Methods of monitoring training load and their relationships to changes in fitness and performance in competitive road cyclists

Purpose: The aim of this study was to assess the dose-response relationships between different training load methods and aerobic fitness and performance in competitive road cyclists. Method: Training data from 15 well-trained competitive cyclists were collected during a 10-week (December – March) pre-season training period. Before and after the training period, participants underwent a laboratory incremental exercise test with gas exchange and lactate measures and a performance assessment using an 8-min time trial (8MT). Internal training load was calculated using Banister’s TRIMP (bTRIMP), Edwards’ TRIMP (eTRIMP), individualized TRIMP (iTRIMP), Lucia’s TRIMP (luTRIMP) and session-RPE (sRPE). External load was measured using Training Stress Score™ (TSS). Results: Large to very large relationships (r = 0.54-0.81) between training load and changes in submaximal fitness variables (power at 2 and 4 mmol·L-1) were observed for all training load calculation methods. The strongest relationships with changes in aerobic fitness variables were observed for iTRIMP (r = 0.81 [95% CI: 0.51 to 0.93, r = 0.77 [95% CI 0.43 to 0.92]) and TSS (r = 0.75 [95% CI 0.31 to 0.93], r = 0.79 [95% CI: 0.40 to 0.94]). The highest dose-response relationships with changes in the 8MT performance test were observed for iTRIMP (r = 0.63 [95% CI 0.17 to 0.86]) and luTRIMP (r = 0.70 [95% CI: 0.29 to 0.89). Conclusions: The results show that training load quantification methods that integrate individual physiological characteristics have the strongest dose-response relationships, suggesting this to be an essential factor in the quantification of training load in cycling

Analysing a cycling grand tour: Can we monitor fatigue with intensity or load ratios?

This study evaluated the changes in ratios of different intensity (rating of perceived exertion; RPE, heart rate; HR, power output; PO) and load measures (session-RPE; sRPE, individualized TRIMP; iTRIMP, Training Stress Score™; TSS) in professional cyclists. RPE, PO and HR data was collected from twelve professional cyclists (VO2max 75 ± 6 ml∙min∙kg-1) during a two-week baseline training period and during two cycling Grand Tours. Subjective:objective intensity (RPE:HR, RPE:PO) and load (sRPE:iTRIMP, sRPE:TSS) ratios and external:internal intensity (PO:HR) and load (TSS:iTRIMP) ratios were calculated for every session. Moderate to large increases in the RPE:HR, RPE:PO and sRPE:TSS ratios (d = 0.79 – 1.79) and small increases in the PO:HR and sRPE:iTRIMP ratio (d = 0.21 – 0.41) were observed during Grand Tours compared to baseline training data. Differences in the TSS:iTRIMP ratio were trivial to small (d = 0.03 – 0.27). Small to moderate weekto- week changes (d = 0.21 – 0.63) in the PO:HR, RPE:PO, RPE:HR, TSS;iTRIMP sRPE:iTRIMP and sRPE:TSS were observed during the Grand Tour. Concluding, this study shows the value of using ratios of intensity and load measures in monitoring cyclists. Increases in ratios could reflect progressive fatigue that is not readily detected by changes in solitary intensity/load measures

Resveratrol as Add-on Therapy in Subjects With Well-Controlled Type 2 Diabetes: A Randomized Controlled Trial

Item does not contain fulltextOBJECTIVE: To determine whether resveratrol supplementation can improve insulin sensitivity and promote overall metabolic health on top of standard diabetes care. RESEARCH DESIGN AND METHODS: Seventeen subjects with well-controlled type 2 diabetes (T2D) were treated with placebo and 150 mg/day resveratrol (resVida) in a randomized double-blind crossover study for 30 days. The main outcome measure was insulin sensitivity by the hyperinsulinemic-euglycemic clamp technique. RESULTS: Hepatic and peripheral insulin sensitivity were not affected by resveratrol treatment. Intrahepatic lipid content also remained unaffected by resveratrol; however, the change in intrahepatic lipid content correlated negatively with plasma resveratrol levels (R = -0.68, P = 0.03). Intramyocellular lipid content increased in type 2 muscle fibers (P = 0.03), and systolic blood pressure tended to decrease (P = 0.09) upon resveratrol treatment. In addition, resveratrol significantly improved ex vivo mitochondrial function (state 3 and state U respiration upon malate with octanoyl-carnitine, P < 0.005). Intriguingly, a correlation was found between plasma levels of a metabolite of resveratrol (dihydroresveratrol) and the metformin dose used by the patients (R = 0.66, P = 0.005), suggesting an interaction between metformin and resveratrol. It could be speculated that the lack of a resveratrol-induced insulin-sensitizing effect is caused by this interaction. CONCLUSIONS: Resveratrol supplementation does not improve hepatic or peripheral insulin sensitivity. Our results question the generalized value of resveratrol as an add-on therapy in the treatment of T2D and emphasize the need to perform studies in drug-naive patients with T2D or subjects with prediabetes.1 december 201

Evidence for a direct effect of the NAD+ precursor acipimox on muscle mitochondrial function in humans.

