Cardiac Output and Performance during a Marathon Race in Middle-Aged Recreational Runners

Purpose. Despite the increasing popularity of marathon running, there are no data on the responses of stroke volume (SV) and cardiac output (CO) to exercise in this context. We sought to establish whether marathon performance is associated with the ability to sustain high fractional use of maximal SV and CO (i.e, cardiac endurance) and/or CO, per meter (i.e., cardiac cost). Methods. We measured the SV, heart rate (HR), CO, and running speed of 14 recreational runners in an incremental, maximal laboratory test and then during a real marathon race (mean performance: 3 hr 30 min ± 45 min). Results. Our data revealed that HR, SV and CO were all in a high but submaximal steady state during the marathon (87.0 ± 1.6%, 77.2 ± 2.6%, and 68.7 ± 2.8% of maximal values, respectively). Marathon performance was inversely correlated with an upward drift in the CO/speed ratio (mL of CO × m−1) (r = −0.65, P < 0.01) and positively correlated with the runner's ability to complete the race at a high percentage of the speed at maximal SV (r = 0.83, P < 0.0002). Conclusion. Our results showed that marathon performance is inversely correlated with cardiac cost and positively correlated with cardiac endurance. The CO response could be a benchmark for race performance in recreational marathon runners

Myostatin is a key mediator between energy metabolism and endurance capacity of skeletal muscle

Myostatin (Mstn) participates in the regulation of skeletal muscle size and has emerged as a regulator of muscle metabolism. Here, we hypothesized that lack of myostatin profoundly depresses oxidative phosphorylation-dependent muscle function. Toward this end, we explored Mstn/ mice as a model for the constitutive absence of myostatin and AAV-mediated overexpression of myostatin propeptide as a model of myostatin blockade in adult wild-type mice. We show that muscles from Mstn/ mice, although larger and stronger, fatigue extremely rapidly. Myostatin deficiency shifts muscle from aerobic toward anaerobic energy metabolism, as evidenced by decreased mitochondrial respiration, reduced expression of PPAR transcriptional regulators, increased enolase activity, and exercise-induced lactic acidosis. As a consequence, constitutively reduced myostatin signaling diminishes exercise capacity, while the hypermuscular state of Mstn/ mice increases oxygen consumption and the energy cost of running. We wondered whether these results are the mere consequence of the congenital fiber-type switch toward a glycolytic phenotype of constitutive Mstn/ mice. Hence, we overexpressed myostatin propeptide in adult mice, which did not affect fiber-type distribution, while nonetheless causing increased muscle fatigability, diminished exercise capacity, and decreased Pparb/d and Pgc1a expression. In conclusion, our results suggest that myostatin endows skeletal muscle with high oxidative capacity and low fatigability, thus regulating the delicate balance between muscle mass, muscle force, energy metabolism, and endurance capacity

A new incremental test for VO2max accurate measurement by increasing VO2max plateau duration, allowing the investigation of its limiting factors

International audienceThe purpose of this study was to (1) validate anew exercise protocol for accurate measurement of VO2max by obtention of a VO2max plateau for all subjects fit and unfit (2) test the hypothesis that VO 2max plateau duration is not correlated with VO2max and (3) verify that limiting factors of VO2max plateau duration are different from those of VO2max amplitude. Therefore, 14 subjects performed two incremental cycling tests (1) a classical incremental test (CIT) to determine VO2max, the power at VO2max (PVO 2max) and at the lactate threshold (PLT) (2) a new incremental test (NIT) in which the power was decreased just after the subject reached VO 2max. During both protocols, heart rate, stroke volume, cardiac output, the arterio-venous difference and the oxygen blood saturation were recorded. The results showed that, with the NIT, subject could maintain along VO2max plateau (6 ± 3 min), even those who could not reach VO2max plateau at the end of CIT (n = 5). The VO2max plateau duration was not correlated with VO2max amplitude which was correlated with the power at SVmax (r = 0.888, pandlt;0.001). The VO2max plateau duration was correlated with the power decrease (W/s) during the VO2max plateau (r = -0.72, p = 0.003) but not with cardiac-related factors nor with PVO2max. In conclusion, these experiments showed that it was possible to get a long VO2max plateau at the end of NIT whatever the individual VO2max amplitude was. The limiting factor of VO2max duration was the power output. © 2011 Springer-Verlag

Validation of a ramp running protocol for determination of the true VO2max in mice

International audienceIn the field of comparative physiology, it remains to be established whether the concept of VO2max is valid in the mouse and, if so, how this value can be accurately determined. In humans, VO2max is generally considered to correspond to the plateau observed when VO2 no longer rises with an increase in workload. In contrast, the concept of VO2peak tends to be used in murine studies. The objectives of the present study were to determine whether (i) a continuous ramp protocol yielded a higher VO2peak than a stepwise, incremental protocol, and (ii) the VO2peak measured in the ramp protocol corresponded to VO2max. The three protocols (based on intensity-controlled treadmill running until exhaustion with eight female FVB/N mice) were performed in random order (a) an incremental protocol that begins at 10 m.min-1 speed and increases by 3 m.min-1 every 3 min. (b) a ramp protocol with slow acceleration (3 m.min-2), and (c) a ramp protocol with fast acceleration (12 m.min-2). Each protocol was performed with two slopes (0 and 25°). Hence, each mouse performed six exercise tests. We found that the value of VO2peak was protocol-dependent (p andlt; 0.05) and was highest (59.0 ml.kg 0.75.min-1) for the 3 m.min-2 0° ramp protocol. In the latter, the presence of a VO2max plateau was associated with the fulfillment of two secondary criteria (a blood lactate concentration andgt; 8 mmol.l-1 and a respiratory exchange ratio andgt; 1). The total duration of the 3 m.min-2 0° ramp protocol was shorter than that of the incremental protocol. Taken as a whole, our results suggest that VO2max in the mouse is best determined by applying a ramp exercise protocol with slow acceleration and no treadmill slope. © 2016 Ayachi, Niel, Momken, Billat and Mille-Hamard