Neither Peristaltic Pulse Dynamic Compressions nor Heat Therapy Accelerate Glycogen Resynthesis after Intermittent Running.

PURPOSE: To investigate the effects of a single session of either peristaltic pulse dynamic leg compressions (PPDC) or local heat therapy (HT) after prolonged intermittent shuttle running on skeletal muscle glycogen content, muscle function, and the expression of factors involved in skeletal muscle remodeling. METHODS: Twenty-six trained individuals were randomly allocated to either a PPDC (n = 13) or a HT (n = 13) group. After completing a 90-min session of intermittent shuttle running, participants consumed 0.3 g·kg-1 protein plus 1.0 g·kg-1 carbohydrate and received either PPDC or HT for 60 min in one randomly selected leg, while the opposite leg served as control. Muscle biopsies from both legs were obtained before and after exposure to the treatments. Muscle function and soreness were also evaluated before, immediately after, and 24 h after the exercise bout. RESULTS: The changes in glycogen content were similar (P > 0.05) between the thigh exposed to PPDC and the control thigh ~90 min (Control: 14.9 ± 34.3 vs PPDC: 29.6 ± 34 mmol·kg-1 wet wt) and ~210 min (Control: 45.8 ± 40.7 vs PPDC: 52 ± 25.3 mmol·kg-1 wet wt) after the treatment. There were also no differences in the change in glycogen content between thighs ~90 min (Control: 35.9 ± 26.1 vs HT: 38.7 ± 21.3 mmol·kg-1 wet wt) and ~210 min (Control: 61.4 ± 50.6 vs HT: 63.4 ± 17.5 mmol·kg-1 wet wt) after local HT. The changes in peak torque and fatigue resistance of the knee extensors, muscle soreness, and the mRNA expression and protein abundance of select factors were also similar (P > 0.05) in both thighs, irrespective of the treatment. CONCLUSIONS: A single 1-h session of either PPDC or local HT does not accelerate glycogen resynthesis and the recovery of muscle function after prolonged intermittent shuttle running.

Heat therapy improves body composition and muscle function but does not affect capillary or collateral growth in a model of obesity and hindlimb ischemia.

Heat therapy (HT) has emerged as a potential adjunctive therapy to alleviate the symptoms of peripheral artery disease (PAD), but the mechanisms underlying the positive effects of this treatment modality remain undefined. Using a model of diet-induced obesity (DIO) and ischemia-induced muscle damage, we tested the hypothesis that HT would alter body composition, promote vascular growth and mitochondrial biogenesis, and improve skeletal muscle function. Male DIO C57Bl/6J mice underwent bilateral ligation of the femoral artery and were randomly allocated to receive HT or a control intervention for 30 min daily over 3 wk. When compared with a group of lean, sham-operated animals, ligated DIO mice exhibited increases in body and fat masses, exercise intolerance, and contractile dysfunction of the isolated soleus (SOL) and extensor digitorum longus (EDL) muscles. Repeated HT averted an increase in body mass induced by high-fat feeding due to reduced fat accrual. Fat mass was ∼25% and 29% lower in the HT group relative to controls after 2 and 3 wk of treatment, respectively. Muscle mass relative to body mass and maximal absolute force of the EDL, but not SOL, were higher in animals exposed to HT. There were no group differences in skeletal muscle capillarization, the expression of angiogenic factors, mitochondrial content, and the diameter of the gracilis arteries. These findings indicate that HT reduces diet-induced fat accumulation and rescues skeletal muscle contractile dysfunction. This practical treatment may prove useful for diabetic and obese PAD patients who are unable to undergo conventional exercise regimens.NEW & NOTEWORTHY The epidemic of obesity-related dyslipidemia and diabetes is a central cause of the increasing burden of peripheral artery disease (PAD), but few accessible therapies exist to mitigate the metabolic and functional abnormalities in these patients. We report that daily exposure to heat therapy (HT) in the form of lower-body immersion in water heated to 39 °C for 3 weeks attenuates fat accumulation and weight gain, and improves muscle strength in obese mice with femoral artery occlusion.

