Mid Sweden University

Background: Sprint events in cross-country skiing are unique not only with respect to their length (0.8–1.8 km), but also in involving four high-intensity heats of ~3 min in duration, separated by a relatively short recovery period (15–60 min). Objective: Our aim was to systematically review the scientific literature to identify factors related to the performance of elite sprint cross-country skiers. Methods: Four electronic databases were searched using relevant medical subject headings and keywords, as were reference lists, relevant journals, and key authors in the field. Only original research articles addressing physiology, biomechanics, anthropometry, or neuromuscular characteristics and elite sprint cross-country skiers and performance outcomes were included. All articles meeting inclusion criteria were quality assessed. Data were extracted from each article using a standardized form and subsequently summarized. Results: Thirty-one articles met the criteria for inclusion, were reviewed, and scored an average of 66 ± 7 % (range 56–78 %) upon quality assessment. All articles except for two were quasi-experimental, and only one had a fully-experimental research design. In total, articles comprised 567 subjects (74 % male), with only nine articles explicitly reporting their skiers’ sprint International Skiing Federation points (weighted mean 116 ± 78). A similar number of articles addressed skating and classical techniques, with more than half of the investigations involving roller-skiing assessments under laboratory conditions. A range of physiological, biomechanical, anthropometric, and neuromuscular characteristics was reported to relate to sprint skiing performance. Both aerobic and anaerobic capacities are important qualities, with the anaerobic system suggested to contribute more to the performance during the first of repeated heats; and the aerobic system during subsequent heats. A capacity for high speed in all the following instances is important for the performance of sprint cross-country skiers: at the start of the race, at any given point when required (e.g., when being challenged by a competitor), and in the final section of each heat. Although high skiing speed is suggested to rely primarily on high cycle rates, longer cycle lengths are commonly observed in faster skiers. In addition, faster skiers rely on different technical strategies when approaching peak speeds, employ more effective techniques, and use better coordinated movements to optimize generation of propulsive force from the resultant ski and pole forces. Strong uphill technique is critical to race performance since uphill segments are the most influential on race outcomes. A certain strength level is required, although more does not necessarily translate to superior sprint skiing performance, and sufficient strength-endurance capacities are also of importance to minimize the impact and accumulation of fatigue during repeated heats. Lastly, higher lean mass does appear to benefit sprint skiers’ performance, with no clear advantage conferred via body height and mass. Limitations: Generalization of findings from one study to the next is challenging considering the array of experimental tasks, variables defining performance, fundamental differences between skiing techniques, and evolution of sprint skiing competitions. Although laboratory-based measures can effectively assess on-snow skiing performance, conclusions drawn from roller-skiing investigations might not fully apply to on-snow skiing performance. A low number of subjects were females (only 17 %), warranting further studies to better understand this population. Lastly, more training studies involving high-level elite sprint skiers and investigations pertaining to the ability of skiers to maintain high-sprint speeds at the end of races are recommended to assist in understanding and improving high-level sprint skiing performance, and resilience to fatigue. Conclusions: Successful sprint cross-country skiing involves well-developed aerobic and anaerobic capacities, high speed abilities, effective biomechanical techniques, and the ability to develop high forces rapidly. A certain level of strength is required, particularly ski-specific strength, as well as the ability to withstand fatigue across the repeated heats of sprint races. Cross-country sprint skiing is demonstrably a demanding and complex sport, where high-performance skiers need to simultaneously address physiological, biomechanical, anthropometric, and neuromuscular aspects to ensure success.

Key points: We investigated whether intramuscular temperature affects the acute recovery of exercise performance following fatigue-induced by endurance exercise. Mean power output was better preserved during an all-out arm-cycling exercise following a 2 h recovery period in which the upper arms were warmed to an intramuscular temperature of ˜ 38°C than when they were cooled to as low as 15°C, which suggested that recovery of exercise performance in humans is dependent on muscle temperature. Mechanisms underlying the temperature-dependent effect on recovery were studied in intact single mouse muscle fibres where we found that recovery of submaximal force and restoration of fatigue resistance was worsened by cooling (16-26°C) and improved by heating (36°C). Isolated whole mouse muscle experiments confirmed that cooling impaired muscle glycogen resynthesis. We conclude that skeletal muscle recovery from fatigue-induced by endurance exercise is impaired by cooling and improved by heating, due to changes in glycogen resynthesis rate.

