The generalized force-velocity relationship explains why the preferred pedaling rate of cyclists exceeds the most efficient one

The most efficient pedaling rate (lowest oxygen consumption) at a workload of 50-300W has been reported to be in the range of 42-60rpm. By contrast, most competitive cyclists prefer a pedaling rate of more than 90rpm. The reason for this difference is still unknown. We assume that the high pedaling rate preferred by cyclists can be explained by the inherent properties of muscle fibers. To obtain statements which do not depend on muscle's cross-section and length, we generalized Hill's characteristic equations where muscle force and heat liberation are related to shortening velocity. A pedaling rate of f ηmax yields to maximal efficiency, whereas the higher pedaling rate f Pmax leads to maximal power. The ratio f Pmax/f ηmax between these two pedaling rates ranges from 1.7 to 2.4, and it depends on the muscle's fiber-type composition. In sprints and competitions of very short duration, f Pmax is more advantageous because energy supply is not the predominant limiting factor. The price to be paid for the most powerful pedaling rate is lower efficiency and higher energy cost. In longer exercises, economy is more important and the optimal pedaling rate shifts toward f ηmax. We conclude that the optimal pedaling rate, representing the fastest race performance, is not fixed but depends on race duration; it ranges between f ηmax and f Pmax. Our results are not only of interest for competitive cyclists but also for investigations using cycle ergometers: maximum power might not be reached by using a pedaling rate near the most efficient on

New fundamental resistance exercise determinants of molecular and cellular muscle adaptations

Physical activity relies on muscular force. In adult skeletal muscle, force results from the contraction of postmitotic, multinucleated myofibres of different contractile and metabolic properties. Myofibres can adapt to (patho-)physiological conditions of altered functional demand by radial growth, longitudinal growth, and regulation of fibre type functional gene modules. The adaptation's specificity depends on the distinct molecular and cellular events triggered by unique combinations of conditional cues. In order to derive effective and tailored exercise prescriptions, it must be determined (1) which mechano-biological condition leads to what molecular/cellular response, and (2) how this molecular/cellular response relates to the structural, contractile, and metabolic adaptation. It follows that a thorough mechano-biological description of the loading condition is imperative. Unfortunately, the definition of (resistance) exercise conditions in the past and present literature is insufficient. It is classically limited to load magnitude, number of repetitions and sets, rest in-between sets, number of interventions/week, and training period. In this review, we show why the current description is insufficient, and identify new determinants of quantitative and/or qualitative effects on skeletal muscle with respect to resistance exercise in healthy, adult humans. These new mandatory determinants comprise the fractional and temporal distribution of the contraction modes per repetition, duration of one repetition, rest in-between repetitions, time under tension, muscular failure, range of motion, recovery time, and anatomical definition. We strongly recommend to standardise the design and description of all future resistance exercise investigations by using the herein proposed set of 13 mechano-biological determinants (classical and new ones

Glycogen reduction in non-exercising muscle depends on blood lactate concentration

The purpose of this study was to determine for the first time by repeated non-invasive 13C-NMR spectrometry whether blood lactate concentration affects glycogen reduction in non-exercising muscle during prolonged (6h) physical exercise in healthy adult males. Such an effect would indirectly show that glycogenolysis independent of nervous activation occurs in non-exercising muscle. After an overnight fast, 12 subjects performed alternating one-leg cycle exercise and arm cranking exercise at an average work load of 106 (SD 26)W [63 (9)% maximum oxygen consumption for one-leg exercise] and 69 (13)W [61 (10)% maximum oxygen consumption for arm cranking exercise], respectively. During the 6-h exercise test, glycogen concentration of the non-exercising calf muscle decreased by 17 (7)% while the glycogen concentration in the exercising calf muscle decreased by 45 (8)%. In a resting control group (n=6), the glycogen concentration did not decrease significantly. The higher the exercise intensity and therefore blood lactate concentration, the smaller was the glycogen reduction in the non-exercising calf muscles. We conclude that during prolonged physical exercise glycogenolysis in non-exercising human muscles decreases as exercise intensity increase contrary to exercising muscles. This observation might be an indirect evidence for a non-exercise induced glycogenolysis in inactive muscle

The energetically optimal cadence decreases after prolonged cycling exercise

This study investigated the change in the energetically optimal cadence after prolonged cycling. The energetically optimal cadence (EOC) was determined in 14 experienced cyclists by pulmonary gas exchange at six different cadences (100-50rpm at 10rpm intervals). The determination of the EOC was repeated after a prolonged cycling exercise of 55min duration, where cadence was fixed either at high (>95rpm) or low (<55rpm) pedalling rates. The EOC decreased after prolonged cycling exercise at a high as well as at a low fixed cadence (P<0.01). According to the generalized muscle equations of Hill, this indicates that most likely more type I muscle fibres contribute to muscular power output after fatiguing cycling exercise compared to cycling in the beginning of an exercise bout. We suggest that the determination of EOC might be a potential non-invasive method to detect the qualitative changes in activated muscle fibres, which needs further investigatio