Effects of repeated local heat therapy on skeletal muscle structure and function in humans.

The purpose of the present study was to examine the effects of repeated exposure to local heat therapy (HT) on skeletal muscle function, myofiber morphology, capillarization, and mitochondrial content in humans. Twelve young adults (23.6 ± 4.8 yr, body mass index 24.9 ± 3.0 kg/m2) had one randomly selected thigh treated with HT (garment perfused with water at ~52°C) for 8 consecutive weeks (90 min, 5 days/wk) while the opposite thigh served as a control. Biopsies were obtained from the vastus lateralis muscle before and after 4 and 8 wk of treatment. Knee extensor strength and fatigue resistance were also assessed using isokinetic dynamometry. The changes in peak isokinetic torque were higher (P = 0.007) in the thigh exposed to HT than in the control thigh at weeks 4 (control 4.2 ± 13.1 Nm vs. HT 9.1 ± 16.1 Nm) and 8 (control 1.8 ± 9.7 Nm vs. HT 7.8 ± 10.2 Nm). Exposure to HT averted a temporal decline in capillarization around type II fibers (P < 0.05), but had no effect on capillarization indexes in type I fibers. The content of endothelial nitric oxide synthase was ~18% and 35% higher in the thigh exposed to HT at 4 and 8 wk, respectively (P = 0.003). Similarly, HT increased the content of small heat shock proteins HSPB5 (P = 0.007) and HSPB1 (P = 0.009). There were no differences between thighs for the changes in fiber cross-sectional area and mitochondrial content. These results indicate that exposure to local HT for 8 wk promotes a proangiogenic environment and enhances muscle strength but does not affect mitochondrial content in humans.NEW & NOTEWORTHY We demonstrate that repeated application of heat therapy to the thigh with a garment perfused with warm water enhances the strength of knee extensors and influences muscle capillarization in parallel with increases in the content of endothelial nitric oxide synthase and small heat shock proteins. This practical method of passive heat stress may be a feasible tool to treat conditions associated with capillary rarefaction and muscle weakness.

Heat therapy improves soleus muscle force in a model of ischemia-induced muscle damage.

Leg muscle ischemia in patients with peripheral artery disease (PAD) leads to alterations in skeletal muscle morphology and reduced leg strength. We tested the hypothesis that exposure to heat therapy (HT) would improve skeletal muscle function in a mouse model of ischemia-induced muscle damage. Male 42-wk-old C57Bl/6 mice underwent ligation of the femoral artery and were randomly assigned to receive HT (immersion in a water bath at 37°C, 39°C, or 41°C for 30 min) or a control intervention for 3 wk. At the end of the treatment, the animals were anesthetized and the soleus and extensor digitorum longus (EDL) muscles were harvested for the assessment of contractile function and examination of muscle morphology. A subset of animals was used to examine the impact of a single HT session on the expression of genes involved in myogenesis and the regulation of muscle mass. Relative soleus muscle mass was significantly higher in animals exposed to HT at 39°C compared with the control group (control: 0.36 ± 0.01 mg/g versus 39°C: 0.40 ± 0.01 mg/g, P = 0.024). Maximal absolute force of the soleus was also significantly higher in animals treated with HT at 37°C and 39°C (control: 274.7 ± 6.6 mN; 37°C: 300.1 ± 7.7 mN; 39°C: 299.5 ± 10 mN, P < 0.05). In the soleus, but not the EDL muscle, a single session of HT enhanced the mRNA expression of myogenic factors as well as of both positive and negative regulators of muscle mass. These findings suggest that the beneficial effects of HT are muscle specific and dependent on the treatment temperature in a model of PAD. NEW & NOTEWORTHY This is the first study to comprehensively examine the impact of temperature and muscle fiber type composition on the adaptations to repeated heat stress in a model of ischemia-induced muscle damage. Exposure to heat therapy (HT) at 37°C and 39°C, but not at 41°C, improved force development of the isolated soleus muscle. These results suggest that HT may be a practical therapeutic tool to restore muscle mass and strength in patients with peripheral artery disease.