Ran across this abstract on pubmed:

OBJECTIVE: To determine the short-term efficacy and security of whole body hyperthermia (WBH) combined with chemotherapy for advanced cancer.

METHODS: Different chemotherapy regimens were applied in 138 patients with advanced cancer. Among them, 68 patients (Group A) didn’t receive any other therapies. The other 70 patients (Group B) received WBH together with chemotherapy. WBH was maintained at 40 degrees C approximately 42 degrees C for 50 approximately 60 min (once or twice every week and 4 times a cycle).

RESULTS: In Group A, the rate of complete remission (CR) was 2.9%, partial remission (PR) was 36.8%, stable disease was 35.3%, progressive disease was 25.0%, the overall response rate (CR + PR) was 39.7%; while in Group B, the corresponding figures were 5.7%, 52.9%, 25.7%, 25.0%, and 58.6%, respectively. There was significant difference between the two groups (P < 0.05). The rates of III + IV gastrointestinal tract andmyelosuppression toxicities were 26.5% and 16.2% in Group A, while 27.1% and 18.6% in Group B. No significant difference was found.

CONCLUSION: WBH combined with chemotherapy is efficient and safe for advanced cancer, and is worth generalizing extensively. (via.)

Mentioned in a previous post, exposure to heat stress has been demonstrated to cause a release of norepinephrine. This is interesting, mostly, because norepinephrine is the target of a line of drugs known as norepinephrine reuptake inhibitors. These drugs prevent the reuptake of norepinephrine, and thereby treat conditions such as ADHD, and depression. Likewise, some studies have hinted at the fact that sauna use may help with depression.

Here’s a study showing that heat acclimation actually increases the amount of norepinephrine stored within the hypothalamus, at least in rats:

The hypothesis that anterior hypothalamic (AH) sensitivity to norepinephrine (NE) is altered by chronic exercise in the heat was tested in male Sprague-Dawley rats. Treadmill exercise 6 days/wk for 3 wk at 21 m/min was performed at 23 degrees C (control; C) or at 35 degrees C (heat acclimated; HA), progressing from 20 to 50 min/day in 2 wk. Time for core temperature (Tco) to rise from 39.5 to 40.5 degrees C during a heat-tolerance test after conditioning increased (P less than 0.05) in the HA group. To test for a change in AH sensitivity, the change in Tco to 2-, 5-, 10-, 20-, and 40-micrograms doses of NE injected bilaterally into the AH was determined after conditioning. Dose-response regression lines showed that exercise in the heat increased the slope and shifted the Tco-NE dose relation to the left. In a separate series of experiments on 6 sedentary(s), 10 C, and 10 HA animals, the amounts of NE, dopamine, and 3,4-dihydroxyphenylglycol (DOPEG) were determined by high-pressure liquid chromatography in the AH, median preoptic area (PO), cortex, and cerebellum after 9 wk of conditioning. Results showed that in the PO there was a significant increase in NE and DOPEG in the HA vs. C group and a trend of increasing NE from the S to C to HA groups. The data indicate that exercise in the heat increases NE-induced peripheral heat-dissipating capacity and increases catecholamine storage in the PO. (via.)

This is too weird. Check it out… Heat acclimation preventing rats from losing their hearing when exposed to loud noises:

Exposure to intense noise stress can cause a permanent noise-induced hearing loss which is thought to be due to elevation of reactive oxygen species in excess of the inherent antioxidant mechanisms of the cell. However, preconditioning to low levels of stress of one type can activate cellular mechanisms leading to the elevation of antioxidant levels so that the cell is then better able to tolerate subsequent severe stress of a different type. This has been called cross-tolerance. Here, we tested this hypothesis by acclimating rats to a moderate heat stress (30 days at 34 degrees C). The rats were exposed to 113 dB SPL noise for 3 days (12 h/day) in three different groups: heat acclimated then noise exposed; noise exposed and then heat acclimated; heat acclimated, then noise exposed and then heat acclimated again. Permanent changes in auditory function–auditory nerve brainstem evoked responses (ABR) and distortion product otoacoustic emissions (DPOAEs)–were evaluated in each of these animals and compared with those in rats exposed to noise only and in control groups of rats. Statistical evaluation of the results showed that when assessed with ABR, each of the heat-acclimated, noise-exposed groups was protected from the noise, even the group that was heat-acclimated after the noise exposure. When assessed with DPOAE, protection was statistically apparent only in the group that was heat acclimated, then exposed to noise, and not in the other groups. Thus, heat acclimation provides protection against permanent noise-induced hearing loss. (via.)

Or, more specifically, heat acclimation reduces the build up of lactate in muscles. Assuming regular use of the sauna, then one might presume that this would result in some level of heat acclimation. Additionally, heat acclimation lowers the aerobic metabolic rate during exercise as well. Perhaps this also plays a role in the enhanced running endurance from heat acclimation mentioned previously.

