Maximal Fat Oxidation During Exercise in Trained Men

Abstract

[Aims] In the present study, we examined effects of exercise training (TR) on high fat diet (HFD)-induced expression changes of prothymosin α (ProTα) and its functions in white adipose tissue (WAT). [Methods] Eight-week-old male C57BL/6J mice were divided randomly into three groups: 1) C mice: control mice; 2) HFD mice: mice fed HFD (60% fat) for 4 months; 3) HFD-TR mice: mice fed HFD with voluntary TR on a running wheel for 4 months. We then investigated the expression of ProTα in WAT. Moreover, to investigate the function of ProTα in adipocytes, ProTα siRNA or recombinant lentivirus containing ProTα cDNA was infected into mouse 3T3-L1 adipocytes. [Results] Although the levels of body and WAT mass in HFD mice were significantly higher than those of C mice, TR inhibited such HFD-induced increases. Moreover, although expression of ProTα in WAT was upregulated by HFD, TR markedly attenuated HFD-induced expression of ProTα. The reduction of ProTα in 3T3-L1 cells resulted in inhibition of adipocyte differentiation with decreased expression of CCAAT-enhancer-binding proteinα (C/EBPα) gene. Conversely, overexpression of ProTα in 3T3-L1 cells enhanced expression of genes for C/EBPα and peroxi-some proliferator-activated receptor γ. [Conclusions] These results suggest that ProTα involves in adipocyte differentiation. Further, TR attenuates HFD-induced increases in expression of ProTα, which is speculated to be implicated in anti-obesity effects of TR. [Aims] Maximal fat oxidation (MFO) in the graded exercise test is considered to be an indicator of the capacity to oxidize fat during exercise. MFO varies widely based on cardiorespiratory fitness and body composition. Fat oxidation at rest (FO rest) positively correlated with MFO in overweight and healthy untrained people. However, it is unclear whether this positive correlation applies to all people with various levels of cardiorespiratory fitness and body composition. The current study examined the correlations between FO rest and MFO in trained, healthy inactive normal weight and overweight men. [Methods] This study included 8 trained, 6 healthy inactive normal weight, and 7 overweight men. All participants rested for 30 min in the supine position and performed a graded exercise test on a treadmill in the morning after a 12 h overnight fast. FO rest , maximal oxygen consumption (V ・ O 2 max), and MFO were measured by indirect calorimetry. Pearson's correlation coefficient was calculated between V ・ O 2 max and FO rest or MFO, FO rest and MFO. [Results] V ・ O 2 max significantly positively correlated with FO rest and MFO (R = 0.51, 0.72; P < 0.05, 0.01, respectively). FO rest significantly positively correlated with MFO (R = 0.71, P < 0.01). [Conclusions] FO rest positively correlated with MFO in trained, healthy inactive normal weight and overweight men. [Aims] Various clinical and epidemiological studies have shown an inverse association between serum high-density lipoprotein (HDL) cholesterol and cardiovascular events. Exercise is an effective treatment for increasin...

Determination of the maximal fat oxidation point in obese children and adolescents: validity of methods to assess maximal aerobic power

“…It is to note that interindividual variations of the maximal fat oxidation point were important with values ranging between 33% and 74% of % _ VO 2max m, a finding which is in agreement with a previous report Meyer et al 2007). These values are lower than the values of 80-85% _ VO 2max beyond which a high glycolytic flux is likely to decrease the bicarbonate pool and increase _ VO 2 due to the buffering of hydrogen ions (Achten and Jeukendrup 2003). A limit of the present study as well as well as several other studies (Achten and Jeukendrup 2003;Brandou et al 2003Brandou et al , 2005Brandou et al , 2006Lazzer et al 2007) measuring the maximal fat oxidation point during an incremental exercise is that we cannot exclude that short duration steps are too short to elicit a steady state of RER (Meyer et al 2007).…”

“…These values are lower than the values of 80-85% _ VO 2max beyond which a high glycolytic flux is likely to decrease the bicarbonate pool and increase _ VO 2 due to the buffering of hydrogen ions (Achten and Jeukendrup 2003). A limit of the present study as well as well as several other studies (Achten and Jeukendrup 2003;Brandou et al 2003Brandou et al , 2005Brandou et al , 2006Lazzer et al 2007) measuring the maximal fat oxidation point during an incremental exercise is that we cannot exclude that short duration steps are too short to elicit a steady state of RER (Meyer et al 2007). However, we used this procedure because it is far more practical for patients and experimenters than determining a maximal fat oxidation point during 30 min to 1 h constant load tests repeated several times within a few days (Meyer et al 2007).…”

“…The maximal fat oxidation point (Bordenave et al 2007) or whole body peak fat oxidation (Nordby et al 2006) is expressed as a percentage of _ VO 2max (Achten and Jeukendrup 2003;Lazzer et al 2007;Nordby et al 2006) or a power output (Brandou et al 2003(Brandou et al , 2006Perez-Martin et al 2001). In the present study we expressed maximal fat oxidation point as (1) % _ VO 2max m, (2) as a percentage of _ VO 2max ACSM; (American College of Sports Medicine 1995) which advise to express _ VO 2 as a linear function of heart rate during at least two stages of submaximal exercise and to extrapolate _ VO 2max from maximal theoretical heart rate [Theoretical maximal heart rate = 220-age (years)], (3) as a percentage of _ VO 2max estimated from Wasserman equations ( _ VO 2max W) (Wasserman et al 1987):…”

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“…Previous studies have shown that maximal fat oxidation often occurs during approximately 50% _ VO 2 max exercise for general population (Venables et al 2005;Achten and Jeukendrup 2004). When exercise intensity further increases, fat oxidation decreases, whereas CHO oxidation is markedly increased (Achten and Jeukendrup 2003;Romijn et al 1993). Therefore, moderate intensity exercise appears to be the most favorable for eliciting a substantial short-term increase in fat oxidation.…”

Can clinicians and scientists explain and prevent unexplained underperformance syndrome in elite athletes: an interdisciplinary perspective and 2016 update

“…It is well described that fat oxidation rates peak at ∼60% to 65% of maximal oxygen consumption (VO 2 max) and once blood lactate is accumulating, fat metabolism dramatically diminishes and may be negligible above 90% of VO 2 max in favour of carbohydrate to fuel a high ATP turnover and maintain workload. 85 This has significant implications for glycogen use, recovery duration and, therefore, EB. Furthermore, training at altitude or in the heat will further increase glycogen turnover and decrease exercise efficiency, 86 as will training in a fatigued or depleted state.…”