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Biological sex does not influence the peak cardiac output response to twelve weeks of sprint interval training.

ABSTRACT: Sprint interval training (SIT) increases peak oxygen uptake (V̇O_2peak) but the mechanistic basis is unclear. We have reported that 12 wk of SIT increased V̇O_2peak and peak cardiac output (Q̇_peak) and the changes in these variables were correlated. An exploratory analysis suggested that Q̇_peak increased in males but not females. The present study incorporated best practices to examine the potential influence of biological sex on the Q̇_peak response to SIT. Male and female participants (n = 10 each; 21 ± 4 y) performed 33 ± 2 sessions of SIT over 12 wk. Each 10-min session involved 3 × 20-s 'all-out' sprints on an ergometer. V̇O_2peak increased after SIT (3.16 ± 1.0 vs. 2.89 ± 1.0 L/min, η²_p = 0.53, p < 0.001) with no sex × time interaction (p = 0.61). Q̇_peak was unchanged after training (15.2 ± 3.3 vs. 15.1 ± 3.0 L/min, p = 0.85), in contrast to our previous study. The peak estimated arteriovenous oxygen difference increased after training (204 ± 30 vs. 187 ± 36 ml/L, p = 0.006). There was no effect of training or sex on measures of endothelial function. We conclude that 12 wk of SIT increases V̇O_2peak but the mechanistic basis remains unclear. The capacity of inert gas rebreathing to assess changes in Q̇_peak may be limited and invasive studies that use more direct measures are needed.

SUBMITTER: Bostad W

PROVIDER: S-EPMC10752867 | biostudies-literature | 2023 Dec

REPOSITORIES: biostudies-literature

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Biological sex does not influence the peak cardiac output response to twelve weeks of sprint interval training.

Bostad William W Williams Jennifer S JS Van Berkel Emily K EK Richards Douglas L DL MacDonald Maureen J MJ Gibala Martin J MJ

Scientific reports 20231227 1

Sprint interval training (SIT) increases peak oxygen uptake (V̇O2peak) but the mechanistic basis is unclear. We have reported that 12 wk of SIT increased V̇O2peak and peak cardiac output (Q̇peak) and the changes in these variables were correlated. An exploratory analysis suggested that Q̇peak increased in males but not females. The present study incorporated best practices to examine the potential influence of biological sex on the Q̇peak re ...[more]

PMID: 38151488

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Project description:Cardiovascular adaptations to exercise, particularly at the individual level, remain poorly understood. Previous group level research suggests the relationship between cardiac output and oxygen consumption ([Formula: see text]-[Formula: see text]) is unaffected by training as submaximal [Formula: see text] is unchanged. We recently identified substantial inter-individual variation in the exercise [Formula: see text]-[Formula: see text] relationship that was correlated to stroke volume (SV) as opposed to arterial oxygen content. Therefore we explored the effects of sprint interval training (SIT) on modulating [Formula: see text]-[Formula: see text] given an individual's specific [Formula: see text]-[Formula: see text] relationship. 22 (21±2 yrs) healthy, recreationally active males participated in a 4-week SIT (8, 20 second sprints; 4x/week, 170% of the work rate at [Formula: see text] peak) study with progressive exercise tests (PET) until exhaustion. Cardiac output ([Formula: see text] L/min; inert gas rebreathe, Finometer Modelflow™), oxygen consumption ([Formula: see text] L/min; breath-by-breath pulmonary gas exchange), quadriceps oxygenation (near infrared spectroscopy) and exercise tolerance (6-20; Borg Scale RPE) were measured throughout PET both before and after training. Data are mean Δ from bsl±SD. Higher [Formula: see text] ([Formula: see text]) and lower [Formula: see text] ([Formula: see text]) responders were identified post hoc (n = 8/group). SIT increased the [Formula: see text]-[Formula: see text] post-training in [Formula: see text] (3.8±0.2 vs. 4.7±0.2; P = 0.02) while [Formula: see text] was unaffected (5.8±0.1 vs. 5.3±0.6; P = 0.5). [Formula: see text] was elevated beyond 80 watts in [Formula: see text] due to a greater increase in SV (all P<0.04). Peak [Formula: see text] (ml/kg/min) was increased in [Formula: see text] (39.7±6.7 vs. 44.5±7.3; P = 0.015) and [Formula: see text] (47.2±4.4 vs. 52.4±6.0; P = 0.009) following SIT, with [Formula: see text] having a greater peak [Formula: see text] both pre (P = 0.02) and post (P = 0.03) training. Quadriceps muscle oxygenation and RPE were not different between groups (all P>0.1). In contrast to [Formula: see text], [Formula: see text] responders are capable of improving submaximal [Formula: see text]-[Formula: see text] in response to SIT via increased SV. However, the increased submaximal exercise [Formula: see text] does not benefit exercising muscle oxygenation.

Project description:BackgroundMany 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.MethodsData 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 ΔVO2max, ΔEI, ΔNEPA, and Δresting metabolic rate.ResultsVery 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 ΔVO2max (p < 0.001) and ΔNEPA (p < 0.001).ConclusionsConsiderable variation exists in response to short-term, low dose interval training. In agreement with prior work, increases in ΔVO2max and ΔNEPA 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.

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Biological sex does not influence the peak cardiac output response to twelve weeks of sprint interval training.

Publications

Biological sex does not influence the peak cardiac output response to twelve weeks of sprint interval training.

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