Muscle and plasma lactate accumulation with exercise was greater (P less than 0.01) in the hot relative to the cool environment both before and after acclimation. Acclimation lowered (P less than 0.01) aerobic metabolic rate as well as muscle and plasma lactate accumulation in both environments. The amount of muscle glycogen utilized during exercise in the hot environment did not differ from that in the cool either before or after acclimation. These findings indicate that accumulation of muscle lactate is increased and aerobic metabolic rate is decreased during exercise in the heat before and after heat acclimation; increased muscle glycogen utilization does not account for the increased muscle lactate accumulation during exercise under extreme heat stress; and heat acclimation lowers the aerobic metabolic rate and muscle and blood lactate accumulation during exercise in a cool as well as a hot environment. (via.)

Saunas induce a unique type of stress in individuals known as heat stress. When the body activates the stress system to respond to heat stress some of the same systems that are used during physical exercise, for example, are also activated.

Mentioned in a previous post was the fact that hyperthermia has been demonstrated to be able to help muscles recover more rapidly and with less oxidative stress after periods of immobilization.

Here’s an interesting study that demonstrated that sauna use specifically might be able to help prevent muscle atrophy from occurring in the first place, and not just assist in the recovery of lost muscle.
See the abstract below:

This study tested the hypothesis that elevation of heat stress proteins by whole body hyperthermia is associated with a decrease in skeletal muscle atrophy induced by reduced contractile activity (i.e., hindlimb unweighting). Female adult rats (6 mo old) were assigned to one of four experimental groups (n = 10/group): 1) sedentary control (Con), 2) heat stress (Heat), 3) hindlimb unweighting (HLU), or 4) heat stress before hindlimb unweighting (Heat+HLU). Animals in the Heat and Heat+HLU groups were exposed to 60 min of hyperthermia (colonic temperature ∼41.6°C). Six hours after heat stress, both the HLU and Heat+HLU groups were subjected to hindlimb unweighting for 8 days. After hindlimb unweighting, the animals were anesthetized, and the soleus muscles were removed, weighed, and analyzed for protein content and the relative levels of heat shock protein 72 (HSP72). Compared with control and HLU animals, the relative content of HSP72 in the soleus muscle was significantly elevated (P < 0.05) in both the Heat and Heat+HLU animals. Although hindlimb unweighting resulted in muscle atrophy in both the HLU and Heat+HLU animals, the loss of muscle weight and protein content was significantly less (P < 0.05) in the Heat+HLU animals. These data demonstrate that heat stress before hindlimb unweighting can reduce the rate of disuse muscle atrophy. We postulate that HSP70 and/or other stress proteins play a role in the control of muscle atrophy induced by reduced contractile activity. (via.)

Skeletal muscle reloading following disuse is characterized by profound oxidative damage. This study tested the hypothesis that intermittent hyperthermia during reloading attenuates oxidative damage and augments skeletal muscle regrowth following immobilization. [...] Heating resulted in ∼25% elevation in heat shock protein expression (P < 0.05) and an ∼30% greater soleus regrowth (P < 0.05) in RH compared with RC. Furthermore, oxidant damage was lower in the RH group compared with RC because nitrotyrosine and 4-hydroxy-2-nonenol were returned to near baseline when heating was combined with reloading. Reduced oxidant damage was independent of antioxidant enzymes (manganese superoxide dismutase, copper-zinc superoxide dismutase, catalase, glutathione peroxidase, glutathione reductase). In summary, these data suggest that intermittent hyperthermia during reloading attenuates oxidative stress and improves the rate of skeletal muscle regrowth during reloading after immobilization. (via.)

The RH group was the group that got “reloaded” (had their hind legs weighted down to induce muscular growth) as well as received heat treatment, while the RC group didn’t get heat treatment. So if you read the abstract they’re saying that increasing that heat shock protein in those mice helped them rapidly regain the muscle they had lost from immobilization, and prevent the oxidative damage that muscles will characteristically experience after having gone through a period of disuse.

According to a recent study by University of Florida researchers, less than a week’s worth of walking, jogging or cycling can help the heart produce enough HSP72 to protect it against the damage done during a heart attack.

“We’ve done studies that indicate that as little as three days of exercise can provide protection,” said Scott Powers, a professor in UF’s department of exercise and sport sciences. In rats tested at UF, as few as five days of exercise produced almost the maximum amount of HSP72 that cells can hold.

“It raises the possibility that this could be true of humans, too, and we think that this is very exciting,” Powers said.

HSP72 is in a family of proteins that form in the cells and protect organs in the body, such as the heart, against the type of extreme stress that a heart attack can cause. During stress, scientists believe, HSP72 can stabilize and refold damaged proteins, which is vital to preserving the heart if blood circulation is cut off.

“The whole problem of a heart attack is that if cells die, they’re gone forever,” Powers said. “What this heat shock protein does is to prevent the cell from dying from stress that would kill cells that didn’t have the same level of stress protein. You’re wounded, but you don’t die.”

Funded by the American Heart Association-Florida Affiliate, the series of studies Powers performed, some of which were published in November’s American Journal of Physiology, were among the first to examine the effects of exercise on the heart “in vivo,” or inside the bodies of live animals.

“A lot of studies take the heart out of the body and study it in an artificially created condition,” Powers said. “Certainly, there’s a lot you can learn from that, but many people argue that it doesn’t mimic normal physiology well.”

