Physiological characteristics of masters-level cyclists.

Although a considerable amount of research is available describing the physiological characteristics of competitive young-adult cyclists, research describing these same characteristics in Masters-level cyclists is rare. Therefore, the purpose of this study was to describe and compare the effect of aging on physiological fitness parameters of Masters-level cyclists in an attempt to provide normative fitness data. Thirty-two male cyclists (35-73 years) completed one 15-minute economy test and one graded exercise test (GXT) on a cycle ergometer. During the GXT, maximal oxygen uptake ([latin capital V with dot above]o2max), maximal heart rate (HRmax), the first (VT1) and second (VT2) ventilatory thresholds, and peak power output (PPO) were recorded. For the purpose of analysis, subjects were allocated into three age groups (35-45 years, 45-54 years, >=55 years). Maximal oxygen uptake and absolute PPO were significantly lower among subjects 55 years and older (45.9 +/- 4.6 mL x kg(-1) x min(-1) and 324 +/- 51 W, respectively) compared with the 45- to 54-year group (54.2 +/- 6.6 mL x kg(-1) x min(-1) and 392 +/- 36 W, respectively), and both were significantly less compared with the 35- to 44-year group (60.7 +/- 5.1 mL x kg(-1) x min(-1) and 434 +/- 32 W, respectively). Maximal heart rate was significantly greater in both the 35- to 44-year and 45- to 54-year age groups compared with the >=55-year group. The first ventilatory threshold was significantly greater in the subjects who were 55 years and older group compared with the 35- to 44-year and 45- to 54-year age groups, and VT2 was significantly greater in subjects 55 years and older compared with the 35- to 44-year group. Economy was not different amongst groups. In conclusion, increases in age resulted in a significant reduction in fitness parameters across age groups. The comparison of the fitness characteristics of Masters-level cyclists with established young-adult cyclist data should be avoided, because this may lead to inaccurate assessments of fitness.

Persistence of baroreceptor control of cerebral blood flow velocity at a simulated altitude of 5000 m.

OBJECTIVE: To assess the effects of acute exposure to simulated high altitude on baroreflex control of mean cerebral blood flow velocity (MCFV). PATIENTS AND METHODS: We compared beat-to-beat changes in RR interval, arterial blood pressure, mean MCFV (by transcranial Doppler velocimetry in the middle cerebral artery), end-tidal CO2, oxygen saturation and respiration in 19 healthy subjects at baseline (Albuquerque, 1779 m), after acute exposure to simulated high altitude in a hypobaric chamber (barometric pressure as at 5000 m) and during oxygen administration (to achieve 100% oxygen saturation) at the same barometric pressure (HOX). Baroreflex control on each signal was assessed by univariate and bivariate power spectral analysis performed on time series obtained during controlled (15 breaths/min) breathing, before and during baroreflex modulation induced by 0.1-Hz sinusoidal neck suction. RESULTS: At baseline, neck suction was able to induce a clear increase in low-frequency power in MCFV (P<0.001) as well as in RR and blood pressure. At high altitude, MCFV, as well as RR and blood pressure, was still able to respond to neck suction (all P<0.001), compared to controlled breathing alone, despite marked decreases in end-tidal CO2 and oxygen saturation at high altitude. A similar response was obtained at HOX. Phase delay analysis excluded a passive transmission of low-frequency oscillations from arterial pressure to cerebral circulation. CONCLUSIONS: During acute exposure to high altitude, cerebral blood flow is still modulated by the autonomic nervous system through the baroreflex, whose sensitivity is not affected by changes in CO2 and oxygen saturation levels.

Reliability and utility of a visual analog scale for the assessment of acute mountain sickness.

Acute mountain sickness (AMS) is a common condition that affects people that ascend too rapidly to high altitude. It is typically assessed with the Lake Louise AMS Self-report Score (LLSelf) that uses a categorical numeric rating scale to answer five questions addressing AMS-related symptoms, such as headache. A 100-mm visual analog scale (VAS) is commonly used to assess subjective phenomena such as pain, but this scale has never been used for the self-assessment of AMS. The purpose of this study was to compare a VAS score to the total LLSelf and to evaluate the test-retest and interrater reliability of the VAS when used as an assessment of AMS. Participants (N = 356) completed both the LLSelf and the VAS on the summit of Mt. Whitney (4419 m). There was a significant relationship (r = 0.65, p < 0.01) between the LLSelf (2.8 +/- 2.0, mean +/- SD) and the VAS (14.4 +/- 14.1 mm). Fifty-seven participants were randomly selected for reliability testing of the VAS. Both test-retest reliability (ICC = 0.996, 95% CI = 0.992 to 0.998) and interrater reliability (ICC = 1.000, 95% CI = 0.999 to 1.000) were high. The mean difference in the VAS score between tests was <1 mm, as was the difference between raters. These results demonstrate excellent reliability for the VAS as an assessment of AMS.

Mitochondrial efficiency and exercise economy following heat stress: a potential role of uncoupling protein 3.