Non-invasive haemodynamic assessments using Innocor™ during standard graded exercise tests

Cardiac output (Q) and stroke volume (V S) represent primary determinants of cardiovascular performance and should therefore be determined for performance diagnostics purposes. Since it is unknown, whether measurements of Q and V S can be performed by means of Innocor™ during standard graded exercise tests (GXTs), and whether current GXT stages are sufficiently long for the measurements to take place, we determined Q and V S at an early and late point in time on submaximal 2min GXT stages. 16 male cyclists (age 25.4±2.9years, body mass 71.2±5.0kg) performed three GXTs and we determined Q and V S after 46 and 103s at 69, 77, and 85% peak power. We found that the rebreathings could easily be incorporated into the GXTs and that Q and V S remained unchanged between the two points in time on the same GXT stage (69% peak power, Q: 18.1±2.1 vs. 18.2±2.3lmin−1, V S: 126±18 vs. 123±21ml; 77% peak power, Q: 20.7±2.6 vs. 21.0±2.3lmin−1, V S: 132±18 vs. 131±18ml; 85% peak power, Q: 21.6±2.4 vs. 21.8±2.7lmin−1, V S: 131±17 vs. 131±22ml). We conclude that Innocor™ may be a useful device for assessing Q and V S during GXTs, and that the adaptation of Q and V S to exercise-to-exercise transitions at moderate to high submaximal power outputs is fast enough for 1 and 2min GXT stage duration

Time to exhaustion at maximal lactate steady state is similar for cycling and running in moderately trained subjects

We compared time to exhaustion (t lim) at maximal lactate steady state (MLSS) between cycling and running, investigated if oxygen consumption, ventilation, blood lactate concentration, and perceived exertion differ between the exercise modes, and established whether MLSS can be determined for cycling and running using the same criteria. MLSS was determined in 15 moderately trained men (30±6years, 77±6kg) by several constant-load tests to exhaustion in cycling and running. Heart rate, oxygen consumption, and ventilation were recorded continuously. Blood lactate concentration and perceived exertion were measured every 5min. t lim (37.7±8.9 vs. 34.4±5.4min) and perceived exertion (7.2±1.7 vs. 7.2±1.5) were similar for cycling and running. Heart rate (165±8 vs. 175±10min−1; P<0.01), oxygen consumption (3.1±0.3 vs. 3.4±0.3lmin−1; P<0.001) and ventilation (93±12 vs. 103±16lmin−1; P<0.01) were lower for cycling compared to running, respectively, whereas blood lactate concentration (5.6±1.7 vs. 4.3±1.3mmoll−1; P<0.05) was higher for cycling. t lim at MLSS is similar for cycling and running, despite absolute differences in heart rate, ventilation, blood lactate concentration, and oxygen consumption. This may be explained by the relatively equal cardiorespiratory demand at MLSS. Additionally, the similar t lim for cycling and running allows the same criteria to be used for determining MLSS in both exercise mode

l -Carnitine and the recovery from exhaustive endurance exercise: a randomised, double-blind, placebo-controlled trial

We hypothesised that l-carnitine could accelerate recovery from exhaustive exercise since increased blood l-carnitine concentrations elicit a vasodilation in isolated animal vessels as well as in patients with peripheral vascular or coronary artery disease during exercise. Twelve subjects received either 2g l-carnitine or a placebo in a study which was double-blind and crossover in design. Two hours after administration, the subjects performed a constant-load exercise test (CET1) cycling at their individual anaerobic threshold to exhaustion. Three hours later this test was repeated (CET2). After 4-14 days, each subject performed the same cycling tests after having taken the other substance. Exercise times of the 12 subjects were identical with l-carnitine (CET1: 21.3±5.7min; CET2: 21.4±5.3min) and placebo (CET1: 21.9±6.2min; CET2: 20.4±4.8min). Also, heart rate, oxygen consumption, respiratory exchange ratio, and blood lactate concentration were identical. In conclusion, 2g of L-carnitine taken 2h before a first of two constant-load exercise tests had no influence on the second tests performed 3h after the first test compared with placeb

Cardiac output but not stroke volume is similar in a Wingate and V˙O2peak \dot{V}{\text{O}}_{{ 2 {\text{peak}}}} test in young men

