. Twelve young (22-34 years) and nine older (63-70 years) adults participated in the study. Blood was sampled pre and immediately post a graded exercise test to exhaustion in both groups. Older participants repeated the process after 8 weeks of SIT (3 × 20 s 'all-out' sprints, 2 × a week). Total CPCs (CD34 ) and endothelial progenitor cells (EPCs: CD34 KDR ) were determined by flow cytometry. Older adults exhibited lower basal total CD34 CPCs (828 ± 314 vs. 1186 ± 272 cells·mL , p = 0.0149) and CD34 KDR EPCs (177 ± 128 vs. 335 ± 92 cells·mL , p = 0.007) than younger adults. The maximal exercise test increased CPCs in young (CD34 : p = 0.004; CD34 KDR : p = 0.017) and older adults (CD34 : p  0.232). This study suggests age per se does not impair exercise-induced CPC counts, but does lower resting CPC counts

Aerobically trained older adults show impaired resting, but preserved exercise-induced circulating progenitor cell count, which was not improved by sprint interval training

Older adults exhibit a reduced number and function of CD34 + circulating progenitor cells (CPC), a known risk factor for cardiovascular disease. Exercise promotes the mobilisation of CPCs from bone marrow, so whether ageing per se or physical inactivity in older age reduces CPCs is unknown. Thus, this study examined the effect of age on resting and exercise-induced changes in CPCs in aerobically trained adults and the effect of 8 weeks of sprint interval training (SIT) on resting and exercise-induced CPCs in older adults. Twelve young (22–34 years) and nine older (63–70 years) adults participated in the study. Blood was sampled pre and immediately post a graded exercise test to exhaustion in both groups. Older participants repeated the process after 8 weeks of SIT (3 × 20 s ‘all-out’ sprints, 2 × a week). Total CPCs (CD34+) and endothelial progenitor cells (EPCs: CD34+KDR+) were determined by flow cytometry. Older adults exhibited lower basal total CD34+ CPCs (828 ± 314 vs. 1186 ± 272 cells·mL−1, p = 0.0149) and CD34+KDR+ EPCs (177 ± 128 vs. 335 ± 92 cells·mL−1, p = 0.007) than younger adults. The maximal exercise test increased CPCs in young (CD34+: p = 0.004; CD34+KDR+: p = 0.017) and older adults (CD34+: p  0.232). This study suggests age per se does not impair exercise-induced CPC counts, but does lower resting CPC counts

High Intensity Interval Training (HIIT) as a Potential Countermeasure for Phenotypic Characteristics of Sarcopenia: A Scoping Review

Background: Sarcopenia is defined as a progressive and generalized loss of skeletal muscle quantity and function associated predominantly with aging. Physical activity appears the most promising intervention to attenuate sarcopenia, yet physical activity guidelines are rarely met. In recent years high intensity interval training (HIIT) has garnered interested in athletic populations, clinical populations, and general population alike. There is emerging evidence of the efficacy of HIIT in the young old (i.e. seventh decade of life), yet data concerning the oldest old (i.e., ninth decade of life onwards), and those diagnosed with sarcopenic are sparse.Objectives: In this scoping review of the literature, we aggregated information regarding HIIT as a potential intervention to attenuate phenotypic characteristics of sarcopenia.Eligibility Criteria: Original investigations concerning the impact of HIIT on muscle function, muscle quantity or quality, and physical performance in older individuals (mean age ≥60 years of age) were considered.Sources of Evidence: Five electronic databases (Medline, EMBASE, Web of Science, Scopus, and the Cochrane Central Register of Controlled Trials [CENTRAL]) were searched.Methods: A scoping review was conducted using the Arksey and O'Malley methodological framework (2005). Review selection and characterization were performed by two independent reviewers using pretested forms.Results: Authors reviewed 1,063 titles and abstracts for inclusion with 74 selected for full text review. Thirty-two studies were analyzed. Twenty-seven studies had a mean participant age in the 60s, two in the 70s, and three in the 80s. There were 20 studies which examined the effect of HIIT on muscle function, 22 which examined muscle quantity, and 12 which examined physical performance. HIIT was generally effective in Improving muscle function and physical performance compared to non-exercised controls, moderate intensity continuous training, or pre-HIIT (study design-dependent), with more ambiguity concerning muscle quantity.Conclusions: Most studies presented herein utilized outcome measures defined by the European Working Group on Sarcopenia in Older People (EWGSOP). However, there are too few studies investigating any form of HIIT in the oldest old (i.e., ≥80 years of age), or those already sarcopenic. Therefore, more intervention studies are needed in this population

Aerobically trained older adults show impaired resting, but preserved exercise-induced circulating progenitor cell count, which was not improved by sprint interval training

Older adults exhibit a reduced number and function of CD34 + circulating progenitor cells (CPC), a known risk factor for cardiovascular disease. Exercise promotes the mobilisation of CPCs from bone marrow, so whether ageing per se or physical inactivity in older age reduces CPCs is unknown. Thus, this study examined the effect of age on resting and exercise-induced changes in CPCs in aerobically trained adults and the effect of 8 weeks of sprint interval training (SIT) on resting and exercise-induced CPCs in older adults. Twelve young (22–34 years) and nine older (63–70 years) adults participated in the study. Blood was sampled pre and immediately post a graded exercise test to exhaustion in both groups. Older participants repeated the process after 8 weeks of SIT (3 × 20 s ‘all-out’ sprints, 2 × a week). Total CPCs (CD34+) and endothelial progenitor cells (EPCs: CD34+KDR+) were determined by flow cytometry. Older adults exhibited lower basal total CD34+ CPCs (828 ± 314 vs. 1186 ± 272 cells·mL−1, p = 0.0149) and CD34+KDR+ EPCs (177 ± 128 vs. 335 ± 92 cells·mL−1, p = 0.007) than younger adults. The maximal exercise test increased CPCs in young (CD34+: p = 0.004; CD34+KDR+: p = 0.017) and older adults (CD34+: p  0.232). This study suggests age per se does not impair exercise-induced CPC counts, but does lower resting CPC counts