UF researchers induced heart attacks in two groups of rats: one that had trained on treadmills and one that had not trained at all. The untrained animals fared much worse after the induced heart attacks, a factor that Powers attributes to the approximately 500 percent increase of HSP72 in the trained rats.

“These experiments are the first to demonstrate that this actually works in the body,” Powers said. “It’s long been believed that exercise protects the heart, but I think these experiments actually provide good evidence that exercise is indeed cardio-protective in terms of being able to withstand a heart attack because of this stress protein.”

Although regular exercise has other health benefits that can prevent heart attacks or protect the body in the event of heart attack, Powers said HSP72 plays a large role in protection, and because it can be synthesized so quickly, it is never too late to begin exercising.

Powers recommends performing endurance exercises such as walking, jogging and cycling for at least 30 minutes a day because the heat generated during endurance exercise plays an important role in the synthesis of heat shock proteins. However, he warns that keeping up with an exercise routine is essential because the proteins can be depleted as quickly as they are created.

“These proteins don’t stay around very long,” he said. “You have to continue with the exercise, or you lose the protection.” (via.)

Since HSP72 is also a protein produced by the sauna, protective effects like these can probably also be had through sauna use. In fact, while this study focused on cardiovascular exercise, the sauna/whole body hyperthermia has been a focus of much heart related research.

One of the effects of sauna use, or actually almost any heating of tissues, is the release of heat shock protein or “HSP” for short. Heat shock protein is a chaperonin and prevents the unfolding of proteins and helps protect the tissues from damage induced by well, heat, and also other stresses.

This study found that not only does HSP induced by “whole body hyperthermia” (sauna use) but also, in fact, protects against damage in the striatum of rats from a compound known as “3-nitropropionic acid” which is toxic to the mitochondria. The striatum is a subcortical region of the forebrain. Notably, Parkinson’s is caused by a loss of dopaminergic neurons in the striatum.

See some of the abstract below:

METHODS: Rats were subjected to WBH (42 degrees C) or normothermia control conditions for 30 min and then treated with 3-NP. Striatum samples were processed and the levels of protein carbonyl groups, biogenic amines, Hsp72 and salicylate hydroxylation (to probe the hydroxyl radical (OH(*)) intervention) were determined.

RESULTS: WBH significantly reduced oxidative stress in the striatum of animals treated with 3-NP, as judged by reductions in protein carbonyl and salicylate hydroxylation derivative levels, whereas striatal Hsp72 expression was significantly increased. The groups treated with 3-NP presented an increased in the dopamine (DA) derivatives 2,3-dihydroxyphenylacetic acid (DOPAC) and norepinephrine (NE) concentration, whereas the striatal relation DOPAC/DA concentration indicate a reduced dopamine turnover. (via.)

… and not just a little bit, but quite a lot.

Eight healthy young men were studied during three periods of heat exposure in a Finnish sauna bath: at 80 degrees C dry bulb (80 D) and 100 degrees C dry bulb (100 D) temperatures until subjective discomfort, and in 80 degrees C dry heat, becoming humid (80 DH) until subjective exhaustion. Oral temperature increased 1.1 degrees C at 80 D, 1.9 degrees C at 100 D and 3.2 degrees C at 80 DH. Heart rate increased about 60% at 80 D, 90% at 100 D and 130% at 80 DH. Plasma noradrenaline increased about 100% at 80 D, 160% at 100 D and 310% at 80 DH. Adrenaline did not change. Plasma prolactin increased 2-fold at 80 D, 7-fold at 100 D and 10-fold at 80 DH. Blood concentrations of the beta-endorphin immunoreactivity at 100 D, adrenocorticotropic hormone (ACTH) at 100 D and 80 DH, growth hormone at 100 D and testosterone at 80 DH also increased, but cortisol at 80 D and 100 D decreased. The plasma prostaglandin E2 and serum thromboxane B2 levels did not change. Patterns related to heat exposure were observed for heart rate, plasma noradrenaline, ACTH and prolactin in the three study periods. (via.)

Drugs exist called “norepinephrine reuptake inhibitors” (see Wikipedia) which are actually intended to treat things like ADHD, and major depression… among other things. Prolactin is also an interesting brain chemical. It’s been demonstrated in mice to actually induce remyelination and treat multiple sclerosis (within the model) (via.).

In the obese leptin is often found to be higher than normal, while ghrelin is found to be below normal. Leptin and ghrelin both are connected with energy intake (eating) and expenditure, and relevant to appetite in particular.

The following study found that sauna use while ghrelin fell in the non-obese, it did not fall in the obese patients. While ordinarily in the non-obese some eating behaviors would upswing while recovering from sauna sessions this did not occur in the obese, and in fact, the obese lost weight after sauna use.

In normal-weight patients with appetite loss, repeated sauna therapy increased plasma ghrelin concentrations and daily caloric intake and improved feeding behavior. In obese patients, the body weight and body fat significantly decreased after 2 weeks of sauna therapy without increase of plasma ghrelin concentrations. On the basis of these data, sauna therapy may be a promising therapy for patients with lifestyle-related diseases. (via.)