Wingate test (WT) training programmes lasting 2-3weeks lead to improved peak oxygen consumption. If a single 30s WT was capable of significantly increasing stroke volume and cardiac output, the increase in peak oxygen consumption could possibly be explained by improved oxygen delivery. Thus, we investigated whether a single WT increases stroke volume and cardiac output to similar levels than those obtained at peak exercise during a graded cycling exercise test (GXT) to exhaustion. Fifteen healthy young men (peak oxygen consumption 45.0±5.3mlkg−1min−1) performed one WT and one GXT on separate days in randomised order. During the tests, we estimated cardiac output using inert gas rebreathing (nitrous oxide and sulphur hexafluoride) and subsequently calculated stroke volume. We found that cardiac output was similar (18.2±3.3 vs. 17.9±2.6lmin−1; P=0.744), stroke volume was higher (127±37 vs. 94±15ml; P<0.001), and heart rate was lower (149±26 vs. 190±12 beatsmin−1; P<0.001) at the end (27±2s) of a WT as compared to peak exercise during a GXT. Our results suggest that a single WT produces a haemodynamic response which is characterised by similar cardiac output, higher stroke volume and lower heart rate as compared to peak exercise during a GX

Task failure from inspiratory resistive loaded breathing: a role for inspiratory muscle fatigue?

The use of non-invasive resistive breathing to task failure to assess inspiratory muscle performance remains a matter of debate. CO2 retention rather than diaphragmatic fatigue was suggested to limit endurance during inspiratory resistive breathing. Cervical magnetic stimulation (CMS) allows discrimination between diaphragmatic and rib cage muscle fatigue. We tested a new protocol with respect to the extent and the partitioning of inspiratory muscle fatigue at task failure. Nine healthy subjects performed two runs of inspiratory resistive breathing at 67 (12)% of their maximal inspiratory mouth pressure, respiratory rate ( f R), paced at 18min-1, with a 15-min pause between runs. Diaphragm and rib cage muscle contractility were assessed from CMS-induced esophageal (P es,tw), gastric (P ga,tw), and transdiaphragmatic (P di,tw) twitch pressures. Average endurance times of the first and second runs were similar [9.1 (6.7)and 8.4 (3.5)min]. P di,tw significantly decreased from 33.1 to 25.9cmH2O in the first run, partially recovered (27.6cmH2O), and decreased further in the second run (23.4cmH2O). P es,tw also decreased significantly (-5.1 and -2.4cmH2O), while P ga,tw did not change significantly (-2.0 and -1.9cmH2O), indicating more pronounced rib cage rather than diaphragmatic fatigue. End-tidal partial pressure of CO2 (P ETCO2) rose from 37.2 to 44.0 and 45.3mmHg, and arterial oxygen saturation (S aO2) decreased in both runs from 98% to 94%. Thus, task failure in mouth-pressure-targeted, inspiratory resistive breathing is associated with both diaphragmatic and rib cage muscle fatigue. Similar endurance times despite different degrees of muscle fatigue at the start of the runs indicate that other factors, e.g. increases in P ETCO2, and/or decreases in S aO2, probably contributed to task-failur

Further glycogen decrease during early recovery after eccentric exercise despite a high carbohydrate intake

Summary. : Background: : Delayed onset muscle soreness (DOMS) is a well-known phenomenon of athletes. It has been reported from muscle biopsies that the rate of muscle glycogen resynthesis is reduced after eccentric compared to concentric exercise. Aim of the study: : Try to compensate by a carbohydrate (CHO)-rich diet the decelerated glycogen resynthesis after eccentric exercise, measured by magnetic resonance spectroscopy. Methods: : Glycogen, phosphocreatine, ATP, and Pi were measured in the human calf muscle. Twenty athletes divided into two groups (DOMS and CONTROL), reduced glycogen in M. gastrocnemius during two different running protocols. Additionally, 12 DOMS subjects performed an eccentric exercise while the CONTROL group rested. Subsequently, subjects consumed a CHO-rich diet (> 10 g/kg body mass/24 h). Results: : In both groups, glycogen has been reduced by about 50%. The first 2 h after exercise, glycogen dropped further (-15.6 ± 15.7 mmol/ kg ww) in the DOMS but rose by +18.4 ± 20.8 mmol/kg ww in the CONTROL group (P < 0.001). CONTROL subjects reached resting glycogen within 24 h (137 ± 47mmol/kg ww), while DOMS subjects needed more than one day (91 ± 23mmol/kgww; P < 0.001). Pi and Pi/PCr, indicators of muscle injury, rose significantly in the DOMS but not in the CONTROL group. Conclusion: : The diet rich in CHO's was not able to refill glycogen stores after eccentric exercise. Glycogen decreased even further during the beginning of recovery. This loss, which to our knowledge has not been measured before is probably the consequence of muscle cell damage and their reparatio