The purpose of this study was to investigate the relationship between muscle and blood lactate concentrations during progressive exercise. Seven endurance-trained male college students performed three incremental bicycle ergometer exercise tests. The first two tests (tests I and II) were identical and consisted of 3-min stage durations with 2-min rest intervals and increased by 50-W increments until exhaustion. During these tests, blood was sampled from a hyperemized earlobe for lactate and pH measurement (and from an antecubital vein during test I), and the exercise intensities corresponding to the lactate threshold (LT), individual anaerobic threshold (IAT), and onset of blood lactate accumulation (OBLA) were determined. The test III was performed at predetermined work loads (50 W below OBLA, at OBLA, and 50 W above OBLA), with the same stage and rest interval durations of tests I and II. Muscle biopsies for lactate and pH determination were taken at rest and immediately after the completion of the three exercise intensities. Blood samples were drawn simultaneously with each biopsy. Muscle lactate concentrations increased abruptly at exercise intensities greater than the "below-OBLA" stage [50.5% maximal O2 uptake (VO2 max)] and resembled a threshold. An increase in blood lactate and [H+] also occurred at the below-OBLA stage; however, no significant change in muscle [H+] was observed. Muscle lactate concentrations were highly correlated to blood lactate (r = 0.91), and muscle-to-blood lactate ratios at below-OBLA, at-OBLA, and above-OBLA stages were 0.74, 0.63, 0.96, and 0.95, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)
"During mild or moderate work intensities below the lactate threshold, the biochemical counterpart of the O2 deficit is the extent of PCr hydrolysis (Di Prampero et al. 2003). Progressive or ramp muscle exercises are characterised by decreases in pH with a significant descent at peak work rates ranging between 60 and 80% (Barstow et al. 1994b; Chwalbinska-Moneta et al. 1989; Knuttgen and Saltin 1972; Marsh et al. 1991). Several previous 31 P-MRS investigations have shown that the linearity between PCr hydrolysis and workload is impaired when the pH in the muscle tissue falls below this so-called intracellular threshold, resulting in an acceleration of PCr hydrolysis via a pH-dependent impairment of creatine kinase activity (Barstow et al. 1994b; Marsh et al. 1991). "
[Show abstract][Hide abstract] ABSTRACT: According to the literature the steady-state level of phosphocreatine (PCr) has a linear relationship to the workload during muscle exercise intensities below the lactate threshold, whereas this linearity is impaired during exercise intensities above the lactate threshold. The purpose of this study was to investigate the linearity between PCr kinetics and workload during two bouts of isotonic incremental calf exercise with transitions from moderate- to high-intensity as well as from high- to moderate-intensity work rates. Using a whole-body 1.5 T MR scanner and a self-built exercise bench, we performed serial phosphorus-31 magnetic resonance spectroscopy ((31)P-MRS) with a time resolution of 30 s in nine healthy male volunteers. Changes in PCr, inorganic phosphate (Pi) and pH were statistically evaluated in comparison to the baseline. The exercise protocol started with a 4.5 W interval of 6 min followed by two bouts of 1.5 W increments. The workload was increased in 2-min intervals up to 9 W during the first bout and up to 7.5 W during the second bout. The second bout was preceded by a 4.5 W interval of 2 min and followed by a 4.5 W interval of 4 min. PCr hydrolysis achieved a steady state during each increment and was highly linear to the work rate (r (2), -0.796; P <0.001). Pi accumulated during each bout, whereas the pH decreased continuously during the first bout and did not exhibit any substantial decrease during the second bout. The metabolite levels and pH were expressed as the median value and the range. Our study confirms that steady-state PCr levels also have a linear relationship to work intensities above the lactate threshold, while pH changes do not have any impact on PCr degradation. The lack of substantial changes in pH during the second exercise bout indicates that prior high-intensity exercise leads to an activation of oxidative phosphorylation.
