The purpose of this study was to develop a standardised maximal treadmill exercise test performed until fatigue in order to find reproducible markers for anaerobic metabolism, specifically adenine nucleotide degradation. Six Standardbred trotters performed an incremental maximal treadmill exercise test in 1 min steps (starting with 7 m l s ) until they could no longer keep pace with the treadmill. The test was performed twice with at least one week between the tests. Heart rate was recorded and venous blood samples were obtained during the test and in the recovery period for determination of plasma lactate, hypoxanthine, xanthine and uric acid. Muscle biopsy samples (m. gluteus) were collected at rest, immediately post exercise, and after 15 min recovery and analysed for their concentrations of glycogen, creatine phosphate (CP), adenosine triphosphate (ATP), adenosine diphosphate (ADP), adenosine monophosphate (AMP), inosine monophosphate (IMP) and muscle lactate (MLa). Significant decreases in glycogen, CP and ATP and significant increases in IMP and MLa were seen immediately post exercise. None of these metabolites had returned to resting levels after 15 min of recovery. A marked increase in plasma lactate @La) occurred during exercise and the peak concentration (mean value = 27.2 mmoyl) was reached within 5 min of recovery. Plasma uric acid concentration did not increase during exercise but rose markedly immediately post exercise, reaching the highest level (mean value = 121.5 ymoY1) a t 20-30 min recovery. The duration of the maximal test was related to peak PLa and the uric acid concentration at 30 min of recovery. A correlation was also found between the ATP and IMP concentrations immediately post exercise and the plasma uric acid concentration at 30 min of recovery. The results show that this treadmill test triggered anaerobic metabolism and also that uric acid concentration post exercise seems to be a marker for the adenine nucleotide degradation that occurs during intense exercise. No significant differences were seen in metabolic response between the 2 test occasions. exercise. Equine vet. J. 17, 439-444. Valberg, S.. Esstn-Gustavsson, B., Lindholm, A. and Penson. S.G.B. (1989) Blood chemistry and skeletal muscle metabolic responses during and after different speeds and durations of trotting. Equine vet. J. 21.91-95.

Summary The aim was to study metabolic response and locomotion pattern in Standardbred trotters during incremental treadmill exercise performed by increasing speed by 1 m/s in 1 min steps (start 7 m/s) until the onset of fatigue. The test protocol included determination of oxygen uptake, heart rate (HR), stride length (SL) and stride frequency (SF). Venous blood samples were collected at rest, at the end of each exercise step and after 30 min of recovery. Muscle biopsies were taken at rest and post exercise and muscle temperature was measured after exercise. As horses fatigued at different speed steps (9–11 m/s), variation was seen in running time (180–300 s), oxygen uptake (109–170 ml/kg bwt min), HR (200–225 beats/min), SL (4.4–5.7 m) and SF (116–130 strides/min) at the last speed step. Increased mean plasma lactate concentration (20.5 mmol/l) was seen at onset of fatigue and increased mean uric acid concentration after 30 min of recovery (112.8 μmol/l). After exercise, a decrease was seen in muscle ATP (7.1 mmol/kg d.w.), creatine phosphate (43.9 mmol/kg d.w.) and glycogen (160 mmol/kg d.w.), and an increase was seen in ADP (0.3 mmol/kg d.w.), AMP (0.18 mmol/kg d.w.), IMP (5.8 mmol/kg d.w.) and lactate (100.8 mmol/kg d.w.). At onset of fatigue, muscle temperature varied from 39.9–41.4°C. Running time correlated with SL (r=0.86), with an increase in IMP (r=0.79) and AMP (r=0.70) post exercise and with plasma uric acid concentration (r=0.74) at 30 min of recovery. SF correlated negatively with the increase in ADP after exercise (r = 0.85). The results of this study indicate that running time during incremental treadmill exercise until the onset of fatigue is related to locomotion pattern and to a marked degree of anaerobic metabolism, especially adenine nucleotide degradation.