Manipulation of muscle temperature is believed to improve post-exercise recovery, with cooling being especially popular among athletes. However, it is unclear whether such temperature manipulations actually have positive effects. Accordingly, we studied the effect of muscle temperature on the acute recovery of force and fatigue resistance after endurance exercise. One hour of moderate-intensity arm cycling exercise in humans was followed by 2 h recovery in which the upper arms were either heated to 38°C, not treated (33°C), or cooled to ∼15°C. Fatigue resistance after the recovery period was assessed by performing 3 × 5 min sessions of all-out arm cycling at physiological temperature for all conditions (i.e. not heated or cooled). Power output during the all-out exercise was better maintained when muscles were heated during recovery, whereas cooling had the opposite effect. Mechanisms underlying the temperature-dependent effect on recovery were tested in mouse intact single muscle fibres, which were exposed to ∼12 min of glycogen-depleting fatiguing stimulation (350 ms tetani given at 10 s interval until force decreased to 30% of the starting force). Fibres were subsequently exposed to the same fatiguing stimulation protocol after 1-2 h of recovery at 16-36°C. Recovery of submaximal force (30 Hz), the tetanic myoplasmic free [Ca2+] (measured with the fluorescent indicator indo-1), and fatigue resistance were all impaired by cooling (16-26°C) and improved by heating (36°C). In addition, glycogen resynthesis was faster at 36°C than 26°C in whole flexor digitorum brevis muscles. We conclude that recovery from exhaustive endurance exercise is accelerated by raising and slowed by lowering muscle temperature.

Abstract: Hyperoxia results from the inhalation of mixtures of gas containing higher partial pressures of oxygen (O2) than normal air at sea level. Exercise in hyperoxia affects the cardiorespiratory, neural and hormonal systems, as well as energy metabolism in humans. In contrast to short-term exposure to hypoxia (i.e. a reduced partial pressure of oxygen), acute hyperoxia may enhance endurance and sprint interval performance by accelerating recovery processes. This narrative literature review, covering 89 studies published between 1975 and 2016, identifies the acute ergogenic effects and health concerns associated with hyperoxia during exercise; however, long-term adaptation to hyperoxia and exercise remain inconclusive. The complexity of the biological responses to hyperoxia, as well as the variations in (1) experimental designs (e.g. exercise intensity and modality, level of oxygen, number of participants), (2) muscles involved (arms and legs) and (3) training status of the participants may account for the discrepancies.

Intense exercise training is a powerful stimulus that activates mitochondrial biogenesis pathways and thus increases mitochondrial density and oxidative capacity. Moderate levels of reactive oxygen species (ROS) during exercise are considered vital in the adaptive response, but high ROS production is a serious threat to cellular homeostasis. Although biochemical markers of the transition from adaptive to maladaptive ROS stress are lacking, it is likely mediated by redox sensitive enzymes involved in oxidative metabolism. One potential enzyme mediating such redox sensitivity is the citric acid cycle enzyme aconitase. In this study, we examined biopsy specimens of vastus lateralis and triceps brachii in healthy volunteers, together with primary human myotubes. An intense exercise regimen inactivated aconitase by 55-72%, resulting in inhibition of mitochondrial respiration by 50-65%. In the vastus, the mitochondrial dysfunction was compensated for by a 15-72% increase in mitochondrial proteins, whereas H2O2 emission was unchanged. In parallel with the inactivation of aconitase, the intermediary metabolite citrate accumulated and played an integral part in cellular protection against oxidative stress. In contrast, the triceps failed to increase mitochondrial density, and citrate did not accumulate. Instead, mitochondrial H2O2 emission was decreased to 40% of the pretraining levels, together with a 6-fold increase in protein abundance of catalase. In this study, a novel mitochondrial stress response was highlighted where accumulation of citrate acted to preserve the redox status of the cell during periods of intense exercise.

