INTRODUCTION:
Impaired metabolism in skeletal muscle and adipose tissue contributes to the pathogenesis of many
metabolic disorders. Endurance exercise training and passive heat acclimation can beneficially remodel
these tissues, thereby reducing metabolic disease risk. However, although oxidative metabolic adaptations in
skeletal muscle are well characterised, many of the adaptations to glucose metabolism and in adipose tissue
remain unclear.
METHODS:
Male Winstar rats (n=26, 8 weeks old) were subject to 6-weeks of endurance exercise training (EXER),
passive heat acclimation (HEAT), or both protocols performed concurrently (BOTH), and compared to a
sedentary control condition (CTRL). Maximal aerobic speed (MAS) and resting metabolic rate (RMR) were
calculated on the last day of conditioning, and animals were euthanised 48 hours after the last test.
Differences in major metabolic pathways were analysed in the plantaris muscle and inguinal white adipose
tissue. Results were analysed by two-way ANOVA.
RESULTS:
XER, but hot HEAT, improved MAS, decreased adipose tissue mass, and reduced resting plasma glucose
concentration (p<0.05). Increased glycogen content, and greater citrate synthase (CS) activity (a marker of
mitochondrial content) in skeletal muscle was observed following both EXER and HEAT (p<0.05), without an
interaction between the interventions. This is accompanied by decreased phosphorylation (increased activity)
of glycogen synthase kinase 3 (GSK3) and decreased carnitine palmitoyltransferase 2 (CPT-2) following
HEAT only (p<0.05). The substrate transporters monocarboxylate trasporter 1 (MCT1) and carnitine
palmitoyltransferase 1 (CPT-1) were increased, and hexokinase (HK) activity decreased, following EXER
only (p<0.05). There was no effect on PFK activity in either condition (p>0.05). HSP70 protein expression
increased in HEAT only, in both muscle and adipose tissue (p<0.05).
CONCLUSION:
As expected, these results indicate a remodelling of skeletal muscle towards oxidative phenotype following
EXER. Decreased plasma glucose utilisation and increased reliance on circulating lactate, fatty acids, and
glycogen stores have previously been reported in endurance trained humans. HEAT induced similar
adaptations to glycogen storage and mitochondrial content, without concomitant increases lactate/fatty acid
transport or decreases in glucose phosphorylation. HEAT was effective at inducing HSP70 expression in
both skeletal muscle and adipose tissue. In general, when both interventions were performed simultaneously
(BOTH), effects were additive, highlighting the potential for combined therapy to benefit metabolism.
Therefore, these interventions could benefit tissue-level substrate metabolism in ways that may contribute to
the maintenance of metabolic health.