Training-induced alterations of carbohydrate metabolism in women: women respond differently from men.

We examined the hypothesis that glucose flux was directly related to relative exercise intensity both before and after a 12-wk cycle ergometer training program [5 days/wk, 1-h duration, 75% peak O2 consumption (VO2 peak)] in healthy female subjects (n = 17; age 23.8 +/- 2.0 yr). Two pretraining trials (45 and 65% of VO2 peak) and two posttraining trials [same absolute workload (65% of old VO2 peak) and same relative workload (65% of new VO2 peak)] were performed on nine subjects by using a primed-continuous infusion of [1-13C]- and [6,6-2H]glucose. Eight additional subjects were studied by using [6, 6-2H]glucose. Subjects were studied postabsorption for 90 min of rest and 1 h of cycling exercise. After training, subjects increased VO2 peak by 25.2 +/- 2.4%. Pretraining, the intensity effect on glucose kinetics was evident between 45 and 65% of VO2 peak with rates of appearance (Ra: 4.52 +/- 0.25 vs. 5.53 +/- 0.33 mg . kg-1 . min-1), disappearance (Rd: 4.46 +/- 0.25 vs. 5.54 +/- 0.33 mg . kg-1 . min-1), and oxidation (Rox: 2.45 +/- 0.16 vs. 4.35 +/- 0.26 mg . kg-1 . min-1) of glucose being significantly greater (P

Training-induced alterations of glucose flux in men.

We examined the hypothesis that glucose flux was directly related to relative exercise intensity both before and after a 10-wk cycle ergometer training program in 19 healthy male subjects. Two pretraining trials [45 and 65% of peak O2 consumption (VO2peak)] and two posttraining trials (same absolute and relative intensities as 65% pretraining) were performed for 90 min of rest and 1 h of cycling exercise. After training, subjects increased VO2peak by 9.4 +/- 1.4%. Pretraining, the intensity effect on glucose kinetics was evident with rates of appearance (R(a); 5.84 +/- 0.23 vs. 4.73 +/- 0.19 mg x kg(-1) x min(-1)), disappearance (R(d); 5.78 +/- 0.19 vs. 4.73 +/- 0.19 mg x kg(-1) x min(-1) x min(-1)), oxidation (R(ox); 5.36 +/- 0.15 vs. 3.41 +/- 0.23 mg x kg(-1) x min(-1)), and metabolic clearance (7.03 +/- 0.56 vs. 5.20 +/- 0.28 ml x kg(-1) x min(-1)) of glucose being significantly greater (P < or = 0.05) in the 65% than the 45% VO2peak trial. When R(d) was expressed as a percentage of total energy expended per minute (R(dE)), there was no difference between the 45 and 65% intensities. Training did reduce R(a) (4.63 +/- 0.25), R(d) (4.65 +/- 0.24), R(ox) (3.77 +/- 0.43), and R(dE) (15.30 +/- 0.40 to 12.85 +/- 0.81) when subjects were tested at the same absolute workload (P < or = 0.05). However, when they were tested at the same relative workload, R(a), R(d), and R(dE) were not different, although R(ox) was lower posttraining (5.36 +/- 0.15 vs. 4.41 +/- 0.42, P < or = 0.05). These results show 1) glucose use is directly related to exercise intensity; 2) training decreases glucose flux for a given power output; 3) when expressed as relative exercise intensity, training does not affect the magnitude of blood glucose use during exercise; 4) training alters the pathways of glucose disposal.

Smoking increases conversion of lactate to glucose during submaximal exercise.

We examined the hypotheses that 1) smoking acutely before exercise (AS) results in a higher rate of lactate production during exercise compared with chronic smoking with preexercise abstinence (CS) and 2) smokers have a higher rate of lactate conversion to glucose during exercise compared with nonsmokers (NS). To test our hypotheses, seven male smokers and seven nonsmokers were studied by using a primed continuous infusion of [3-13C]lactate during 90 min of rest and 60 min of exercise on a cycle ergometer at 50% peak O2 consumption; smokers were studied twice: once after an overnight smoking abstinence and once after smoking three cigarettes before exercise. The rates of lactate appearance and conversion to glucose were increased markedly with exercise compared with rest in all groups (P < 0.05); the rate of lactate appearance for AS was significantly greater (7.87 +/- 0.77 mg.kg-1.min-1) than for both CS (4.64 +/- 0.33 mg.kg-1.min-1) and NS (5.57 +/- 0.60 mg.kg-1.min-1) (P < 0.05). The rate of lactate conversion to glucose was similar between CS and AS (6.49 +/- 1.82 and 6.30 +/- 1.69 mg.kg-1.min-1, respectively) during exercise; NS had a significantly lower rate (3.31 +/- 0.90 mg.kg-1.min-1) compared with CS and AS (P < 0.05). In summary, acute smoking increases lactate flux during exercise; in addition, smokers have a higher rate of lactate to glucose conversion during exercise compared with nonsmokers, which may indicate an increased glucose dependency.

An acute myocardial infarction occurring in an anabolic steroid user.

Anabolic-androgenic steroid abuse is prevalent and has been associated with numerous adverse effects. The case being presented is of an amateur weight trainer, who suffered an acute myocardial infarction; his only significant risk factor was his nonmedical use of an anabolic steroid, nandrolone decanoate. This case presentation discusses the hematologic effects of this class of drugs and the subsequent impact on ischemic heart disease.