No abstract

Black athletes currently dominate long-distance running events in South Africa. In an attempt to explain an apparently superior running ability of black South African athletes at distances > 3 km, we compared physiological measurements in the fastest 9 white and 11 black South African middle-to long-distance runners. Whereas both groups ran at a similar percentage of maximal O2 uptake (%VO2max) over 1.65-5 km, the %VO2max sustained by black athletes was greater than that of white athletes at distances > 5 km (P < 0.001). Although both groups had similar training volumes, black athletes reported that they completed more exercise at > 80% VO2max (36 +/- 18 vs. 14 +/- 7%: P < 0.005). When corrections were made for the black athletes' smaller body mass, their superior ability to sustain a high %VO2max could not be explained by any differences in VO2max, maximal ventilation, or submaximal running economy. Superior distance running performance of the black athletes was not due to a greater (+/- 50%) percentage of type I fibers but was associated with lower blood lactate concentrations during exercise. Time to fatigue during repetitive isometric muscle contractions was also longer in black runners (169 +/- 65 vs. 97 +/- 69 s; P < 0.05), but whether this observation explains the superior endurance or was due to the lower peak muscle strength (46.3 +/- 10.3 vs. 67.5 +/- 18.0 Nm/l lean thigh volume; P < 0.01) remains to be established.

The female hormones, oestrogen and progesterone, fluctuate predictably across the menstrual cycle in naturally cycling eumenorrhoeic women. Other than reproductive function, these hormones influence many other physiological systems, and their action during exercise may have implications for exercise performance. Although a number of studies have found exercise performance - and in particular, endurance performance - to vary between menstrual phases, there is an equal number of such studies reporting no differences. However, a comparison of the increase in the oestrogen concentration (E) relative to progesterone concentration (P) as the E/P ratio (pmol/nmol) in the luteal phase in these studies reveals that endurance performance may only be improved in the mid-luteal phase compared with the early follicular phase when the E/P ratio is high in the mid-luteal phase. Furthermore, the late follicular phase, characterized by the pre-ovulatory surge in oestrogen and suppressed progesterone concentrations, tends to promote improved performance in a cycling time trial and future studies should include this menstrual phase. Menstrual phase variations in endurance performance may largely be a consequence of changes to exercise metabolism stimulated by the fluctuations in ovarian hormone concentrations. The literature suggests that oestrogen may promote endurance performance by altering carbohydrate, fat and protein metabolism, with progesterone often appearing to act antagonistically. Details of the ovarian hormone influences on the metabolism of these macronutrients are no longer only limited to evidence from animal research and indirect calorimetry but have been verified by substrate kinetics determined with stable tracer methodology in eumenorrhoeic women. This review thoroughly examines the metabolic perturbations induced by the ovarian hormones and, by detailed comparison, proposes reasons for many of the inconsistent reports in menstrual phase comparative research. Often the magnitude of increase in the ovarian hormones between menstrual phases and the E/P ratio appear to be important factors determining an effect on metabolism. However, energy demand and nutritional status may be confounding variables, particularly in carbohydrate metabolism. The review specifically considers how changes in metabolic responses due to the ovarian hormones may influence exercise performance. For example, oestrogen promotes glucose availability and uptake into type I muscle fibres providing the fuel of choice during short duration exercise; an action that can be inhibited by progesterone. A high oestrogen concentration in the luteal phase augments muscle glycogen storage capacity compared with the low oestrogen environment of the early follicular phase. However, following a carbo-loading diet will super-compensate muscle glycogen stores in the early follicular phase to values attained in the luteal phase. Oestrogen concentrations of the luteal phase reduce reliance on muscle glycogen during exercise and although not as yet supported by ...

This study examined effects of ingesting a 10% carbohydrate (CHO) drink (CI) or placebo (PI) at 500 ml/h on total (splanchnic) glucose appearance (endogenous+exogenous; Ra), blood glucose oxidation, and muscle glycogen utilization in 14 male endurance-trained cyclists who rode for 180 min at 70% of maximal O2 uptake after CHO loading [starting muscle glycogen 203 +/- 7 (SE) mmol/kg wet wt]. Total CHO oxidation was similar in CI and PI, but Ra increased significantly during the trial in both groups with CI reaching a plateau after 75 min. Ra was significantly greater in CI than in PI at the end of exercise. Blood glucose oxidation also increased significantly during the trial to a plateau in CI and was significantly higher in CI than in PI at the end of exercise. However, mean endogenous Ra was significantly lower in CI than in PI throughout exercise, as was oxidation of endogenous blood glucose, which remained almost constant in CI and reached 43 +/- 8 and 73 +/- 13 mumol.min-1.kg fat-free mass-1 in CI and PI, respectively, at the end of exercise. At 0.83 g/min of CHO ingestion, 0.77 +/- 0.03 g/min was oxidized. Muscle glycogen utilization was identical in both groups and was higher during the 1st h of exercise.(ABSTRACT TRUNCATED AT 250 WORDS)