"Interestingly, in HSP patients , we also observed a significant increment of mean lactate precociously with respect to the LT, at the exe rcise interstep 30-40% of the pnPO max . This increment, may be the expression of an " early threshold " , has previously been observed in normal subjects    and has been attributed to additional recruitment of glycogenolitic fibres at low levels of muscle contraction   during incremental exercise . This threshold makes it possible to distinguish between patients and controls. "
[Show abstract][Hide abstract] ABSTRACT: Hereditary spastic paraplegia (HSP) is a group of familial neurodegenerative disorders cha-racterized by progressive lower limb spasticity and weakness due to degeneration of corti-cospinal axons. These disorders are classified both genetically, according to the mode of inheritance, and clinically, as pure and complicated forms. Recently the discovery that pa-raplegin, the defective protein in autosomal recessive HSP-SPG7, localizes in mitochondria allowed to foster the hypothesis that some mitochondrial dysfunctions can play a pathoge-nic role in HSP. The aim of our study was to indirectly evaluate oxidative metabolism in contracting mu s-cle, by assessing the anaerobic lactate threshold in 7 patients (5 M and 2 F, mean age 48.0±13.9 yrs) affected by HSP, both autosomal dominant or sporadic, during an incre-mental bicycle exercise. Analysis of venous lactate curve showed that lactate levels were significantly higher than in controls (peak normalised lactate: 378.8 vs. 271%, p<0.01). Furthermore, an early threshold of lactate was detected only in HSP patients. Even if other factors such as chronic spasticity or muscle deconditioning have to be taken into account in the interpretation of our data, these results suggest possible occurrence of mitochondrial involvement in skeletal muscle of HSP patients. Hereditary spastic paraplegia (HSP) is a group of fa-milial neurodegenerative disorders characterized by progressive lower limb spasticity. These disorders are classified both genetically, according to the mode of in-heritance, as autosomal dominant, autosomal recessive and X linked, and clinically, as pure and complicated forms [7, 8]. The complicated form is characterized by the association of progressive lower limb spasticity and other neurological abnormalities such as optic neuropa-thy, retinopathy, extrapyramidal disturbances, dementia, ataxia, ichthyosis, mental retardation and deafness. Also sporadic cases of spastic paraplegia can be included in HSP group, when other possible causes of pyramidal system involvement are ruled out. There is evidence that HSP can be, at least in some in-stances, a mitochondrial dysfunction . This is the case of the autosomal recessive SPG7 form in which a mutation of a nuclear gene encoding for a mitochondrial protein has been reported . In fact, the product of the SPG7 gene is a protein of 795 amino acids, called para-plegin, which is highly homologous to a class of yeast ATP-dependent zinc metalloproteases  and has been demonstrated to specifically localize into the mitochon-dria in immunofluorescence transfected COS-7 cells . Furthermore, analysis of muscle biopsies demo n-strated that individuals with paraplegin mutation show typical signs of mitochondrial involvement suggesting the presence of impaired oxidative phosphorylation in these cases [5, 16]. Therefore aim of this study was to evaluate in patients affected by HSP oxidative metabolism in exercising muscle by the assessment of blood lactate kinetics dur-ing an incremental workload exercise.
[Show abstract][Hide abstract] ABSTRACT: Pyruvate dehydrogenase (PDH) is an important regulator of carbohydrate oxidation during exercise and its activity can be down-regulated by an increase in dietary fat. The purpose of this study was to determine the acute metabolic effects of differential dietary fatty acids on the activation of PDH in its active form (PDHa) at rest and at the onset of moderate-intensity exercise. University-aged male subjects (n=7) underwent 2 fat loading trials spaced at least 2 weeks apart. Subjects consumed saturated (SFA) or polyunsaturated (PUFA) fat over the course of 5 hours. Following this, participants cycled at 65% VO2 max for 15 min. Muscle biopsies were taken prior to and following fat loading and at 1 min exercise. Plasma free fatty acids increased from 0.15 ± 0.07 to 0.54 ± 0.19 mM over 5 hours with SFA and from 0.1 1 ± 0.04 to 0.35 ±0.13 mM with PUFA. PDHa activity was unchanged following fat loading, but increased at the onset of exercise in the SFA trial, from 1 .4 ± 0.4 to 2.2 ± 0.4 /xmol/min/kg wet wt. This effect was negated in the PUFA trial (1 .2 ± 0.3 to 1 .3 ± 0.3 pimol/min/kg wet wt.). PDH kinase (PDK) was unchanged in both trials, suggesting that the attenuation of PDHa activity with PUFA was a result of changes in the concentrations of intramitochondrial effectors, more specifically intramitochondrial NADH or Ca^*. Our findings suggest that attenuated PDHa activity participates in the preferential oxidation of PUFA during moderateintensity exercise.
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