Exercise metabolism was examined in 13 endurance athletes who exercised on three occasions for 40 min at 70% of maximal O2 uptake in an environmental chamber at either 20 degrees C and 20% relative humidity (RTT) or 40 degrees C and 20% relative humidity before (PRE ACC) or after (POST ACC) 7 days of acclimation. Exercise in the heat resulted in a lower (P < 0.05) mean O2 uptake (0.13 l/min) and higher (P < 0.01) heart rate and respiratory exchange ratio. Acclimation resulted in a lower (P < 0.01) mean heart rate and respiratory exchange ratio. Postexercise rectal temperature, muscle temperature, muscle and blood lactate, and blood glucose were higher (P < 0.01) in the PRE ACC than in the RTT trial, but all were reduced (P < 0.01) in the POST ACC compared with the PRE ACC trial. Muscle glycogenolysis and percentage of type I muscle fibers showing glycogen depletion were greater (P < 0.05) in the PRE ACC than in the RTT trial. Muscle glycogenolysis was unaffected by acclimation during exercise in the heat, although the percentage of depleted type I fibers was higher (P < 0.05) in the unacclimated state. Plasma epinephrine was higher (P < 0.01) during exercise in the heat in the unacclimated individual relative to RTT but was lower (P < 0.01) in the POST ACC than in the PRE ACC trial. The greater reliance on carbohydrate as a fuel source during exercise in the heat appears to be partially reduced after acclimation. These alterations are consistent with the observed changes in plasma epinephrine concentrations.

Although WP and/or CrM seem to promote greater strength gains and muscle morphology during RE training, the hypertrophy responses within the groups varied. These differences in skeletal muscle morphology may have important implications for various populations and, therefore, warrant further investigation.

This study examined the effects of elevated muscle temperature on muscle metabolism during exercise. Seven active but untrained men completed two cycle ergometer trials for 2 min at a workload estimated to require 115% maximal oxygen uptake (VO2) either without pretreatment (CT) or after having their thigh wrapped in a heating blanket for 60 min before exercise (HT). HT increased (P < 0.01) muscle temperature (Tm) and resulted in a difference in Tm between the two trials before (delta = 1.9 +/- 0.1 degrees C, P < 0.01) and after exercise (delta = 0.6 +/- 0.2 degree C, P < 0.05). HT did not affect rectal temperature or plasma catecholamines. In addition, these parameters were not different between CT and HT either before or after exercise. No differences in resting intramuscular concentrations of the adenine nucleotides (ATP, ADP, AMP) or their degradation products (inosine 5'-monophosphate, ammonia), lactate, glycogen, creatine phosphate, or creatine were observed between HT and CT. During exercise, the magnitude of ATP degradation and inosine 5'-monophosphate and ammonia accumulation was higher (P < 0.05) in HT compared with CT. Although preexercise concentrations of glycogen and lactate were not different between the two trials, postexercise lactate concentration was higher (P < 0.05) and glycogen lower (P < 0.05) in HT compared with CT. In addition, net muscle glycogen use was higher (P < 0.05) in HT. It is concluded that an elevated Tm per se increases muscle glycogenolysis, glycolysis, and high-energy phosphate degradation during exercise. These alterations may be the result of an increased rate of ATP turnover associated with the exercise and/or changes in the anaerobic/aerobic contribution to ATP resynthesis.

AimThis study explored the effects of blood flow restriction (BFR) on mRNA responses of PGC‐1α (total, 1α1, and 1α4) and Na+,K+‐ATPase isoforms (NKA; α1‐3, β1‐3, and FXYD1) to an interval running session and determined whether these effects were related to increased oxidative stress, hypoxia, and fibre type‐specific AMPK and CaMKII signalling, in human skeletal muscle.MethodsIn a randomized, crossover fashion, 8 healthy men (26 ± 5 year and 57.4 ± 6.3 mL kg−1 min−1) completed 3 exercise sessions: without (CON) or with blood flow restriction (BFR), or in systemic hypoxia (HYP, ~3250 m). A muscle sample was collected before (Pre) and after exercise (+0 hour, +3 hours) to quantify mRNA, indicators of oxidative stress (HSP27 protein in type I and II fibres, and catalase and HSP70 mRNA), metabolites, and α‐AMPK Thr172/α‐AMPK, ACC Ser221/ACC, CaMKII Thr287/CaMKII, and PLBSer16/PLB ratios in type I and II fibres.ResultsMuscle hypoxia (assessed by near‐infrared spectroscopy) was matched between BFR and HYP, which was higher than CON (~90% vs ~70%; P < .05). The mRNA levels of FXYD1 and PGC‐1α isoforms (1α1 and 1α4) increased in BFR only (P < .05) and were associated with increases in indicators of oxidative stress and type I fibre ACC Ser221/ACC ratio, but dissociated from muscle hypoxia, lactate, and CaMKII signalling.ConclusionBlood flow restriction augmented exercise‐induced increases in muscle FXYD1 and PGC‐1α mRNA in men. This effect was related to increased oxidative stress and fibre type‐dependent AMPK signalling, but unrelated to the severity of muscle hypoxia, lactate accumulation, and modulation of fibre type‐specific CaMKII signalling.