Muscle metabolites and performance during high-intensity, intermittent exercise

Six men were studied during four 30-s all-out exercise bouts on an air-braked cycle ergometer. The first three exercise bouts were separated by 4 min of passive recovery; after the third bout, subjects rested for 4 min, exercised for 30 min at 30-35% peak O-2 consumption, and rested for a further 60 min before completing the fourth exercise bout. Peak power and total work were reduced (P < 0.05) during bout 3 [765 +/- 60 (SE) W; 15.8 +/- 1.0 kJ] compared with bout 1 (1,168 +/- 55 mT, 23.8 +/- 1.2 kJ), but no difference in exercise performance was observed between bouts 1 and 4 (1,094 +/- 64 W, 23.2 +/- 1.4 kJ). Before bout 3, muscle ATP, creatine phosphate (CP), glycogen, pH, and sarcoplasmic reticulum (SR) Ca2+ uptake were reduced, while muscle lactate and inosine 5'-monophosphate were increased. Muscle ATP and glycogen before bout 4 remained lower than values before bout I (P < 0.05), but there were no differences in muscle inosine 5'-monophosphate, lactate, pH, and SR Ca2+ uptake. Muscle CP levels before bout 4 had increased above resting levels. Consistent with the decline in muscle ATP were increases in hypoxanthine and inosine before bouts 3 and 4. The decline in exercise performance does not appear to be related to a reduction in muscle glycogen. Instead, it may be caused by reduced CP availability, increased H+ concentration, impairment in SR function, or some other fatigue-inducing agent.

Factors affecting the rate of phosphocreatine resynthesis following intense exercise

Within the skeletal muscle cell at the onset of muscular contraction, phosphocreatine (PCr) represents the most immediate reserve for the rephosphorylation of adenosine triphosphate (ATP). As a result, its concentration can be reduced to less than 30% of resting levels during intense exercise. As a fall in the level of PCr appears to adversely affect muscle contraction, and therefore power output in a subsequent bout, maximising the rate of PCr resynthesis during a brief recovery period will be of benefit to an athlete involved in activities which demand intermittent exercise. Although this resynthesis process simply involves the rephosphorylation of creatine by aerobically produced ATP (with the release of protons), it has both a fast and slow component, each proceeding at a rate that is controlled by different components of the creatine kinase equilibrium. The initial fast phase appears to proceed at a rate independent of muscle pH. Instead, its rate appears to be controlled by adenosine diphosphate (ADP) levels; either directly through its free cytosolic concentration, or indirectly, through its effect on the free energy of ATP hydrolysis. Once this fast phase of recovery is complete, there is a secondary slower phase that appears almost certainly rate-dependant on the return of the muscle cell to homeostatic intracellular pH. Given the importance of oxidative phosphorylation in this resynthesis process, those individuals with an elevated aerobic power should be able to resynthesise PCr at a more rapid rate than their sedentary counterparts. However, results from studies that have used phosphorus nuclear magnetic resonance (P-31-NMR) spectroscopy, have been somewhat inconsistent with respect to the relationship between aerobic power and PCr recovery following intense exercise. Because of the methodological constraints that appear to have limited a number of these studies, further research in this area is warranted.

A practical guide to exercise training for heart failure patients

Background: Exercise training has been shown to improve exercise capacity in patients with heart failure. We sought to examine the optimal strategy of exercise training for patients with heart failure. Methods: Review of the published data on the characteristics of the training program, with comparison of physiologic markers of exercise capacity in heart failure patients and healthy individuals and comparison of the change in these characteristics after all exercise training program. Results: Many factors, including the duration, supervision, and venue of exercise training; the volume of working muscle; the delivery mode (eg, continuous vs. intermittent exercise), training intensity; and the concurrent effects of medical treatments may influence the results of exercise training in heart failure. Starting in an individually prescribed and safely monitored hospital-based program, followed by progression to an ongoing and progressive home program of exercise appears to be the best solution to the barriers of anxiety, adherence, and ease of access encountered by the heart failure patient. Conclusions: Various exercise training programs have been shown to improve exercise capacity and symptom status in heart failure, but these improvements may only be preserved with an ongoing maintenance program.