This study compared liver glucose turnover, blood glucose oxidation, and muscle glycogen utilization in 15 male endurance-trained cyclists who rode for 180 min at 70% of maximal O2 consumption in either a carbohydrate-(CHO) loaded (CL) or a non-CHO-loaded (NL) state. Total CHO oxidation during exercise was similar in the CL and NL subjects (492 +/- 77 vs. 448 +/- 43 g, respectively), as were blood glucose oxidation (103 +/- 19 vs. 99 +/- 7 g, respectively) and liver glucose appearance (110 +/- 15 vs. 127 +/- 16 g, respectively). However, total muscle glycogen utilization was greater in CL than NL subjects (134 +/- 11 vs. 95 +/- 12 mmol/kg wet wt; P < 0.05), the former of which had higher muscle glycogen content at the start (194 +/- 4 vs. 124 +/- 7 mmol/kg wet wt; P < 0.05) and throughout the trial. Whereas high rates of muscle glycogen breakdown were maintained throughout the trial in CL subjects, rates of muscle glycogenolysis in NL subjects decreased to 26 mmol.kg wet wt-1.h-1 after 60 min of exercise (P < 0.05) when their muscle glycogen content had declined to 70 mmol/kg wet wt. Comparable rates of blood glucose and overall CHO oxidation in CL and NL subjects, despite a slowing of muscle glycogenolysis in the NL group, could be explained by an accelerated breakdown of glycogen in the nonworking muscles to redistribute CHO (lactate) to the working muscles for oxidation.(ABSTRACT TRUNCATED AT 250 WORDS)

To determine whether the reduced blood lactate concentrations [La] during submaximal exercise in humans after endurance training result from a decreased rate of lactate appearance (Ra) or an increased rate of lactate metabolic clearance (MCR), interrelationships among blood [La], lactate Ra, and lactate MCR were investigated in eight untrained men during progressive exercise before and after a 9-wk endurance training program. Radioisotope dilution measurements of L-[U-14C]lactate revealed that the slower rise in blood [La] with increasing O2 uptake (VO2) after training was due to a reduced lactate Ra at the lower work rates [VO2 less than 2.27 l/min, less than 60% maximum VO2 (VO2max); P less than 0.01]. At power outputs closer to maximum, peak lactate Ra values before (215 +/- 28 mumol.min-1.kg-1) and after training (244 +/- 12 mumol.min-1.kg-1) became similar. In contrast, submaximal (less than 75% VO2max) and peak lactate MCR values were higher after than before training (40 +/- 3 vs. 31 +/- 4 ml.min-1.kg-1, P less than 0.05). Thus the lower blood [La] values during exercise after training in this study were caused by a diminished lactate Ra at low absolute and relative work rates and an elevated MCR at higher absolute and all relative work rates during exercise.

To determine why black distance runners currently out-perform white distance runners in South Africa, we measured maximum oxygen consumption (VO2max), maximum workload during a VO2max test (Lmax), ventilation threshold (VThr), running economy, inspiratory ventilation (VI), tidal volume (VT), breathing frequency (f) and respiratory exchange ratio (RER) in sub-elite black and white runners matched for best standard 42.2 km marathon times. During maximal treadmill testing, the black runners achieved a significantly lower (P less than 0.05) Lmax (17 km h-1, 2% grade, vs 17 km h-1, 4% grade) and VI max (6.21 vs 6.82 l kg-2/3 min-1), which was the result of a lower VT (101 vs 119 ml kg-2/3 breath-1) as fmax was the same in both groups. The lower VT in the black runners was probably due to their smaller body size. The VThr occurred at a higher percentage VO2max in black than in white runners (82.7%, SD 7.7% vs 75.6%, SD 6.2% respectively) but there were no differences in the VO2max. However, during a 42.2-km marathon run on a treadmill, the black athletes ran at the higher percentage VO2max (76%, SD 7.9% vs 68%, SD 5.3%), RER (0.96, SD 0.07 vs 0.91, SD 0.04) and f (56 breaths min-1, SD 11 vs 47 breaths min-1, SD 10), and at lower VT (78 ml kg-2/3 breath-1, SD 15 vs 85 ml kg-2/3 breath-1, SD 19). The combination of higher f and lower VT resulted in an identical VI.(ABSTRACT TRUNCATED AT 250 WORDS)

Euglycemia was maintained in 13 subjects with low muscle glycogen [low glycogen, euglycemic (LGE), n = 8; low glycogen, euglycemic, hyperinsulinemic (LGEI), n = 5] and 6 subjects with normal muscle glycogen (NGE), whereas hyperglycemia was maintained in 8 low muscle glycogen subjects (LGH). All subjects cycled for 145 min at 70% of maximal oxygen uptake during the infusions. Insulin was infused in LGEI at 0.2 mU ⋅ kg−1 ⋅ min−1. During exercise, respiratory exchange ratio (RER) was lower and norepinephrine higher in LGE than in NGE. In LGEI and LGH, RER at the start of exercise was the same as in LGE but did not decrease as in LGE. Free fatty acids (FFA) were higher and plasma insulin concentrations lower in LGE than NGE, LGEI, or LGH over the first 45 min of exercise. Rate of glucose infusion (Ri) and rate of glucose oxidation (Rox) were higher in LGH and LGEI than in NGE or LGE, and Ri matched Rox in all groups except LGH, in which Ri was greater than Rox. Muscle glycogen disappearance was greater in NGE than LGE, LGEI, or LGH, but the latter three groups did not differ. In conclusion, this study showed that low muscle glycogen content results in a decrease in RER, an increase in FFA, fat oxidation, and norepinephrine both at rest and during exercise, and does not affect Rox when euglycemia is maintained by infusion of glucose alone. Rox was increased only during insulin and hyperglycemia.