P. B. Laursen

THE SCIENTIFIC BASIS FOR HIGH-INTENSITY INTERVAL TRAINING: OPTIMISING TRAINING PROGRAMMES AND MAXIMISING PERFORMANCE IN HIGHLY TRAINED ENDURANCE ATHLETES

While the physiological adaptations that occur following endurance training in previously sedentary and recreationally active individuals are relatively well understood, the adaptations to training in already highly trained endurance athletes remain unclear. While significant improvements in endurance performance and corresponding physiological markers are evident following submaximal endurance training in sedentary and recreationally active groups, an additional increase in submaximal training (i.e. volume) in highly trained individuals does not appear to further enhance either endurance performance or associated physiological variables [e.g. peak oxygen uptake (V̇O2peak), oxidative enzyme activity]. It seems that, for athletes who are already trained, improvements in endurance performance can be achieved only through high-intensity interval training (HIT). The limited research which has examined changes in muscle enzyme activity in highly trained athletes, following HIT, has revealed no change in oxidative or glycolytic enzyme activity, despite significant improvements in endurance performance (p < 0.05). Instead, an increase in skeletal muscle buffering capacity may be one mechanism responsible for an improvement in endurance performance. Changes in plasma volume, stroke volume, as well as muscle cation pumps, myoglobin, capillary density and fibre type characteristics have yet to be investigated in response to HIT with the highly trained athlete. Information relating to HIT programme optimisation in endurance athletes is also very sparse. Preliminary work using the velocity at whichV̇O2max is achieved (Vmax) as the interval intensity, and fractions (50 to 75%) of the time to exhaustion at Vmax (Tmax) as the interval duration has been successful in eliciting improvements in performance in long-distance runners. However, Vmax and Tmax have not been used with cyclists. Instead, HIT programme optimisation research in cyclists has revealed that repeated supramaximal sprinting may be equally effective as more traditional HIT programmes for eliciting improvements in endurance performance. Further examination of the biochemical and physiological adaptations which accompany different HIT programmes, as well as investigation into the optimal HIT programme for eliciting performance enhancements in highly trained athletes is required.

Relationship of exercise test variables to cycling performance in an Ironman triathlon.

Abstract. The purpose of this study was, firstly, to investigate the intensity of exercise performanceof highly trained ultra-endurance triathletes during the cycling portion of an Ironman triathlon, and, secondly, to examine the anaerobic threshold and its relationship to this performance. Following a peak oxygen consumption (VO2peak) test on a cycle ergometer to determine the heart rate (HRTh,vent) and power output (POTh,vent) at the ventilatory threshold (Thvent), 11xa0highly trained male triathletes [mean (SEM) age 35.8xa0(1.6)xa0years, body fat 11.7xa0(1.2)%. VO2peak 67.5xa0(1.0)xa0ml·kg–1·min–1] who were participating in an Ironman triathlon, in random order: (1) cycled at their POTh,vent (BiTh,vent) until they were exhausted, and (2) cycled for 5xa0h at a self-selected intensity (BiSSI). Cycling power output (PO), oxygen uptake (VO2), heart rate (HR) and blood lactate concentration ([La–]b) were recorded at regular intervals during these trials, while performance HR was recorded during the cycling phase of the Ironman triathlon. Significantly greater (P<0.05) values were attained during BiTh,vent than during BiSSI for PO [274xa0(9) compared to 188xa0(9)xa0W], VO2 [3.61xa0(0.15) compared to 2.64xa0(0.09)xa0l·min–1], and [La–]b [6.7xa0(0.8) compared to 2.8xa0(0.4)xa0mmol·l–1]. Moreover, mean HR during the Ironman triathlon cycle phase [146.3xa0(2.4)xa0beats·min–1; n=7] was significantly greater than mean HR during BiSSI [130xa0(4)xa0beats·min–1], and significantly less than mean HR during BiTh,vent [159xa0(3)xa0beats·min–1; all P<0.05]. However, HR during the cycle portion of the Ironman triathlon was highly related to (r=0.873; P<0.05) and not significantly different to HRTh,vent [150xa0(4)xa0beats·min–1]. These data suggest that ultra-endurance triathletes cycle during the Ironman triathlon at a HR intensity that approximates to HRTh,vent, but at a PO that is significantly below POTh,vent.