Leukocyte subset responses during exercise under heat stress with carbohydrate or water intake

Purpose: This study investigated leukocyte subset responses to moderate-intensity exercise under heat stress, with water (W) or carbohydrate (CHO) drink ingestion. Methods: In repeated trials, 13 soldiers consumed either a W or CHO drink during 3 h of walking at 4.4 km center dot h(-1) with a 5% gradient (15 min rest per hour) under heat stress (35 C and 55% relative humidity). The soldiers wore combat uniforms and carried water bottles and dummy rifles and ammunition, altogether weighing about 11.5 +/- 1.0 kg. Results: Plasma glucose concentration was significantly higher with CHO than W ingestion during exercise (p < 0.01). There were no significant differences between W and CHO conditions in exercise performance, plasma cortisol concentration, heart rate, or core temperature. CHO ingestion significantly moderated the increases in leukocyte (83% in W, 28% in CHO; p < 0.001), monocyte (60% in W, 34% in CHO; p < 0.05), and granulocyte counts (120% in W, 30% in CHO; p < 0.001), but not in lymphocyte count (41% in W, 25% in CHO). Conclusions: The increases in leukocyte and subset counts during moderate-intensity exercise under heat stress may be comparable to those observed during intense exercise in cool conditions. The response of immune cell counts is blunted by CHO intake during moderate-intensity exercise in the heat, and may not occur through the cortisol pathway.

Muscle metabolism during constant- and alternating-intensity exercise around critical power

Few studies have focused on the metabolic responses to alternating high- and low-intensity exercise and, specifically, compared these responses to those seen during constant-load exercise performed at the same average power output. This study compared muscle metabolic responses between two patterns of exercise during which the intensity was either constant and just below critical power (CP) or that oscillated above and below CP. Six trained males (mean +/- SD age 23.6 +/- 2.6 y) completed two 30-minute bouts of cycling (alternating and constant) at an average intensity equal to 90% of CR The intensity during alternating exercise varied between 158% CP and 73% CP. Biopsy samples from the vastus lateralis muscle were taken before (PRE), at the midpoint and end (POST) of exercise and analysed for glycogen, lactate, PCr and pH. Although these metabolic variables in muscle changed significantly during both patterns of exercise, there were no significant differences (p > 0.05) between constant and alternating exercise for glycogen (PRE: 418.8 +/- 85 vs. 444.3 +/- 70; POST: 220.5 +/- 59 vs. 259.5 +/- 126mmol.kg(-1) dw), lactate (PRE: 8.5 +/- 7.7 vs. 8.5 +/- 8.3; POST: 49.9 +/- 19.0 vs. 42.6 +/- 26.6 mmol.kg(-1)dw), phosphocreatine (PRE: 77.9 +/- 11.6 vs. 75.7 +/- 16.9; POST: 65.8 +/- 12.1 vs. 61.2 +/- 12.7mmol.kg(-1)dw) or pH (PRE: 6.99 +/- 0.12 vs. 6.99 +/- 0.08; POST: 6.86 +/- 0.13 vs. 6.85 +/- 0.06), respectively. There were also no significant differences in blood lactate responses to the two patterns of exercise. These data suggest that, when the average power output is similar, large variations in exercise intensity exert no significant effect on muscle metabolism.

Long-term metabolic and skeletal muscle adaptations to short-sprint training: Implications for sprint training and tapering

The adaptations of muscle to sprint training can be separated into metabolic and morphological changes. Enzyme adaptations represent a major metabolic adaptation to sprint training, with the enzymes of all three energy systems showing signs of adaptation to training and some evidence of a return to baseline levels with detraining. Myokinase and creatine phosphokinase have shown small increases as a result of short-sprint training in some studies and elite sprinters appear better able to rapidly breakdown phosphocreatine (PCr) than the sub-elite. No changes in these enzyme levels have been reported as a result of detraining. Similarly, glycolytic enzyme activity (notably lactate dehydrogenase, phosphofructokinase and glycogen phosphorylase) has been shown to increase after training consisting of either long (> 10-second) or short (< 10-second) sprints. Evidence suggests that these enzymes return to pre-training levels after somewhere between 7 weeks and 6 months of detraining. Mitochondrial enzyme activity also increases after sprint training, particularly when long sprints or short recovery between short sprints are used as the training stimulus. Morphological adaptations to sprint training include changes in muscle fibre type, sarcoplasmic reticulum, and fibre cross-sectional area. An appropriate sprint training programme could be expected to induce a shift toward type Ha muscle, increase muscle cross-sectional area and increase the sarcoplasmic reticulum volume to aid release of Ca2+. Training volume and/or frequency of sprint training in excess of what is optimal for an individual, however, will induce a shift toward slower muscle contractile characteristics. In contrast, detraining appears to shift the contractile characteristics towards type IIb, although muscle atrophy is also likely to occur. Muscle conduction velocity appears to be a potential non-invasive method of monitoring contractile changes in response to sprint training and detraining. In summary, adaptation to sprint training is clearly dependent on the duration of sprinting, recovery between repetitions, total volume and frequency of training bouts. These variables have profound effects on the metabolic, structural and performance adaptations from a sprint-training programme and these changes take a considerable period of time to return to baseline after a period of detraining. However, the complexity of the interaction between the aforementioned variables and training adaptation combined with individual differences is clearly disruptive to the transfer of knowledge and advice from laboratory to coach to athlete.