Summary The aim of the present study was to investigate the effect of creatine (Cr) supplementation on muscle metabolic response in connection with a maximal treadmill exercise test, known to cause a marked anaerobic metabolic response and adenine nucleotide degradation. First, 6 Standardbred trotters performed a standardised maximal exercise test until fatigue (baseline test). The test used was an inclined incremental treadmill test in which the speed was increased by 1 m/s, starting at 7 m/s, every 60 s until the horse could no longer keep pace with the treadmill. After this baseline test, the horses were separated into 2 equal groups. One half received a dose of 25 g creatine monohydrate twice daily, and the other group were given the same dose of lactose (placebo). The supplementation period was 6.5 days, after which the maximal treadmill exercise test was performed again. A washout period of 14 days was allowed before treatments were switched between groups and a new supplementation period started. After this second supplementation period a new maximal exercise test was performed. After supplementation with creatine or placebo, horses were stopped after performing the same number of speed steps and duration of exercise as they had in the baseline test. Blood samples for analysis of plasma lactate, creatine (Cr), creatinine, hypoxanthine, xanthine and uric acid concentrations were collected at rest, during each speed step and during recovery. The total blood volume (TBV) was also determined. Muscle biopsies for analysis of muscle metabolites (adenosine triphosphate [ATP], adenosine diphosphate [ADP], adenosine monophosphate [AMP], inosine monophosphate [IMP], creatine phosphate [CP], lactate [La] and glycogen) were taken at rest, immediately post exercise and after 15 min recovery. The results showed no significant increase in plasma Cr or muscle total creatine concentration (TCr) after supplementation with Cr. At the end of exercise ATP and CP concentrations had decreased and IMP and lactate concentrations increased in muscle in all groups. Plasma lactate concentration increased during exercise and recovery and plasma uric acid concentration increased during recovery in all groups. No influence could be found in TBV after supplementation with creatine. These results show that creatine supplementation in the dosage used in this study had no influence on muscle metabolic response or TBV.

Administration of bicarbonate has been shown to cause metabolic alkalosis both in man and in horses and is, therefore, thought to increase the buffering capacity of the body and thereby delay the onset of fatigue. However, results regarding the influence of sodium bicarbonate loading on performance both in human athletes and in horses are conflicting. The aim of this study was, therefore, to investigate the metabolic response to a standardised treadmill exercise test to fatigue, in horses given bicarbonate (0.6 g/kg bwt), in comparison to horses given placebo (water). Five Standardbred trotters performed the test on 2 occasions. Venous blood samples were collected before and after administration of test substance, during exercise and during recovery. Muscle biopsy specimens were taken at rest, postexercise and at 15 min of recovery. The increases in pH and concentration of bicarbonate in the blood and the shift seen in base excess showed that the administration of sodium bicarbonate caused metabolic alkalosis. Exercise caused similar decreases in muscle ATP, CP and glycogen and similar increases in muscle IMP, lactate and plasma lactate and uric acid concentrations both in the placebo- and bicarbonate-treated group. The effect upon postexercise muscle and plasma metabolites was similar with both test treatments. Duration of exercise did not change after sodium bicarbonate intake. In conclusion, sodium bicarbonate caused metabolic alkalosis, but did not affect the metabolic response or duration of exercise.

SummaryThe purpose was to investigate the degradation of proglycogen and macroglycogen in skeletal muscle during intense exercise. Ten Standardbred trotters performed a maximal treadmill exercise test comprising a warm-up period, an exercise period, starting at 7 m/s with increments of 1 m/s every 60 s until the onset of fatigue (mean ± s.d. 246 ± 32 s) and a walking recovery period. Muscle biopsies were taken at rest, immediately after exercise and 15 min postexercise. The exercise caused a marked anaerobic metabolism as shown by the decrease in both muscle ATP and creatine phosphate and increase in muscle lactate. Free muscle glucose increased immediately postexercise and a further increase was noted 15 min later. There was a significant decrease (P<0.05) in proglycogen (57.1 ± 22.2 mmol/kg dw) and macroglycogen (63.0 ± 65.5 mmol/kg dw) during exercise. The proglycogen concentration tended to increase 15 min after exercise (19.9 ± 27.3 mmol/kg dw; P = 0.06). The results from this study demonstrate that both proglycogen and macroglycogen contribute equally to glycogenolysis during intense exercise and suggest that glycogen resynthesis starts in the proglycogen pool.