Physiological responses to repeated bouts of high-intensity ultraendurance cycling - a field study case report

The present study aimed to 1) examine the relationship between laboratory-based measures and high-intensity ultraendurance (HIU) performance during an intermittent 24-h relay ultraendurance mountain bike race (approximately 20 min cycling, approximately 60 min recovery), and 2) examine physiological and performance based changes throughout the HIU event. Prior to the HIU event, four highly-trained male cyclists (age = 24.0 +/- 2.1 yr; mass = 75.0 +/- 2.7 kg; VO2peak = 70 +/- 3 ml x kg(-1) x min(-1)) performed 1) a progressive exercise test to determine peak volume of oxygen uptake (VO2peak), peak power output (PPO), and ventilatory threshold (T(vent)), 2) time-to-fatigue tests at 100% (TF100) and 150% of PPO (TF150), and 3) a laboratory simulated 40-km time trial (TT40). Blood lactate (Lac(-)), haematocrit and haemoglobin were measured at 6-h intervals throughout the HIU event, while heart rate (HR) was recorded continuously. Intermittent HIU performance, performance HR, recovery HR, and Lac(-) declined (P < 0.05), while plasma volume expanded (P < 0.05) during the HIU event. TF100 was related to the decline in lap time (r = -0.96; P < 0.05), and a trend (P = 0.081) was found between TF150 and average intermittent HIU speed (r = 0.92). However, other measures (VO2peak, PPO, T(vent), and TT40) were not related to HIU performance. Measures of high-intensity endurance performance (TF100, TF150) were better predictors of intermittent HIU performance than traditional laboratory-based measures of aerobic capacity.

Bcl-2 levels are increased in endothelial cells by antioxidant supplementation but not exercise training

The efficacy of antioxidant supplementation in the prevention of cardiovascular disease appears equivocal, however the use of more potent antioxidant combinations than those traditionally used may exert a more positive effect. We have shown previously that supplementation of vitamin E and α-lipoic acid increases cardiac performance during post-ischemia reperfusion in older rats and increases Bcl-2 levels in endothelial cells. The purpose of this study was to examine the effects of vitamin E and α-lipoic acid supplementation on myocardial gene expression with a view to determine their mechanism of action. Young male rats received either a control (n=7) or vitamin E and α-lipoic acid supplemented diet (n=8) for 14 weeks. RNA from myocardial tissue was then amplified and samples were pooled within groups and competitively hybridized to 8.5K oligonucleotide rat microarrays. The relative expression of each gene was then compared to the control sample. Animals that received the antioxidant-supplemented diet exhibited upregulation (>1.5×) of 13 genes in the myocardium with 2 genes downregulated. Upregulated genes include those involved in cell growth and maintenance (LynB, Csf1r, Akt2, Tp53), cell signaling (LynB, Csf1r) and signal transduction (Pacsin2, Csf1r). Downregulated genes encode thyroid (Thrsp) and F-actin binding proteins (Nexilin).Duchenne muscular dystrophy (DMD) is a fatal neuromuscular condition affecting approximately one in 3500 live male births resulting from the lack of the myocyte protein dystrophin. The absence of dystrophin in cardiac myocytes is associated with calcium overload which in turn activates calcium-dependent proteolytic enzymes contributing to congestive heart failure, muscle necrosis and fibrosis. To date, the basis for the calcium overload has not been determined. Since L-type calcium channels are a major mediator of calcium influx we determined their potential contribution to the calcium overload. Male muscular dystrophy (mdx) mice and control C57BL10ScSn (C57) mice aged 12– 16 weeks were used in all experiments. In tissue bath studies, isolated contracting left atria from mdx revealed a reduced potency to the dihydropyridine (DHP) agonist BayK8644 and antagonist nifedipine (P < 0.05). Similarly, radioligand binding studies using the DHP antagonist [3H]-PN 200-110 showed a reduced potency (P < 0.05) in isolated membranes, associated with an increased receptor density (P < 0.05). The increased receptor density was supported by RT-PCR experiments revealing increased RNAfor the DHP receptor. Patch clamp studies revealed the presence of a diltiazem sensitive calcium current that showed delayed inactivation in isolated mdx myocytes (P < 0.01). In conclusion, the increased number of DHP binding sites and the delay in L-type current inactivation may both contribute to increased calcium influx and hence calcium overload in the dystrophin deficient mdx cardiac myocytes.