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 (similar to20 min cycling, similar to60min 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; (V)over dot O-2peak = 70 +/- 3 ml.kg(-1).min(-1)) performed 1) a progressive exercise test to determine peak Volume of oxygen uptake ((V)over dot O-2peak), 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 (V)over dot O-2peak, 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.

Tennis, incidence of URTI and salivary IgA

Tennis played at an elite level requires intensive training characterized by repeated bouts of brief intermittent high intensity exercise over relatively long periods of time (1 - 3 h or more). Competition can place additional stress on players. The purpose of this study was to investigate the temporal association between specific components of tennis training and competition, the incidence of upper respiratory tract infections (URT1), and salivary IgA, in a cohort of seventeen elite female tennis players. Timed, whole unstimulated saliva samples were collected before and after selected 1-h training sessions at 2 weekly intervals, over 12 weeks. Salivary IgA concentration was measured by ELISA and IgA secretion rate calculated (mug IgA x ml(-1) x ml saliva x min(-1)). Players reported URTI symptoms and recorded training and competition in daily logs. Data analysis showed that higher incidence of URTI was significantly associated with increased training duration and load, and competition level, on a weekly basis. Salivary IgA secretion rate (S-IgA) dropped significantly after 1 hour of tennis play. Over the 12-week period, pre-exercise salivary IgA concentration and secretion rate were directly associated with the amount of training undertaken during the previous day and week (p < 0.05). However, the decline in S-IgA after 1 h of intense tennis play was also positively related to the duration and load of training undertaken during the previous day and week (p < 0.05). Although exercise-induced suppression of salivary IgA may be a risk factor, it could not accurately predict the occurrence of URTI in this cohort of athletes.

Effect of propionyl-L-carnitine on exercise performance in peripheral arterial disease

Background: Supplementation with propionyl-L-carnitine (PLC) may be of use in improving the exercise capacity of people with peripheral arterial disease. Methods: After a 2-wk exercise familiarization phase, seven subjects displaying intermittent claudication were studied over a 12-wk period consisting of three 4-wk phases, baseline (B), supplementation (S), and placebo (P). PLC was supplemented at 2 g(.)d(-1), and subjects were blinded to the order of supplementation. Unilateral calf strength and endurance were assessed weekly. Walking performance was assessed at the end of each phase using an incremental protocol, during which respiratory gases were collected. Results: Although there was not a significant increase in maximal walking time (similar to 14%) in the whole group, walking time improved to a greater extent than the individual baseline coefficient of variation in four of the seven subjects. The changes in walking performance were correlated with changes in the respiratory exchange ratio both at steady state (r = 0.59) and maximal exercise (r = 0.79). Muscle strength increased significantly from 695 +/- 198 N to 812 +/- 249 N by the end of S. Changes in calf strength from B to S were modestly related to changes in walking performance (r = 0.56). No improvements in calf endurance were detected throughout the study. Conclusions: These preliminary data suggest that, in addition to walking performance, muscle strength can be increased in PAD patients after 4 wk of supplementation with propionyl-L-carnitine.

Pharmacotherapy of intermittent claudication

Intermittent claudication (IC) is leg muscle pain, cramping and fatigue brought on by exercise and is the primary symptom of peripheral arterial disease. The goals of pharmacotherapy for IC are to increase the walking capacity/quality of life and to decrease rates of amputation. In 1988, pentoxifylline was the only drug that had reasonable supportive clinical trial evidence for being beneficial in IC. Since then a number of drugs have shown benefit or potential in IC. Cilostazol, a specific inhibitor of phosphodiesterase 3 and activator of lipoprotein lipase, clearly increases pain-free and absolute walking distances in claudicants. However, cilostazol does cause minor side effects including headache, diarrhoea, loose stools and flatulence. Naftidrofuryl, a serotonin (5-HT2) receptor antagonist and antiplatelet drug, is beneficial in claudicants. Inhibitors of platelet aggregation (including nitric oxide from L-arginine or glyceryl trinitrate) and anticoagulants (low molecular weight heparin, defibrotide) probably have both short and long-term benefits in IC. In addition, intravenous infusions of prostaglandins (PGs) PGE1 and PGI2 have an established role in severe peripheral arterial disease and the recent introduction of longer lasting and/or oral forms of the PGs makes them more likely to be useful in the IC associated with less severe forms of the disease. There are some exciting new approaches to the treatment of IC, including propionyl-L-carnitine and basic fibroblast growth factor (bFGF).