To elucidate the mechanisms underlying the differences in adaptation of arm and leg muscles to sprint training, over a period of 11 days 16 untrained men performed six sessions of 4-6 x 30-s all-out sprints (SIT) with the legs and arms, separately, with a 1-h interval of recovery. Limb-specific VO(2)peak, sprint performance (two 30-s Wingate tests with 4-min recovery), muscle efficiency and time-trial performance (TT, 5-min all-out) were assessed and biopsies from the m. vastus lateralis and m. triceps brachii taken before and after training. VO(2)peak and Wmax increased 3-11% after training, with a more pronounced change in the arms (P < 0.05). Gross efficiency improved for the arms (+8.8%, P < 0.05), but not the legs (-0.6%). Wingate peak and mean power outputs improved similarly for the arms and legs, as did TT performance. After training, VO2 during the two Wingate tests was increased by 52 and 6% for the arms and legs, respectively (P < 0.001). In the case of the arms, VO2 was higher during the first than second Wingate test (64 vs. 44%, P < 0.05). During the TT, relative exercise intensity, HR, VO2, VCO2, V-E, and V-t were all lower during arm-cranking than leg-pedaling, and oxidation of fat was minimal, remaining so after training. Despite the higher relative intensity, fat oxidation was 70% greater during leg-pedaling (P = 0.017). The aerobic energy contribution in the legs was larger than for the arms during the Wingate tests, although VO2 for the arms was enhanced more by training, reducing the O-2 deficit after SIT. The levels of muscle glycogen, as well as the myosin heavy chain composition were unchanged in both cases, while the activities of 3-hydroxyacyl-CoA-dehydrogenase and citrate synthase were elevated only in the legs and capillarization enhanced in both limbs. Multiple regression analysis demonstrated that the variables that predict TT performance differ for the arms and legs. The primary mechanism of adaptation to SIT by both the arms and legs is enhancement of aerobic energy production. However, with their higher proportion of fast muscle fibers, the arms exhibit greater plasticity.

Introduction

This study was designed to determine whether elevated muscle temperature allows muscles to recover their force or power more rapidly following fatigue

Methods

Intact single fibers from mouse flexor digitorum brevis muscle were fatigued at 31˚C (70-Hz 350-ms tetani once every 10s until initial force decreased to 30%).  During a subsequent 2-hr recovery period, the fibers were perfused in Tyrode solution at either 31°C (physiological temperature) or 36°C and isometric force and cytoplasmic free [Ca²⁺] ([Ca²⁺]_i) were measured during 30-Hz tetani evoked periodically.  In addition, seven human subjects performed fatiguing arm exercise consisting of 3 x 5min maximal effort arm cycling at 100 rpm followed by 4 x 15 min at an intensity of 50% of VO_2peak. Then followed 2hr of recovery during which both arms were either heated or not heated at 5˚C above physiological temperatures using arm cuffs continuously perfused with temperature-regulated water; the order of heating vs. not heating was randomized between two visits. Intramuscular temperature was recorded with probes inserted 1.5 cm into the lateral head of the triceps brachii muscle. During the recovery period, subjects consumed 1.0 g/hr/kg body weight carbohydrates to support glycogen repletion. After recovery, the subjects repeated the 3 x 5 min time trials to evaluate the effect of the recovery intervention.

Results

Recovery from fatigue in mouse single fibers was dependent on muscle glycogen restoration since fibers perfused with glucose-free Tyrode did not recover contractile force (P<0.05). After 30 min of recovery, the tetanic [Ca²⁺]_i was 107±10% and 92 ± 8% and the corresponding forces were 69±15% vs.49±14% of the initial values for the heated and non-heated muscles, respectively.  In seven human subjects, 2h of muscle heating also appeared to improve muscle recovery, leading to higher mean power output in the post-recovery arm cycling time trial than without muscle heating.

