Effects of high-intensity training on muscle lactate transporters and postexercise recovery of muscle lactate and hydrogen ions in women

Abstract

Bishop D, Edge J, Thomas C, Mercier J. Effects of high-intensity training on muscle lactate transporters and postexercise recovery of muscle lactate and hydrogen ions in women. Am J Physiol Regul Integr Comp Physiol 295: R1991-R1998, 2008. First published October 1, 2008 doi:10.1152/ajpregu.00863.2007.-The purpose of this study was to investigate the effects of high-intensity interval training (3 days/wk for 5 wk), provoking large changes in muscle lactate and pH, on changes in intracellular buffer capacity (␤min vitro), monocarboxylate transporters (MCTs), and the decrease in muscle lactate and hydrogen ions (H ϩ ) after exercise in women. Before and after training, biopsies of the vastus lateralis were obtained at rest and immediately after and 60 s after 45 s of exercise at 190% of maximal O2 uptake. Muscle samples were analyzed for ATP, phosphocreatine (PCr), lactate, and H ϩ ; MCT1 and MCT4 relative abundance and ␤min vitro were also determined in resting muscle only. Training provoked a large decrease in postexercise muscle pH (pH 6.81). After training, there was a significant decrease in ␤min vitro (Ϫ11%) and no significant change in relative abundance of MCT1 (96 Ϯ 12%) or MCT4 (120 Ϯ 21%). During the 60-s recovery after exercise, training was associated with no change in the decrease in muscle lactate, a significantly smaller decrease in muscle H ϩ , and increased PCr resynthesis. These results suggest that increases in ␤m in vitro and MCT relative abundance are not linked to the degree of muscle lactate and H ϩ accumulation during training. Furthermore, training that is very intense may actually lead to decreases in ␤m in vitro. The smaller postexercise decrease in muscle H ϩ after training is a further novel finding and suggests that training that results in a decrease in H ϩ accumulation and an increase in PCr resynthesis can actually reduce the decrease in muscle H ϩ during the recovery from supramaximal exercise.

Extremely low-volume, high-intensity interval training improves exercise capacity and increases mitochondrial protein content in human skeletal muscle

“…While others have also failed to observe an increase in MCT1 and MCT4 following HIT [36] it is possible that MCT4 increased following training in the current study, resulting in improved lactate export. While we were unable to measure MCT4 this explanation seems unlikely as MCT1 and MCT4 typically change in concert [5,36]. Alternatively, the observed increases in anaerobic power may be a result of improved muscle buffering capacity.…”

“…Alternatively, the observed increases in anaerobic power may be a result of improved muscle buffering capacity. While increases in buffering capacity have been observed following HIT training [2], no changes in buffering capacity have also been reported following HIT [36]. The mechanisms underlying the increases in anaerobic power induced by the Tabata protocol, and HIT in general, remain unclear.…”

The relationship between monocarboxylate transporters 1 and 4 expression in skeletal muscle and endurance performance in athletes

“…This could explain the contrasting results of these studies and the present investigation. At the same time, other training studies both performed in athletes have shown that MCT1 and MCT4 remain unchanged after a period of intensified training (Clark et al 2004;Bishop et al 2008). Also, other studies have shown that the expression of MCT1 and MCT4 acutely decreased following a single bout of high-intensity exercise ).…”

Análise da cinética de remoção de lactato em atletas de canoagem slalom

“…Para ser utilizado, o lactato produzido na fibra muscular deve ser transportado para a corrente sanguínea. Para isto, uma proteína presente na membrana da célula muscular, conhecida como transportador de monocarboxilato (MCT), transporta o lactato de dentro da célula para o sangue (JUEL et al, 2004;BONEN et al, 1998;BONEN, 2000;GLADDEN, 2007;BISHOP et al, 2008). O transporte do lactato para a corrente sanguínea através dos MCTs somente é realizado em co-transporte com H + , constituindo-se, dessa forma, como um dos processos que mais contribui para a manutenção do pH intracelular (BISHOP et al, 2001;JUEL et al, 2004;THOMAS et al, 2005;GLADDEN, 2007;BISHOP et al, 2008);BOGDANIS, 2012).…”

“…Neste contexto, estudos prévios reportados na literatura objetivaram analisar a cinética de remoção de lactato frente a esforços de alta intensidade (BRET et al, 2003;MESSONNIER et al, 2006;BISHOP et al 2008;MENZIES et al, 2010). A produção de lactato indica a magnitude da capacidade de produção de ATP via metabolismo anaeróbico lático, e sua remoção para o sangue uma capacidade de regulação de pH intramuscular.…”