Heat stress has been reported to reduce uncoupling proteins (UCP) expression, which in turn should improve mitochondrial efficiency. Such an improvement in efficiency may translate to the systemic level as greater exercise economy. However, neither the heat-induced improvement in mitochondrial efficiency (due to decrease in UCP), nor its potential to improve economy has been studied. Determine: (i) if heat stress in vitro lowers UCP3 thereby improving mitochondrial efficiency in C2C12 myocytes; (ii) whether heat acclimation (HA) in vivo improves exercise economy in trained individuals; and (iii) the potential improved economy during exercise at altitude. In vitro, myocytes were heat stressed for 24 h (40°C), followed by measurements of UCP3, mitochondrial uncoupling, and efficiency. In vivo, eight trained males completed: (i) pre-HA testing; (ii) 10 days of HA (40°C, 20% RH); and (iii) post-HA testing. Pre- and posttesting consisted of maximal exercise test and submaximal exercise at two intensities to assess exercise economy at 1600 m (Albuquerque, NM) and 4350 m. Heat-stressed myocytes displayed significantly reduced UCP3 mRNA expression and, mitochondrial uncoupling (77.1 ± 1.2%, P < 0.0001) and improved mitochondrial efficiency (62.9 ± 4.1%, P < 0.0001) compared to control. In humans, at both 1600 m and 4350 m, following HA, submaximal exercise economy did not change at low and moderate exercise intensities. Our findings indicate that while heat-induced reduction in UCP3 improves mitochondrial efficiency in vitro, this is not translated to in vivo improvement of exercise economy at 1600 m or 4350 m.

The science of cycling: physiology and training - part 1.

The aim of this review is to provide greater insight and understanding regarding the scientific nature of cycling. Research findings are presented in a practical manner for their direct application to cycling. The two parts of this review provide information that is useful to athletes, coaches and exercise scientists in the prescription of training regimens, adoption of exercise protocols and creation of research designs. Here for the first time, we present rationale to dispute prevailing myths linked to erroneous concepts and terminology surrounding the sport of cycling. In some studies, a review of the cycling literature revealed incomplete characterisation of athletic performance, lack of appropriate controls and small subject numbers, thereby complicating the understanding of the cycling research. Moreover, a mixture of cycling testing equipment coupled with a multitude of exercise protocols stresses the reliability and validity of the findings. Our scrutiny of the literature revealed key cycling performance-determining variables and their training-induced metabolic responses. The review of training strategies provides guidelines that will assist in the design of aerobic and anaerobic training protocols. Paradoxically, while maximal oxygen uptake (V-O(2max)) is generally not considered a valid indicator of cycling performance when it is coupled with other markers of exercise performance (e.g. blood lactate, power output, metabolic thresholds and efficiency/economy), it is found to gain predictive credibility. The positive facets of lactate metabolism dispel the 'lactic acid myth'. Lactate is shown to lower hydrogen ion concentrations rather than raise them, thereby retarding acidosis. Every aspect of lactate production is shown to be advantageous to cycling performance. To minimise the effects of muscle fatigue, the efficacy of employing a combination of different high cycling cadences is evident. The subconscious fatigue avoidance mechanism 'teleoanticipation' system serves to set the tolerable upper limits of competitive effort in order to assure the athlete completion of the physical challenge. Physiological markers found to be predictive of cycling performance include: (i) power output at the lactate threshold (LT2); (ii) peak power output (W(peak)) indicating a power/weight ratio of > or =5.5 W/kg; (iii) the percentage of type I fibres in the vastus lateralis; (iv) maximal lactate steady-state, representing the highest exercise intensity at which blood lactate concentration remains stable; (v) W(peak) at LT2; and (vi) W(peak) during a maximal cycling test. Furthermore, the unique breathing pattern, characterised by a lack of tachypnoeic shift, found in professional cyclists may enhance the efficiency and metabolic cost of breathing. The training impulse is useful to characterise exercise intensity and load during training and competition. It serves to enable the cyclist or coach to evaluate the effects of training strategies and may well serve to predict the cyclist's performance. Findings indicate that peripheral adaptations in working muscles play a more important role for enhanced submaximal cycling capacity than central adaptations. Clearly, relatively brief but intense sprint training can enhance both glycolytic and oxidative enzyme activity, maximum short-term power output and V-O(2max). To that end, it is suggested to replace approximately 15% of normal training with one of the interval exercise protocols. Tapering, through reduction in duration of training sessions or the frequency of sessions per week while maintaining intensity, is extremely effective for improvement of cycling time-trial performance. Overuse and over-training disabilities common to the competitive cyclist, if untreated, can lead to delayed recovery.

The science of cycling: factors affecting performance - part 2.

This review presents information that is useful to athletes, coaches and exercise scientists in the adoption of exercise protocols, prescription of training regimens and creation of research designs. Part 2 focuses on the factors that affect cycling performance. Among those factors, aerodynamic resistance is the major resistance force the racing cyclist must overcome. This challenge can be dealt with through equipment technological modifications and body position configuration adjustments. To successfully achieve efficient transfer of power from the body to the drive train of the bicycle the major concern is bicycle configuration and cycling body position. Peak power output appears to be highly correlated with cycling success. Likewise, gear ratio and pedalling cadence directly influence cycling economy/efficiency. Knowledge of muscle recruitment throughout the crank cycle has important implications for training and body position adjustments while climbing. A review of pacing models suggests that while there appears to be some evidence in favour of one technique over another, there remains the need for further field research to validate the findings. Nevertheless, performance modelling has important implications for the establishment of performance standards and consequent recommendations for training.