Physiological and symptomatic responses to cycling and walking in intermittent claudication

To shed light on the potential efficacy of cycling as a resting modality in the treatment of intermittent claudication (IC), this study compared physiological and symptomatic responses to graded walking and cycling tests in claudicants. Sixteen subjects with peripheral arterial disease (resting ankle:brachial index (ABI) < 0.9) and IC completed a maximal graded treadmill walking (T) and cycle (C) Lest after three familiarization tests on each mode. During cacti test, symptoms, oxygen uptake (VO2), minute ventilation (V-E), (respiratory exchange ratio) (RER) and heart rate (HR) were measured, and for 10 min after each Lest the brachial and ankle systolic pressures were recorded, All but One subject experienced calf pain as the primary limiting symptom during T whereas the symptoms were more varied during C and included thigh pain, calf pain and dyspnoea, Although maximal exercise time was significantly longer on C than T (690 +/- 67 vs, 495 +/- 57 s), peak VO2, peak, V-E and peak heart rate during C and T were not different; whereas peak RER was higher during C. These responses during C and T were also positively 1, (P < 0.05) with each other, with the exception of RER. The postexercise systolic pressures were also not different between C and T. However, the peak decline ill ankle pressures from resting values after C and T were not correlated with each other. Thew data demonstrate that cycling and walking induce a similar level of metabolic and cardiovascular strain, but that the primary limiting symptoms and haemodynamic response in an individual's extremity, measured after exercise, can differ substantially between these two modes.

Optimising exercise training in peripheral arterial disease

Peripheral arterial disease (PAD) is an obstructive condition where the flow of blood through peripheral arteries is impeded. During periods of increased oxygen demand (e.g. during exercise), peripheral limb ischaemia occurs, resulting in the sensation of muscle pain termed 'claudication'. As a result of claudication, subjects' ability to exercise is greatly reduced affecting their quality of life. Although many treatment options for patients with PAD exist, exercise training is an effective and low-cost means of improving functional ability and quality of life. Currently, there are limited specific recommendations to assist the exercise prescription and programming of these individuals. This review summarises data from 28 exercise training studies conducted in patients with PAD and formulates recommendations based on their results. Exercise training for patients with PAD should involve three training sessions per week comprising 45 minutes of intermittent treadmill walking in a supervised environment for a time period of 20 weeks or more. Encouragement and direction is given to further research aimed at investigating the effectiveness of training programmes in these patients.

Short-term effects of cycle and treadmill training on exercise tolerance in peripheral arterial disease

Background. To explore the efficacy of cycle training in the treatment of intermittent claudication, the present study compared performance and physiologic effects of cycle training with more conventional treadmill walking training in a group of patients with claudication. Method: Forty-two individuals with peripheral arterial disease and intermittent claudication (24 men, 18 women) were stratified by gender and the presence or absence of type 2 diabetes mellitus and then randomized to a treadmill (n = 13), cycle (n = 15), or control group (n = 14). Treadmill and cycle groups trained three times a week for 6 weeks, whereas the control group did not train during this period. Maximal and pain-free exercise times were measured on graded treadmill and cycle tests before and after training. Results. Treadmill training significantly improved maximal and pain-free treadmill walking times but did not improve cycle performance. Cycle training significantly improved maximal cycle time but did not improve treadmill performance. However, there was evidence of a stronger cross-transfer effect between the training modes for patients who reported a common limiting symptom during cycling and walking at baseline. There was also considerable variation in the training response to cycling, and a subgroup of responsive patients in the cycle group improved their walking performance by more than the average response observed in the treadmill group. Conclusion: These findings suggest that cycle exercise is not effective in improving walking performance in all claudication patients but might be an effective alternative to walking in those who exhibit similar limiting symptoms during both types of exercise.

Effect of training on the response of plasma vascular endothelial growth factor to exercise in patients with peripheral arterial disease

Expansion of the capillary network, or angiogenesis, occurs following endurance training. This process, which is reliant on the presence of VEGF (vascular endothelial growth factor), is an adaptation to a chronic mismatch between oxygen demand and supply. Patients with IC (intermittent claudication) experience pain during exercise associated with an inadequate oxygen delivery to the muscles. Therefore the aims of the present study were to examine the plasma VEGF response to acute exercise, and to establish whether exercise training alters this response in patients with IC. In Part A, blood was collected from patients with IC (n = 18) before and after (+ 20 and + 60 min post-exercise) a maximal walking test to determine the plasma VEGF response to acute exercise. VEGF was present in the plasma of patients (45.11 +/- 29.96 pg/ml) and was unchanged in response to acute exercise. Part B was a training study to determine whether exercise training altered the VEGF response to acute exercise. Patients were randomly assigned to a treatment group (TMT; n = 7) that completed 6 weeks of high-intensity treadmill training, or to a control group (CON; n = 6). All patients completed a maximal walking test before and after the intervention, with blood samples drawn as for Part A. Training had no effect on plasma VEGF at rest or in response to acute exercise, despite a significant increase in maximal walking time in the TMT group (915 + 533 to 1206 + 500 s; P = 0.009) following the intervention. The absence of a change in plasma VEGF may reflect altered VEGF binding at the endothelium, although this cannot be confirmed by the present data.