Recent preclinical studies showed the potential of nicotinamide adenine dinucleotide (NAD(+)) precursors to increase oxidative phosphorylation and improve metabolic health, but human data are lacking. We hypothesize that the nicotinic acid derivative acipimox, an NAD(+) precursor, would directly affect mitochondrial function independent of reductions in nonesterified fatty acid (NEFA) concentrations. In a multicenter randomized crossover trial, 21 patients with type 2 diabetes (age 57.7 +/- 1.1 years, BMI 33.4 +/- 0.8 kg/m(2)) received either placebo or acipimox 250 mg three times daily dosage for 2 weeks. Acipimox treatment increased plasma NEFA levels (759 +/- 44 vs. 1,135 +/- 97 mumol/L for placebo vs. acipimox, P < 0.01) owing to a previously described rebound effect. As a result, skeletal muscle lipid content increased and insulin sensitivity decreased. Despite the elevated plasma NEFA levels, ex vivo mitochondrial respiration in skeletal muscle increased. Subsequently, we showed that acipimox treatment resulted in a robust elevation in expression of nuclear-encoded mitochondrial gene sets and a mitonuclear protein imbalance, which may indicate activation of the mitochondrial unfolded protein response. Further studies in C2C12 myotubes confirmed a direct effect of acipimox on NAD(+) levels, mitonuclear protein imbalance, and mitochondrial oxidative capacity. To the best of our knowledge, this study is the first to demonstrate that NAD(+) boosters can also directly affect skeletal muscle mitochondrial function in humans

The lipid droplet coat protein perilipin 5 also localizes to muscle mitochondria

Perilipin 5 (PLIN5/OXPAT) is a lipid droplet (LD) coat protein mainly present in tissues with a high fat-oxidative capacity, suggesting a role for PLIN5 in facilitating fatty acid oxidation. Here, we investigated the role of PLIN5 in fat oxidation in skeletal muscle. In human skeletal muscle, we observed that PLIN5 (but not PLIN2) protein content correlated tightly with OXPHOS content and in rat muscle PLIN5 content correlated with mitochondrial respiration rates on a lipid-derived substrate. This prompted us to examine PLIN5 protein expression in skeletal muscle mitochondria by means of immunogold electron microscopy and Western blots in isolated mitochondria. These data show that PLIN5, in contrast to PLIN2, not only localizes to LD but also to mitochondria, possibly facilitating fatty acid oxidation. Unilateral overexpression of PLIN5 in rat anterior tibialis muscle augmented myocellular fat storage without increasing mitochondrial density as indicated by the lack of change in protein content of five components of the OXPHOS system. Mitochondria isolated from PLIN5 overexpressing muscles did not possess increased fatty acid respiration. Interestingly though, 14C-palmitate oxidation assays in muscle homogenates from PLIN5 overexpressing muscles revealed a 44.8% (P = 0.05) increase in complete fatty acid oxidation. Thus, in mitochondrial isolations devoid of LD, PLIN5 does not augment fat oxidation, while in homogenates containing PLIN5-coated LD, fat oxidation is higher upon PLIN5 overexpression. The presence of PLIN5 in mitochondria helps to understand why PLIN5, in contrast to PLIN2, is of specific importance in fat oxidative tissues. Our data suggests involvement of PLIN5 in directing fatty acids from the LD to mitochondrial fatty acid oxidation

Paradoxical Increase in TAG and DAG Content Parallel the Insulin Sensitizing Effect of Unilateral DGAT1 Overexpression in Rat Skeletal Muscle

BACKGROUND: The involvement of muscle triacylglycerol (TAG) storage in the onset of insulin resistance is questioned and the attention has shifted towards inhibition of insulin signalling by the lipid intermediate diacylglycerol (DAG). The enzyme 1,2-acylCoA:diacylglyceroltransferase-1 (DGAT1) esterifies a fatty acyl-CoA on DAG to form TAG. Therefore, the aim of the present study was to investigate if unilateral overexpression of DGAT1 in adult rat Tibialis anterior (TA) muscle will increase conversion of the lipid intermediate DAG into TAG, thereby improving muscle insulin sensitivity. METHODOLOGY/PRINCIPAL FINDINGS: The DGAT1 gene construct was injected in the left TA muscle of male rats on chow or high-fat (45% kcal) diet for three weeks, followed by application of one 800 V/cm and four 80 V/cm pulses, using the contralateral leg as sham-electroporated control. Seven days after electroporation, muscle specific insulin sensitivity was assessed with a hyperinsulinemic euglycemic clamp using 2-deoxy-[3H]glucose. Here, we provide evidence that unilateral overexpression of DGAT1 in TA muscle of male rats is associated with an increased rather than decreased DAG content. Strikingly, this increase in DAG content was accompanied by improved muscle insulin sensitivity. Interestingly, markers of muscle lipolysis and mitochondrial function were also increased in DGAT1 overexpressing muscle. CONCLUSIONS/SIGNIFICANCE: We conclude that unilateral DGAT1 overexpression can rescue insulin sensitivity, possibly by increasing DAG and TAG turnover in skeletal muscle. In case of a proper balance between the supply and oxidation of fatty acids in skeletal muscle, the lipid intermediate DAG may not exert harmful effects on insulin signalling