Mt. Whitney: determinants of summit success and acute mountain sickness.

PURPOSE: The aim of this study was to determine the prevalence of summit success and acute mountain sickness (AMS) on Mt. Whitney (4419 m) and to identify variables that contribute to both. METHODS: Hikers (N = 886) attempting the summit were interviewed at the trailhead upon their descent. Questionnaires included demographic and descriptive data, acclimatization and altitude history, and information specific to the ascent. The Lake Louise Self-Assessment Score was used to make a determination about the occurrence of AMS. Logistic regression techniques were used to calculate odds ratios (OR) for AMS and summit success. RESULTS: Forty-three percent of the sample met the criteria for AMS, and 81% reached the summit. The odds of experiencing AMS were reduced with increases in age (adjusted 10-yr OR = 0.78; P < 0.001), number of hours spent above 3000 m in the 2 wk preceding the ascent (adjusted 24-h OR = 0.71; P < 0.001), and for females (OR = 0.68; P = 0.02). Climbers who had a history of AMS (OR = 1.41; P = 0.02) and those taking analgesics (OR = 2.39; P < 0.001) were more likely to experience AMS. As climber age increased, the odds of reaching the summit decreased (adjusted 10-yr OR = 0.75; P < 0.001). However, increases in the number of hours per week spent training (adjusted 5-h OR = 1.24; P = 0.05), rate of ascent (adjusted 50 m x h(-1) OR = 1.13; P = 0.04), and previous high-altitude record (adjusted 500 m OR = 1.26; P < 0.001) were all associated with increased odds for summit success. CONCLUSIONS: A high percentage of trekkers reached the summit despite having symptoms of AMS.

Variables contributing to acute mountain sickness on the summit of Mt Whitney.

OBJECTIVE: The interaction of 15 variables representing physical characteristics, previous altitude exposure, and ascent data was analyzed to determine their contribution to acute mountain sickness (AMS). METHODS: Questionnaires were obtained from 359 volunteers upon reaching the summit of Mt Whitney (4419 m). Heart rate and arterial oxygen saturation were measured with a pulse oximeter, and AMS was identified by Lake Louise Self-Assessment scoring. Multiple logistic regression analysis was used to identify significant protective and risk factors for AMS. RESULTS: Thirty-three percent of the sample met the criteria for AMS. The odds of experiencing AMS were greater for those who reported a previous altitude illness (adjusted odds ratio [OR] = 2.00, P < .01) or who were taking analgesics during the ascent (adjusted OR = 2.09, P < .01). Odds for AMS decreased with increasing age (adjusted OR = 0.82, P < .0001), a greater number of climbs above 3000 m in the past month (adjusted OR = 0.92, P < .05), and use of acetazolamide during the ascent (adjusted OR = 0.33, P < .05). CONCLUSIONS: The significant determinants of AMS on the summit of Mt Whitney were age, a history of altitude illness, number of climbs above 3000 m in the past month, and use of acetazolamide and analgesics during ascent.

Biochemistry of exercise-induced metabolic acidosis.

The development of acidosis during intense exercise has traditionally been explained by the increased production of lactic acid, causing the release of a proton and the formation of the acid salt sodium lactate. On the basis of this explanation, if the rate of lactate production is high enough, the cellular proton buffering capacity can be exceeded, resulting in a decrease in cellular pH. These biochemical events have been termed lactic acidosis. The lactic acidosis of exercise has been a classic explanation of the biochemistry of acidosis for more than 80 years. This belief has led to the interpretation that lactate production causes acidosis and, in turn, that increased lactate production is one of the several causes of muscle fatigue during intense exercise. This review presents clear evidence that there is no biochemical support for lactate production causing acidosis. Lactate production retards, not causes, acidosis. Similarly, there is a wealth of research evidence to show that acidosis is caused by reactions other than lactate production. Every time ATP is broken down to ADP and P(i), a proton is released. When the ATP demand of muscle contraction is met by mitochondrial respiration, there is no proton accumulation in the cell, as protons are used by the mitochondria for oxidative phosphorylation and to maintain the proton gradient in the intermembranous space. It is only when the exercise intensity increases beyond steady state that there is a need for greater reliance on ATP regeneration from glycolysis and the phosphagen system. The ATP that is supplied from these nonmitochondrial sources and is eventually used to fuel muscle contraction increases proton release and causes the acidosis of intense exercise. Lactate production increases under these cellular conditions to prevent pyruvate accumulation and supply the NAD(+) needed for phase 2 of glycolysis. Thus increased lactate production coincides with cellular acidosis and remains a good indirect marker for cell metabolic conditions that induce metabolic acidosis. If muscle did not produce lactate, acidosis and muscle fatigue would occur more quickly and exercise performance would be severely impaired.