Impacts of high‐intensity exercise on the metabolomics profile of human skeletal muscle tissue

Abstract

The study aimed to identify and quantify the metabolites profile and metabolic pathways in human muscle tissue engaged during exhaustive high‐intensity cycling exercise. Seven healthy physically active men performed a graded exercise test and an exhaustive supramaximal effort at 115% of maximal aerobic power with muscles biopsies performed in rest and immediately after exhaustion for quantifying of muscle metabolites changes by 1H‐NMR spectroscopy. The time until exhaustion (tlim) recorded was 224.7 ± 35.5 s whereas the muscle pH at exhaustion was 6.48 ± 0.05. A total of 54 metabolites were identified and quantified. The most enriched and impacted pathways included: beta oxidation of very long chain fatty acids, mitochondrial electron transport chain, alanine aspartate, and glutamate metabolism, citric acid cycle, arginine biosynthesis, propanoate metabolism, threonine and 2‐oxobutanoate degradation and pyruvate metabolism. In addition, the muscle concentrations in Post exercise, compared to Pre increased significantly (p < 0.0398) for fumarate (42.0%), succinate (101.2%), glucose (249.7%), lactate (122.8%), O‐acetylcarnitine (164.7%), glycerol (79.3%), AMP (288.2%), 2‐oxobutyrate (121.0%), and methanol (58.5%), whereas decreased significantly (p < 0.010) for creatine phosphate (−70.2%), ADP (−56.5%), carnitine (−33.5%), and glutamate (−42.3%). Only the succinate was significantly correlated with tlim (r = −0.76; p = 0.0497). Besides the classical expected contribution of glycolytic and phosphagen energetic pathways, it was demonstrated that the high‐intensity exercise is also associated with pathways indicatives of amino acid and fatty acid oxidation metabolisms, highlighting the inverse relation between changes in the intramuscular succinate levels and tlim.

Effects of 12-week combined training versus high intensity interval training on cardiorespiratory fitness, body composition and fat metabolism in obese male adults

“…Contrary to the theory that above 80% of V’O 2 max, the contribution of fat oxidation is near negligible, 45 , 67 recent studies have shown that during HIIT, fat oxidation rates increase (i.e., threefold higher in well-trained athletes than in moderately active people), 18 as confirmed by metabolomics analysis. 68 In fact, fat oxidation during HIIT, compared to continuous exercise, occurred mainly due to increased levels of fatty acid transport proteins taking up plasmatic free fatty acids 69 in type II fibres of human skeletal muscle. 70 On the other hand, in COMB training, increased fat oxidation during MICT 34 primarily occurs in type I fibres 71 that exhibit high rates of intramuscular fatty acid oxidation.…”

Mechanical energy on anaerobic capacity during a supramaximal treadmill running in men: Is there influence between runners and active individuals?

“…Prior to each constant‐load supramaximal trial, the participants remained at rest seated in a chair for 10 min in order to determine the resting values of V̇O 2 (assuming the V̇O 2 average of the last 2 min of rest) and the [La − ]. After a warm up (abovementioned), the individuals performed the constant‐load supramaximal effort at 115% of vV̇O 2max until the task failure, which was assumed as the incapacity to keep the running intensity (Zagatto, Bertuzzi, et al, 2016; Zagatto, Leite, et al, 2016; Zagatto, Miyagi, et al, 2017; Zagatto, Nakamura, et al, 2017; Zagatto et al, 2022). The TTE was recorded.…”

“…The oxygen equivalent from glycolytic energy pathway ( E [La − ] ) was estimated by net lactate concentration accumulation (i.e., difference between peak [La − ] and the baseline [La − ]; ∆[La − ]), assuming an oxygen equivalent 3.0 ml·kg −1 for each ∆[La − ] of 1 mmol·L −1 (Brisola et al, 2015; Di Prampero & Ferretti, 1999; Miyagi et al, 2017; Zagatto, Bertuzzi, et al, 2016; Zagatto, Leite, et al, 2016; Zagatto, Miyagi, et al, 2017; Zagatto, Nakamura, et al, 2017; Zagatto et al, 2022). Therefore, the anaerobic capacity was assumed as the sum of E PCr and E [La − ] (Brisola et al, 2015; Milioni et al, 2016, 2017; Miyagi et al, 2017; Zagatto & Gobatto, 2012; Zagatto, Bertuzzi, et al, 2016; Zagatto, Leite, et al, 2016; Zagatto, Miyagi, et al, 2017; Zagatto, Nakamura, et al, 2017; Zagatto et al, 2022). The oxygen equivalent from oxidative metabolism ( E OXID ) also was estimated considering the V̇O 2 area under the curve by trapezoidal method (Brisola et al, 2015; Milioni et al, 2017; Miyagi et al, 2017; Zagatto, Bertuzzi, et al, 2016; Zagatto, Leite, et al, 2016; Zagatto, Miyagi, et al, 2017; Zagatto, Nakamura, et al, 2017; Zagatto et al, 2022).…”

“…Therefore, the anaerobic capacity was assumed as the sum of E PCr and E [La − ] (Brisola et al, 2015;Milioni et al, 2016Milioni et al, , 2017Miyagi et al, 2017;Zagatto & Gobatto, 2012;Zagatto, Bertuzzi, et al, 2016;Zagatto, Leite, et al, 2016;Zagatto, Nakamura, et al, 2017;Zagatto et al, 2022). The oxygen equivalent from oxidative metabolism (E OXID ) also was estimated considering the VȮ 2 area under the curve by trapezoidal method (Brisola et al, 2015;Milioni et al, 2017;Miyagi et al, 2017;Zagatto, Bertuzzi, et al, 2016;Zagatto, Leite, et al, 2016;Zagatto, Nakamura, et al, 2017;Zagatto et al, 2022).…”

“…The anaerobic capacity is defined as the maximal amount of energy which can be resynthesized by non‐mitochondrial metabolic pathways (i.e., glycolytic and phosphagen pathways) in a specific effort performed until failure (Zagatto, Bertuzzi, et al, 2016; Zagatto, Leite, et al, 2016). Considering the non‐mitochondrial metabolic pathways have actions predominant in the first seconds of an effort acting until approximately 45 s for a maximal effort (Hargreaves & Spriet, 2020; Zagatto et al, 2022), the anaerobic capacity has been significantly correlated with the performance recorded in short‐term events (Nevill et al, 2008; Ramsbottom et al, 1994, 2001; Zagatto, Miyagi, et al, 2017; Zagatto, Nakamura, et al, 2017).…”