Discussion

Elevating muscle temperature by 5°C above physiological temperature accelerates recovery in mouse muscle in-vitro and in human skeletal muscle in-vivo and this appears to depend on faster muscle glycogen resynthesis following fatigue.

Splenic contraction induced by repeated apneas has been shown to increase oxygen availability. Our aim was to determine whether repeated maximal voluntary apnea enhances the performance of cyclists in a subsequent 4-km time trial. Seven male cyclists [age: 27.1 +/- A 2.1 years; height: 182 +/- A 8 cm; body mass: 74.8 +/- A 9.2 kg; peak oxygen uptake: 56.9 +/- A 6.6 mL min(-1) kg(-1) (mean +/- A SD)] performed a 4-km time trial on an ergometer with and without four prior maximal bouts of apnea interspersed with 2 min of recovery. The average power output during the time trial was similar with (293 +/- A 48 W) and without (305 +/- A 42 W) prior apnea (P = 0.11, d = 0.27). The spleen was reduced in size after the fourth bout of apnea (-12.4 +/- A 9.0 %), as well as one (-36.6 +/- A 10.3 %) and 10 min (-19.5 +/- A 17.9 %) after the time trial, while with normal breathing the spleen was smaller one (-35.0 +/- A 11.3 %) and 10 min (-23.4 +/- A 19.7 %) after the time trial. Heart rate; oxygen uptake and carbon dioxide production; tissue oxygen saturation; and the lactate concentration, pH, oxygen saturation, level of hemoglobin and hematocrit of the blood were similar under both conditions. Our present findings reveal that four apneas by cyclists prior to a 4-km time trial led to splenic contraction, but no change in mean power output, the level of hemoglobin, hematocrit, oxygen saturation of the m. vastus lateralis or oxygen uptake.

Introduction

Interval cycle sprint training (SIT) has been shown to improve anaerobic capacity, VO₂max and biomarkers of muscle oxidative capacity in as little as 2 weeks in previously untrained adults. The present study was designed to characterize and compare systemic VO₂ and exercise performance after SIT engaging the arms and legs.

Methods

Sixteen healthy, untrained men (23.9 ± 3.7 yrs; 183.8 ± 6.8 cm; 80.3 ± 14.1 kg) performed six sessions of 4-6x30 sec all-out sprints with the legs then arms (or vice versa) separated by a 1-h recovery over an 11-day period. Limb-specific VO₂peak, anaerobic capacity (2x30-sec Wingate tests with 4 min of recovery), a 4-min submaximal work economy test, and a 5-min all-out time trial (TT) were conducted before and after the training program. Muscle biopsies (from the m. vastus lateralis and m. triceps brachii) were taken before and after the training period.

Results

VO₂peak increased by 10.6% and 5.9% with arm and leg training, respectively (p<0.05), with the increase in the arms significantly greater than in the legs (p=0.02). Work economy was improved for the arms (-9.8%, p<0.05), but not for the legs (-0.9%). Mean power during the TT rose by 13.5% for the arms and 11.8% for the legs (p<0.05). Peak power output and mean power during the two Wingate tests were elevated in both the arms (PPO: 6.7% (p<0.01) and 13.3% (p<0.01); MPO: 6.1% (p<0.01) and 8.4% (p<0.01)) and legs (PPO: 3.1% (p=0.07) and 7.1% (p=0.02); MPO: 3.3% (p<0.01) and 5.6% (p<0.01)). The activity of 3-hydroxyacyl-CoA dehydrogenase (HAD) and levels of muscle glycogen were unchanged in both limbs.

Discussion

Sprint interval training with arm or leg cycling exercise increased peak pulmonary VO₂ during their respective modes over an 11-day training period with a greater increase in the arms. Sprint performance rose to a similar extent in both extremities, yet work economy was improved only in the arms. These findings suggest some limb-specific responsiveness to SIT training.