The therapeutic effects of heat have been harnessed for centuries to treat skeletal muscle disorders and other pathologies. However, the fundamental mechanisms underlying the well-documented clinical benefits associated with heat therapy (HT) remain poorly defined. Foundational studies in cultured skeletal muscle and endothelial cells, as well as in rodents, revealed that episodic exposure to heat stress activates a number of intracellular signaling networks and promotes skeletal muscle remodeling. Renewed interest in the physiology of HT in recent years has provided greater understanding of the signals and molecular players involved in the skeletal muscle adaptations to episodic exposures to HT. It is increasingly clear that heat stress promotes signaling mechanisms involved in angiogenesis, muscle hypertrophy, mitochondrial biogenesis, and glucose metabolism through not only elevations in tissue temperature but also other perturbations, including increased intramyocellular calcium and enhanced energy turnover. The few available translational studies seem to indicate that the earlier observations in rodents also apply to human skeletal muscle. Indeed, recent findings revealed that both local and whole-body HT may promote capillary growth, enhance mitochondrial content and function, improve insulin sensitivity and attenuate disuse-induced muscle wasting. This accumulating body of work implies that HT may be a practical treatment to combat skeletal abnormalities in individuals with chronic disease who are unwilling or cannot participate in traditional exercise-training regimens.

A single session of leg heat therapy (HT) has been shown to elicit increases in leg blood flow and reduce blood pressure (BP) and the circulating levels of endothelin-1 (ET-1) in patients with symptomatic peripheral artery disease (PAD). We assessed whether 6 weeks of supervised leg HT (3 times/wk) using water-circulating trousers perfused with water at 48ºC improved 6-minute walk distance in people with PAD, compared to a sham treatment. Secondary outcomes included the assessment of leg vascular function, BP, quality of life and the serum ET-1 and nitrite plus nitrate (NOx) levels. Of thirty-two PAD patients randomized, thirty (age: 68±8 yrs; ankle-brachial index (ABI): 0.6±0.1) completed the 3 and 6-week follow ups. Participants completed 98.7% of the treatment sessions. When compared to the sham treatment, exposure to HT did not improve 6-minute walk distance, BP, popliteal artery reactive hyperemia, cutaneous microvascular reactivity, resting ABI or the serum NOx levels. The change from baseline to 6 weeks in scores of the physical functioning subscale of the 36-item Short Form Health Survey was significantly higher in the HT group (Control: -6.9±10 versus HT: 6.8±15; 95% confidence interval: 2.5-24.3, p=0.017). Similarly, the change in ET-1 levels after 6 weeks was different between groups, with the HT group experiencing a 0.4 decrease (95% confidence interval: -0.8,-0.0, p=0.03). These preliminary results indicate that leg HT may improve perceived physical function in symptomatic PAD patients. Additional, larger studies are needed to confirm these findings and determine the optimal treatment regimen for symptomatic PAD patients.

The prolonged impairment in muscle strength, power and fatigue resistance following eccentric exercise has been ascribed to a plethora of mechanisms, including delayed muscle refueling and microvascular and mitochondrial dysfunction. This review will explore the hypothesis that local heat therapy (HT) hastens functional recovery following strenuous eccentric exercise by facilitating glycogen resynthesis, reversing vascular derangements, augmenting mitochondrial function and stimulating muscle protein synthesis.

Lower‐extremity peripheral artery disease (PAD) is associated with increased risk of cardiovascular events and impaired exercise tolerance. We have previously reported that leg heat therapy (HT) applied using liquid‐circulating trousers perfused with warm water increases leg blood flow and reduces blood pressure (BP) and the circulating levels of endothelin‐1 (ET‐1) in patients with symptomatic PAD. In this sham‐controlled, randomized, crossover study, sixteen patients with symptomatic PAD (age 65 ± 5.7 years and ankle‐brachial index: 0.69 ± 0.1) underwent a single 90‐min session of HT or a sham treatment prior to a symptom‐limited, graded cardiopulmonary exercise test on the treadmill. The primary outcome was the peak walking time (PWT) during the exercise test. Secondary outcomes included the claudication onset time (COT), resting and exercise BP, calf muscle oxygenation, pulmonary oxygen uptake (V̇O2), and plasma levels of ET‐1, interleukin‐6 (IL‐6) and tumor necrosis factor‐alpha (TNF‐α). Systolic, but not diastolic BP, was significantly lower (~7 mmHg, p < .05) during HT when compared to the sham treatment. There was also a trend for lower SBP throughout the exercise and the recovery period following HT (p = .057). While COT did not differ between treatments (p = .77), PWT tended to increase following HT (CON: 911 ± 69 s, HT: 954 ± 77 s, p = .059). Post‐exercise plasma levels of ET‐1 were also lower in the HT session (CON: 2.0 ± 0.1, HT: 1.7 ± 0.1, p = .02). Calf muscle oxygenation, V̇O2, COT, IL‐6, and TNF‐α did not differ between treatments. A single session of leg HT lowers BP and post‐exercise circulating levels of ET‐1 and may enhance treadmill walking performance in symptomatic PAD patients.

Monroe, JC, Naugle, KM, and Naugle, KE. Effect of acute bouts of volume-matched high-intensity resistance training protocols on blood glucose levels. J Strength Cond Res 34(2): 445–450, 2020—Resistance exercise has the capability to alter glucose metabolism in healthy adults; however, to what extent single sessions of varying intensities of resistance exercise affect capillary glucose levels is not completely understood. The purpose of this study was to compare the effect of different resistance training intensities on capillary blood glucose levels in healthy adults. Thirteen resistance-trained men (age 24.4 ± 2.7 years) participated in an evaluation and 2 separate experimental resistance training sessions. The experimental sessions were a high-intensity resistance training session (HT) consisting of 7 sets of 3 repetitions at 90% of the participant's estimated 1 repetition maximum (e1RM), and a moderate-/high-intensity resistance training session (MT) consisting of 3 sets of 9 repetitions at 70% of the participant's e1RM. At least 7 days separated the completion of each session. Four glucose readings during each session were recorded using a capillary glucometer: G1 (baseline); G2 (pre-exercise); G3 (after exercise); and G4 (10 minutes after exercise). Results were analyzed using repeated-measures analysis of variances. Analysis revealed a significant decrease in blood glucose levels between G2 and G3, and G2 and G4 in both the HT and MT experimental sessions (p = 0.045). In addition, there was a significant difference in the magnitude of change in glucose levels from G2 to G3 between HT and MT (HT = −38.2 ± 5.3% SE, p = 0.042, MT = −22.2 ± 5.9% SE). Although both of the acute resistance exercise protocols decreased blood glucose levels in healthy men, a greater decrease in blood glucose levels from pre-exercise to post-exercise was observed in HT group compared with MT group.