RESUMO
We tested the hypothesis that AMPK activation and peroxisome proliferator gamma coactivator 1 alpha (PGC-1α) expression are not augmented as exercise intensity (power output) increases from maximal to supramaximal intensities and conducted an exploratory analysis comparing AMPK activation and PGC-1α expression in males and females. Seventeen (n = 9 males; n = 8 females) recreationally active, healthy, young individuals volunteered to participate in the current study. Participants completed work matched interval exercise at 100% (Max) and 133% (Supra) of peak work rate (WRpeak). Intervals were 1 min in duration and participants were prescribed 6 and 8 intervals of Max and Supra, respectively, to equate external work across protocols. PGC-1α mRNA expression and activation of AMPK (p-ACC) were examined in muscle biopsy samples. Interval WR (watts; W), intensity (%WRpeak) and average HR (bpm), blood lactate (mmol/L) and rating of perceived exertion were all higher (all p < 0.05) in Supra. Fatigue was greater (p < 0.05) in Supra. PGC-1α mRNA expression significantly increased after exercise in Max (p < 0.01) and Supra (p < 0.01), but was not significantly different (p = 0.71) between intensities. A main effect of time (Pre - 0 h) (p < 0.01) was observed for p-ACC; however, no effect of intensity (p = 0.08) or interaction (p = 0.97) was observed. No significant effects of time (p = 0.05) intensity (p = 0.42), or interaction (p = 0.97) were observed for p-AMPK (Thr172). Exploratory sex analysis demonstrated a main effect of sex for p-ACC (greater p-ACC in males; p < 0.05) but not for p-AMPK or PGC-1α expression. Our results confirm that AMPK-PGC-1α signalling is not augmented following supramaximal exercise and provide novel data demonstrating a decrease in AMPK activation (p-ACC) in females compared to men. Trial registration: https://doi.org/10.17605/OSF.IO/U7PX9.
Assuntos
Proteínas Quinases Ativadas por AMP , Músculo Esquelético , Masculino , Humanos , Feminino , Proteínas Quinases Ativadas por AMP/genética , Proteínas Quinases Ativadas por AMP/metabolismo , Estudos Cross-Over , Músculo Esquelético/fisiologia , Exercício Físico/fisiologia , RNA Mensageiro/genética , RNA Mensageiro/metabolismo , Coativador 1-alfa do Receptor gama Ativado por Proliferador de Peroxissomo/genética , Coativador 1-alfa do Receptor gama Ativado por Proliferador de Peroxissomo/metabolismoRESUMO
The purpose of this review is to explore and discuss the impacts of augmented training volume, intensity, and duration on the phosphorylation/activation of key signaling protein - AMPK, CaMKII and PGC-1α - involved in the initiation of mitochondrial biogenesis. Specifically, we explore the impacts of augmented exercise protocols on AMP/ADP and Ca2+ signaling and changes in post exercise PGC - 1α gene expression. Although AMP/ADP concentrations appear to increase with increasing intensity and during extended durations of higher intensity exercise AMPK activation results are varied with some results supporting and intensity/duration effect and others not. Similarly, CaMKII activation and signaling results following exercise of different intensities and durations are inconsistent. The PGC-1α literature is equally inconsistent with only some studies demonstrating an effect of intensity on post exercise mRNA expression. We present a novel meta-analysis that suggests that the inconsistency in the PGC-1α literature may be due to sample size and statistical power limitations owing to the effect of intensity on PGC-1α expression being small. There is little data available regarding the impact of exercise duration on PGC-1α expression. We highlight the need for future well designed, adequately statistically powered, studies to clarify our understanding of the effects of volume, intensity, and duration on the induction of mitochondrial biogenesis by exercise.
Assuntos
Proteínas Quinases Ativadas por AMP , Proteína Quinase Tipo 2 Dependente de Cálcio-Calmodulina , Proteínas Quinases Ativadas por AMP/genética , Proteínas Quinases Ativadas por AMP/metabolismo , Proteína Quinase Tipo 2 Dependente de Cálcio-Calmodulina/genética , Proteína Quinase Tipo 2 Dependente de Cálcio-Calmodulina/metabolismo , Exercício Físico/fisiologia , Músculo Esquelético/metabolismo , Fosforilação , RNA Mensageiro/genética , HumanosRESUMO
INTRODUCTION: High-intensity interval training and sprint interval training significantly increase maximal oxygen uptake (VÌO 2max ), which enhances endurance performance and health status. Whether this response is due to increases in central cardiovascular function (cardiac output (CO) and blood volume) or peripheral factors is unknown. PURPOSE: This study aimed to conduct a systematic review and meta-analysis to assess the effects of high-intensity interval training and sprint interval training (referred to as intense interval training) on changes in central cardiovascular function. METHODS: We performed a systematic search of eight databases for studies denoting increases in VÌO 2max in which CO, stroke volume (SV), blood volume, plasma volume, end-diastolic/systolic volume, or hematocrit were measured. RESULTS: Forty-five studies were included in this analysis, comprising 946 men and women of various health status (age and VÌO 2max , 20-76 yr and 13-61 mL·kg -1 ·min -1 ) who performed 6-96 sessions of interval training. Results showed an increase in VÌO 2max with intense interval training that was classified as a large effect ( d = 0.83). SV ( d = 0.69), and CO ( d = 0.49) had moderate effect sizes in response to intense interval training. Of 27 studies in which CO was measured, 77% exhibited significant increases in resting CO or that obtained during exercise. Similarly, 93% of studies revealed significant increases in SV in response to intense interval training. Effect sizes for these outcomes were larger for clinical versus healthy populations. Plasma volume, blood volume, and hematocrit had small effect sizes after training ( d = 0.06-0.14). CONCLUSIONS: Increases in VÌO 2max demonstrated with intense interval training are attendant with increases in central O 2 delivery with little contribution from changes in hematocrit, blood volume, or plasma volume.